StemCell Therapy

Hospitals will begin contacting people over the age of 16, who have very weakened immune systems due to certain medical conditions, to offer them an additional Covid-19 vaccine.

Hospitals will identify the people who need an additional dose, the HSE said. You dont need to register or contact anyone.

People who need an additional dose will receive a text message with an appointment for their vaccine.

These additional doses will be given through a HSE vaccination centre near you, or your hospital if you are an inpatient. GPs may also vaccinate some people.

The HSE said this would happen from this week for those aged 16 and over.

As the vaccination programme for 12- to 15-year-olds started later, those aged 12 to 15 who have been identified for an additional dose will be offered an appointment at a later date.

This is to facilitate the two-month minimum interval from their last dose of Covid-19 vaccine.

Dr Colm Henry, Chief Clinical Officer of the HSE, said: It has been shown that people with weakened immune systems do not generate a full immune response to their first two doses of the Covid-19 vaccine.

This additional dose we are offering will mean they will get the maximum benefit from their primary vaccination course, giving them better protection against the serious effects of Covid-19.

It follows recommendations from the National Immunisation Advisory Committee (Niac) that people aged 12 years and older, who are immunocompromised at the time of vaccination due to disease or treatment, should receive one additional dose of a Covid-19 vaccine.

They will be offered a single dose of either Pfizer/BioNTech Covid-19 vaccine or Moderna vaccine. They need to continue to follow anti-Covid protection measures.

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Over-16s with weakened immune system to be offered third jab - Independent.ie

A new, sustainable immune health ingredient derived from carrot pomace is set to launch at the SupplySide West trade show in Las Vegas this October. Introduced by Dutch ingredients company NutriLeads (Wageningen, the Netherlands), BeniCaros is an ingredient suited for both dietary supplements and functional foods and beverages.

BeniCaros is a soluble fiber produced from upcycled carrot pomace, which is a byproduct of carrot juice production, making it a sustainable ingredient that is also label friendly.

NutriLeadss proprietary extraction process ensures the ingredient is rich in the immune-supporting polysaccharide rhamnogalacturonan-I (RG-I). The company says BeniCaros was shown in a clinical trial to help the immune system become more responsive to potential challenges as well as to stimulate beneficial gut microorganisms and their metabolites, at a daily dose of 0.3 grams. The firm says there is robust preclinical and clinical research showing the efficacy of BeniCaros.

In a press release, Ruud Albers, PhD, chief scientific officer for NutriLeads, said, I have been active in this field for more than 25 years and have never seen another ingredient with such distinctive data supporting its effectiveness. He added, There are many immune health ingredient options out there but very few that work like BeniCaros and even fewer that work with the same efficacy to support immune function.

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Immune health ingredient from carrots debuting at SupplySide West 2021 - Nutritional Outlook

Lots of people these days are asking what they feel is a completely legitimate question, "Is it safe to get the COVID vaccine and get my flu shot?" The quick answer is: Yes. ABSOLUTELY...According to the Centers For Disease Control and Prevention.

WWLP/News 22 Springfield is reporting that, according to the CDC,its safe for other vaccines to be administered at the same time as the COVID-19 vaccine.

This new guidance is a definite change from previous CDC recommendations which said that other vaccinations should not be administered within a 2-week window before or after the COVID-19 vaccine.

With colder weather on the horizon, many people are starting to think about the flu shot in addition to COVID vaccinations. But there are also many who are wondering, after last year's very mild flu season, if getting a flu shot is even essential.

Health officials caution that substantial flu activity happening at the same time as COVID-19 activity could seriously overwhelm our health care systems.

The Centers For Disease Control and Prevention estimates that every year, anywhere between 12,000 to 61,000 people die due to the flu. Last year, however, the combination of social distancing and wearing masks prevented the majority of cases.

In summation, you can get your flu shot at the same time you get your COVID vaccination or vice versa. The CDC recommends getting the flu vaccine by the end of October and to get the COVID-19 vaccine as soon as you can.

For more information, check out WWLP's website here.

KEEP READING: See 25 natural ways to boost your immune system

Here are some tips for self-care during the pandemic:

KEEP READING: 15 Natural Ways to Improve Your Sleep

Read the original here:
Health Officials Addressing Concerns Over Flu Shot, COVID Shot - Live 95.9

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A patient at The Ottawa Hospitals General campus has been diagnosed with legionellosis, forcing the hospital to turn off the water supply to a portion of the hospital in order to disinfect it.

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In a brief statement, the hospital said the water system at the General campus is undergoing hyperchlorination.

Ottawa Public Health said its infection prevention and control team was made aware of one case of legionellosis affecting a patient at the General campus and has worked closely with the hospital, locating the source and ensuring steps are taken to protect patients and staff.

There have been no further reports of legionellosis infection at The Ottawa Hospital, according to Ottawa Public Health. All cases must be reported to public health for follow up with the patient as well as investigation.

Ottawa Public Health performed environmental testing, with support from Public Health Ontario. The hospital continues to work with public health and has hired its own environmental consultants to lead the remediation.

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The illness is a form of pneumonia caused by exposure to Legionella, the common name for the bacterium L. pneumophila. It lives in water and may infect some people who inhale water droplets from a contaminated water supply, although most people will be unaffected.

For people with healthy immune systems the risk is low, but for those that have a suppressed immune system, there is a greater risk of infection, said the hospital.

The hospital said Tuesday it immediately turned off the water on the unit where the patient was, and the issue is being addressed.

During this time, water will be temporarily unavailable on certain units. We are working with care teams to ensure alternative water sources are available during this time, to minimize the impact on patient care.

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Rachel Muir, The Ottawa Hospital bargaining unit president with the Ontario Nurses Association, said the water has been shut off between the hospitals fourth and eight floors since the case of legionellosis was identified last Friday. She said the water isnt expected to be back on until later this week, possibly the weekend.

She said staff was notified last Friday that there was a case of legionellosis and the source was located in the water system in the unit.

Muir said drinking water and ice are being supplied to all the units affected and wipes and clean water are being provided for cleaning.

Patients will be freshened up but not showered until the system is back on.

Muir called it an inconvenience but said the hospital is working hard to minimize that and keep staff and patients informed.

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The hospital said it is working closely with public health and environmental experts to remediate the issue and to turn the water back on as soon as possible.

Legionnaires disease, named after a severe pneumonia outbreak at a convention centre in the U.S. in 1976, is the most common form of legionellosis. It can also cause less severe illness. According to the U.S. Centers for Disease Control and Prevention, healthy people usually get better after being sick with Legionnaires disease, but hospitalization is often required. About 15 out of 100 people who get it will die from the infection.

Many hospital patients have compromised immune systems because of illness, age or treatment. The General campus is home to The Ottawa Hospital Cancer Program where many patients are undergoing treatment that affects their immune systems ability to fight off infection.

Safety is our top priority, and we will continue to update patients and families to ensure they have all the information they need, said the hospital.

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Hospital disinfecting water system after patient at the General diagnosed with legionellosis - Ottawa Citizen

A recent study has found that despite effective antiretroviral therapy, low CD4/CD8 ratios and high CD8 counts are associated with a higher risk of Kaposis sarcoma and non-Hodgkin lymphoma, respectively. This increased risk is particularly present in people living with HIV who have CD4 cell counts above 500.

As expected, virological failure was a strong risk factor for both cancers. Findings are published in Clinical Infectious Diseases.

Kaposis sarcoma is a cancer that forms in the lining of blood and lymph vessels. The tumours can appear as painless purplish spots on the legs, feet or face, in the genital area, mouth or lymph nodes, and may also develop at a later stage in the digestive tract or lungs. The underlying cause of Kaposis sarcoma is infection with a virus called human herpes virus-8 (HHV-8). This virus causes no symptoms in healthy people. However, in people with a damaged immune system CD4 loss, but also an imbalance between CD4 and CD8 cell counts which allows it to multiply, HHV-8 has the potential to trigger Kaposis sarcoma.

Non-Hodgkin lymphoma is a type of cancer that begins in the lymphatic system, which is part of the bodys germ-fighting immune system. In non-Hodgkin lymphoma, lymphocytes grow abnormally and can form tumours throughout the body. Signs and symptoms may include swollen lymph nodes, abdominal pain, persistent fatigue, night sweats, fever, chest pain, coughing or trouble breathing. Non-Hodgkin lymphoma can be induced by the Epstein-Barr virus (EBV), herpes virus-8 (HHV-8) or human T-cell leukaemia/lymphoma virus-1 (HTLV-1) when the damaged immune system cannot regulate them adequately.

A molecule on the surface of some white blood cells. Some of these cells can kill other cells that are infected with foreign organisms.

Lesions on the skin and/or internal organs caused by abnormal growth of blood vessels. In people living with HIV, Kaposis sarcoma is an AIDS-defining cancer.

