StemCell Therapy

Have you been told that steroid injections or invasive surgery are your only options to treat your knee pain? Interventional orthopedics provides a non-surgical alternative that uses your own cells to repair the damage.

Recent researchshows that some of the most popularorthopedic kneesurgeriesincluding meniscectomies have no benefit and are not more effective than placebo or sham surgery. Moreover, knee replacement is extremely traumatic and carries associated risks, and even successful surgeries minimally require months of painful rehab to regain strength and mobility. Most surgeries also accelerate degeneration that leads toosteoarthritis and exacerbate the biomechanical problems that initially led to the need for the surgery. Regenexx urges patients suffering from knee injuries or degenerative conditions to consider all of their options.

At Regenexx we inventeda new approachto orthopedic care we call Interventional Orthopedics. This approach involves the use ofimage guidance (flouroscopy and ultrasound) to precisely placehigh-dose stem cells or platelets from your body directly where they are needed in a specific joint structure. These cells then work in the site of your injury to grow into new, healthy tissue, a process that will only occur if the cells have been placed exactly where they need to go in order to achieve positive outcomes for the patient.This precise approach to orthopedic care cant be replicated by a surgeon or nurse in a chiropractors office. Interventional Orthopedics requiresthousands of hours of trainingfollowing a standardized protocol process to become a licensed Regenexx physician.

The innovative Regenexx procedures restore knee function and mobility and decrease pain without the need for surgery by regenerating damaged tissue. Duringthis outpatient procedure, ourexpert physiciansuseprecise image guidanceto injectcustom concentrationsofyour bodys natural healing agentsinto the exact areas of damage to tighten and stabilize your knee joint for better function and mobility.

This page contains an extensive library of educational resources on kneeconditions and our patented kneeprocedures created by Regenexx and our founder, Chris Centeno, M.D.. We encourage you to research your options.

GET RELIEF. 855-330-5818

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Stem Cell Therapy For Knees | Relief Without Surgery!

Are Stem Cells Good or Bad?

Do you know what a stem cell is? Stems cells are the undifferentiated biological cells, which have the potential to develop into different types of cells with specialized functions. They also help to repair the damaged cells in our body. These cells also have the ability to renew themselves via cell division even after remaining inactive for a long period of time. Due to their regenerative properties, stem cells are nowadays being experimented to treat the various diseases.

Though these cells are present in all our bodies, they function more effectively in a fetus. Hence, there are two types of stem cells adult stem cells and embryonic stem cells. Bone marrow transplantation is the only stem cell therapy, which is being used widely today. The use of stem cells for treatments and other experiments have always been the topics of controversy. Like all the medicines and treatments, the stem cell therapy also will cause both positive and negative effects on our body. Some of them are mentioned below:

There are many people who consider the treatments using the stem cells as unethical. The government authorities also do not extend a wide support to these experiments. The various states in the US have even banned the research activities of the embryonic stem cells. The destruction of the blastocytes which happen during the stem cell research is also considered to be immoral by many people.

Moreover, most of the treatments and research on the stem cell therapies are based on theories. Though more than 3500 research studies are happening on the stem cells and the treatments using them, there are no proven results on them. Some of the stem cells, even use immunosuppressant on patients before doing the transplantation in order to prevent the chances of rejection of these cells by the body. This can cause various harmful side effects on the patients after the treatment.

Though the stem cells provide solutions to a wide number of diseases, the therapies done using them cannot be trusted completely. As it remains unproven, it has to be decided by the people, if they want to subject their lives to such experiments with no certain outcomes.

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Positive and negative Impacts of Stem Cells - Essay and ...

Here are the three possibilities: 1. Multiplying with -1 2. Formatting to minus(-) sign3. ABS() Function

Method 1: Multiplying with -11. Enter the numbers as usual, after finishing all entries, do the following:2. Go to any other empty cell, and type -1 and copy it, now select the entire column you want to make negative.3. Right-click on the selection and select Paste Special..4. Choose All and Multiply and click OK, as shown in the picture below: Now all the selected cells will be negative. Now delete the cell value-1 you copied from.

1. Select the entire column you want it to be negative, by clicking on the column header.2. MAC users Hold down Command key and click in any cell(with selection), WINDOWS users right-click, then click Format cells in the context menu.3. Click Number tab, click Custom Option, on right-hand side, under Type text box select General, and in the Type text box, enter a minus sign like this: -General and click OK.

Note: Positive values will be from D1 to D50 and Negative values will be from E1 to E50 as the above example is concerned

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How to automatically make all entered numbers in a row ...

This randomized phase III trial studies rituximab after stem cell transplant and to see how well it works compared with rituximab alone in treating patients with in minimal residual disease-negative mantle cell lymphoma in first complete remission. Monoclonal antibodies, such as rituximab, may interfere with the ability of cancer cells to grow and spread. Giving chemotherapy before a stem cell transplant helps kill any cancer cells that are in the body and helps make room in the patient's bone marrow for new blood-forming cells (stem cells) to grow. After treatment, stem cells are collected from the patient's blood and stored. More chemotherapy is then given to prepare the bone marrow for the stem cell transplant. The stem cells are then returned to the patient to replace the blood-forming cells that were destroyed by the chemotherapy. Giving rituximab with or without stem cell transplant may work better in treating patients with mantle cell lymphoma.

PRIMARY OBJECTIVES:

I. To compare overall survival in mantle cell lymphoma (MCL) patients in minimal residual disease (MRD)-negative first remission who undergo autologous hematopoietic stem cell transplantation (auto-HCT) followed by maintenance rituximab versus (vs.) maintenance rituximab alone (without auto-HCT).

SECONDARY OBJECTIVES:

I. To compare progression-free survival in MCL patients in MRD-negative first remission who undergo auto-HCT followed by maintenance rituximab vs. maintenance rituximab alone.

II. To define the overall survival and progression-free survival at 2 and 5 years of chemosensitive but MRD-positive (or MRD-indeterminate) patients who undergo auto-HCT followed by 2 years of maintenance rituximab.

III. To describe the rate of complications (serious infection, hospitalization, need for intravenous immune globulin) in MCL patients undergoing maintenance rituximab following auto-HCT.

IV. To determine the prognostic impact of MRD status at day 100, in MCL patients who were MRD-positive prior to auto-HCT.

OUTLINE: Patients are randomized to 1 of 2 groups.

GROUP I: Patients receive standard of care preparative chemotherapy and undergo auto-HCT. Beginning 60-120 days after transplant, patients receive rituximab intravenously (IV) once every 8 weeks for up to 12 courses in the absence of disease progression or unacceptable toxicity.

GROUP II: Patients receive standard of care induction chemotherapy. Beginning 40-120 days after completion of chemotherapy, patients receive rituximab as in Group I.

After completion of study treatment, patients are followed up every 3 and 6 months for 10 years.

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Rituximab With or Without Stem Cell Transplant in Treating ...

Stem Cell Therapy for Neuropathy Concerning Foot and Ankle Conditions

For many people, especially those who have diabetes, peripheral neuropathy most often occurs in the feet. The discomfort caused by peripheral neuropathy in people, whether they are diabetic or not, is most commonly described as a sharpness, shooting, or burning. Some describe the nerve pain as feeling as if they were getting electric shocks.

No matter how the pain or tingling is described, the core reason for it is nerve damage, and an effective neuropathy pain treatment must address damage to the nerve cells. Stem cell-based therapy for peripheral neuropathy works to repair damaged nerves and rebuild new nerve connections, even in diabetic patients.

This new stem cell therapy for neuropathy does more than just heal nerve damage; stem cell treatment for neuropathy also addresses glial cells and cytokine inflammation, which has a significant role in both the development of and the progression of neuropathy.

Neuropathic pain, including that produced by idiopathic peripheral neuropathy, doesnt always respond well to pain medication or other pharmaceutical drugs. Even when it does, there are often unwelcome side effects that accompany the response to such forms of neuropathy pain treatment, including weight gain, drowsiness, dry mouth, or negative mood changes.

The National Stem Cell Institutes proprietary stem cell therapy for neuropathy uses mesenchymal stem cells (MSCs) derived from the patients adipose tissue or bone marrow, so you dont have to worry that our new therapy for neuropathy is adding to the risks and side effects of any medication.

The stem cells used in our stem cell therapy for neuropathy are not embryonic stem cells or cells from fetuses. Instead, these regenerative cells come straight from fat stores in your own body just a few hours before they are injected back into your body and put to work to heal disease or dysfunction such as peripheral neuropathy. The safety of stem cell therapy procedures has been well established in countless studies and research, and it extends to our stem cell therapy for peripheral neuropathy.

After stem cell therapy for neuropathy, patients experience relief from Neuropathy Pain.* Scar tissues begin to heal and reverse to healthy tissue while inflammation and pain are relieved. This relief to peripheral neuropathy after a stem cell transplant allows patients to increase their daily activities and movement, getting them back to a healthier, happier life.

NSIs proprietary stem cell therapy for neuropathy requires no overnight stays in a hospital. Its done on an outpatient basis with little to minimal downtime post-procedure. Most people return to their usual, everyday activities the very same day that they undergo stem cell treatment for neuropathy.

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Stem Cell Therapy for Neuropathy | NSI Stem Cell

It's not so much the acutal medical risks, but the ehtical and moral implications of conducting research in the field.

The following is an excerpt from a research paper I recently wrote concerning stem cell research:

Embryonic stem cell research raises immense ethical and religious concern: The issue of research involving stem cells derived from human embryos is increasingly the subject of a national debate and dinner table discussions. The issue is confronted every day in laboratories as scientists ponder the ethical ramifications of their work. It is agonized over by parents and many couples as they try to have children or to save children already born. The issue is debated within the church, with people of different faiths- even many of the same faith- coming to different conclusions. Many people are finding the more they know about stem cell research, the less certain they are about the right ethical and moral conclusions. (Bush Embryonic Stem Cell Decision 1) Quite often, the status of an embryo is debated among scientists, politicians, theologians, philosophers, and even everyday people. There are many ideas circulating the globe as some vie to protect the embryo and others hope to use it to benefit society. Those that oppose stem cell research claim that the methods scientists use are not morally justifiable. Human embryos, in their minds, are not mere biological tissues or clusters of cells; they are the tiniest of human beings (Espejo 49). According to the Human Embryo Research Panel and the National Bioethics Commission, the embryo should be considered a living organism from its earliest stages (Espejo 46-50). People therefore claim that scientists are alienating the rights of living human beings by performing experiments on embryos: The painful lessons of the past should have taught us that human beings must not be conscripted for research without their permission- no matter what the alleged justification- especially when that research means the forfeiture of their health or lives. Even if an individuals death is believed to be otherwise imminent, we still do not have a license to engage in lethal experimentation- just as we may not experiment on death row prisoners or harvest their organs without their consent. (Espejo 49) The widespread Christian view that life begins at the moment of conception has caused many to believe that the destruction of the human embryo is murder (Espejo 4). People also believe that is irrelevant whether the embryos are capable of implanting in a uterus and developing, as they are embryos nonetheless (Morris 2). As Morris questions, are we willing to recognize life, even if its living in a Petri dish? (2). Those that sympathize with these concerns feel that research requiring the destruction of a human embryo should be banned. Others argue that since IVF procedures often generate more embryos than needed, the excess embryos should be used for potentially life-saving research rather than being discarded (Espejo 36-37). Also, they claim embryos do not have the same rights as adult humans. The suggestion that a mass of 50-100 cells with no heart and no brain is entitled to the same protections is unprecedented and not embodied in American law (Espejo 38). With this in mind, it seems that embryonic stem cell research should not be undermined by the aforementioned arguments. There are additional concerns however. The use of SCNT is often criticized by those opposed to cloning, as a majority of people view cloning as morally wrong. SCNT has been used in reproductive cloning, such as the cloning of Dolly the sheep. In the publics mind, the distinction between this form of cloning and therapeutic cloning, which involves SCNT used for medical purposes, has blurred. The two should not be confused however, as they are completely separate procedures. Outlawing the use of SCNT would prevent the development of very promising techniques for curing disease, such as the one mentioned earlier (Scott 49-56). Finally, there are claims that the science will not live up to the hope that has been generated. Opponents of stem cell research are quick to point out that stem cell technologies are still at a developmental stage and it is virtually impossible to predict the eventual outcomes of innovation in the field (Stem Cell Controversy 2). Some have even claimed that researchers have falsely raised peoples expectations in an attempt to secure funding and support (Stem Cell Controversy 2). Such statements should not be regarded as wholly true, but with ideas such as these spreading around the globe, it is no wonder why the topic has become so controversial.

Granted, it's somewhat lengthy, but there is alot of information in there. If you want me to send you the whole paper sometime, just let me know. But please, if you're using this for your own schoolwork, avoid plagarism.

Hope this helps!

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what are the negative aspects to stem cell therapy ...

Debates over the ethics of embryonic stem cell research have divided scientists, politicians, and religious groups for years. However, promising developments in other areas of stem cell research have led to solutions that help bypass these ethical barriers and win more support from those against embryonic stem cell research; the newer methods don't require the destruction of blastocysts.

In 1998, the first published research paper on the topic reported that stem cells could be taken from human embryos. Subsequent research led to the ability to maintain undifferentiated stem cell lines (pluripotent cells) and techniques for differentiating them into cells specific to various tissues and organs.

The debates over the ethics of stem cell research began almost immediately in 1999, despite reports that stem cells cannot grow into complete organisms.

In 20002001, governments worldwide were beginning to draft proposals and guidelines to control stem cell research and the handling of embryonic tissues and reach universal policies. The Canadian Institutes of Health Research (CIHR) drafted a list of recommendations for stem cell research in 2001. In the U.S., the Clinton administration drafted guidelines for stem cell research in 2000. Australia, Germany, the United Kingdom, and other countries followed suit and formulated their own policies.

Debates over the ethics of studying embryonic stem cells continued for nearly a decade until the use of adult-derived stem cellsknown as induced pluripotent stem cells (IPSCs)became more prevalent and alleviated those concerns.

In the U.S. since 2011, federal funds can be used to study embryonic stem cells, but such funding cannot be used to destroy an embryo.

The excitement about stem cell research is primarily due to the medical benefits in areas ofregenerative medicineand therapeutic cloning. Stem cells provide huge potential for finding treatments and cures to a vast array of medical issues:

Stem cell research presents problems like any form of research, but most opposition to stem cell research is philosophical and theological, focusing on questions of whether we should be taking science this far:

Use of adult-derived stem cellsknown as induced pluripotent stem cells (IPSCs)from blood, cord blood, skin, and other tissues has been demonstrated as effective in treating different diseases in animal models. Umbilical cord-derived stem cells obtained from the cord blood also have been isolated and used for various experimental treatments. Another option is uniparental stem cells. Although these cell lines are shorter-lived than embryonic cell lines, uniparental stem cells hold vast potential if enough research money can be directed that way: pro-life advocates do not technically consider them individual living beings.

Two recent developments from stem cell research involve the heart and the blood it pumps. In 2016, researchers in Scotland began working on the possibility of generating red blood cells from stem cells in order to create a large supply of blood for transfusions. A few years earlier, researchers in England began working on polymers derived from bacteria that can be used to repair damaged heart tissue.

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Pros and Cons of Stem Cell Research - The Balance

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EasySep Human Nave CD4+ T Cell Isolation Kit

EasySep Human Nave CD4+ T Cell Isolation Kit

For even faster cell isolations, we recommend the new EasySep Human Nave CD4+ T Cell Isolation Kit II (17555) which isolates cells in just 11 minutes.

Advantages:

Fast, easy-to-use and column-free Up to 96% purity Isolated cells are untouched

Magnet Compatibility:

EasySep Magnet (Catalog #18000)

The Big Easy EasySep Magnet (Catalog #18001)

Easy 50 EasySep Magnet (Catalog #18002)

EasyEights EasySep Magnet (Catalog #18103)

RoboSep-S (Catalog #21000)

Subtype:

Cell Isolation Kits

Cell Type:

T Cells; T Cells, CD4+

Selection Method:

Negative

Application:

Cell Isolation

Area of Interest:

Immunology

Document Type

Product Name

Catalog #

Lot #

Language

Yes. The EasySep kits use either a negative selection approach by targeting and removing unwanted cells or a positive selection approach targeting desired cells. Depletion kits are also available for the removal of cells with a specific undesired marker (e.g. GlyA).

Magnetic particles are crosslinked to cells using Tetrameric Antibody Complexes (TAC). When placed in the EasySep Magnet, labeled cells migrate to the wall of the tube. The unlabeled cells are then poured off into a separate fraction.

The EasySep procedure is column-free. That's right - no columns!

The Product Information Sheet provided with each EasySep kit contains detailed staining information.

Yes. RoboSep, the fully automated cell separator, automates all EasySep labeling and cell separation steps.

Yes. We recommend a cell concentration of 2x108 cells/mL and a minimum working volume of 100 L. Samples containing 2x107 cells or fewer should be suspended in 100 L of buffer.

Yes, the EasySep particles are flow cytometry-compatible, as they are very uniform in size and about 5000X smaller than other commercially available magnetic beads used with column-free systems.

No, but due to the small size of these particles, they will not interfere with downstream applications.

Yes; however, this may impact the kit's performance. The provided EasySep protocols have already been optimized to balance purity, recovery and time spent on the isolation.

Yes, the purity of targeted cells will increase with additional rounds of separations; however, cell recovery will decrease.

If particle binding is a key concern, we offer two options for negative selection. The EasySep negative selection kits can isolate untouched cells with comparable purities, while RosetteSep can isolate untouched cells directly from whole blood without using particles or magnets.

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This product is designed for use in the following research area(s) as part of the highlighted workflow stage(s). Explore these workflows to learn more about the other products we offer to support each research area.

Research Area Workflow Stages for

Workflow Stages

Figure 1. Typical EasySep Human Nave CD4+ T Cell Isolation Profile

Starting with a single-cell suspension of PBMCs, the nave CD4+ T cell (CD3+CD4+CD45RA+CD45RO-) content of the isolated fraction typically ranges from 91.3% - 96.9%. In the example above, the purities of the start and isolated fraction are 11.1% and 93.2%, respectively.

Bjö et al.

Staphylococcus aureus (S. aureus) is a human pathogen as well as a frequent colonizer of skin and mucosa. This bacterium potently activates conventional T-cells through superantigens and it is suggested to induce T-cell cytokine-production as well as to promote a regulatory phenotype in T-cells in order to avoid clearance. This study aimed to investigate how S. aureus impacts the production of regulatory and pro-inflammatory cytokines and the expression of CD161 and HELIOS by peripheral CD4(+)FOXP3(+) T-cells. Stimulation of PBMC with S. aureus 161:2-cell free supernatant (CFS) induced expression of IL-10, IFN- and IL-17A in FOXP3(+) cells. Further, CD161 and HELIOS separated the FOXP3(+) cells into four distinct populations regarding cytokine-expression. Monocyte-depletion decreased S. aureus 161:2-induced activation of FOXP3(+) cells while pre-stimulation of purified monocytes with S. aureus 161:2-CFS and subsequent co-culture with autologous monocyte-depleted PBMC was sufficient to mediate activation of FOXP3(+) cells. Together, these data show that S. aureus potently induces FOXP3(+) cells and promotes a diverse phenotype with expression of regulatory and pro-inflammatory cytokines connected to increased CD161-expression. This could indicate potent regulation or a contribution of FOXP3(+) cells to inflammation and repression of immune-suppression upon encounter with S. aureus.

STEMCELL TECHNOLOGIES INC.S QUALITY MANAGEMENT SYSTEM IS CERTIFIED TO ISO 13485. PRODUCTS ARE FOR RESEARCH USE ONLY AND NOT INTENDED FOR HUMAN OR ANIMAL DIAGNOSTIC OR THERAPEUTIC USES UNLESS OTHERWISE STATED.

Internal Search Keywords: 19555|19555RF|19555C|19515|19155|19155RF|19155C|19115|Easy sep naive CD-4|Easy sep naive CD4 T

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EasySep Human Nave CD4+ T Cell Isolation Kit

Stem Cell Therapy for Autoimmune Diseases

Today, new treatments and advances in research are giving new hope to people affected by Autoimmune Diseases. StemGenexStem Cell Research Centre provides stem cell therapy for Autoimmune Diseases to help those with unmet clinical needs achieve optimum health and better quality of life.

Stem cell therapy for Autoimmune Diseases is being studied for efficacy in improving the complications in patients through the use of their own stem cells.These autoimmune disorder treatments may help patients who dont respond to typical drug treatment, want to reduce their reliance on medication, or are looking to try stem cell therapy before starting drug treatment.

To learn more about becoming a patient and receiving treatment for autoimmune diseases through the use of stem cells at StemGenex, please contact one of our Patient Advocates at (800) 609-7795. Below are some frequently asked questions aboutstem cell therapy for Autoimmune Diseases.

The bodys immune system is a complex network of special cells and organs that defends the body from germs and other foreign invaders. In order for the immune system to function properly, it needs the ability to tell the difference between what's you and what's foreign. When the immune system cannot, it attacks normal cells by mistake. The result of these misguided attacks is what is known as autoimmune disease.

Millions of people suffer from over eighty different types of known autoimmune diseases. Common autoimmune diseases include:

Stem cells that come from your adipose (fat) tissue have distinct functional properties including immunomodulatory and anti-inflammatory functional properties which have the capability of repairing and regenerating damaged tissue associated with disease and injury.

Upholding the highest levels of ethical conduct, safety and efficacy is our primary focus. Five clinical stem cell studies for Parkinson's Disease, Multiple Sclerosis, Osteoarthritis, Rheumatoid Arthritis and Chronic Obstructive Pulmonary Disease (COPD) are registered through the National Institutes of Health (NIH) at http://www.clinicaltrials.gov/stemgenex. Each clinical study is reviewed and approved by an independent Institutional Review Board (IRB) to ensure proper oversight and protocols are being followed.

Stem cells are the basic building blocks of human tissue and have the ability to repair, rebuild, and rejuvenate tissues in the body. When a disease or injury strikes, stem cells respond to specific signals and set about to facilitate the healing process by differentiating into specialized cells required for the bodys repair.

There are four known types of stem cells which include:

StemGenex provides autologous adult stem cells (from fat tissue) where the stem cells come from the person receiving treatment.

StemGenex provides autologous adult adipose-derived stem cells (from fat tissue) where the stem cells come from the person receiving treatment.

We tap into our bodys stem cell reserve daily to repair and replace damaged or diseased tissue. When the bodys reserve is limited and as it becomes depleted, the regenerative power of our body decreases and we succumb to disease and injury.

Three sources of stem cells from a patients body are used clinically which include adipose tissue (fat), bone marrow and peripheral blood.

Performed by Board Certified Physicians, dormant stem cells are extracted from the patients adipose tissue (fat) through a minimally invasive mini-liposuction procedure with little to no downtime.

During the liposuction procedure, a small area (typically the abdomen) is numbed with an anesthetic and patients receive mild to moderate sedation. Next, the extracted dormant stem cells are isolated from the fat and activated, and then comfortably infused back into the patient intravenously (IV) and via other directly targeted methods of administration. The out-patient procedure takes approximately four to five hours.

StemGenex provides multiple administration methods for patients with Autoimmune Diseases to best target the disease related conditions and symptoms which include:

Since each condition and patient are unique, there is no guarantee of what results will be achieved or how quickly they may be observed. According to patient feedback, some patients report results in one to three months, however, it may take as long as six to nine months. Individuals interested in stem cell therapy are urged to consult with their physician before choosing investigational autologous adipose-derived stem cell therapy as a treatment option.

In order to determine if you are a good candidate for adult stem cell treatment, you will need to complete a medical history form which will be provided by your StemGenex Patient Advocate. Once you complete and submit your medical history form, our medical team will review your records and determine if you are a qualified candidate for adult stem cell therapy.

StemGenex team members are here to help assist and guide you through the patient process.

Patients travel to StemGenex located in Del Mar, California located in San Diego County for stem cell treatment from all over the United States, Canada and around the globe. Treatment will consist of one visit lasting a total of three days. The therapy is minimally invasive and there is little to no down time. Majority of patients fly home the day after treatment.

The side effects of the mini-liposuction procedure are minimal and may include but are not limited to: minor swelling, bruising and redness at the procedure site, minor fever, headache, or nausea. However, these side effects typically last no longer than 24 hours and are experienced mostly by people with sensitivity to mild anesthesia. No long-term negative side effects or risks have been reported.

The side effects of adipose-derived stem cell therapy are minimal and may include but are not limited to: infection, minor bleeding at the treatment sites and localized pain. However, these side effects typically last no longer than 24 hours. No long-term negative side effects or risks have been reported.

StemGenex provides adult stem cell treatment with mesenchymal stem cells which come from the person receiving treatment. Embryonic stem cells are typically associated with ethical and political controversies.

The FDA is currently in the process of defining a regulatory path for cellular therapies. A Scientific Workshop and Public Hearing Draft Guidances Relating to the Regulation of Human Cells, Tissues or Cellular or Tissue-Based Products was held in September 2016 at the National Institutes of Health (NIH) in Bethesda, MD. Currently, stem cell treatment is not FDA approved.

In March 2016, bipartisan legislation, the REGROW Act was introduced to the Senate and House of Representatives to develop and advance stem cell therapies.

Stem cell treatment is not covered by health insurance at this time. The cost for standard preoperative labs are included. Additional specific labs may be requested at the patients expense.

With over 80 different types of Autoimmune Diseases and hundreds of symptoms, some of the most common symptoms include:

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Autoimmune Disorder Treatment - Stem Cell Therapy, Stem ...