A type of cancer that starts in the tissues of the lymphatic system, including the lymph nodes, spleen, and bone marrow. In people who have HIV, certain lymphomas, such as Burkitt lymphoma, are AIDS-defining conditions.

A group of lymphomas (cancers of the lymphatic system). The many types of non-Hodgkin lymphoma (NHL) are classified according to how fast the cancer spreads. Although the symptoms of NHLs vary, they often include swollen lymph nodes, fever, and weight loss. Certain types of NHLs, such as Burkitt lymphoma and immunoblastic lymphoma, are AIDS-defining cancers in people with HIV.

A type of lymphoma. Lymphoma is a cancer of a part of the immune system called the lymph system. The first sign of Hodgkin disease is often an enlarged lymph node. The disease can spread to nearby lymph nodes, the lungs, liver, or bone marrow. The exact cause is unknown. See also non-Hodgkin lymphoma.

Despite the widespread use of effective antiretroviral therapy and the resulting long-term viral suppression and CD4 restoration, a higher incidence of Kaposis sarcoma and non-Hodgkin lymphoma persists in people living with HIV, compared to the general population. These events seem to be driven by immune activation and inflammation that even viral suppression may not control.

CD8 cells are part of the immune system: also known as T killer cells, they recognise and destroy cells infected with viruses or bacteria. CD8 cell counts increase in response to acute infections. However, they can remain high in chronic infections such as HIV and respond to treatment more slowly than CD4 cell counts.

The CD4/CD8 ratio is considered a reliable marker of immune activation during successful antiretroviral therapy. Its normal value ranges between 1 and 4. When it is lower than 1 in people with HIV receiving antiretroviral therapy, it correlates with the risk of AIDS-related mortality and non-AIDS defining events, especially cancers.

However, the impact of the CD4/CD8 ratio on the risk of AIDS-defining cancers, such as Kaposis sarcoma and non-Hodgkin lymphoma, had never been studied before.

Dr Fabienne Caby and colleagues from COHERE (Collaboration of Observational HIV Epidemiological Research Europe, composed of several major cohorts) used data from over 50,000 people living with HIV who were receiving effective antiretroviral therapy to assess the impact of the CD4/CD8 ratio on Kaposis sarcoma or non-Hodgkin lymphoma risks in this population. This analysis focused specifically on whether or not this biomarker provided additional information to the CD4 count, which is the usual immunological predictor for both cancers.

As starting antiretroviral therapy with a high CD4 count is more and more common, the investigators conducted a secondary analysis that focused only on people with CD4 cell counts above 500 after they achieved virological control.

To be included in the study, individuals had to be at least sixteen years old, to have started antiretroviral therapy in the 2000-2014 period and to have achieved virological control defined as viral load below 500 copies within nine months after starting their treatment. At least one CD4/CD8 measurement, done in the six months following virological control, was needed.

For both analyses, the baseline was considered as the time of the very first CD4/CD8 ratio measurement within six months after virological control. Individuals with a diagnosis of Kaposis sarcoma or non-Hodgkin lymphoma at baseline or before could not be included in the study.

To better understand the impact of immune factors on the risk of the two cancers, three statistical models were tested, respectively adjusted for the CD4/CD8 ratio; both the CD4 and the CD8 cell counts; and for both the CD4/CD8 ratio and the CD4 cell count. All models were also adjusted for virological failure, demographics and year.

Overall, 57,708 people living with HIV from twenty cohorts in twelve Western European countries were eligible for the study. Men who have sex with men accounted for 49% of these participants, and women for 25%. Most participants were of European origin (69%), whereas 15% were of sub-Saharan origin (5770 women and 2691 men).

At baseline, the median age was 38 years (interquartile range 32-45) and the median CD4 and CD8 counts were 414 (IQR = 296-552) and 936 (IQR = 670-1304), respectively. The median CD4/CD8 ratio was low at 0.43 (IQR = 0.28-0.65) and reached 1 in only 8% of participants. Also, a very low CD4/CD8 ratio (<0.5) was found in 59% of participants.

Finding these low CD4/CD8 ratios in people with a suppressed viral load is not uncommon. As explained above, CD8 cells take time to respond to HIV treatment, except when treatment is started during acute HIV infection.

Participants were followed up for a median of 59 (IQR = 30-96) months from baseline, accounting for 307,700 persons-years. Two years after baseline, the CD4/CD8 ratio was restored to 1 in only 28% of participants (46% of those with a baseline CD4 count over 500).

In the primary analysis, Caby and colleagues found that during follow-up, Kaposis sarcoma and non-Hodgkin lymphoma had been diagnosed in 221 and 187 cases, respectively. This corresponded to incidence rates of 72/100,000 persons-years for the former and to 61/100,000 persons-years (95% CI; 46-76) for the latter. Most cases of Kaposis sarcoma were diagnosed between 2 to 37 months after baseline, whereas non-Hodgkin lymphoma was diagnosed between 7 to 42 months.

Of note, 15% (33/221) of Kaposis sarcoma cases and 12% (23/187) of non-Hodgkin lymphoma cases occurred in a context of virological failure.

The secondary analysis showed that among the 19,133 participants with CD4 cell counts above 500 at baseline, 65 were diagnosed with Kaposis sarcoma and 50 with non-Hodgkin lymphoma. However, this time, occurrence of the two cancers in a context of virological failure amounted to 14/65 cases (21%) of Kaposis sarcoma and 11/50 cases (22%) of non-Hodgkin lymphoma, despite the patients high CD4 cell counts.

What were the risk factors associated with Kaposis sarcoma? In all three models described above, virological failure was the strongest, with a nearly 3-fold higher risk (hazard ratio 2.77 in the third model).

When the CD4/CD8 ratio was looked at as the only immune factor, the lower it was, the higher the risk. When CD4 and CD8 counts were looked at separately, their independent associations with the risk of Kaposis sarcoma were confirmed.

In the third model which was found to be the most accurate CD4 counts and CD4/CD8 ratios were found to be independently associated with Kaposis sarcoma. The better the CD4 restoration was, the lower the risk: hazard ratio from 1.57 with 350 CD4 cells, to 0.71 with 650 CD4 cells, when compared to 500 CD4 cells. Furthermore, the association between the CD4/CD8 ratio and the risk of Kaposis sarcoma was gradual: hazard ratio from 1.18 in participants with a CD4/CD8 ratio of 0.8, to 2.02 in those with a CD4/CD8 ratio of 0.3, when compared to a normal CD4/CD8 ratio of 1.

The investigators highlight that in participants with CD4 cell counts above 500, the association between the CD4/CD8 ratio and the Kaposis sarcoma risk was stronger than that seen in the entire study population. They also found that being a man who has sex with men and being older were associated with a higher Kaposis sarcoma risk.

As observed with Kaposis sarcoma, virological failure was a strong factor for non-Hodgkin lymphoma risk, increasing it two-fold. Contrary to what was seen with Kaposis sarcoma, the CD4/CD8 ratio was not as predictive as the CD4 count for non-Hodgkin lymphoma.

However, the model adjusted for the CD4 and the CD8 counts showed that the risk for non-Hodgkin lymphoma strongly increased when the CD8 count was very high: hazard ratio from 1.61 for 2000 CD8 cells, to 3.14 for 3000 CD8 cells, compared to 1000 CD8 cells. This association was even stronger among participants with CD4 cell counts above 500 at baseline.

The investigators identified being older and male sex as other independent factors associated with a higher non-Hodgkin lymphoma risk.

These results confirm that HIV-related diseases still occur in people living with HIV despite a suppressed viral load and a relative immune response restoration. HIV-related inflammation is reflected in persistently high CD8 cell counts and leads to unbalanced CD4/CD8 ratios, raising the risk of AIDS and non-AIDS-related diseases.

Caby and colleagues say that CD4/CD8 ratios and high CD8 counts may be biomarkers of particular interest to people living with HIV who have high CD4 counts. For those with persisting low CD4/CD8 ratios despite efficient antiretroviral therapy, closer monitoring could be beneficial.

However, they add, further studies are needed to clarify the impact of the CD4/CD8 ratio on the risk of other HIV-related diseases, to know which specific preventative measures could be implemented.

See the article here:
Increased risk of Kaposi's sarcoma with low CD4/CD8 ratios and of non-Hodgkin lymphoma with high CD8 counts despite effective HIV treatment - aidsmap

RESEARCHERS have discovered a "cold environment" in a form of cancer which hides it from the immune system.

The findings mean immunotherapy- an emerging and advanced treatment which triggers the bodys own immune system to attack cancer cells - is unlikely to be effective in treating neuroendocrine tumours, a form of cancer which goes undetected by the immune system.