Cancer Stem Cells-Emanated Therapy Resistance: Implications for Liposomal Drug Delivery SystemsDianat-Moghadam,H; Heydarifard, M; Jahanban-Esfahlan, R; Panahi, Y; Hamishehkar, H; Pouremamali, F; Rahbarghazi, R; Nouri, M J Control Release 2018-09-02 7.36 | Sep 12 Cytokines, Breast Cancer Stem Cells (BCSCs) and ChemoresistanceChen, W; Qin, Y; Liu, S Clin Transl Med 2018-09-03 7.35 | Sep 5 Role of Tumor Microenvironment in Cancer Stem Cell Chemoresistance and RecurrenceDas, M; Law, S Int J Biochem Cell Biol 2018-08-25 7.34 | Aug 29 The Next Generation of Anticancer Metallopharmaceuticals: Cancer Stem Cell-Active InorganicsLaws, K; Suntharalingam, K Chembiochem 2018-08-15 7.33 | Aug 22 Targeting Molecular Pathways in Cancer Stem Cells by Natural Bioactive CompoundsCianciosi, D; Varela-Lopez, A; Forbes-Hernandez, TY; Gasparrini, M; Afrin, S; Reboredo-Rodriguez, P; Zhang, J; Quiles, JL; Nabav, SF; Battino, M; Giampieri, F Pharmacol Res 2018-08-10 7.32 | Aug 15 Hypoxia-Inducible Factor 2: A Novel Target in GliomasRenfrow, JJ; 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De Maria, RCancer Immunol Immunother2014-08-083.31 | Aug 13Stem Cells and Gliomas: Past, Present, and FutureGermano, IM; Binello, EJ Neurooncol2014-08-013.30 | Aug 6The Emerging Role of Tumor-Suppressive MicroRNA-218 in Targeting Glioblastoma StemnessGao, X; Jin, WCancer Lett2014-07-173.29 | Jul 30Cancer Stem Cell Detection and IsolationMoghbeli, M; Moghbeli, F; Forghanifard, MM; Abbaszadegan, MRMed Oncol2014-07-273.29 | Jul 30Helicobacter pylori Infection and Stem Cells at the Origin of Gastric CancerBessede, E; Dubus, P; Megraud, F; Varon, COncogene2014-07-213.28 | Jul 23Cancer Stem Cells, Cancer Cell Plasticity and Radiation TherapyVlashi, E; Pajonk, FSemin Cancer Biol2014-07-123.27 | Jul 16MET-Mediated Resistance to EGFR Inhibitors: An Old Liaison Rooted in Colorectal Cancer Stem CellsBoccaccio, C; Luraghi, P; Comoglio, PMCancer Res2014-07-013.26 | Jul 9Breast Cancer Stem Cells and the Immune System: Promotion, Evasion and TherapyBoyle, ST; Kochetkova, MJ Mammary Gland Biol Neoplasia2014-07-063.26 | Jul 9MicroRNAs in Cancer Stem Cells: Current Status and Future DirectionsChhabra, R; 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Barbieri, F; Florio, TFront Cell Neurosci2014-05-283.22 | Jun 11Breast Cancer Stem Cells: Regulatory Networks, Stem Cell Niches, and Disease RelevanceGuo, WStem Cells Transl Med2014-06-053.22 | Jun 11The Non-Reverse Transcriptase Activity of the Human Telomerase Reverse Transcriptase Promotes Tumor ProgressionQin, Y; Guo, H; Tang, B; Yang, SMInt J Oncol2014-05-283.21 | Jun 4Role of Fbxw7 in the Maintenance of Normal Stem Cells and Cancer-Initiating CellsTakeishi, S; Nakayama, KIBr J Cancer2014-05-223.20 | May 28Brain Metastasis-Initiating Cells: Survival of the FittestSingh, M; Manoranjan, B; Mahendram, S; McFarlane, N; Venugopal, C; Singh, SKInt J Mol Sci2014-05-223.20 | May 28ZNF281/ZBP-99: A New Player in EpithelialMesenchymal Transition, Stemness, and CancerHahn, S; Hermeking, HJ Mol Med2014-05-183.19 | May 21Gastric Cancer Stem Cells in Gastric Carcinogenesis, Progression, Prevention and TreatmentLi, K; Dan, Z; Nie, YQWorld J Gastroenterol2014-05-143.19 | May 21Immunotherapy of Cancer Stem Cells in Solid Tumors: Initial Findings and Future ProspectiveGammaitoni, L; Leuci, V; Mesiano, G; Giraudo, L; Todorovic, M; Carnevale-Schianca, F; Aglietta, M; Sangiolo, DExpert Opin Biol Ther2014-05-163.19 | May 21Circulating Tumor Cells-A Bona Fide Cause of Metastatic CancerCaixeiro, NJ; Kienzle, N; Lim, SH; Spring, KJ; Tognela, A; Scott, KF; de Souza, P; Becker, TMCancer Metastasis Rev2014-05-103.18 | May 14Chemical Approaches to Targeting Drug Resistance in Cancer Stem CellsSotiropouloua, PA; Christodouloub, MS; Silvanib, A; Herold-Mendec, C; Passarella, DDrug Discov Today2014-05-103.18 | May 14Cancer Stem Cells: Biological Functions and Therapeutically TargetingCiurea, ME; Georgescu, AM; Purcaru, SO; Artene, SA; Emami, GH; Boldeanu, MV; Tache, DE; Dricu, AInt J Mol Sci2014-05-093.18 | May 14Epithelial-to-Mesenchymal Transition and the Cancer Stem Cell Phenotype: Insights from Cancer Biology with Therapeutic Implications for Colorectal CancerFindlay, VJ; Wang, C; Watson, DK; Camp, ERCancer Gene Ther2014-05-023.17 | May 7Cancer Stem-Like Cells and Thyroid CancerLloyd, R; Guo, Z; Hardin, HEndocr Relat Cancer2014-04-303.17 | May 7Maternal Embryonic Leucine Zipper Kinase: Key Kinase for Stem Cell Phenotype in Glioma and Other CancersGanguly, R; Hong, CS; Smith, LGF; Kornblum, HI; Nakano, IMol Cancer Ther2014-05-023.17 | May 7Cancer Stem Cells and Their Implication in Breast CancerCarrasco, E; Alvarez, PJ; Prados, J; Melguizo, C; Rama, AR; Aranega, A; Rodriguez-Serrano, FEur J Clin Invest2014-04-273.16 | Apr 30Hallmarks in Colorectal Cancer: Angiogenesis and Cancer Stem-Like CellsMathonnet, M; Perraud, A; Christou, N; Akil, H; Melin, C; Battu, S; Jauberteau, MO; Denizot, YWorld J Gastroenterol2014-04-213.16 | Apr 30Chemopreventive Drugs: Mechanisms via Inhibition of Cancer Stem Cells in Colorectal CancerKim, TIWorld J Gastroenterol2014-04-143.15 | Apr 23Cancer Stem Cells: Constantly Evolving and Functionally Heterogeneous Therapeutic TargetsYang, T; Rycaj, K; Liu, Z; Tang, DGCancer Res2014-04-083.14 | Apr 16Cancer Stem Cells and Tumor MetastasisLi, S; Li, QInt J Oncol2014-04-023.14 | Apr 16Glioma Stem Cells: Turpis Omen in Nomen? (The Evil in the Name?)Binda, E; Reynolds, BA; Vescovi, ALJ Intern Med2014-04-073.13 | Apr 9Nanomaterials for Targeted Drug Delivery to Cancer Stem CellsOrza, A; Casciano, D; Biris, ADrug Metab Rev2014-04-043.13 | Apr 9Cancer Cell Dormancy in Novel Mouse Models for Reversible Pancreatic Cancer: A Lingering Challenge in the Development of Targeted TherapiesLin, WC; Rajbhandari, N; Wagner, KUCancer Res2014-03-213.12 | Apr 2The Paradigm of Mutant p53-Cancer Stem Cells and Drug ResistanceShetzer, Y; Solomon, H; Koifman, G; Molchadsky, A; Horesh, S; Rotter, VCarcinogenesis2014-03-213.11 | Mar 26Glioblastoma Cancer Stem Cells: Biomarker and Therapeutic AdvancesPointer, KB; Clark, PA; Zorniak, M; Alrfaei, BM; Kuo, JSNeurochem Int2014-03-193.11 | Mar 26Contributions of Epithelial-Mesenchymal Transition and Cancer Stem Cells to the Development of Castration Resistance of Prostate CancerLi, P; Yang, R; Gao, WQMol Cancer2014-03-123.10 | Mar 19Cancer Stem Cells and RadioresistanceRycaj, K; Tang, DGInt J Radiat Biol2014-03-073.09 | Mar 12CD133-Targeted Niche-Dependent Therapy in Cancer: A Multipronged ApproachMak, AB; Schnegg, C; Lai, CY; Ghosh, S; Yang, MH; Moffat, J; Hsu, MYAm J Pathol2014-03-033.08 | Mar 5p53: The Barrier to Cancer Stem Cell FormationAloni-Grinstein, R; Shetzer, Y; Kaufman, T; Rotter, VFEBS Lett2014-02-193.07 | Feb 26Dedifferentiation and Reprogramming: Origins of Cancer Stem CellsFriedmann-Morvinski, D; Verma, IMEMBO Rep2014-02-143.06 | Feb 19Cell Adhesion Molecules and Their Relation to (Cancer) Cell StemnessFarahani, E; Patra, HK; Jangamreddy, JR; Rashedi, I; Kawalec, M; Rao Pariti, RK; Batakis, P; Wiechec, ECarcinogenesis2014-02-153.06 | Feb 19MicroRNA Control of Epithelial-Mesenchymal Transition in Cancer Stem CellsHao, J; Zhang, Y; Deng, M; Ye, R; Zhao, S; Wang, Y; Li, J; Zhao, ZInt J Cancer2014-02-053.05 | Feb 12Discontinuation of Tyrosine Kinase Inhibitors and New Approaches to Target Leukemic Stem Cells: Treatment-Free Remission as a New Goal in Chronic Myeloid LeukemiaBreccia, M; Alimena, GCancer Lett2014-02-043.05 | Feb 12Role of p75 Neurotrophin Receptor in Stem Cell Biology: More than Just a MarkerTomellini, E; Lagadec, C; Polakowska, R; Le Bourhis, XCell Mol Life Sci2014-01-313.04 | Feb 5Defining and Targeting Myeloma Stem Cell-Like CellsAbe, M; Harada, T; Matsumoto, TStem Cells2014-01-223.03 | Jan 29Targeting Cancer Stem Cells by Curcumin and Clinical ApplicationsLi, Y; Zhang, TCancer Lett2014-01-233.03 | Jan 29The ID Proteins: Master Regulators of Cancer Stem Cells and Tumor AggressivenessLasorella, A; Benezra, R; Iavarone, ANat Rev Cancer2014-01-203.02 | Jan 22The Cancer Stem Cell Niche: Cross Talk between Cancer Stem Cells and Their MicroenvironmentYe, J; Wu, D; Wu, P; Chen, Z; Huang, JTumor Biol2014-01-143.01 | Jan 15Oncogenic Somatic Events in Tissue-Specific Stem Cells: A Role in Cancer Recurrence?Hartwig, F; Collares, T; Nedel, F; Tarquinio, S; Demarco, F; Nr, JEAgeing Res Rev2013-12-253.00 | Jan 8Kinase-Inhibitor-Insensitive Cancer Stem Cells in Chronic Myeloid LeukemiaMorotti, A; Panuzzo, C; Fava, C; Saglio, GExp Opin Biol Ther2014-01-033.00 | Jan 8The Roles of FOXM1 in Pancreatic Stem Cells and CarcinogenesisQuan, M; Wang, P; Cui, J; Gao, Y; Xie, KMol Cancer2013-12-102.50 | Dec 18Immunology of Cancer Stem Cells in Solid Tumors. A ReviewMaccalli, C; Volont, A; Cimminiello, C; Parmiani, GEur J Cancer2013-12-122.50 | Dec 18Fact or Fiction Identifying the Elusive Multiple Myeloma Stem CellKellner, J; Liu, B; Kang, Y; Li, ZJ Hematol Oncol2013-12-072.49 | Dec 11Circadian Disruption and Cancer Risk: A New Concept of Stromal NicheIzumi, H; Wang, K; Morimoto, Y; Sasaguri, Y; Kohno, KInt J Oncol2013-11-292.48 | Dec 4VEGF Targets the Tumour CellGoel, HL; Mercurio, AMNat Rev Cancer2013-11-222.47 | Nov 27Molecular Biomarkers of Cancer Stem/Progenitor Cells Associated with Progression, Metastases and Treatment Resistance of Aggressive CancersMimeault, M; Batra, SKCancer Epidemiol Biomarkers Prev2013-11-222.47 | Nov 27MicroRNAs and Cancer Stem Cells: The Sword and the ShieldSun, X; Jiao, X; Pestell, TG; Fan, C; Qin, S; Mirabelli, E; Ren, H; Pestell, RGOncogene2013-11-182.46 | Nov 20Alteration of Pancreatic Cancer Cell Functions by Tumor-Stromal Cell InteractionHamada, S; Masamune, A; Shimosegawa, TFront Physiol2013-11-012.45 | Nov 13Nuclear Receptors as Regulators of Stem Cell and Cancer Stem Cell MetabolismSimandi, Z; Cuaranta-Monroy, I; Nagy, LSemin Cell Dev Biol2013-10-312.44 | Nov 6Regulation of Angiogenesis via Notch Signaling in Breast Cancer and Cancer Stem CellsZhou, W; Wang, G; Guo, SBiochim Biophys Acta2013-10-302.44 | Nov 6Embryonic Stem Cell-Specific Signature in Cervical CancerOrganista-Nava, J; Gmez-Gmez, Y; Gariglio, PTumour Biol2013-10-282.43 | Oct 30Stem Cells and Targeted Approaches to Melanoma CureMurphy, GF; Wilson, BJ; Girouard, SD; Frank, NY; Frank, MHMol Asp Med2013-10-192.42 | Oct 23MicroRNAs Are Involved in the Self-Renewal and Differentiation of Cancer Stem CellsWang, ZM; Du, WJ; Piazza, GA; Xi, YActa Phramacol Sin2013-10-142.41 | Oct 16Targeting Cancer Stem Cells to Suppress Acquired Chemotherapy ResistanceVidal, SJ; Rodriguez-Bravo, V; Galsky, M, Cordon-Cardo, C; Domingo-Domenech, JOncogene2013-10-072.40 | Oct 9Stem Cells in the Skin and Their Role in OncogenesisSingh, R; Chen, C; Phelps, RG; Elston, DMJ Eur Acad Dermatol Venereol2013-10-012.40 | Oct 9Molecular Insight in Gastric Cancer Induction: An Overview of Cancer Stemness GenesPhay, J; Ringel, MDCell Biochem Biophys2013-09-282.39 | Oct 2Tumor Heterogeneity and Cancer Cell PlasticityMeacham, CE; Morrison, SJNature2013-09-192.38 | Sep 25Metastatic Mechanism in Follicular Cell-Derived Thyroid CancerPhay, J; Ringel, MDEndocr Relat Cancer2013-09-132.37 | Sep 18Lung Cancer Stem Cells: Molecular Features and Therapeutic TargetsSingh, S; Chellappan, SMol Aspects Med2013-09-072.36 | Sep 11Therapy Targets in Glioblastoma and Cancer Stem Cells: Lessons from Hematopoietic NeoplasmsCruceru, ML; Neagu, M; Demoulin, JB; Constantinescu, SNJ Cell Mol Med2013-09-022.36 | Sep 11Breast Cancer Adaptive Resistance: HER2 and Cancer Stem Cell Repopulation in a Heterogeneous Tumor SocietyDuru, N; Candas, D; Jiang, G; Li, JJJ Cancer Res Clin Oncol2013-08-302.35 | Sep 4Deadly Crosstalk: Notch Signaling at the Intersection of EMT and Cancer Stem CellsEspinoza, I; Miele, LCancer Lett2013-08-212.34 | Aug 28Omic-Profiling in Breast Cancer Metastasis to Bone: Implications for Mechanisms, Biomarkers and TreatmentWood, SL; Westbrook, JA; Brown, JECancer Treat Rev2013-08-192.33 | Aug 21Colorectal Cancer Defeating? Challenge Accepted!Di Franco, S; Todaro, M; Dieli, F; Stassi, GMol Aspect Med2013-08-052.32 | Aug 14The Role of Cancer Stem Cells in the Anti-Carcinogenicity of CurcuminNorris, L; Karmokar, A; Howells, L; Steward, WP; Gescher, A; Brown, KMol Nutr Food Res2013-07-132.31 | Aug 7Targeting Cancer Stem Cells with Sulforaphane, a Dietary Component from Broccoli and Broccoli SproutsLi, Y; Zhang, TFuture Oncol2013-08-012.31 | Aug 7Role of Integrated Cancer Nanomedicine in Overcoming Drug ResistanceIyer, AK; Singh, A; Ganta, S; Amiji, MMAdv Drug Deliv Rev2013-07-202.30 | Aug 31Relevance of Cancer Initiating/Stem Cells in Carcinogenesis and Therapy Resistance in Oral CancerSinha, N; Mukhopadhyay, S; Das, DN; Panda, PK; Bhutia, SKOral Oncol2013-07-222.29 | Jul 24The Role of MicroRNAs in Breast Cancer Stem CellsSchwarzenbacher, D; Balic, M; Pichler, MInt J Mol Sci2013-07-152.29 | Jul 24Unravelling Stem Cell Dynamics by Lineage TracingBlanpain, C; Simons, BNat Rev Mol Cell Biol2013-07-172.28 | Jul 17Cancer Stem Cells, Epithelial-Mesenchymal Transition, and Drug Resistance in High-Grade Ovarian Serous CarcinomaChen, X; Zhang, J; Zhang, Z; Li, H; Cheng, W; Liu, JHum Pathol2013-07-112.28 | Jul 17The Yin and Yang of Intestinal (Cancer) Stem Cells and Their ProgenitorsStange, D; Clevers, HStem Cells2013-07-082.27 | Jul 10The Variety of Leukemic Stem Cells in Myeloid MalignancyWiseman, DH; Greystoke, BF; Somervaille, TCPOncogene2013-07-082.27 | Jul 10Ovarian Cancer Stem Cells: Molecular Concepts and Relevance as Therapeutic TargetsAhmed, N; Abubaker, K; Findlay, JMol Aspects Med2013-06-252.26 | Jul 3Searching for Prostate Cancer Stem Cells: Markers and MethodsSharpe, B; Beresford, M; Bowen, R; Mitchard, J; Chalmers, ADStem Cell Rev Rep2013-06-192.25 | Jun 26The Evolution of the Cancer Niche during Multistage CarcinogenesisBarcellos-Hoff, MH; Lyden, D; Wang, TNat Rev Cancer2013-06-132.24 | Jun 19HER2 and Breast Cancer Stem Cells: More than Meets the EyeKorkaya, H; Wicha, MCancer Res2013-06-052.23 | Jun 12HIF Expression and the Role of Hypoxic Microenvironments within Primary Tumors as Protective Sites Driving Cancer Stem Cell Renewal and Metastatic ProgressionPhilip, B; 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'); jQuery('.cart-remove-box a').on('click', function(){ link = jQuery(this).attr('href'); jQuery.ajax({ url: link, cache: false }); jQuery('.cart-remove-box').remove(); setTimeout(function(){window.location.reload();}, 800); }); }); //jQuery('#ajax_loader').hide(); // clear being added addToCartButton.text(defaultText).removeAttr('disabled').removeClass('disabled'); addToCartButton.parent().find('.disabled-blocker').remove(); loadingDots.remove(); clearInterval(loadingDotId); jQuery('body').append(""); setTimeout(function () {jQuery('.add-to-cart-success').slideUp(500)}, 5000); }); } try { jQuery.ajax( { url : url, dataType : 'json', type : 'post', data : data, complete: function(){ if(jQuery('body').hasClass('product-edit') || jQuery('body').hasClass('wishlist-index-configure')){ jQuery.ajax({ url: "https://www.stemcell.com/meigeeactions/updatecart/", cache: false }).done(function(html){ jQuery('header#header .top-cart').replaceWith(html); }); jQuery('#ajax_loader').hide(); jQuery('body').append(""); setTimeout(function () {jQuery('.add-to-cart-success').slideUp(500)}, 5000); } }, success : function(data) { if(data.status == 'ERROR'){ jQuery('body').append(''); }else{ ajaxComplete(); } } }); } catch (e) { } // End of our new ajax code this.form.action = oldUrl; if (e) { throw e; } } }.bind(productAddToCartForm); productAddToCartForm.submitLight = function(button, url){ if(this.validator) { var nv = Validation.methods; delete Validation.methods['required-entry']; delete Validation.methods['validate-one-required']; delete Validation.methods['validate-one-required-by-name']; if (this.validator.validate()) { if (url) { this.form.action = url; } this.form.submit(); } Object.extend(Validation.methods, nv); } }.bind(productAddToCartForm); function setAjaxData(data,iframe,name,image){ if(data.status == 'ERROR'){ jQuery('body').append(''); }else{ if(data.sidebar && !iframe){ if(jQuery('.top-cart').length){ jQuery('.top-cart').replaceWith(data.sidebar); } if(jQuery('.sidebar .block.block-cart').length){ if(jQuery('#cart-sidebar').length){ jQuery('#cart-sidebar').html(jQuery(data.sidebar).find('#mini-cart')); jQuery('.sidebar .block.block-cart .subtotal').html(jQuery(data.sidebar).find('.subtotal')); }else{ jQuery('.sidebar .block.block-cart p.empty').remove(); content = jQuery('.sidebar .block.block-cart .block-content'); jQuery('').appendTo(content); jQuery('').appendTo(content); content.find('#cart-sidebar').html(jQuery(data.sidebar).find('#mini-cart').html()); content.find('.actions').append(jQuery(data.sidebar).find('.subtotal')); content.find('.actions').append(jQuery(data.sidebar).find('.actions button.button')); } cartProductRemove('#cart-sidebar li.item a.btn-remove', { confirm: 'Are you sure you would like to remove this item from the shopping cart?', submit: 'Ok', calcel: 'Cancel' }); } jQuery.fancybox.close(); jQuery('body').append(''); }else{ jQuery.ajax({ url: "https://www.stemcell.com/meigeeactions/updatecart/", cache: false }).done(function(html){ jQuery('header#header .top-cart').replaceWith(html); jQuery('.top-cart #mini-cart li.item a.btn-remove').on('click', function(event){ event.preventDefault(); jQuery('body').append('Are you sure you would like to remove this item from the shopping cart?OkCancel'); jQuery('.cart-remove-box a').on('click', function(){ link = jQuery(this).attr('href'); jQuery.ajax({ url: link, cache: false }); jQuery('.cart-remove-box').remove(); setTimeout(function(){window.location.reload();}, 800); }); }); jQuery.fancybox.close(); jQuery('body').append(''); }); } } setTimeout(function () {jQuery('.add-to-cart-success').slideUp(500)}, 5000); } // The EasySep Human CD4+ T Cell Enrichment Kit is designed to isolate CD4+ T cells from fresh or previously frozen peripheral mononuclear cells by negative selection. Unwanted cells are targeted for removal with Tetrameric Antibody Complexes recognizing non-CD4+ T cells and dextran-coated magnetic particles. Labeled cells are separated using an EasySep magnet without the use of columns. Desired cells are poured off into a new tube.

For even faster cell isolations, we recommend the new EasySep Human CD4+ T Cell Isolation Kit (17952) which isolates cells in just 8 minutes.

Advantages:

Fast, easy-to-use and column-free Up to 97% purity Untouched, viable cells

Magnet Compatibility:

EasySep Magnet (Catalog #18000)

The Big Easy EasySep Magnet (Catalog #18001)

Easy 50 EasySep Magnet (Catalog #18002)

EasyPlate EasySep Magnet (Catalog 18102)

EasyEights EasySep Magnet (Catalog #18103)

RoboSep-S (Catalog #21000)

Subtype:

Cell Isolation Kits

Cell Type:

T Cells; T Cells, CD4+

Sample Source:

Leukapheresis; PBMC

Selection Method:

Negative

Application:

Cell Isolation

Area of Interest:

Immunology

Document Type

Product Name

Catalog #

Lot #

Language

Yes. The EasySep kits use either a negative selection approach by targeting and removing unwanted cells or a positive selection approach targeting desired cells. Depletion kits are also available for the removal of cells with a specific undesired marker (e.g. GlyA).

Magnetic particles are crosslinked to cells using Tetrameric Antibody Complexes (TAC). When placed in the EasySep Magnet, labeled cells migrate to the wall of the tube. The unlabeled cells are then poured off into a separate fraction.

The EasySep procedure is column-free. That's right - no columns!

The Product Information Sheet provided with each EasySep kit contains detailed staining information.

Yes. RoboSep, the fully automated cell separator, automates all EasySep labeling and cell separation steps.

Yes. We recommend a cell concentration of 2x108 cells/mL and a minimum working volume of 100 L. Samples containing 2x107 cells or fewer should be suspended in 100 L of buffer.

Yes, the EasySep particles are flow cytometry-compatible, as they are very uniform in size and about 5000X smaller than other commercially available magnetic beads used with column-free systems.

No, but due to the small size of these particles, they will not interfere with downstream applications.

Yes; however, this may impact the kit's performance. The provided EasySep protocols have already been optimized to balance purity, recovery and time spent on the isolation.

Yes, the purity of targeted cells will increase with additional rounds of separations; however, cell recovery will decrease.

If particle binding is a key concern, we offer two options for negative selection. The EasySep negative selection kits can isolate untouched cells with comparable purities, while RosetteSep can isolate untouched cells directly from whole blood without using particles or magnets.

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Figure 1. FACS Histogram Results Using EasySep Human CD4+ T Cell Enrichment Kit

Starting with frozen mononuclear cells, the CD4+ T cell content of the enriched fraction typically ranges from 92% - 97%.

Huang S-H et al.

The presence of persistent, latent HIV reservoirs in CD4+ T cells obstructs current efforts to cure infection. The so-called kick-and-kill paradigm proposes to purge these reservoirs by combining latency-reversing agents with immune effectors such as cytotoxic T lymphocytes. Support for this approach is largely based on success in latency models, which do not fully reflect the makeup of latent reservoirs in individuals on long-term antiretroviral therapy (ART). Recent studies have shown that CD8+ T cells have the potential to recognize defective proviruses, which comprise the vast majority of all infected cells, and that the proviral landscape can be shaped over time due to in vivo clonal expansion of infected CD4+ T cells. Here, we have shown that treating CD4+ T cells from ART-treated individuals with combinations of potent latency-reversing agents and autologous CD8+ T cells consistently reduced cell-associated HIV DNA, but failed to deplete replication-competent virus. These CD8+ T cells recognized and potently eliminated CD4+ T cells that were newly infected with autologous reservoir virus, ruling out a role for both immune escape and CD8+ T cell dysfunction. Thus, our results suggest that cells harboring replication-competent HIV possess an inherent resistance to CD8+ T cells that may need to be addressed to cure infection.

Albert BJ et al.

Current antiretroviral therapy (ART) for HIV/AIDS slows disease progression by reducing viral loads and increasing CD4 counts. Yet ART is not curative due to the persistence of CD4+ T-cell proviral reservoirs that chronically resupply active virus. Elimination of these reservoirs through the administration of synergistic combinations of latency reversing agents (LRAs), such as histone deacetylase (HDAC) inhibitors and protein kinase C (PKC) modulators, provides a promising strategy to reduce if not eradicate the viral reservoir. Here, we demonstrate that largazole and its analogues are isoform-targeted histone deacetylase inhibitors and potent LRAs. Significantly, these isoform-targeted HDAC inhibitors synergize with PKC modulators, namely bryostatin-1 analogues (bryologs). Implementation of this unprecedented LRA combination induces HIV-1 reactivation to unparalleled levels and avoids global T-cell activation within resting CD4+ T-cells.

Hultquist JF et al.

New genetic tools are needed to understand the functional interactions between HIV and human host factors in primary cells. We recently developed a method to edit the genome of primary CD4(+) T cells by electroporation of CRISPR/Cas9 ribonucleoproteins (RNPs). Here, we adapted this methodology to a high-throughput platform for the efficient, arrayed editing of candidate host factors. CXCR4 or CCR5 knockout cells generated with this method are resistant to HIV infection in a tropism-dependent manner, whereas knockout of LEDGF or TNPO3 results in a tropism-independent reduction in infection. CRISPR/Cas9 RNPs can furthermore edit multiple genes simultaneously, enabling studies of interactions among multiple host and viral factors. Finally, in an arrayed screen of 45 genes associated with HIV integrase, we identified several candidate dependency/restriction factors, demonstrating the power of this approach as a discovery platform. This technology should accelerate target validation for pharmaceutical and cell-based therapies to cure HIV infection.

Vanwalscappel B et al.

Treatment of HIV-infected patients with IFN- results in significant, but clinically insufficient, reductions of viremia. IFN induces the expression of several antiviral proteins including BST-2, which inhibits HIV by multiple mechanisms. The viral protein Vpu counteracts different effects of BST-2. We thus asked if Vpu proteins from IFN-treated patients displayed improved anti-BST-2 activities as compared to Vpu from baseline. Deep-sequencing analyses revealed that in five of seven patients treated by IFN- for a concomitant HCV infection in the absence of antiretroviral drugs, the dominant Vpu sequences differed before and during treatment. In three patients, vpu alleles that emerged during treatment improved virus replication in the presence of IFN-, and two of them conferred improved virus budding from cells expressing BST-2. Differences were observed for the ability to down-regulate CD4, while all Vpu variants potently down-modulated BST-2 from the cell surface. This report discloses relevant consequences of IFN-treatment on HIV properties.

Hrecka K et al.

HIV replication in nondividing host cells occurs in the presence of high concentrations of noncanonical dUTP, apolipoprotein B mRNA-editing, enzyme-catalytic, polypeptide-like 3 (APOBEC3) cytidine deaminases, and SAMHD1 (a cell cycle-regulated dNTP triphosphohydrolase) dNTPase, which maintains low concentrations of canonical dNTPs in these cells. These conditions favor the introduction of marks of DNA damage into viral cDNA, and thereby prime it for processing by DNA repair enzymes. Accessory protein Vpr, found in all primate lentiviruses, and its HIV-2/simian immunodeficiency virus (SIV) SIVsm paralogue Vpx, hijack the CRL4(DCAF1) E3 ubiquitin ligase to alleviate some of these conditions, but the extent of their interactions with DNA repair proteins has not been thoroughly characterized. Here, we identify HLTF, a postreplication DNA repair helicase, as a common target of HIV-1/SIVcpz Vpr proteins. We show that HIV-1 Vpr reprograms CRL4(DCAF1) E3 to direct HLTF for proteasome-dependent degradation independent from previously reported Vpr interactions with base excision repair enzyme uracil DNA glycosylase (UNG2) and crossover junction endonuclease MUS81, which Vpr also directs for degradation via CRL4(DCAF1) E3. Thus, separate functions of HIV-1 Vpr usurp CRL4(DCAF1) E3 to remove key enzymes in three DNA repair pathways. In contrast, we find that HIV-2 Vpr is unable to efficiently program HLTF or UNG2 for degradation. Our findings reveal complex interactions between HIV-1 and the DNA repair machinery, suggesting that DNA repair plays important roles in the HIV-1 life cycle. The divergent interactions of HIV-1 and HIV-2 with DNA repair enzymes and SAMHD1 imply that these viruses use different strategies to guard their genomes and facilitate their replication in the host.

STEMCELL TECHNOLOGIES INC.S QUALITY MANAGEMENT SYSTEM IS CERTIFIED TO ISO 13485. PRODUCTS ARE FOR RESEARCH USE ONLY AND NOT INTENDED FOR HUMAN OR ANIMAL DIAGNOSTIC OR THERAPEUTIC USES UNLESS OTHERWISE STATED.

Internal Search Keywords: 19052|19052RF|19052C.2|19012|14052 |Easy sep CD-4 T|Easy sep CD4|CD4+ T cell isolation|CD4 T cell isolation|T cell isolation

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EasySep Human CD4+ T Cell Enrichment Kit

A T cell, or T lymphocyte, is a type of lymphocyte (a subtype of white blood cell) that plays a central role in cell-mediated immunity. T cells can be distinguished from other lymphocytes, such as B cells and natural killer cells, by the presence of a T-cell receptor on the cell surface. They are called T cells because they mature in the thymus from thymocytes[1] (although some also mature in the tonsils[2]). The several subsets of T cells each have a distinct function. The majority of human T cells rearrange their alpha and beta chains on the cell receptor and are termed alpha beta T cells ( T cells) and are part of the adaptive immune system. Specialized gamma delta T cells, (a small minority of T cells in the human body, more frequent in ruminants), have invariant T-cell receptors with limited diversity, that can effectively present antigens to other T cells[3] and are considered to be part of the innate immune system.

Effector cells are the superset of all the various T cell types that actively respond immediately to a stimulus, such as co-stimulation. This includes helper, killer, regulatory, and potentially other T cell types. Memory cells are their opposite counterpart that are longer lived to target future infections as necessary.

T helper cells (TH cells) assist other white blood cells in immunologic processes, including maturation of B cells into plasma cells and memory B cells, and activation of cytotoxic T cells and macrophages. These cells are also known as CD4+ T cells because they express the CD4 glycoprotein on their surfaces. Helper T cells become activated when they are presented with peptide antigens by MHC class II molecules, which are expressed on the surface of antigen-presenting cells (APCs). Once activated, they divide rapidly and secrete small proteins called cytokines that regulate or assist in the active immune response. These cells can differentiate into one of several subtypes, including TH1, TH2, TH3, TH17, TH9, or TFH, which secrete different cytokines to facilitate different types of immune responses. Signalling from the APC directs T cells into particular subtypes.[4]

Cytotoxic T cells (TC cells, CTLs, T-killer cells, killer T cells) destroy virus-infected cells and tumor cells, and are also implicated in transplant rejection. These cells are also known as CD8+ T cells since they express the CD8 glycoprotein at their surfaces. These cells recognize their targets by binding to antigen associated with MHC class I molecules, which are present on the surface of all nucleated cells. Through IL-10, adenosine, and other molecules secreted by regulatory T cells, the CD8+ cells can be inactivated to an anergic state, which prevents autoimmune diseases.

Antigen-nave T cells expand and differentiate into memory and effector T cells after they encounter their cognate antigen within the context of an MHC molecule on the surface of a professional antigen presenting cell (e.g. a dendritic cell). Appropriate co-stimulation must be present at the time of antigen encounter for this process to occur. Historically, memory T cells were thought to belong to either the effector or central memory subtypes, each with their own distinguishing set of cell surface markers (see below).[5] Subsequently, numerous new populations of memory T cells were discovered including tissue-resident memory T (Trm) cells, stem memory TSCM cells, and virtual memory T cells. The single unifying theme for all memory T cell subtypes is that they are long-lived and can quickly expand to large numbers of effector T cells upon re-exposure to their cognate antigen. By this mechanism they provide the immune system with "memory" against previously encountered pathogens. Memory T cells may be either CD4+ or CD8+ and usually express CD45RO.[6]

Memory T cell subtypes:

Regulatory T cells (suppressor T cells) are crucial for the maintenance of immunological tolerance. Their major role is to shut down T cell-mediated immunity toward the end of an immune reaction and to suppress autoreactive T cells that escaped the process of negative selection in the thymus. Suppressor T cells along with Helper T cells can collectively be called Regulatory T cells due to their regulatory functions.[12]

Two major classes of CD4+ Treg cells have been described FOXP3+ Treg cells and FOXP3 Treg cells.