As a result, attention can now turn to understanding why this type of cancer is not recognised and finding ways to trigger an immune response to enable further treatments to be developed.

In this study, Dr Lulu Tanno, NETs research fellow at the University of Southampton, and her team studied samples of the tumours of 192 patients with pancreatic and small intestinal NETs at University Hospital Southampton.

The results, presented at the European Neuroendocrine Tumours Society, showed neither of these tumours contained any immune cells, known as tumour infiltrating lymphocytes (TILs), compared to hundreds found in the most common form of lung cancer.

Prior to this study very little was known about the quality and significance of the immune (anti-tumour) response in NETs but it is vital we know more with the emergence of immunotherapy as a potential treatment option, explained Dr Tanno.

What we have established is that there is no evidence of immune cells in pancreatic and small intestinal NETs, making it an immunologically cold environment and, therefore, unlikely to respond to current immunotherapy.

NETs are rare types of cancer which are usually found in the pancreas, bowel or lungs but can also develop in other parts of the body.

They arise from cells found throughout the body which form a link between the nervous system and the endocrine system, a collection of glands which produce hormones.

Around 4,000 new cases are diagnosed every year in the UK, though it is thought that a larger number of people are affected but remain undiagnosed as the cancers are slow growing.

If detected early they can often be cured with surgery but, at present, most are diagnosed at a later stage when they have already spread to other parts of the body.

Dr Tannos research programme was founded by the Robert White Legacy Fund and is part-funded by PLANETS Charity, which helps patients with pancreatic, liver, colorectal, abdominal and neuroendocrine cancer by funding patient support groups, innovative treatments and research.

She said NET patients curiosity and enthusiasm for knowing more about their condition was one of the major driving forces behind this research project.

See the article here:
Researchers discover 'cold environment cancer' which hides from the immune system - Daily Echo

As the subject of the 2018 Nobel Prize in Medicine, tumor immunotherapy has proven to be an exciting cancer treatment strategy. Most immunotherapies to date have focused on T cell function; however, more natural killer (NK) cell-based therapies that involve monoclonal antibodies (mAbs) that target tumor antigens are emerging. mAbs have shown clinical success for the treatment of both hematological cancers and previously difficult to treat solid tumors. One fundamental mechanism through which mAbs can kill tumor cells is antibody-dependent cellular cytotoxicity (ADCC). ADCC refers to when mAbs elicit an immune response through the activation of NK cells and is triggered by the bi-specific binding of an antibody to both a NK cell activation receptor (CD16) and a target cancer cell protein antigen. This binding results in the release of cyto-toxic molecules that lead to targeted cancer cell death. While promising, mAbs are potentially immunogenic, can degrade in vivo and experience difficulties trafficking to the site of solid tumors. Furthermore, large doses of the mAb need to be administered intravenously. This increases manufacturing costs, resulting in higher drug prices and limiting general patient accessibility. An approach to utilize tumor immunotherapeutic antibodies directly in vivo using small immune recruiting molecules coined as covalent immune recruiters (CIRs) was developed. CIRs selectively link to naturally abundant serum antibodies and redirect them to the sur-face of tumor cells. The resultant display of tumor coated antibodies activates stimulatory receptors on innate immune cells, such as CD16 on NK cells, and triggers an antitumor immune response. The efficacy of these CIRs as modulators of protein proximity can be characterized by the Octet Bio-Layer Interferometry (BLI) platform. Octet systems are capable of real-time, high-throughput analysis of small molecule and biomolecule binding kinetics under equilibrium conditions. Due to its flexibility and compatibility for alternative assay format arrangements, it is a powerful tool for characterizing the CIR dependent binding equilibrium (e.g., tumor antigen:CIR:Ab) in addition to its use in determining CIR-antibody covalent recruitment kinetics. The label-free and highly sensitive nature of the Octet BLI technology also enables analysis under dilute conditions, conserving expensive biologic reagents and attenuating aggregation phenomena intrinsic to isothermal titration calorimetry (ITC) and fluorescence polarization (FP) assays. Octet systems also present a unique method to simultaneously characterize multiple protein binding and covalent labeling processes and discern reversible binding from a covalent reaction. Octet system can be employed to efficiently characterize CIR binding affinities against both a prostate tumor antigen and human serum antibodies, as well as measure the selective covalent recruitment of these antibodies to the tumor antigen. These assays can accelerate the advancement of lead compounds to in vivo validation studies, and have additional utility in characterizing emerging classes of covalent inhibitor drugs.

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Synthetic Immune Recruitment - A New Way to Fight Tumors - Technology Networks

Every person, every mouse, every dog, has one unmistakable sign of aging: hair loss. But why does that happen?

Rui Yi, a professor of pathology at Northwestern University, set out to answer the question.

A generally accepted hypothesis about stem cells says they replenish tissues and organs, including hair, but they will eventually be exhausted and then die in place. This process is seen as an integral part of aging.

Instead Dr. Yi and his colleagues made a surprising discovery that, at least in the hair of aging animals, stem cells escape from the structures that house them.

Its a new way of thinking about aging, said Dr. Cheng-Ming Chuong, a skin cell researcher and professor of pathology at the University of Southern California, who was not involved in Dr. Yis study, which was published on Monday in the journal Nature Aging.

The study also identifies two genes involved in the aging of hair, opening up new possibilities for stopping the process by preventing stem cells from escaping.

Charles K.F. Chan, a stem cell researcher at Stanford University, called the paper very important, noting that in science, everything about aging seems so complicated we dont know where to start. By showing a pathway and a mechanism for explaining aging hair, Dr. Yi and colleagues may have provided a toehold.

Stem cells play a crucial role in the growth of hair in mice and in humans. Hair follicles, the tunnel-shaped miniature organs from which hairs grow, go through cyclical periods of growth in which a population of stem cells living in a specialized region called the bulge divide and become rapidly growing hair cells.

Sarah Millar, director of the Black Family Stem Cell Institute at the Icahn School of Medicine at Mount Sinai, who was not involved in Dr. Yis paper, explained that those cells give rise to the hair shaft and its sheath. Then, after a period of time, which is short for human body hair and much longer for hair on a persons head, the follicle becomes inactive and its lower part degenerates. The hair shaft stops growing and is shed, only to be replaced by a new strand of hair as the cycle repeats.

But while the rest of the follicle dies, a collection of stem cells remains in the bulge, ready to start turning into hair cells to grow a new strand of hair.

Dr. Yi, like most scientists, had assumed that with age the stem cells died in a process known as stem cell exhaustion. He expected that the death of a hair follicles stem cells meant that the hair would turn white and, when enough stem cells were lost, the strand of hair would die. But this hypothesis had not been fully tested.

Together with a graduate student, Chi Zhang, Dr. Yi decided that to understand the aging process in hair, he needed to watch individual strands of hair as they grew and aged.

Ordinarily, researchers who study aging take chunks of tissue from animals of different ages and examine the changes. There are two drawbacks to this approach, Dr. Yi said. First, the tissue is already dead. And it is not clear what led to the changes that are observed or what will come after them.

He decided his team would use a different method. They watched the growth of individual hair follicles in the ears of mice using a long wavelength laser that can penetrate deep into tissue. They labeled hair follicles with a green fluorescent protein, anesthetized the animals so they did not move, put their ear under the microscope and went back again and again to watch what was happening to the same hair follicle.

What they saw was a surprise: When the animals started to grow old and gray and lose their hair, their stem cells started to escape their little homes in the bulge. The cells changed their shapes from round to amoeba-like and squeezed out of tiny holes in the follicle. Then they recovered their normal shapes and darted away.

Sometimes, the escaping stem cells leapt long distances, in cellular terms, from the niche where they lived.

If I did not see it for myself I would not have believed it, Dr. Yi said. Its almost crazy in my mind.

The stem cells then vanished, perhaps consumed by the immune system.

Dr. Chan compared an animal's body to a car. If you run it long enough and dont replace parts, things wear out, he said. In the body, stem cells are like a mechanic, providing replacement parts, and in some organs like hair, blood and bone, the replacement is continual.

But with hair, it now looks as if the mechanic the stem cells simply walks off the job one day.

But why? Dr. Yi and his colleagues next step was to ask if genes are controlling the process. They discovered two FOXC1 and NFATC1 that were less active in older hair follicle cells. Their role was to imprison stem cells in the bulge. So the researchers bred mice that lacked those genes to see if they were the master controllers.

By the time the mice were 4 to 5 months old, they started losing hair. By age 16 months, when the animals were middle-aged, they looked ancient: They had lost a lot of hair and the sparse strands remaining were gray.

Now the researchers want to save the hair stem cells in aging mice.

This story of the discovery of a completely unexpected natural process makes Dr. Chuong wonder what remains to be learned about living creatures.

Nature has endless surprises waiting for us, he said. You can see fantastic things.

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Losing Your Hair? You Might Blame the Great Stem Cell Escape. - The New York Times

A lung transplant can mean the difference between life and death for people with diseases such as pulmonary fibrosis, chronic obstructive pulmonary disease (COPD) and even severe COVID-19. Yet, recipients of donor lungs must take daily medications to stave off damage caused by their own immune system, which attacks the organs it recognizes as foreigna process known as rejection.

A new University of Michigan Health study, published in the Journal of Clinical Investigation, has identified cells that appear to play a pivotal role in creating the scarring, or fibrosis, characteristic of chronic rejection following a lung transplant.

Almost 15 years ago, Vibha Lama, MBBS, M.S., a professor in the Division of Pulmonary Disease and Critical Care Medicine, and her lab described the presence of stem-cell-like cells, called mesenchymal stromal cells, in lung sample fluid from lung transplant recipients.

We found that even ten years post-transplant, these cells belonged to the donor, not the recipient, she explained. At that time, we had no clue where in the lung they were coming from or what role they played.

To figure this out, her lab generated a mouse model to recreate what happens within a lung transplant recipient. With the model, they followed a transcription factor known as FOXF1 as a sort of trail of breadcrumbs back to the cells original location.

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They discovered that these cells formed a reservoir of stem cells within the bronchovascular bundle deep inside the lung. These bundles contain a bronchus (airway), arteries, connective tissue and other structures and is the part of the lung which connects it to the outside environment.

In this study, explained Lama, who is senior author on the paper, they show that these specific stem cells are interacting with neighboring epithelial cells within that airway niche.

Epithelial cells line and protect the airways and produce a protein known as Sonic hedgehog. Via this protein, epithelial cells signal the stem-cell-like mesenchymal cells, which make up the scaffolding of the lungs, to make FOXF1, a repressor that keeps the stem cells in check.

We are just recently understanding that there are many different kinds of mesenchymal cells in the lung, said Lama. What we describe here is not only are there many kinds of mesenchymal cells, FOXF1 is retained only in these specific stem-cell-like cells.

In the case of lung transplant rejection, Lama hypothesized that immune cells from the recipient attack the epithelial cells which disrupts the balance between them and the mesenchymal cells.

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Because of the damage caused by rejection, the epithelial cells get damaged, Sonic hedgehog is reduced and that interrupts the signaling to the mesenchymal cells to keep quiet, she said. Because of that, these cells start dividing and they lay down more collagen, which leads to fibrotic scarring.

The work sets the stage for more research into the interaction of these cells with epithelial and other cells it their vicinity to further characterize what happens during chronic rejection and potentially how to prevent it. Furthermore, discovery of these cells is also important in understanding other airway diseases like asthma and COPD.

Paper cited: Transcription factor FOXF1 identifies compartmentally distinct mesenchymal cells with a role in lung allograft fibrogenesis, J Clin Invest. DOI: 10.1172/JCI147343

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Stem cells and their role in lung transplant rejection - Michigan Medicine

If you are human, you are going to die. This isn't the most comforting thought, but death is the inevitable price we must pay for being alive. Humans are, however, getting better at pushing back our expiration date, as our medicines and technologies advance.

If the human life span continues to stretch, could we one day become immortal? The answer depends on what you think it means to be an immortal human.

"I don't think when people are even asking about immortality they really mean true immortality, unless they believe in something like a soul," Susan Schneider, a philosopher and founding director of the Center for the Future Mind at Florida Atlantic University, told Live Science. "If someone was, say, to upgrade their brain and body to live a really long time, they would still not be able to live beyond the end of the universe."

Scientists expect the universe will end, which puts an immediate dampener on a mystery about the potential for human immortality. Some scientists have speculated about surviving the death of the universe, as science journalist John Horgan reported for Scientific American, but it's unlikely that any humans alive today will experience the universe's demise anyway.

Related: What happens when you die?

Many humans grow old and die. To live indefinitely, we would need to stop the body from aging. A group of animals may have already solved this problem, so it isn't as far-fetched as it sounds.

Hydra are small, jellyfish-like invertebrates with a remarkable approach to aging. They are largely made up of stem cells that constantly divide to make new cells, as their older cells are discarded. The constant influx of new cells allows hydra to rejuvenate themselves and stay forever young, Live Science previously reported.

"They don't seem to age, so, potentially they are immortal," Daniel Martnez, a biology professor at Pomona College in Claremont, California, who discovered the hydra's lack of aging, told Live Science. Hydra show that animals do not have to grow old, but that doesn't mean humans could replicate their rejuvenating habits. At 0.4 inches (10 millimeters) long, hydra are small and don't have organs. "It's impossible for us because our bodies are super complex," Martnez said.

Humans have stem cells that can repair and even regrow parts of the body, such as in the liver, but the human body is not made almost entirely of these cells, like hydra are. That's because humans need cells to do things other than just divide and make new cells. For example, our red blood cells transport oxygen around the body. "We make cells commit to a function, and in doing that, they have to lose the ability to divide," Martnez said. As the cells age, so do we.

We can't simply discard our old cells like hydra do, because we need them. For example, the neurons in the brain transmit information. "We don't want those to be replaced," Martnez said. "Because otherwise, we won't remember anything." Hydra could inspire research that allows humans to live healthier lives, for example, by finding ways for our cells to function better as they age, according to Martnez. However, his gut feeling is that humans will never achieve such biological immortality.

Though Martnez personally doesn't want to live forever, he thinks humans are already capable of a form of immortality. "I always say, 'I think we are immortal,'" he said. "Poets to me are immortal because they're still with us after so many years and they still influence us. And so I think that people survive through their legacy."

The oldest-living human on record is Jeanne Calment from France, who died at the age of 122 in 1997, according to Guinness World Records. In a 2021 study published in the journal Nature Communications, researchers reported that humans may be able to live up to a maximum of between 120 and 150 years, after which, the researchers anticipate a complete loss of resilience the body's ability to recover from things like illness or injury. To live beyond this limit, humans would need to stop cells from aging and prevent disease.

Related: What's the oldest living thing alive today?

Humans may be able to live beyond their biological limits with future technological advancements involving nanotechnology. This is the manipulation of materials on a nanoscale, less than 100 nanometers (one-billionth of a meter or 400-billionths of an inch). Machines this small could travel in the blood and possibly prevent aging by repairing the damage cells experience over time. Nanotech could also cure certain diseases, including some types of cancer, by removing cancerous cells from the body, according to the University of Melbourne in Australia.

Preventing the human body from aging still isn't enough to achieve immortality; just ask the hydra. Even though hydra don't show signs of aging, the creatures still die. They are eaten by predators, such as fish, and perish if their environment changes too much, such as if their ponds freeze in winter, Martnez said.

Humans don't have many predators to contend with, but we are prone to fatal accidents and vulnerable to extreme environmental events, such as those intensified by climate change. We'll need a sturdier vessel than our current bodies to ensure our survival long into the future. Technology may provide the solution for this, too.

As technology advances, futurists anticipate two defining milestones. The first is the singularity, in which we will design artificial intelligence (A.I.) smart enough to redesign itself, and it will get progressively smarter until it is vastly superior to our own intelligence, Live Science previously reported. The second milestone is virtual immortality, where we will be able to scan our brains and transfer ourselves to a non-biological medium, like a computer.

Researchers have already mapped the neural connections of a roundworm (Caenorhabditis elegans). As part of the so-called OpenWorm project, they then simulated the roundworm's brain in software replicating the neural connections, and programmed that software to direct a Lego robot, according to Smithsonian Magazine. The robot then appeared to start behaving like a roundworm. Scientists aren't close to mapping the connections between the 86 billion neurons of the human brain (roundworms have only 302 neurons), but advances in artificial intelligence may help us get there.

Once the human mind is in a computer and can be uploaded to the internet, we won't have to worry about the human body perishing. Moving the human mind out of the body would be a significant step on the road to immortality but, according to Schneider, there's a catch. "I don't think that will achieve immortality for you, and that's because I think you'd be creating a digital double," she said.

Schneider, who is also the author of "Artificial You: AI and the Future of Your Mind" (Princeton University Press, 2019), describes a thought experiment in which the brain either does or doesn't survive the upload process. If the brain does survive, then the digital copy can't be you as you're still alive; conversely, the digital copy also can't be you if your brain doesn't survive the upload process, because it wouldn't be if you did the copy can only be your digital double.

Related: What is consciousness?

According to Schneider, a better route to extreme longevity, while also preserving the person, would be through biological enhancements compatible with the survival of the human brain. Another, more controversial route would be through brain chips.