Regulatory T cells can develop either during normal development in the thymus, and are then known as thymic Treg cells, or can be induced peripherally and are called peripherally derived Treg cells. These two subsets were previously called "naturally occurring", and "adaptive" or "induced", respectively.[13] Both subsets require the expression of the transcription factor FOXP3 which can be used to identify the cells. Mutations of the FOXP3 gene can prevent regulatory T cell development, causing the fatal autoimmune disease IPEX.

Several other types of T cell have suppressive activity, but do not express FOXP3. These include Tr1 cells and Th3 cells, which are thought to originate during an immune response and act by producing suppressive molecules. Tr1 cells are associated with IL-10, and Th3 cells are associated with TGF-beta. Recently, Treg17 cells have been added to this list.[14]

Natural killer T cells (NKT cells not to be confused with natural killer cells of the innate immune system) bridge the adaptive immune system with the innate immune system. Unlike conventional T cells that recognize peptide antigens presented by major histocompatibility complex (MHC) molecules, NKT cells recognize glycolipid antigen presented by a molecule called CD1d. Once activated, these cells can perform functions ascribed to both Th and Tc cells (i.e., cytokine production and release of cytolytic/cell killing molecules). They are also able to recognize and eliminate some tumor cells and cells infected with herpes viruses.[15]

MAIT cells display innate, effector-like qualities.[16][17] In humans, MAIT cells are found in the blood, liver, lungs, and mucosa, defending against microbial activity and infection.[16] The MHC class I-like protein, MR1, is responsible for presenting bacterially-produced vitamin B metabolites to MAIT cells.[18][19][20] After the presentation of foreign antigen by MR1, MAIT cells secretes pro-inflammatory cytokines and are capable of lysing bacterially-infected cells.[16][20] MAIT cells can also be activated through MR1-independent signaling.[20] In addition to possessing innate-like functions, this T cell subset supports the adaptive immune response and has a memory-like phenotype.[16] Furthermore, MAIT cells are thought to play a role in autoimmune diseases, such as multiple sclerosis, arthritis and inflammatory bowel disease,[21][22] although definitive evidence is yet to be published.[23][24][25][26]

Gamma delta T cells ( T cells) represent a small subset of T cells that possess a distinct T cell receptor (TCR) on their surfaces. A majority of T cells have a TCR composed of two glycoprotein chains called - and - TCR chains. However, in T cells, the TCR is made up of one -chain and one -chain. This group of T cells is much less common in humans and mice (about 2% of total T cells); and are found mostly in the gut mucosa, within a population of lymphocytes known as intraepithelial lymphocytes. In rabbits, sheep, and chickens, the number of T cells can be as high as 60% of total T cells. The antigenic molecules that activate T cells are still widely unknown. However, T cells are not MHC-restricted and seem to be able to recognize whole proteins rather than requiring peptides to be presented by MHC molecules on APCs. Some murine T cells recognize MHC class IB molecules, though. Human V9/V2 T cells, which constitute the major T cell population in peripheral blood, are unique in that they specifically and rapidly respond to a set of nonpeptidic phosphorylated isoprenoid precursors, collectively named phosphoantigens, which are produced by virtually all living cells. The most common phosphoantigens from animal and human cells (including cancer cells) are isopentenyl pyrophosphate (IPP) and its isomer dimethylallyl pyrophosphate (DMPP). Many microbes produce the highly active compound hydroxy-DMAPP (HMB-PP) and corresponding mononucleotide conjugates, in addition to IPP and DMAPP. Plant cells produce both types of phosphoantigens. Drugs activating human V9/V2 T cells comprise synthetic phosphoantigens and aminobisphosphonates, which upregulate endogenous IPP/DMAPP.

All T cells originate from haematopoietic stem cells in the bone marrow. Haematopoietic progenitors (lymphoid progenitor cells) from haematopoietic stem cells populate the thymus and expand by cell division to generate a large population of immature thymocytes.[27] The earliest thymocytes express neither CD4 nor CD8, and are therefore classed as double-negative (CD4CD8) cells. As they progress through their development, they become double-positive thymocytes (CD4+CD8+), and finally mature to single-positive (CD4+CD8 or CD4CD8+) thymocytes that are then released from the thymus to peripheral tissues. There is some evidence of double-positive T-cells in the periphery, though their prevalence and function is uncertain.[28][29] In laboratory, T-cells can be converted into functional neurons within three weeks. [30]

About 98% of thymocytes die during the development processes in the thymus by failing either positive selection or negative selection, whereas the other 2% survive and leave the thymus to become mature immunocompetent T cells. Increasing evidence indicates microRNAs, which are small noncoding regulatory RNAs, could impact the clonal selection process during thymic development. For example, miR-181a was found to play a role in the positive selection of T lymphocytes.[31]

The thymus contributes fewer cells as a person ages. As the thymus shrinks by about 3%[32] a year throughout middle age, a corresponding fall in the thymic production of nave T cells occurs, leaving peripheral T cell expansion to play a greater role in protecting older subjects.

Common lymphoid precursor cells that migrate to the thymus become known as T-cell precursors (or thymocytes) and do not express a T cell receptor. Broadly speaking, the double negative (DN) stage is focused on producing a functional -chain whereas the double positive (DP) stage is focused on producing a functional -chain, ultimately producing a functional T cell receptor. As the developing thymocyte progresses through the four DN stages (DN1, DN2, DN3, and DN4), the T cell expresses an invariant -chain but rearranges the -chain locus. If the rearranged -chain successfully pairs with the invariant -chain, signals are produced which cease rearrangement of the -chain (and silence the alternate allele) and result in proliferation of the cell.[33] Although these signals require this pre-TCR at the cell surface, they are independent of ligand binding to the pre-TCR. These thymocytes will then express both CD4 and CD8 and progresses to the double positive (DP) stage where selection of the -chain takes place. If a rearranged -chain does not lead to any signalling (e.g. as a result of an inability to pair with the invariant -chain), the cell may die by neglect (lack of signalling).

Positive selection "selects for" T cells capable of interacting with MHC. Positive selection involves the production of a signal by double-positive precursors that express either MHC Class I or II restricted receptors. The signal produced by these thymocytes result in RAG gene repression, long-term survival and migration into the medulla, as well as differentiation into mature T cells. The process of positive selection takes a number of days.[34]

Double-positive thymocytes (CD4+/CD8+) move deep into the thymic cortex, where they are presented with self-antigens. These self-antigens are expressed by thymic cortical epithelial cells on MHC molecules on the surface of cortical epithelial cells. Only those thymocytes that interact with MHC-I or MHC-II appropriately (i.e., not too strongly or too weakly) will receive a vital "survival signal". All that cannot (i.e., if they do not interact strongly enough, or if they bind too strongly) will die by "death by neglect" (no survival signal). This process ensures that the selected T-cells will have an MHC affinity that can serve useful functions in the body (i.e., the cells must be able to interact with MHC and peptide complexes to effect immune responses). The vast majority of all thymocytes will die during this process.

A thymocyte's fate is determined during positive selection. Double-positive cells (CD4+/CD8+) that interact well with MHC class II molecules will eventually become CD4+ cells, whereas thymocytes that interact well with MHC class I molecules mature into CD8+ cells. A T cell becomes a CD4+ cell by down-regulating expression of its CD8 cell surface receptors. If the cell does not lose its signal, it will continue downregulating CD8 and become a CD4+, single positive cell.[35] But, if there is a signal interruption, the cell stops downregulating CD8 and switches over to downregulating CD4 molecules, instead, eventually becoming a CD8+, single positive cell.

This process does not remove thymocytes that may cause autoimmunity. The potentially autoimmune cells are removed by the process of negative selection, which occurs in the thymic medulla (discussed below).

Negative selection removes thymocytes that are capable of strongly binding with "self" MHC peptides. Thymocytes that survive positive selection migrate towards the boundary of the cortex and medulla in the thymus. While in the medulla, they are again presented with a self-antigen presented on the MHC complex of medullary thymic epithelial cells (mTECs).[36] mTECs must be AIRE+ to properly express self-antigens from all tissues of the body on their MHC class I peptides. Some mTECs are phagocytosed by thymic dendritic cells; this allows for presentation of self-antigens on MHC class II molecules (positively selected CD4+ cells must interact with MHC class II molecules, thus APCs, which possess MHC class II, must be present for CD4+ T-cell negative selection). Thymocytes that interact too strongly with the self-antigen receive an apoptotic signal that leads to cell death. However, some of these cells are selected to become Treg cells. The remaining cells exit the thymus as immature nave T cells (also known as recent thymic emigrants [37]). This process is an important component of central tolerance and serves to prevent the formation of self-reactive T cells that are capable of inducing autoimmune diseases in the host.

In summary, -selection is the first checkpoint, where the T cells that are able to form a functional pre-TCR with an invariant alpha chain and a functional beta chain are allowed to continue development in the thymus. Next, positive selection checks that T cells have successfully rearranged their TCR locus and are capable of recognizing peptide-MHC complexes with appropriate affinity. Negative selection in the medulla then obliterates T cells that bind too strongly to self-antigens expressed on MHC molecules. These selection processes allow for tolerance of self by the immune system. Typical T cells that leave the thymus (via the corticomedullarly junction) are self-restricted, self-tolerant, and singly positive.

Activation of CD4+ T cells occurs through the simultaneous engagement of the T-cell receptor and a co-stimulatory molecule (like CD28, or ICOS) on the T cell by the major histocompatibility complex (MHCII) peptide and co-stimulatory molecules on the APC. Both are required for production of an effective immune response; in the absence of co-stimulation, T cell receptor signalling alone results in anergy. The signalling pathways downstream from co-stimulatory molecules usually engages the PI3K pathway generating PIP3 at the plasma membrane and recruiting PH domain containing signaling molecules like PDK1 that are essential for the activation of PKC, and eventual IL-2 production. Optimal CD8+ T cell response relies on CD4+ signalling.[39] CD4+ cells are useful in the initial antigenic activation of nave CD8 T cells, and sustaining memory CD8+ T cells in the aftermath of an acute infection. Therefore, activation of CD4+ T cells can be beneficial to the action of CD8+ T cells.[40][41][42]

The first signal is provided by binding of the T cell receptor to its cognate peptide presented on MHCII on an APC. MHCII is restricted to so-called professional antigen-presenting cells, like dendritic cells, B cells, and macrophages, to name a few. The peptides presented to CD8+ T cells by MHC class I molecules are 813 amino acids in length; the peptides presented to CD4+ cells by MHC class II molecules are longer, usually 1225 amino acids in length,[43] as the ends of the binding cleft of the MHC class II molecule are open.

The second signal comes from co-stimulation, in which surface receptors on the APC are induced by a relatively small number of stimuli, usually products of pathogens, but sometimes breakdown products of cells, such as necrotic-bodies or heat shock proteins. The only co-stimulatory receptor expressed constitutively by nave T cells is CD28, so co-stimulation for these cells comes from the CD80 and CD86 proteins, which together constitute the B7 protein, (B7.1 and B7.2, respectively) on the APC. Other receptors are expressed upon activation of the T cell, such as OX40 and ICOS, but these largely depend upon CD28 for their expression. The second signal licenses the T cell to respond to an antigen. Without it, the T cell becomes anergic, and it becomes more difficult for it to activate in future. This mechanism prevents inappropriate responses to self, as self-peptides will not usually be presented with suitable co-stimulation. Once a T cell has been appropriately activated (i.e. has received signal one and signal two) it alters its cell surface expression of a variety of proteins. Markers of T cell activation include CD69, CD71 and CD25 (also a marker for Treg cells), and HLA-DR (a marker of human T cell activation). CTLA-4 expression is also up-regulated on activated T cells, which in turn outcompetes CD28 for binding to the B7 proteins. This is a checkpoint mechanism to prevent over activation of the T cell. Activated T cells also change their cell surface glycosylation profile.[44]

The T cell receptor exists as a complex of several proteins. The actual T cell receptor is composed of two separate peptide chains, which are produced from the independent T cell receptor alpha and beta (TCR and TCR) genes. The other proteins in the complex are the CD3 proteins: CD3 and CD3 heterodimers and, most important, a CD3 homodimer, which has a total of six ITAM motifs. The ITAM motifs on the CD3 can be phosphorylated by Lck and in turn recruit ZAP-70. Lck and/or ZAP-70 can also phosphorylate the tyrosines on many other molecules, not least CD28, LAT and SLP-76, which allows the aggregation of signalling complexes around these proteins.

Phosphorylated LAT recruits SLP-76 to the membrane, where it can then bring in PLC-, VAV1, Itk and potentially PI3K. PLC- cleaves PI(4,5)P2 on the inner leaflet of the membrane to create the active intermediaries diacylglycerol (DAG), inositol-1,4,5-trisphosphate (IP3); PI3K also acts on PIP2, phosphorylating it to produce phosphatidlyinositol-3,4,5-trisphosphate (PIP3). DAG binds and activates some PKCs. Most important in T cells is PKC, critical for activating the transcription factors NF-B and AP-1. IP3 is released from the membrane by PLC- and diffuses rapidly to activate calcium channel receptors on the ER, which induces the release of calcium into the cytosol. Low calcium in the endoplasmic reticulum causes STIM1 clustering on the ER membrane and leads to activation of cell membrane CRAC channels that allows additional calcium to flow into the cytosol from the extracellular space. This aggregated cytosolic calcium binds calmodulin, which can then activate calcineurin. Calcineurin, in turn, activates NFAT, which then translocates to the nucleus. NFAT is a transcription factor that activates the transcription of a pleiotropic set of genes, most notable, IL-2, a cytokine that promotes long-term proliferation of activated T cells.