"There's been a lot of talk about gradually replacing parts of the brain with chips. So, eventually, one becomes like an artificial intelligence," Schneider said. In other words, slowly transitioning into a cyborg and thinking in chips rather than neurons. But if the human brain is intimately connected to you, then replacing it could mean suicide, she added.

The human body appears to have an expiration date, regardless of how it is upgraded or uploaded. Whether humans are still human without their bodies is an open question.

"To me, it's not even really an issue about whether you're technically a human being or not," Schneider said. "The real issue is whether you're the same self of a person. So, what really matters here is, what is it to be a conscious being? And when is it that changes in the brain change which conscious being you are?" In other words, at what point does changing what we can do with our brains change who we are?

Schneider is excited by the potential brain and body enhancements of the future and likes the idea of ridding ourselves of death by old age, despite some of her reservations. "I would love that, absolutely, she said. "And I would love to see science and technology cure ailments, make us smarter. I would love to see people have the option of upgrading their brains with chips. I just want them to understand what's at stake."

Originally published on Live Science.

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Will humans ever be immortal? - Livescience.com

RJ Pierce, Tech Times 05 October 2021, 09:10 am

Healthcare research has gone a long way from the dark days of old, when today's simplest illnesses can be a death sentence. And now, there's reason to look forward to a brighter future because of this news.

(Photo : Getty Images )

According to BigThink, a team from Iowa State University claimed that they've found a way to integrate human immune systems in pigs, as a way to study illnesses much closer.

In other words, they basically "humanized" the pigs to try and find out how to better treat human diseases in the future.

The implications of their research are quite profound, too. As per the researchers, this breakthrough could theoretically advance healthcare research in areas such as virus and vaccines, cancer, and even stem cell treatments.

Before this, scientists often used mice in their biotech and biomedical experiments. However, the problem is that mice-based results don't translate well to humans.

Aside from mice, primates have also been used in related fields of healthcare research due to their direct biological connections with humans. Nevertheless, a lot of ethical issues popped up, thus leading to the retirement of primates, including chimpanzees, from this type of research eight years ago.

This won't be the first time that healthcare research has produced what's basically human-animal hybrids to study illnesses.

Three years ago, a team of scientists from Rockefeller University in New York managed to create a human-chicken embryo, in an attempt to take a closer look at the intricacies of stem cell therapies.

Read also: Scientists Want To Create Part-Human Part-Animal Chimeras To Find Cure For Diseases

It started when the same scientists from Iowa State University discovered a genetic mutation in pigs that caused an illness called SCID (Severe Combined Immunodeficiency).

Some people may know this from the film "The Boy In The Plastic Bubble" from 1976, which tells the story of a child whose immune system never fully developed. As such, he was forced to literally live inside a sterile bubble because even the slightest cold would kill him.

Upon this discovery, the researchers then developed a pig that's far more immunocompromised compared to a person with SCID, then successfully "humanized" it by injecting human immune stem cells into the livers of piglets.

The researchers were able to do this by using ultrasound imaging as a guide.

Ultrasound imaging, also known as sonography, makes use of high-frequency waves to look inside the body.

(Photo : Getty Images )

The resulting pigs had excellent healthcare research potential, because they were found to have human immune cells in their blood, thymus gland, spleen, and liver.

However, the SCID-afflicted pigs are in constant danger of infections. As such, they have to be housed in so-called bubble biocontainment facilities. These facilities work by maintaining high positive pressure, which keeps dangerous pathogens out. All staff members have to wear sterile protective gear at all times.

They've basically turned into their own versions of the boy in the bubble.

Before this research, pigs have often been used to know more about the human body because of how strikingly similar their anatomy is to humans.

In fact, a few scientists even believe that with how biologically similar pigs are to humans, they might be classified into an animal family occupied by primates, reportedScience.org.au.

But of course, there have been ethical issues involving the use of these human-animal hybrids for healthcare research. Eventually, though, the National Institutes of Health (NIH) relaxed their regulations a bit back in 2016, which made it easier for scientists to transfer human stem cells into animal embryos.

Related: Scientists Grow Sheep Embryos With Human Cells To Revolutionize Organ Transplant

This article is owned by Tech Times

Written by RJ Pierce

2021 TECHTIMES.com All rights reserved. Do not reproduce without permission.

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Healthcare Researchers Are Putting HUMAN Immune Systems In Pigs To Study Illnesses-Here's The Tech Behind It - Tech Times

ORLANDO, Fla., Oct. 4, 2021 /PRNewswire/ --Billions of dollars are spent every year because of complications of wound healing. Researchers at the College of Medicine at the University of Central Florida (UCF) in Orlando have discovered a new technology to accelerate wound healing. Their research is published in the Life Cell Biology and Tissue Engineering Journal (https://pubmed.ncbi.nlm.nih.gov/34575027/). The UCF lab's research focus is to develop stem cell therapies for neurodegenerative diseases, including Alzheimer's disease, Parkinson's disease, wound healing and ALS.

Researchers at the College of Medicine at UCF in Orlando have discovered a new technology to accelerate wound healing.

Dr. Frederick R Carrick, Professor of Neurology at the College of Medicine at UCF, reported that animals with wounds and injured stem cells that were placed on a special ceramic blanket healed much faster than controls. Gladiator Therapeutics manufactured the therapeutic ceramic blanket that was used in this research. The researchers reported that wounds in animals and in stem cells were both repaired significantly faster when they treated them with the ceramic blankets.

This research was designed and accepted for presentation at the USA Department of Defense's premier scientific meeting, the Military Health System Research Symposium (MHSRS). Dr Carrick stated that the new ceramic blankets do not need a power supply and are ideally suited for use in both combat and civilian wound treatments. Large wounds, such as those suffered in combat are easily infected and may result in increased suffering, disability and death amongst Warfighters. Faster healing of wounds can decrease pain and suffering and save lives.

The UCF College of Medicine research team is conducting ongoing research on the use of the Gladiator ceramic blanket in animal models of Alzheimer's and Parkinson's disease, traumatic brain injury and wound care. They have recently developed a new Alzheimer's therapy combining drugs that affect stem cells that increase the development of brain cells and improve brain function. The UCF lab is also the first to transplant stem cells isolated from the human brain to aged rats where they showed increased development of new brain cells and improvement of cognition.

Dr. Kiminobu Sugaya, Professor of Medicine at the UCF College of Medicine is excited about their findings. Dr. Sugaya stated that the benefits of using the Gladiator ceramic blanket are that it can be used anywhere without a power supply or the side effects that are commonly found when injecting chemicals or drugs.

Further information about this study:

drfrcarrick@post.harvard.edu 321-868-6464

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Faster healing of wounds can decrease pain and suffering and save lives - ABC 12 News

Almost two months after Jeff Bezosblasted off into space debuting his rocket along with a new, plumper face the Amazon honcho announced anew investmentinAltos Labs, a startupdedicated todiscovering how to reverse the aging process.

While non-Botoxed eyebrows were raised around the world, Bezos isnt the only mega-wealthy man who wants to become Dorian Gray.

Eternal life has become the new space quest for the tech overlords.

Its a little bit juvenile,Rami Kaminski, MD,Kaminski, who is the founder and director of The Institute of Integrative Psychiatry(TiiPS). You may go to Mars, but you cannot go out into the solar system. [These wealthy men] are limited. What theyre trying to do is get away from the mortal coil. Every day when you look in the mirror you are reminded you are made of carbon. It is degrading and has to be recycled.

Peter Thiel, the PayPal co-foundertoldBusiness Insiderin 2012.,There are all these people who say that death is natural, its just part of life, and I think that nothing can be further from the truth, noting that death is a problem that can be solved.

Also on the hunt for the Fountain of Youth is Larry Page, one of the co-founders of Google. In 2013,Google founded Calico, a biology company with the stated goal of solv[ing] death. The company, according to itsWeb site, Seek(s) to answer the most challenging biological questions of our time how humans age and can we develop interventions to allow people. To live longer, healthier lives.

Keith Campbell, a psychology and social personality professor at the University of Georgia, told The Post: I call this process rebuilding Frankenstein [The desire]comes from a radical misunderstanding of the human condition, [where] materialism and behaviorism are mashed up with AI. That coupled with egoand fear and lots of money leads to the search.

Silicon Valleyentrepreneur Serge Faguet founder of the video platform TokBox and the Russian booking Web site Ostrovok has spent more than $250,000 on biohacking. Hes also a fan of microdosing with MDMA, telling The Guardian its all helped him become calmer, thinner, extroverted, healthier and happier. Oh, and its increased his sex drive, helping him (pick) up girls.

Meanwhile, lets not leave out TeslasElon Musk, who doesnt care about his body he simply wants his thoughts and brain to live forever via his new company,Neuralink.

The quest for the Fountain of Youth is not a new one. Ponce De Len never found it. In modern times, you have men like Peter Nygard. The disgraced fashion execbuilt a bio science lab in the Bahamasas part of a scheme to gather stem cells from the aborted fetuses of women hed impregnate all to elongate his life. (Hes now in jail in Canada, facing trial for sex trafficking and racketeering, amid several sexual assault allegations.)

Why are so many powerful men eager to, seemingly, live forever?

Death is the great equalizer the only thing that can bring [these men] down is death and you can not do anything about it. Unless you can,Kaminski told the Post. They are literally scared to die and immortality is the ultimate defense.

They want to defeat the only thing they cannot. They have the means and the power. When you have limitless amount of money you start pushing the boundaries. For the super billionaires, its not surprising they are choosing the ultimate limit.

And because these men have done the seemingly impossible in their work lives, and are treated like demigods on social media, their ego has morphed into a Dr. Frankenstein-esque manner, where they think they can now control the one thing man has never been able to control: death.

People with big egos think they matter more than their organizations, Campbell said. They think that, if they were gone, the world would fall apart because they are smarter than others and they were put here for a reason. Because theyve been so successful in putting their will on reality they think, Why cant I beat [death]? I can beat anything.

This feeling of being able to master the universe and manipulate all in their realm leads to a very real God Complex.

When an individual is exposed to excess wealth and power over an extended period of time it can alter their entire worldview; (they believe) they are special and better than others because of their ability to amass and hoard money, Dr.BethanyCook, a licensed psychotherapist told the Post. If one has vast amounts of money and power, along with a God complex, its easy to see why they may invest in discovering the secret to eternal life; they wish to retain their power and wealth for as long as possible.

The psychologists and psychiatrists The Post spoke to also noted that while these men think they are masters of the universe, their actions suggest immaturity and a fear of the inevitable.

Our old elites had some life experiences, like going to war or even doing sales, and were not psychological children like this new crowd, said Campbell. These arent spiritually grounded individuals. They may have a high IQ, but they are linear and very detached from reality.

And while some see the billionaires continued quest for everlasting life as interesting, Campbell finds it worrisome.

Im utterly terrified of people who think they know better than everyone else and who have power and arent afraid to use it, he said. Thats what a tyrant is. People who think they can control the world, who have power without humility makes me nervous.

And once the Fountain of Youth is discovered, how do we stop it? Already scientists are predicting humans can live to 130 years and that its not improbable to think we could live forever and the consequences have already been dire. This week, 23 more species, including the ivory-billed woodpecker, were declared extinct due to human activity. What will happen if we all live forever and keep reproducing?

Kaminski warns, Maybe there will be a breakthrough [for longevity] but then what do we do with humanity? If they had a pill to stop everyone from dying, people would be crawling all over the planet there wouldnt be a place to sit. The problem is the defiance of nature.

That, thus far, has never really worked out for humans.

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Why Bezos, Musk, Page and other billionaires want to live forever - New York Post

SANTA MONICA, Calif.--(BUSINESS WIRE)--Kite, a Gilead Company (Nasdaq: GILD), today announced the U.S. Food and Drug Administration (FDA) has granted approval for Tecartus (brexucabtagene autoleucel) for the treatment of adult patients (18 years and older) with relapsed or refractory B-cell precursor acute lymphoblastic leukemia (ALL). Following FDA Breakthrough Therapy Designation and a priority review, Tecartus is the first and only chimeric antigen receptor (CAR) T-cell therapy approved for adults (18 years and older) with ALL. There is a high unmet need, as half of this patient population will relapse, and median overall survival (OS) is only approximately eight months with current standard-of-care treatments. Patients can access Tecartus through 109 authorized treatment centers across the U.S.

Adults with ALL face a significantly poorer prognosis compared to children, and roughly half of all adults with B-ALL will relapse on currently available therapies, said Bijal Shah, MD, ZUMA-3 investigator and medical oncologist, Moffitt Cancer Center, Tampa, Florida. We now have a new meaningful advancement in treatment for these patients. A single infusion of Tecartus has demonstrated durable responses, suggesting the potential for long-term remission and a new approach to care.

The approval is based on results from ZUMA-3, a global, multicenter, single-arm, open-label study in which 65% of the evaluable patients (n=54) achieved complete remission (CR) or CR with incomplete hematological recovery (CRi) at a median actual follow-up of 12.3 months. The duration of CR was estimated to exceed 12 months for more than half the patients. Among efficacy-evaluable patients, median duration of remission (DOR) was 13.6 months. Among the patients treated with Tecartus at the target dose (n=78), Grade 3 or higher cytokine release syndrome (CRS) and neurologic events occurred in 26% and 35% of patients, respectively, and were generally well-managed.

Today marks Kites fourth FDA approved indication in cell therapy in under four years, demonstrating our commitment to advancing CAR T for patients across many different hematologic malignancies, said Christi Shaw, Chief Executive Officer of Kite. Tecartus has already transformed outcomes for adults living with mantle cell lymphoma, and we look forward to offering the hope for a cure to patients with ALL.

Adults with relapsed or refractory ALL often undergo multiple treatments including chemotherapy, targeted therapy and stem cell transplant. CAR T-cell therapy works differently, by harnessing a patients own immune system to fight cancer. With CAR T, the patients blood is drawn and the T cells are separated. Then the T cells are genetically engineered with a specific receptor that enables them to identify and attack cancer cells, and put back into the patients body.

Roughly half of all ALL cases actually occur in adults, and unlike pediatric ALL, adult ALL has historically had a poor prognosis, said Lee Greenberger, PhD, Chief Scientific Officer of The Leukemia & Lymphoma Society (LLS). Developing new therapies that would be life-changing for people with cancer has been a dream of LLS. We are proud to see the potential of CAR T realized for even more people with this approval for brexucabtagene autoleucel.

Tecartus is also currently under review in the European Union and United Kingdom for the treatment of adult patients with relapsed or refractory B-cell precursor ALL.

The Tecartus U.S. Prescribing Information has a BOXED WARNING for the risks of CRS and neurologic toxicities, and Tecartus is approved with a Risk Evaluation and Mitigation Strategy (REMS) due to these risks; see below for Important Safety Information.

Additional Information About ZUMA-3 Trial

Further efficacy results from the ZUMA-3 trial have been published and presented in scientific forums. Published Phase 1 data showed 32% of responders (n=22) were still in remission at the median follow-up of 22.1 months. In Phase 2 data presented at the 2021 American Society of Clinical Oncology (ASCO) Annual Meeting, investigators reported that among treated patients (n=54), 31% of these patients were in ongoing response at a median follow-up of 16.4 months. 97% of responders had deep molecular remission, with undetectable minimal residual disease (MRD), and median OS among all responders has not yet been reached. A safety analysis, reported in the Lancet, showed among all patients who experienced a neurologic event, 94% of CRS events and 88% of neurologic events were resolved.

ZUMA-3 is an international multicenter, registrational Phase 1/2 study in adult patients (18 years old) with ALL whose disease is refractory to or has relapsed following first standard systemic therapy with remission of 12 months or less, after two or more lines of systemic therapy or at least 100 days after allogeneic stem cell transplantation. Seventy-one patients were enrolled (and leukapheresed) in the study, and the primary endpoint was overall complete remission rate (OCR, equaling complete remission plus complete remission with incomplete hematologic recovery) as determined by an independent review.

About ALL

ALL is an aggressive type of blood cancer that can also involve the lymph nodes, spleen, liver, central nervous system and other organs. Approximately 1,000 adults are treated annually for relapsed or refractory ALL. B-cell precursor ALL is the most common form, accounting for approximately 75% of cases, and treatment is typically associated with inferior outcomes compared with other types of ALL. Survival rates remain very poor in adult patients with relapsed or refractory ALL, with median OS at less than eight months.

About Tecartus

Tecartus is an autologous, anti-CD19 CAR T-cell therapy. Tecartus uses the XLP manufacturing process that includes T cell enrichment, a necessary step in certain B-cell malignancies in which circulating lymphoblasts are a common feature. Tecartus is also being evaluated in pediatric ALL, where its use is investigational, and its safety and efficacy have not been established.

About Kite

Kite, a Gilead Company, is a global biopharmaceutical company based in Santa Monica, California, with commercial manufacturing operations in North America and Europe. Kites singular focus is cell therapy to treat and potentially cure cancer. As the cell therapy leader, Kite has more approved CAR T indications to help more patients than any other company. For more information on Kite, please visit http://www.kitepharma.com.

About Gilead Sciences

Gilead Sciences, Inc. is a biopharmaceutical company that has pursued and achieved breakthroughs in medicine for more than three decades, with the goal of creating a healthier world for all people. The company is committed to advancing innovative medicines to prevent and treat life-threatening diseases, including HIV, viral hepatitis and cancer. Gilead operates in more than 35 countries worldwide, with headquarters in Foster City, California.