PLC can also initiate the NF-B pathway. DAG activates PKC, which then phosphorylates CARMA1, causing it to unfold and function as a scaffold. The cytosolic domains bind an adapter BCL10 via CARD (Caspase activation and recruitment domains) domains; that then binds TRAF6, which is ubiquitinated at K63.:513523[45] This form of ubiquitination does not lead to degradation of target proteins. Rather, it serves to recruit NEMO, IKK and -, and TAB1-2/ TAK1.[46] TAK 1 phosphorylates IKK-, which then phosphorylates IB allowing for K48 ubiquitination: leads to proteasomal degradation. Rel A and p50 can then enter the nucleus and bind the NF-B response element. This coupled with NFAT signaling allows for complete activation of the IL-2 gene.[45]

While in most cases activation is dependent on TCR recognition of antigen, alternative pathways for activation have been described. For example, cytotoxic T cells have been shown to become activated when targeted by other CD8 T cells leading to tolerization of the latter.[47]

In spring 2014, the T-Cell Activation in Space (TCAS) experiment was launched to the International Space Station on the SpaceX CRS-3 mission to study how "deficiencies in the human immune system are affected by a microgravity environment".[48]

T cell activation is modulated by reactive oxygen species.[49]

A unique feature of T cells is their ability to discriminate between healthy and abnormal (e.g. infected or cancerous) cells in the body.[50] Healthy cells typically express a large number of self derived pMHC on their cell surface and although the T cell antigen receptor can interact with at least a subset of these self pMHC, the T cell generally ignores these healthy cells. However, when these very same cells contain even minute quantities of pathogen derived pMHC, T cells are able to become activated and initiate immune responses. The ability of T cells to ignore healthy cells but respond when these same cells contain pathogen (or cancer) derived pMHC is known as antigen discrimination. The molecular mechanisms that underlie this process are controversial.[50][51]

Causes of T cell deficiency include lymphocytopenia of T cells and/or defects on function of individual T cells. Complete insufficiency of T cell function can result from hereditary conditions such as severe combined immunodeficiency (SCID), Omenn syndrome, and cartilagehair hypoplasia.[52] Causes of partial insufficiencies of T cell function include acquired immune deficiency syndrome (AIDS), and hereditary conditions such as DiGeorge syndrome (DGS), chromosomal breakage syndromes (CBSs), and B-cell and T-cell combined disorders such as ataxia-telangiectasia (AT) and WiskottAldrich syndrome (WAS).[52]

The main pathogens of concern in T cell deficiencies are intracellular pathogens, including Herpes simplex virus, Mycobacterium and Listeria.[53] Also, fungal infections are also more common and severe in T cell deficiencies.[53]

Cancer of T cells is termed T-cell lymphoma, and accounts for perhaps one in ten cases of non-Hodgkin lymphoma.[54] The main forms of T cell lymphoma are:

T cell exhaustion is the progressive loss of T cell function. It can occur during sepsis and after other acute or chronic infections.[55][56]

T cell exhaustion is mediated by several inhibitory receptors including programmed cell death protein 1 (PD1), TIM3, and lymphocyte activation gene 3 protein (LAG3).[57]CD8+ T cell exhaustion occurs in some tumours, and can be partly reversed by blocking the inhibitory receptors (e.g. PD1).[58]

T cell exhaustion is associated with epigenetic changes in the T cells.[59]

( See also Immunosenescence#T cell functional dysregulation as a biomarker for immunosenescence ).

In 2015, a team of researchers led by Dr. Alexander Marson[60] at the University of California, San Francisco successfully edited the genome of human T cells using a Cas9 ribonucleoprotein delivery method.[61] This advancement has potential for applications in treating "cancer immunotherapies and cell-based therapies for HIV, primary immune deficiencies, and autoimmune diseases".[61]

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T cell - Wikipedia

"Type O" redirects here. It is not to be confused with type 0.

A blood type (also called a blood group) is a classification of blood based on the presence and absence of antibodies and also based on the presence or absence of inherited antigenic substances on the surface of red blood cells (RBCs). These antigens may be proteins, carbohydrates, glycoproteins, or glycolipids, depending on the blood group system. Some of these antigens are also present on the surface of other types of cells of various tissues. Several of these red blood cell surface antigens can stem from one allele (or an alternative version of a gene) and collectively form a blood group system.[1] Blood types are inherited and represent contributions from both parents. A total of 36 human blood group systems are now recognized by the International Society of Blood Transfusion (ISBT).[2] The two most important ones are ABO and the Rh blood group systems; they determine someone's blood type (A, B, AB and O, with +, or null denoting RhD status) for suitability in blood transfusion.

A complete blood type would describe a full set of 30 substances on the surface of red blood cells, and an individual's blood type is one of many possible combinations of blood-group antigens.[3] Across the 36 blood groups, over 340 different blood-group antigens have been found.[2] Almost always, an individual has the same blood group for life, but very rarely an individual's blood type changes through addition or suppression of an antigen in infection, malignancy, or autoimmune disease.[4][5][6][7] Another more common cause in blood type change is a bone marrow transplant. Bone-marrow transplants are performed for many leukemias and lymphomas, among other diseases. If a person receives bone marrow from someone who is a different ABO type (e.g., a type A patient receives a type O bone marrow), the patient's blood type will eventually convert to the donor's type.

Some blood types are associated with inheritance of other diseases; for example, the Kell antigen is sometimes associated with McLeod syndrome.[8] Certain blood types may affect susceptibility to infections, an example being the resistance to specific malaria species seen in individuals lacking the Duffy antigen.[9] The Duffy antigen, presumably as a result of natural selection, is less common in ethnic groups from areas with a high incidence of malaria.[10]

The ABO blood group system involves two antigens and two antibodies found in human blood. The two antigens are antigen A and antigen B. The two antibodies are antibody A and antibody B. The antigens are present on the red blood cells and the antibodies in the serum. Regarding the antigen property of the blood all human beings can be classified into 4 groups, those with antigen A (group A), those with antigen B (group B), those with both antigen A and B (group AB) and those with neither antigen (group O). The antibodies present together with the antigens are found as follows:

1. Antigen A with antibody B2. Antigen B with antibody A3. Antigen AB has no antibodies4. Antigen nil (group O) with antibody A and B.

There is an agglutination reaction between similar antigen and antibody (for example, antigen A agglutinates the antibody A and antigen B agglutinates the antibody B). Thus, transfusion can be considered safe as long as the serum of the recipient does not contain antibodies for the blood cell antigens of the donor.

The ABO system is the most important blood-group system in human-blood transfusion. The associated anti-A and anti-B antibodies are usually immunoglobulin M, abbreviated IgM, antibodies. ABO IgM antibodies are produced in the first years of life by sensitization to environmental substances such as food, bacteria, and viruses.[citation needed] The original terminology used by Karl Landsteiner in 1901 for the classification was A/B/C; in later publications "C" became "O".[11] "O" is often called 0 (zero, or null) in other languages.[11][12]

The Rh system (Rh meaning Rhesus) is the second most significant blood-group system in human-blood transfusion with currently 50 antigens. The most significant Rh antigen is the D antigen, because it is the most likely to provoke an immune system response of the five main Rh antigens. It is common for D-negative individuals not to have any anti-D IgG or IgM antibodies, because anti-D antibodies are not usually produced by sensitization against environmental substances. However, D-negative individuals can produce IgG anti-D antibodies following a sensitizing event: possibly a fetomaternal transfusion of blood from a fetus in pregnancy or occasionally a blood transfusion with D positive RBCs.[13] Rh disease can develop in these cases.[14] Rh negative blood types are much less common in Asian populations (0.3%) than they are in European populations (15%).[15] The presence or absence of the Rh(D) antigen is signified by the + or sign, so that, for example, the A group is ABO type A and does not have the Rh (D) antigen.

As with many other genetic traits, the distribution of ABO and Rh blood groups varies significantly between populations.

Thirty-three blood-group systems have been identified by the International Society for Blood Transfusion in addition to the common ABO and Rh systems.[16] Thus, in addition to the ABO antigens and Rh antigens, many other antigens are expressed on the RBC surface membrane. For example, an individual can be AB, D positive, and at the same time M and N positive (MNS system), K positive (Kell system), Lea or Leb negative (Lewis system), and so on, being positive or negative for each blood group system antigen. Many of the blood group systems were named after the patients in whom the corresponding antibodies were initially encountered.

Transfusion medicine is a specialized branch of hematology that is concerned with the study of blood groups, along with the work of a blood bank to provide a transfusion service for blood and other blood products. Across the world, blood products must be prescribed by a medical doctor (licensed physician or surgeon) in a similar way as medicines.

Much of the routine work of a blood bank involves testing blood from both donors and recipients to ensure that every individual recipient is given blood that is compatible and is as safe as possible. If a unit of incompatible blood is transfused between a donor and recipient, a severe acute hemolytic reaction with hemolysis (RBC destruction), renal failure and shock is likely to occur, and death is a possibility. Antibodies can be highly active and can attack RBCs and bind components of the complement system to cause massive hemolysis of the transfused blood.

Patients should ideally receive their own blood or type-specific blood products to minimize the chance of a transfusion reaction. Risks can be further reduced by cross-matching blood, but this may be skipped when blood is required for an emergency. Cross-matching involves mixing a sample of the recipient's serum with a sample of the donor's red blood cells and checking if the mixture agglutinates, or forms clumps. If agglutination is not obvious by direct vision, blood bank technicians usually check for agglutination with a microscope. If agglutination occurs, that particular donor's blood cannot be transfused to that particular recipient. In a blood bank it is vital that all blood specimens are correctly identified, so labelling has been standardized using a barcode system known as ISBT 128.

The blood group may be included on identification tags or on tattoos worn by military personnel, in case they should need an emergency blood transfusion. Frontline German Waffen-SS had blood group tattoos during World War II.

Rare blood types can cause supply problems for blood banks and hospitals. For example, Duffy-negative blood occurs much more frequently in people of African origin,[19] and the rarity of this blood type in the rest of the population can result in a shortage of Duffy-negative blood for these patients. Similarly for RhD negative people, there is a risk associated with travelling to parts of the world where supplies of RhD negative blood are rare, particularly East Asia, where blood services may endeavor to encourage Westerners to donate blood.[20]

Pregnant women may carry a fetus with a blood type which is different from their own. In those cases, the mother can make IgG blood group antibodies. This can happen if some of the fetus' blood cells pass into the mother's blood circulation (e.g. a small fetomaternal hemorrhage at the time of childbirth or obstetric intervention), or sometimes after a therapeutic blood transfusion. This can cause Rh disease or other forms of hemolytic disease of the newborn (HDN) in the current pregnancy and/or subsequent pregnancies. Sometimes this is lethal for the fetus; in these cases it is called hydrops fetalis.[21] If a pregnant woman is known to have anti-D antibodies, the Rh blood type of a fetus can be tested by analysis of fetal DNA in maternal plasma to assess the risk to the fetus of Rh disease.[22] One of the major advances of twentieth century medicine was to prevent this disease by stopping the formation of Anti-D antibodies by D negative mothers with an injectable medication called Rho(D) immune globulin.[23][24] Antibodies associated with some blood groups can cause severe HDN, others can only cause mild HDN and others are not known to cause HDN.[21]

To provide maximum benefit from each blood donation and to extend shelf-life, blood banks fractionate some whole blood into several products. The most common of these products are packed RBCs, plasma, platelets, cryoprecipitate, and fresh frozen plasma (FFP). FFP is quick-frozen to retain the labile clotting factors V and VIII, which are usually administered to patients who have a potentially fatal clotting problem caused by a condition such as advanced liver disease, overdose of anticoagulant, or disseminated intravascular coagulation (DIC).

Units of packed red cells are made by removing as much of the plasma as possible from whole blood units.

Clotting factors synthesized by modern recombinant methods are now in routine clinical use for hemophilia, as the risks of infection transmission that occur with pooled blood products are avoided.

Table note1. Assumes absence of atypical antibodies that would cause an incompatibility between donor and recipient blood, as is usual for blood selected by cross matching.

An Rh D-negative patient who does not have any anti-D antibodies (never being previously sensitized to D-positive RBCs) can receive a transfusion of D-positive blood once, but this would cause sensitization to the D antigen, and a female patient would become at risk for hemolytic disease of the newborn. If a D-negative patient has developed anti-D antibodies, a subsequent exposure to D-positive blood would lead to a potentially dangerous transfusion reaction. Rh D-positive blood should never be given to D-negative women of child bearing age or to patients with D antibodies, so blood banks must conserve Rh-negative blood for these patients. In extreme circumstances, such as for a major bleed when stocks of D-negative blood units are very low at the blood bank, D-positive blood might be given to D-negative females above child-bearing age or to Rh-negative males, providing that they did not have anti-D antibodies, to conserve D-negative blood stock in the blood bank. The converse is not true; Rh D-positive patients do not react to D negative blood.

This same matching is done for other antigens of the Rh system as C, c, E and e and for other blood group systems with a known risk for immunization such as the Kell system in particular for females of child-bearing age or patients with known need for many transfusions.

Blood plasma compatibility is the inverse of red blood cell compatibility.[28] Type AB plasma carries neither anti-A nor anti-B antibodies and can be transfused to individuals of any blood group; but type AB patients can only receive type AB plasma. Type O carries both antibodies, so individuals of blood group O can receive plasma from any blood group, but type O plasma can be used only by type O recipients.

Table note1. Assumes absence of strong atypical antibodies in donor plasma

Rh D antibodies are uncommon, so generally neither D negative nor D positive blood contain anti-D antibodies. If a potential donor is found to have anti-D antibodies or any strong atypical blood group antibody by antibody screening in the blood bank, they would not be accepted as a donor (or in some blood banks the blood would be drawn but the product would need to be appropriately labeled); therefore, donor blood plasma issued by a blood bank can be selected to be free of D antibodies and free of other atypical antibodies, and such donor plasma issued from a blood bank would be suitable for a recipient who may be D positive or D negative, as long as blood plasma and the recipient are ABO compatible.[citation needed]

In transfusions of packed red blood cells, individuals with type O Rh D negative blood are often called universal donors. Those with type AB Rh D positive blood are called universal recipients. However, these terms are only generally true with respect to possible reactions of the recipient's anti-A and anti-B antibodies to transfused red blood cells, and also possible sensitization to Rh D antigens. One exception is individuals with hh antigen system (also known as the Bombay phenotype) who can only receive blood safely from other hh donors, because they form antibodies against the H antigen present on all red blood cells.[29][30]

Blood donors with exceptionally strong anti-A, anti-B or any atypical blood group antibody may be excluded from blood donation. In general, while the plasma fraction of a blood transfusion may carry donor antibodies not found in the recipient, a significant reaction is unlikely because of dilution.

Additionally, red blood cell surface antigens other than A, B and Rh D, might cause adverse reactions and sensitization, if they can bind to the corresponding antibodies to generate an immune response. Transfusions are further complicated because platelets and white blood cells (WBCs) have their own systems of surface antigens, and sensitization to platelet or WBC antigens can occur as a result of transfusion.

For transfusions of plasma, this situation is reversed. Type O plasma, containing both anti-A and anti-B antibodies, can only be given to O recipients. The antibodies will attack the antigens on any other blood type. Conversely, AB plasma can be given to patients of any ABO blood group, because it does not contain any anti-A or anti-B antibodies.

Typically, blood type tests are performed through addition of a blood sample to a solution containing antibodies corresponding to each antigen. The presence of an antigen on the surface of the blood cells is indicated by agglutination. An alternative system for blood type determination involving no antibodies was developed in 2017 at Imperial College London which makes use of paramagnetic molecularly imprinted polymer nanoparticles with affinity for specific blood antigens.[31] In these tests, rather than agglutination, a positive result is indicated by decolorization as red blood cells which bind to the nanoparticles are pulled toward a magnet and removed from solution.