Tecartus Indication

Tecartus is a CD19-directed genetically modified autologous T cell immunotherapy indicated for the treatment of:

This indication is approved under accelerated approval based on overall response rate and durability of response. Continued approval for this indication may be contingent upon verification and description of clinical benefit in a confirmatory trial.

U.S. IMPORTANT SAFETY INFORMATION

BOXED WARNING: CYTOKINE RELEASE SYNDROME and NEUROLOGIC TOXICITIES

Cytokine Release Syndrome (CRS), including life-threatening reactions, occurred following treatment with Tecartus. In ZUMA-2, CRS occurred in 91% (75/82) of patients receiving Tecartus, including Grade 3 CRS in 18% of patients. Among the patients who died after receiving Tecartus, one had a fatal CRS event. The median time to onset of CRS was three days (range: 1 to 13 days) and the median duration of CRS was ten days (range: 1 to 50 days). Among patients with CRS, the key manifestations (>10%) were similar in MCL and ALL and included fever (93%), hypotension (62%), tachycardia (59%), chills (32%), hypoxia (31%), headache (21%), fatigue (20%), and nausea (13%). Serious events associated with CRS included hypotension, fever, hypoxia, tachycardia, and dyspnea.

Ensure that a minimum of two doses of tocilizumab are available for each patient prior to infusion of Tecartus. Following infusion, monitor patients for signs and symptoms of CRS daily for at least seven days at the certified healthcare facility, and for four weeks thereafter. Counsel patients to seek immediate medical attention should signs or symptoms of CRS occur at any time. At the first sign of CRS, institute treatment with supportive care, tocilizumab, or tocilizumab and corticosteroids as indicated.

Neurologic Events, including those that were fatal or life-threatening, occurred following treatment with Tecartus. Neurologic events occurred in 81% (66/82) of patients with MCL, including Grade 3 in 37% of patients. The median time to onset for neurologic events was six days (range: 1 to 32 days) with a median duration of 21 days (range: 2 to 454 days) in patients with MCL. Neurologic events occurred in 87% (68/78) of patients with ALL, including Grade 3 in 35% of patients. The median time to onset for neurologic events was seven days (range: 1 to 51 days) with a median duration of 15 days (range: 1 to 397 days) in patients with ALL. For patients with MCL, 54 (66%) patients experienced CRS before the onset of neurological events. Five (6%) patients did not experience CRS with neurologic events and eight patients (10%) developed neurological events after the resolution of CRS. Neurologic events resolved for 119 out of 134 (89%) patients treated with Tecartus. Nine patients (three patients with MCL and six patients with ALL) had ongoing neurologic events at the time of death. For patients with ALL, neurologic events occurred before, during, and after CRS in 4 (5%), 57 (73%), and 8 (10%) of patients; respectively. Three patients (4%) had neurologic events without CRS. The onset of neurologic events can be concurrent with CRS, following resolution of CRS or in the absence of CRS.

The most common neurologic events (>10%) were similar in MCL and ALL and included encephalopathy (57%), headache (37%), tremor (34%), confusional state (26%), aphasia (23%), delirium (17%), dizziness (15%), anxiety (14%), and agitation (12%). Serious events including encephalopathy, aphasia, confusional state, and seizures occurred after treatment with Tecartus.

Monitor patients daily for at least seven days for patients with MCL and at least 14 days for patients with ALL at the certified healthcare facility and for four weeks following infusion for signs and symptoms of neurologic toxicities and treat promptly.

REMS Program: Because of the risk of CRS and neurologic toxicities, Tecartus is available only through a restricted program under a Risk Evaluation and Mitigation Strategy (REMS) called the Yescarta and Tecartus REMS Program which requires that:

Hypersensitivity Reactions: Serious hypersensitivity reactions, including anaphylaxis, may occur due to dimethyl sulfoxide (DMSO) or residual gentamicin in Tecartus.

Severe Infections: Severe or life-threatening infections occurred in patients after Tecartus infusion. Infections (all grades) occurred in 56% (46/82) of patients with MCL and 44% (34/78) of patients with ALL. Grade 3 or higher infections, including bacterial, viral, and fungal infections, occurred in 30% of patients with ALL and MCL. Tecartus should not be administered to patients with clinically significant active systemic infections. Monitor patients for signs and symptoms of infection before and after Tecartus infusion and treat appropriately. Administer prophylactic antimicrobials according to local guidelines.

Febrile neutropenia was observed in 6% of patients with MCL and 35% of patients with ALL after Tecartus infusion and may be concurrent with CRS. The febrile neutropenia in 27 (35%) of patients with ALL includes events of febrile neutropenia (11 (14%)) plus the concurrent events of fever and neutropenia (16 (21%)). In the event of febrile neutropenia, evaluate for infection and manage with broad spectrum antibiotics, fluids, and other supportive care as medically indicated.

In immunosuppressed patients, life-threatening and fatal opportunistic infections have been reported. The possibility of rare infectious etiologies (e.g., fungal and viral infections such as HHV-6 and progressive multifocal leukoencephalopathy) should be considered in patients with neurologic events and appropriate diagnostic evaluations should be performed.

Hepatitis B virus (HBV) reactivation, in some cases resulting in fulminant hepatitis, hepatic failure, and death, can occur in patients treated with drugs directed against B cells. Perform screening for HBV, HCV, and HIV in accordance with clinical guidelines before collection of cells for manufacturing.

Prolonged Cytopenias: Patients may exhibit cytopenias for several weeks following lymphodepleting chemotherapy and Tecartus infusion. In patients with MCL, Grade 3 or higher cytopenias not resolved by Day 30 following Tecartus infusion occurred in 55% (45/82) of patients and included thrombocytopenia (38%), neutropenia (37%), and anemia (17%). In patients with ALL who were responders to Tecartus treatment, Grade 3 or higher cytopenias not resolved by Day 30 following Tecartus infusion occurred in 20% (7/35) of the patients and included neutropenia (12%) and thrombocytopenia (12%); Grade 3 or higher cytopenias not resolved by Day 60 following Tecartus infusion occurred in 11% (4/35) of the patients and included neutropenia (9%) and thrombocytopenia (6%). Monitor blood counts after Tecartus infusion.

Hypogammaglobulinemia: B cell aplasia and hypogammaglobulinemia can occur in patients receiving treatment with Tecartus. Hypogammaglobulinemia was reported in 16% (13/82) of patients with MCL and 9% (7/78) of patients with ALL. Monitor immunoglobulin levels after treatment with Tecartus and manage using infection precautions, antibiotic prophylaxis, and immunoglobulin replacement.

The safety of immunization with live viral vaccines during or following Tecartus treatment has not been studied. Vaccination with live virus vaccines is not recommended for at least six weeks prior to the start of lymphodepleting chemotherapy, during Tecartus treatment, and until immune recovery following treatment with Tecartus.

Secondary Malignancies may develop. Monitor life-long for secondary malignancies. In the event that one occurs, contact Kite at 1-844-454-KITE (5483) to obtain instructions on patient samples to collect for testing.

Effects on Ability to Drive and Use Machines: Due to the potential for neurologic events, including altered mental status or seizures, patients are at risk for altered or decreased consciousness or coordination in the 8 weeks following Tecartus infusion. Advise patients to refrain from driving and engaging in hazardous activities, such as operating heavy or potentially dangerous machinery, during this period.

Adverse Reactions: The most common non-laboratory adverse reactions ( 20%) were fever, cytokine release syndrome, hypotension, encephalopathy, tachycardia, nausea, chills, headache, fatigue, febrile neutropenia, diarrhea, musculoskeletal pain, hypoxia, rash, edema, tremor, infection with pathogen unspecified, constipation, decreased appetite, and vomiting. The most common serious adverse reactions ( 2%) were cytokine release syndrome, febrile neutropenia, hypotension, encephalopathy, fever, infection with pathogen unspecified, hypoxia, tachycardia, bacterial infections, respiratory failure, seizure, diarrhea, dyspnea, fungal infections, viral infections, coagulopathy, delirium, fatigue, hemophagocytic lymphohistiocytosis, musculoskeletal pain, edema, and paraparesis.

Please see full Prescribing Information, including BOXED WARNING and Medication Guide.