In addition to the current practice of serologic testing of blood types, the progress in molecular diagnostics allows the increasing use of blood group genotyping. In contrast to serologic tests reporting a direct blood type phenotype, genotyping allows the prediction of a phenotype based on the knowledge of the molecular basis of the currently known antigens. This allows a more detailed determination of the blood type and therefore a better match for transfusion, which can be crucial in particular for patients with needs for many transfusions to prevent allo-immunization.[32][33]

Blood types were first discovered by an Austrian Physician Karl Landsteiner working at the Pathological-Anatomical Institute of the University of Vienna (now Medical University of Vienna). In 1900, he found that blood sera from different persons would clump together (agglutinate) when mixed in test tubes, and not only that some human blood also agglutinated with animal blood.[34] He wrote a two-sentence footnote:

The serum of healthy human beings not only agglutinates animal red cells, but also often those of human origin, from other individuals. It remains to be seen whether this appearance is related to inborn differences between individuals or it is the result of some damage of bacterial kind.[35]

This was the first evidence that blood variation exists in humans. The next year, in 1901, he made a definitive observation that blood serum of an individual would agglutinate with only those of certain individuals. Based on this he classified human bloods into three groups, namely group A, group B, and group C. He defined that group A blood agglutinates with group B, but never with its own type. Similarly, group B blood agglutinates with group A. Group C blood is different in that it agglutinates with both A and B.[36] This was the discovery of blood groups for which Landsteiner was awarded the Nobel Prize in Physiology or Medicine in 1930. (C was later renamed to O after the German Ohne, meaning without, or zero, or null.[37]) The group AB was discovered a year later by Landsteiner's students Adriano Sturli, and Alfred von Decastello.[38][39]

In 1927, Landsteiner, with Philip Levine, discovered the MN blood group system,[40] and the P system.[41] Development of the Coombs test in 1945,[42] the advent of transfusion medicine, and the understanding of ABO hemolytic disease of the newborn led to discovery of more blood groups. As of 2018, the International Society of Blood Transfusion (ISBT) recognizes 346 blood group antigens which are assigned to 36 blood groups.[2]

A popular belief in Japan is that a person's ABO blood type is predictive of their personality, character, and compatibility with others. This belief is also widespread in South Korea[43] and Taiwan. The theory reached Japan in a 1927 psychologist's report, and the government of the time commissioned a study aimed at breeding better soldiers.[43] Interest in the theory faded in the 1930s. Ultimately, the discovery of DNA in the following decades indicated that DNA instead had an important role in both heredity generally and personality specifically. Interest in the theory was revived in the 1970s by Masahiko Nomi, a broadcaster with a background in law rather than science.[43] The theory is widely accepted in Japanese and South Korean popular culture.[44]

Originally posted here:
Blood type - Wikipedia

September 6, 2017 - By Clifton Ray

Avalon Advisors Llc decreased Comcast Corporation Cmn Class (CMCSA) stake by 3.04% reported in 2016Q4 SEC filing. Avalon Advisors Llc sold 4,568 shares as Comcast Corporation Cmn Class (CMCSA)s stock rose 3.16%. The Avalon Advisors Llc holds 145,911 shares with $10.08M value, down from 150,479 last quarter. Comcast Corporation Cmn Class now has $194.05B valuation. The stock increased 1.23% or $0.5 during the last trading session, reaching $41.17. About 14.24M shares traded. Comcast Corporation (NASDAQ:CMCSA) has risen 28.96% since September 6, 2016 and is uptrending. It has outperformed by 12.26% the S&P500.

Neuralstem, Inc. is a clinical-stage biopharmaceutical company. The company has market cap of $13.81 million. The Firm is engaged in research, development and commercialization of central nervous system therapies based on its human neuronal stem cells and its stem-cell derived small molecule compounds. It currently has negative earnings. The Firm has approximately three assets: its NSI-189 small molecule program, its NSI-566 stem cell therapy program and its chemical entity screening platform.

Investors sentiment decreased to 1.01 in Q4 2016. Its down 11.82, from 12.83 in 2016Q3. It turned negative, as 58 investors sold CMCSA shares while 518 reduced holdings. 123 funds opened positions while 431 raised stakes. 1.89 billion shares or 0.35% more from 1.88 billion shares in 2016Q3 were reported. Quantitative Investment Mgmt Ltd Liability Co reported 0.19% in Comcast Corporation (NASDAQ:CMCSA). 88 were reported by Sun Life Incorporated. Moreover, Twin Tree Mngmt LP has 0.01% invested in Comcast Corporation (NASDAQ:CMCSA) for 15,085 shares. North Carolina-based Bb&T has invested 0.48% in Comcast Corporation (NASDAQ:CMCSA). Wetherby Asset Mngmt owns 38,194 shares or 0.52% of their US portfolio. Fiduciary Wi has invested 4.13% of its portfolio in Comcast Corporation (NASDAQ:CMCSA). Janus Capital Mgmt Limited Company has 18.62M shares for 1.08% of their portfolio. Roberts Glore Co Il invested in 5,382 shares or 0.26% of the stock. Tower Bridge Advsrs reported 65,524 shares or 0% of all its holdings. Van Hulzen Asset Mngmt Limited Liability has 274,360 shares. Pacad Inv accumulated 138,501 shares. Dumont & Blake Invest Advsr Lc stated it has 0.5% in Comcast Corporation (NASDAQ:CMCSA). The New Hampshire-based Tru Advisors Ltd has invested 3.17% in Comcast Corporation (NASDAQ:CMCSA). Grisanti Mgmt Ltd Com reported 189,525 shares. Delphi Management Inc Ma invested in 32,962 shares.

Among 26 analysts covering Comcast Corporation (NASDAQ:CMCSA), 21 have Buy rating, 1 Sell and 4 Hold. Therefore 81% are positive. Comcast Corporation had 56 analyst reports since July 27, 2015 according to SRatingsIntel. As per Monday, January 4, the company rating was maintained by Macquarie Research. The stock of Comcast Corporation (NASDAQ:CMCSA) earned Buy rating by Pivotal Research on Thursday, January 26. Telsey Advisory Group maintained Comcast Corporation (NASDAQ:CMCSA) on Tuesday, January 24 with Outperform rating. The firm has Buy rating given on Wednesday, May 4 by Goldman Sachs. The stock of Comcast Corporation (NASDAQ:CMCSA) earned Buy rating by Oppenheimer on Thursday, July 27. The stock has Buy rating by Macquarie Research on Wednesday, July 5. Nomura maintained Comcast Corporation (NASDAQ:CMCSA) rating on Monday, June 27. Nomura has Buy rating and $73 target. The firm has Buy rating by Pivotal Research given on Tuesday, September 27. The stock of Comcast Corporation (NASDAQ:CMCSA) earned Buy rating by Wunderlich on Wednesday, September 16. Suntrust Robinson initiated the stock with Neutral rating in Wednesday, November 11 report.

Since March 20, 2017, it had 0 buys, and 6 selling transactions for $12.52 million activity. 20,572 shares valued at $762,193 were sold by BLOCK ARTHUR R on Wednesday, March 22. The insider BURKE STEPHEN B sold $10.07 million. On Thursday, May 25 BACON KENNETH J sold $303,713 worth of Comcast Corporation (NASDAQ:CMCSA) or 7,500 shares.

Avalon Advisors Llc increased Intl Business Machines Corp Cm (NYSE:IBM) stake by 65,901 shares to 239,076 valued at $39.68 million in 2016Q4. It also upped Chevron Corporation Cmn (NYSE:CVX) stake by 27,633 shares and now owns 377,867 shares. Asml Holding N V N Y Registry (NASDAQ:ASML) was raised too.

About 121,853 shares traded. Neuralstem, Inc. (CUR) has risen 3.35% since September 6, 2016 and is uptrending. It has underperformed by 13.35% the S&P500.

Ratings analysis reveals 100% of Neuralstems analysts are positive. Out of 2 Wall Street analysts rating Neuralstem, 2 give it Buy, 0 Sell rating, while 0 recommend Hold. CUR was included in 2 notes of analysts from August 29, 2016. The rating was initiated by Roth Capital with Buy on Monday, August 29. The rating was initiated by Aegis Capital on Monday, November 7 with Buy.

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Avalon Advisors Has Decreased Its Comcast Cmn Class (CMCSA) Position; Neuralstem (CUR)'s Sentiment Is 0 - High Point Observer

In developing fetuses, infection by the Zika virus can result in devastating neurological damage, most notably microcephaly and other brain malformations. In a new study, published today in The Journal of Experimental Medicine, researchers at the University of California San Diego School of Medicine and Washington University School of Medicine in St. Louis report the virus specifically targets and kills brain cancer stem cells.

The findings suggest the lethal power of the virus notorious for causing infected babies to be born with under-sized, misshapen heads could be directed at malignant cells in adult brains. Doing so might potentially improve survival rates for patients diagnosed with glioblastomas, the most common and aggressive form of brain cancer, with a median survival rate of just over 14 months after diagnosis.

The Zika virus specifically targets neuroprogenitor cells in fetal and adult brains. Our research shows it also selectively targets and kills cancer stem cells, which tend to be resistant to standard treatments and a big reason why glioblastomas recur after surgery and result in shorter patient survival rates, said Jeremy Rich, MD, professor of medicine at UC San Diego School of Medicine. Rich is co-senior author of the study with Michael S. Diamond, MD, PhD, professor, and Milan G. Chheda, MD, assistant professor, both at Washington University School of Medicine in St. Louis.

Transmission electron microscope image of negative-stained, Fortaleza-strain Zika virus (red), isolated from a microcephaly case in Brazil. Image courtesy of NIAID.

This year, more than 12,000 Americans will be diagnosed with glioblastomas, according to the American Brain Tumor Association. Among them: U.S. Senator John McCain, who announced his diagnosis in July. They are highly malignant. The two-year survival rate is 30 percent.

Standard treatment is aggressive: surgery, followed by chemotherapy and radiation. Yet most tumors recur within six months, fueled by a small population of glioblastoma stem cells that resist and survive treatment, continuing to divide and produce new tumor cells to replace those killed by cancer drugs.

For Zhe Zhu, MD, PhD, a postdoctoral scholar in Richs lab and first author of the study, the hyper-reproductive capabilities of glioblastoma stem cells reminded him of neuroprogenitor cells, which fuel the explosive growth of developing brains. Zika virus specifically targets and kills neuroprogenitor cells.

So Zhu, with Rich, Diamond, Chheda and other collaborators, investigated whether the Zika virus might also target and kill cultured glioblastoma stem cells derived from patients being treated for the disease. They infected cultured tumors with one of two strains of the virus. Both strains spread through the tumors, infecting and killing stem cells while largely avoiding other tumor cells.

The findings, the authors said, suggest that chemotherapy-radiation treatment and a Zika infection appear to produce complementary results. Standard treatment kills most tumor cells but typically leaves stem cells intact. The Zika virus attacks stem cells but bypasses ordinary tumor cells.

We see Zika one day being used in combination with current therapies to eradicate the whole tumor, said Chheda, an assistant professor of medicine and of neurology at Washington University School of Medicine.

To find out whether the virus could boost treatment efficacy in a live animal, researchers injected either the Zika virus or a saltwater placebo directly into glioblastoma tumors in 18 and 15 mice, respectively. Two weeks after injection, tumors were significantly smaller in the Zika-treated mice, who survived significantly longer than those given the placebo.

The scientists note that the idea of injecting a virus notorious for causing brain damage into patients brains seems alarming, but they say Zika may prove a safe therapy with further testing because its primary target neuroprogenitor cells are rare in adult brains. The opposite is true of fetal brains, which is part of the reason why a Zika infection before birth produces widespread and severe brain damage while a normal Zika infection in adults typically causes mild symptoms or none at all.

The researchers also conducted studies of the virus using brain tissue from epilepsy patients that showed the virus does not infect non-cancerous brain cells.

As an additional safety feature, the research team introduced two mutations that weakened the viruss ability to combat natural cellular defenses against infection, reasoning that while the mutated virus would still be able to grow in tumor cells, which have a poor anti-viral defense system, it would be quickly eliminated in healthy cells with a robust anti-viral response.

When they tested the mutated viral strain and the original parental strain in glioblastoma stem cells, they found that the original strain was more potent, but that the mutant strain also succeeded in killing the cancerous cells.

Were going to introduce additional mutations to sensitize the virus even more to the innate immune response and prevent the infection from spreading, said Diamond, a professor of molecular microbiology, pathology and immunology. Once we add a couple more, I think its going to be impossible for the virus to overcome them and cause disease.

Co-authors of the study include: Matthew Gorman, Estefania Fernandez, Lisa McKenzie, Jiani Chai, Justin M. Richner, and Rong Zhang, Washington University, St. Louis; Christopher Hubert, and Briana Prager, Cleveland Clinic; Chao Shan, and Pei-Yong Shi, University of Texas Medical Branch; and Xiuxing Wang, UC San Diego.

Funding for this research came, in part, from the National Institutes of Health (R01 AI073755, R01 AI104972, CA197718, CA154130, CA169117, CA171652, NS087913, NS089272), the Pardee Foundation, the Concern Foundation, the Cancer Research Foundation and the McDonnell Center for Cellular and Molecular Neurobiology of Washington University.

Read more:
Zika Virus Targets and Kills Brain Cancer Stem Cells - UC San Diego Health

Shares of US Stem Cell Inc (USRM) opened the last session at 0.0200, touching a high of 0.0200 and a low of 0.0200 , yielding a change of0.0011. The latest reading places the stock below the Ichimoku cloud which indicates negative momentum and a potential sellsignal for the equity.

The Ichimoku cloud is a favorite technical indicator used primarily in Asian markets. The cloud is one of the only indicators that is both forward and backward looking. The cloud produces better levels of support and resistance and is a breakout traders best friend. The cloud is also one of the easiest indicators to use. Any trader, regardless of skill level or expertise, can use the cloud to quickly and efficiently analyze any product on any time frame. The cloud shines in the fact that it can be universally applied to any trading plan by any trader.

It is a type of chart used in technical analysis to display support and resistance, momentum, and trend in one view. TenkanSen and KijunSen are similar to moving averages and analyzed in relationship to one another. When the shorter term indicator, TenkanSen, rises above the longer term indicator, KijunSen, the securities trend is typically positive. When TenkanSen falls below KijunSen, the securities trend is typically negative. TenkanSen and KijunSen as a group are then analyzed in relationship to the Cloud, which is composed of the area between Senkou A and Senkou B.A multi-faceted indicator designed to give support/resistance levels, trend direction, and entry/exit points of varying strengths. General theory behind this indicator states that if price action is above the cloud, the overall trend is bullish, and if below the cloud, the overall trend is bearish. There are also moving averages (the Tenkan and Kijun lines) which act like the MACD crossover signals with the Tenkan crossing from underneath the Kijun as a bullish signal, while crossing overhead giving a bearish signal.

It is no secret that most investors have the best of intentions when diving into the equity markets. Making sound, informed decisions can help the investor make the most progress when dealing with the markets. Often times, investors may think they have everything in order, but they still come out on the losing end. Investors may need to figure out ways to keep emotion out of stock picking. Sometimes trading on emotions can lead to poor results. Making hasty decisions and not paying attention to the correct data can lead to poor performing portfolios in the long-term.

Checking on some popular technical levels, US Stem Cell Inc (USRM) has a 14-day Commodity Channel Index (CCI) of -84.33. The CCI technical indicator can be employed to help figure out if a stock is entering overbought or oversold territory. CCI may also be used to help discover divergences that may signal reversal moves. A CCI closer to +100 may provide an overbought signal, and a CCI near -100 may provide an oversold signal.

Tracking other technical indicators, the 14-day RSI is presently standing at 38.60, the 7-day sits at 38.88, and the 3-day is resting at 48.14 for US Stem Cell Inc (USRM). The Relative Strength Index (RSI) is a highly popular technical indicator. The RSI is computed base on the speed and direction of a stocks price movement. The RSI is considered to be an internal strength indicator, not to be confused with relative strength which is compared to other stocks and indices. The RSI value will always move between 0 and 100. One of the most popular time frames using RSI is the 14-day.

Moving averages have the ability to be used as a powerful indicator for technical stock analysis. Following multiple time frames using moving averages can help investors figure out where the stock has been and help determine where it may be possibly going. The simple moving average is a mathematical calculation that takes the average price (mean) for a given amount of time. Currently, the 7-day moving average is sitting at 0.02.

Lets take a further look at the Average Directional Index or ADX. The ADX measures the strength or weakness of a particular trend. Investors and traders may be looking to figure out if a stock is trending before employing a specific trading strategy. The ADX is typically used along with the Plus Directional Indicator (+DI) and Minus Directional Indicator (-DI) which point to the direction of the trend. The 14-day ADX for US Stem Cell Inc (USRM) is currently at 69.43. In general, and ADX value from 0-25 would represent an absent or weak trend. A value of 25-50 would support a strong trend. A value of 50-75 would signify a very strong trend, and a value of 75-100 would point to an extremely strong trend.

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US Stem Cell Inc (USRM) Holds Negative Momentum As Price is Below the Cloud - Rockville Register

Scott McIntyre calls himself a walking miracle, and he wants to tell the world about it.

I was given three to six months to survive and Im 16 months in remission, said the 53-year-old South Bend man. I would love to get the story out and let people have hope. Dont give up. You never know.

On Friday, a University of Chicago Medicine marketing team shot video and still images of Scott at Shamrock Truck Sales, the semi-truck sales and service business he co-owns near LaPaz. His face will adorn billboards, digital and print ads in Chicagoland and northwest Indiana as soon as the U.S. Food and Drug Administration approves what UCM is calling a revolutionary breakthrough in cancer treatment.

If that FDA approval comes and UCM is preparing for it to come very soon UCM will have one of the only facilities in the Midwest certified to administer chimeric antigen receptor T-cell infusion, or CAR T-cell, a newer form of immunotherapy.

Video: CAR T treatment gives hope in cancer fight

In CAR T-cell therapy, a type of white blood cell called T-cells are extracted from the patients blood and modified in the lab to recognize specific cancer cells. These supercharged T-cells are then infused back into the patient, where they search out and destroy cancer cells.

The therapy, often described as a living drug because it is customized with each patients T-cells, will be marketed as Kymriah by Swiss pharmaceutical maker Novartis.

Scott was excited to hear news Wednesday that the FDA approved the same treatment for a form of childhood leukemia, meaning, he hopes, that it won't be long before it's approved for his form of cancer, diffuse large B-cell lymphoma. The FDA called the approval "historic" because it marks the first cell-based gene therapy approved in the United States.

Scott is one of 130 patients nationally in the clinical trial for his form of lymphoma, and he was the first to receive the treatment at UCM. That happened in May 2016, when he had exhausted all other options.

Scott has been feeling good for just less than a year. Chemotherapy has taken his hair three times but he has a full head of it once again. He can play an entire round of golf with his son. An avid Notre Dame football fan and season ticket holder, he had to miss each game in 2015, but plans to attend every game this season.

In May 2013, Scott noticed a painful growth in his groin area. His family doctor, Dr. Joseph Caruso, said he had developed a swollen lymph node, which could have resulted from his body trying to fight off an infection. Caruso asked him if he had recently had an infection, and Scott recounted recently stepping on a rusty nail while the roof on his home was being replaced. Caruso prescribed an antibiotic and the swelling seemed to go away.

But four months later, while in the shower, Scott noticed another lump under his arm. He went back to Caruso, who referred him to South Bend-based Beacon Health System oncologist Dr. Thomas Reid. After some scans, Reid diagnosed Stage 3 lymphoma.

Reid administered the standard treatment, four cycles of a chemotherapy regimen known as R-CHOP, an effective but highly toxic blend of drugs causing severe side effects. The fourth cycle had to be delayed because he developed appendicitis, and it was tougher than the first three.

After all of that, the cancer started growing again just two months later.

Reid referred him to Dr. Sonali Smith, professor of medicine and director of UCMs lymphoma program. Smith and her team knew the CAR T-cell therapy was being investigated in a few select centers. Their short-term goal was to keep him alive until they could be cleared to administer the clinical trial.

In February 2015, Scott received a stem-cell transplant, which went smoothly. But three months later, the cancer again started growing. Participation in two more clinical trials and some precisely targeted radiation therapy bought a little more time, but by late 2015, his lymphoma was gaining on him.

Then, in early February 2016, the UCM team received the go-ahead for the CAR T-cell treatment and began harvesting his T cells, a process that resembles dialysis. Scott said another patient had been slated to receive the treatment first, but that patient died.

It was during an appointment in May 2016, just a week before the treatment, that Scott first grasped how close he was to dying. Smith told him the treatment could cause severe side effects, including death. Five people in the trial had died.

I said, I understand. What other options do I have? Scott recalled. She says, Oh youve already surpassed all expectations. I said, What do you mean by that? And thats when she said, after the stem cell, if it comes back, life expectancy is six months. It was a rough day. On the way home I was pretty shaken up.

A little after 9:30 a.m. on May 18, 2016, Scott, sporting a Notre Dame baseball cap, was prepared for the treatment. Carefully observing was Dr. Michael Bishop, professor of medicine and director of the Hematopoietic Cellular Therapy Program at UCM, and about a dozen members of his team. A technician brought in his modified T-cells, thawed them out and infused them into Scott intravenously.

Ten minutes later, the treatment was finished. Afterward, he and his wife Cindy spent 28 days in the hospital and then were required to live in an apartment within 10 minutes of the university hospital. They were allowed to move back home to South Bend in July, about two months after the treatment.

Its incredible, Cindy said of Scotts recovery thus far. We did not realize what we were getting into, all of the risks, until days before. She (Dr. Smith) may have mentioned it but it didnt sink in. We both realized that win, lose or draw, theyre going to learn so much, just from how he responds to it.

Cindy praised how well Drs. Reid and Smith worked together between South Bend and Chicago, and how they told them just enough to be informed without telling them so much that they panicked.

She said, theres this trial, Cindy said. This is for you. You were designed for this trial and it was designed for you. We just have to keep you going until we can give it to you.

The treatment was on a Wednesday. By Friday night, his first fever came and it wasnt a surprise. Once they enter the body, each T cell multiplies rapidly, producing thousands of offspring. Then they launch a vigorous assault. All of that warfare occurring inside the body can cause severe flu-like symptoms: fever, swelling, low blood pressure.

On Sunday his fever spiked to 104 degrees. They packed him in ice around his neck and under his arms, and managed to break the fever without sending him into intensive care.

He also experienced some neurological effects, including tremors, cognitive delays and blurred vision.

Now, more than a year later, Smith still wants to see Scott every three months, and he remains very susceptible to infections because his immunity will always be compromised not from the CAR T-cell but from all of the chemotherapy. He still has some swelling because the scar tissue from three surgeries restricts the flow of lymphotic fluids.

I feel it all the time and I have very limited range of movements but it doesnt stop me, he said.

Unless the lawn needs to be mowed, then it really bothers him, she said. Some things will never change.

She said she never imagined she had married a pioneer.

I knew I had married somebody very unique, very special, but definitely not a pioneer, she said. He was the last person you ever thought would be sick. Doesnt drink. Doesnt smoke. Never had ventured on the wild side. This wasnt supposed to happen.

So far the FDA has only approved T-cell treatments for blood cancers, such as lymphoma and leukemia, but not solid tumor cancers, such as breast and colon cancer, which kill many more people. But Bishop of UCM said that day is coming. He expects those clinical trials to begin within a year or two, and receive FDA approval within about five years.

Its very exciting, Bishop said. The technology is a little more complicated but it has the potential to treat a broad spectrum of cancers. Ive been doing this for 25 years and this is one of the most significant advances Ive seen in my career.

Meanwhile, Scott will keep telling his story of hope to everyone he can, including himself. Bishop said Scott's cancer has a 10- to 20-percent chance to recur.

Youre still thinking that the other shoe can drop, Scott said. The mantra I use when negative thoughts enter my head is, Alright Scott, are you giving up? No. Are you quitting? No. Then shut up. I dont know if that will ever go away.

Read the original:
South Bend man a 'walking miracle' after cancer treatment breakthrough - South Bend Tribune

AsianScientist (Aug. 30, 2017) - In a study published in Cell Stem Cell, scientists in Japan and Switzerland have found that bacterial infections can stress blood-producing stem cells in the bone marrow and reduce their ability to self-replicate.

When a person becomes infected with a virus or bacteria, immune cells in the blood or lymph react to the infection. Some of these immune cells use sensors on their surfaces, called Toll-like receptors (TLR), to distinguish invading pathogens from molecules that are expressed by the host. By doing so, they can attack and ultimately destroy pathogens thereby protecting the body without attacking host cells.

Bone marrow contains hematopoietic stem cells which create blood cells, such as lymphocytes and erythrocytes, throughout the lifetime of an individual. When infection occurs, a large number of immune cells are activated and consumed. Hence, it is necessary to replenish these immune cells by increasing blood production in bone marrow.

Recent studies have revealed that immune cells are not the only cells that detect the danger signals associated with infection. Hematopoietic stem cells also identify these signals and use them to adjust blood production. However, little was known about how hematopoietic stem cells respond to bacterial infection or how it affected their function.

In this study, researchers from Kumamoto University and the University of Zurich analyzed the role of TLRs in hematopoietic stem cells upon bacterial infection, given that both immune cells and hematopoietic stem cells have TLRs.

To generate a model of bacterial infection, researchers injected one of the key molecules found in the outer membrane of gram negative bacteria and known to cause sepsislipopolysaccharide (LPS)into lab mice. They then analyzed the detailed role of TLRs in hematopoietic stem cell regulation by combining genetically modified animals that do not have TLR and related molecules, or agents that inhibit these molecules.

The results showed that LPS spread throughout the body, with some eventually reaching the bone marrow. This stimulated the TLRs of the hematopoietic stem cells and induced them to proliferate. They also discovered that while LPS promoted stem cell proliferation, it also induced stressed the stem cells, impairing their ability to successfully self-replicate and resulting in diminished blood production. Similar results were obtained after infection with Escherichia coli bacteria.

Fortunately we were able to confirm that this molecular reaction can be inhibited by drugs, said Professor Hitoshi Takizawa of Kumamoto University who led the study. The medication maintains the production of blood and immune cells without weakening the immune reaction against pathogenic bacteria. It might be possible to simultaneously prevent blood diseases and many bacterial infections in the future.

The article can be found at: Takizawa et al. (2017) Pathogen-Induced TLR4-TRIF Innate Immune Signaling in Hematopoietic Stem Cells Promotes Proliferation but Reduces Competitive Fitness.

Source: Kumamoto University.Disclaimer: This article does not necessarily reflect the views of AsianScientist or its staff.

Originally posted here:
Bacterial Infection Stresses Blood Stem Cells - Asian Scientist Magazine

Spinal injuries are oftenpermanent, but new research suggests such injuries may be healed, at least in part.Researchers were able to stimulate limb function in paralyzed mice by implanting human stem cells into theirspinal cords. We're not close to repeating the test in people, but the study shows it may be possible some day with further research.

The University of California-San Diego team grafted human neural stem cells (NSCs) into the spinal cord injuries of mice who were purposely injuredto impair the use of their front legs. The stem cells grew slowly, yet steadily, over the course of 18 months, retaining their original function despite being in a strange and challenging environment for an extended period of time. Whats more, eventually the rodents were able to use their front legs again.

"The bottom line is that clinical outcome measures for future trials need to be focused on long time points after grafting," said study researcher Mark Tuszynskiin a recent statement. Relying on shorter time frames might produce misleadingly negative results considering how long it takes neural stem cells to develop, he added.

For the study, the team used H9 human NSCs, which are a type of stem cell derived from human embryonic stem cells, as commonly used in scientific research, the statement reported. They then grafted these human stem cells into the spinal injuries of mice. The researchers observed the rodents recovery over the course of 18 months, noting that significant cellgrowth did occur soon after grafting, and continued up to a year after the initial implantation.

The most important observation was that these cells were able to continue to do what they were designed to doregrow neural cellsdespite the fact that they were transplanted into an entirely different species. This suggests the cells have resilience and similar experiments mayalso work in human subjects.

Before you get too excited about these results, the researchers emphasized that there were a number of caveats. First, humans and mice are entirely different species, and though the results observed in the rodents are promising, we don't know if they could be repeated in people.

Also, the researchers observed that some astrocytes, star-shaped neural cells associated with electrical impulse transmission, did migrate from the original implantation site to other areas of the rodents. These brain cells are classified as glial cells, which are noted to lead to devastating and difficult to treat cancers when they are dysregulated, Harvard University reported. However, there were no tumors or abnormal growths observed in the mice in the study and the researchers are trying to figure out way to make sure cancer doesn't develop.

Ultimately, the team believe that these results stand as a good foundation on which to buildfurther research.

Success, it would seem, will take time," concluded Tuszynski.

Source: Lu P, Ceto S, Wang Y, et al. Prolonged human neural stem cell maturation supports recovery in injured rodent CNS. The Journal of Clinical Investigation . 2017

See the original post:
Stem Cell Graft Repairs Spinal Cord Injury, Helps Paralyzed Mice Move Again - Medical Daily

A human stem cell replicating itself.

Hal X. Nguyen and Aileen J. Anderson

But when it comes to spinal cord injuries, the healing process goes awry.

Immune cells rush in and cause a scar that blocks the ability of neurons to regrow and reconnect. However, recent studies have shown that the immune system can also aid regeneration.

The immune system has both positive and a negative impact what it does is really context specific, says Jan Kaslin, who studies neural regeneration in zebrafish at the Australian Regenerative Institute of Medicine in Melbourne, Australia.

Stem cells provide a great hope for damaged spinal cords and brain injury but it has not been clear on how the immune system may affect the regrowth.

Now a new study has taken a look at how stem cells and the immune system interact in the repair of the spinal cord. Led by Aileen Anderson from the University of California, Irvine and published in the Journal of Neuroscience, the study suggests that whether or not the immune system hinders or helps transplanted stem cells to regrow lost tissue may be influenced by the presence of certain kinds of immune cells.

The study used stem cells derived from human foetal brain tissue and transplanted them into mice with a wound in their spinal cord. They then blocked the invasion of a specific population of immune cells called neutrophils and observed how well the wound was repaired by transplanted stem cells.

In contrast to earlier research, Andersons team found with that with neutrophils out of the way the transplanted stem cells behaved differently and were more able to repair the damage.

This is the first data to show that the immune environment can be altered to allow stem cell populations to perform better in terms of restoring function, according to Anderson.

Can other immune cells be manipulated to increase the effectiveness of stem cell transplantation in spinal cord regeneration?

These findings are an important of piece of the puzzle, says Kaslin, that may significantly improve future stem cell transplantation approaches.

Originally posted here:
Immune cells may prevent stem cell growth in spinal cord repair - Cosmos