Forward-Looking Statements

This press release includes forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995 that are subject to risks, uncertainties and other factors, including the risk that physicians and patients may not see the potential benefits of Tecartus for the treatment of adult patients with relapsed or refractory B-cell ALL; the possibility of unfavorable results from ongoing and additional clinical trials involving Tecartus; and the possibility that Tecartus may not receive regulatory approvals in the European Union and United Kingdom for the treatment of adult patients with relapsed or refractory B-cell ALL in the anticipated timelines or at all, and the risk that any such approvals, if granted, may have sigfniciant limitationon its use. These and other risks, uncertainties and other factors are described in detail in Gileads Quarterly Report on Form 10-Q for the quarter ended June 30, 2021, as filed with the U.S. Securities and Exchange Commission. These risks, uncertainties and other factors could cause actual results to differ materially from those referred to in the forward-looking statements. All statements other than statements of historical fact are statements that could be deemed forward-looking statements. Investors are cautioned that any such forward-looking statements are not guarantees of future performance and involve risks and uncertainties and are cautioned not to place undue reliance on these forward-looking statements. All forward-looking statements are based on information currently available to Kite and Gilead, and Kite and Gilead assume no obligation and disclaim any intent to update any such forward-looking statements.

U.S. Prescribing Information for Tecartus including BOXED WARNING, is available at http://www.kitepharma.com and http://www.gilead.com.

Kite, the Kite logo, Yescarta, Tecartus, XLP and GILEAD are trademarks of Gilead Sciences, Inc. or its related companies.

For more information on Kite, please visit the companys website at http://www.kitepharma.com or call Gilead Public Affairs at 1-800-GILEAD-5 or 1-650-574-3000. Follow Kite on social media on Twitter (@KitePharma) and LinkedIn.

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U.S. FDA Approves Kite's Tecartus as the First and Only Car T for Adults With Relapsed or Refractory B-cell Acute Lymphoblastic Leukemia - Business...

For the first time, a type of CRISPR/Cas9 genome editing, called prime editing, has been performed in mini-organs to correct the mutation causing cystic fibrosis.

Cystic fibrosis is thought to affect more than 70,000 people worldwide.It is a genetic disease caused by a mutation in a single gene, called the CFTR gene, which result in a dysfunctional CFTR protein. This dysfunctional protein aspect is what causes the main symptom of cystic fibrosis; a sticky mucus buildup in the respiratory tract and lungs.

Published in Life Science Alliance, researchers from the Hubrecht Institute, in collaboration with UMC Utrecht and Oncode Institute, demonstrated that they were able to correct a mutation in CFTR that causes cystic fibrosis by performing genome editing in a mini-organ called an organoid. The organoids, mini intestines, had been grown from stem cells originally collected from patients with cystic fibrosis.

Prime editing is different than traditional CRISPR genome editing. Instead of acting as a pair of scissors, prime editing uses a modified Cas9 protein to make a direct change to the DNA sequence. In doing so, the researchers are able to change the underlying DNA sequence without cutting the DNA. This also reduces the risk of Cas9 cutting randomly elsewhere in the genome.

To test if the prime editing was successful, the researchers, led by Hans Clever, added a treatment called forskolin to the organoids. In healthy organoids, addition of forskolin causes the mini-intestines to swell up due to movement of fluids into the center. The researchers found that this happened in some of the prime edited organoids as well, suggesting that the mutation had been corrected. Organoids that carried a CFTR gene with a mutation however, did not respond to forskolin treatment.

Prime editing efficiency is variable between organoids and cell types, an important consideration in the developments towards gene therapy for cystic fibrosis and other diseases. Moreover, significant research effort should be invested into ensuring that prime editing techniques do not cause any unintended off-target effects. Despite this, these proof-of-principle research findings provide a step forward for the understanding and future developments of gene therapy for cystic fibrosis treatment.

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Skeletons' broken clavicles tell a centuries-old tale of humans and horses - Massive Science

IN 2016, INVENTOR and scientist Erik Gentalen reached out to a former colleague with exciting news, and a proposition.

"I started a company, and we could use some help," Gentalen said. The former colleague, Lena Wu, had worked with him around 15 years earlier as the director of business development at Caliper Technologies, a Mountain View, California-based bioresearch firm. Gentalen's new company, Intabio, would launch his latest invention, an instrument to analyze and ensure the efficacy and safety of biopharmaceutical drugs. Called the Blaze System, the machine could reduce the analysis time from weeks in some cases to less than 30 minutes per sample, dramatically shortening a drug's development period.

Wu joined Intabio's board later that year and became CEO the next. It was a hire that paid dividends in unexpected ways. When it came time to raise startup capital, Gentalen turned to Genoa Ventures managing director Jenny Rooke, whom he'd met through other investors in the life sciences industry.

"It was Erik's openness to bringing in Lena's complementary strengths that attracted me to the company," Rooke says. "When Lena joined forces with Erik as his business partner and Intabio's CEO, I knew the time was right."

In 2017, Rooke's San Francisco-based venture capital firm led Intabio's $3.2 million seed financing.

"It was clear from the earliest meeting that Jenny had great technical expertise, was willing to be collaborative in solving issues, and was thoughtful and strategic," Wu says. "Many people in Jenny's position are super supportive but not critical. She's the rare combination of both."

Rooke honed her expertise while earning a PhD in genetics at Yale, after which she worked at McKinsey advising pharmaceutical and biotech companies on business strategy. She also served in the executive ranks of U.S. Genomics (later called PathoGenetix), leading R&D and corporate development. Rooke knew the business. According to Wu, she had a keen eye for burnout, a common affliction among entrepreneurs. "She would say, 'You need to take a break. Now, go on vacation,' " Wu recalls. "I've never had another VC tell me to go on vacation."

Though Genoa didn't lead Intabio's Series A or Series B funding rounds, which brought the company's total funding to $30 million, Rooke introduced Wu to other investors and identified VCs to target. "We gained a great deal of credibility as a good investment given Jenny's reputation and the fact that she led our seed round," Wu says.

Intabio's first non-founder hire after raising capital was principal scientist Scott Mack, who helped develop the company's technology and was the first author of the company's published scientific paper describing the technology. (Mack's dog is also the Blaze System's namesake.) As of early 2021, Intabio had more than 40 employees.

Mack and Blaze (the system, not the dog) had their work cut out for them. Getting from a prototype that was tested only in-house at Intabio to a pre-commercial beta system took three years of development. Pharmaceutical companies Pfizer and Janssen Pharmaceuticals beta-tested the Blaze system, while Merck was an "early access collaborator" that sent samples to Intabio to analyze at the company's lab and return the results. Wu developed Intabio's go-to-market strategy and early access program, with Rooke helping refine and pressure-test aspects of the strategy.

When all was said and done, the proof-of-concept method worked. In January 2021, the life sciences company Sciex announced it had acquired Intabio for an undisclosed sum, just three and half years after the startup began operations. And when negotiating the deal, Wu relied on Rooke to play the role of not just investor but true partner.

"Jenny's input was, as always, both supportive and rigorous," Wu says. "It gave me the confidence that as a management team, we were making the right decision."

From the October 2021 issue of Inc. Magazine

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How a Venture Investor with a PhD in Genetics Helped This Biotech Firm Get Started, Funded, and Acquired - Inc.

MCLEAN, Va., Oct. 1, 2021 /PRNewswire-PRWeb/ --The Multiple System Atrophy ("MSA") Coalition announces a ground-breaking million-dollar multi-year collaborative project focused on exploring the genetics of up to 1,200 people with either a diagnosis of probable MSA, in the case of living patients, or postmortem pathological confirmation of multiple system atrophy, aimed at locating commonalities in their genes that might contribute to the development of multiple system atrophy. The aim of this collaborative study is to sequence and organize the genomes of existing genetic samples as well as to organize previously sequenced whole-genome data into a single database that is accessible to researchers worldwide. While many researchers have looked at the genetics of MSA, this will be the first time such a large number of genomes from ethnically diverse populations have been sequenced and organized in such a way as to facilitate thorough analysis and collaborative enterprise.

"MSA is not typically passed from parent to child, except in extremely rare cases. However, there are still important clues about the underlying cause of MSA that can be found by examining the genetic code of a large population of MSA patients and looking for commonalities. Because MSA is a such a rare disease, there is a need for multiple researchers to work together and pool their data. Until now there has not been a concerted effort among genetic labs to combine these rare genetic samples from MSA patients with diverse backgrounds into a large, shared database," said Pam Bower, chair of the MSA Coalition's research committee. "The MSA Coalition is proud to be the driver of this ground-breaking study."

University of Florida will perform genetic sequencing under the direction of Matt Farrer, PhD, while storage, analysis and visualization of data will occur at Harvard Medical School in the Clinical Genome Analysis Platform ("CGAP") under the direction of Dana Vuzman, PhD. Additional genomic information will be provided by University College of London, Queen Square Institute of Neurology under the direction of Henry Houlden, MBBS, MRCP, PhD; by Translational Genomics Research Institute (TGen) under the direction of Matt Huentelman, PhD (Funded in part by the Rex Griswold Foundation, a grant from the NIH NINDS (R21-NS093222, PI: Huentelman), and through institutional support of TGen.); and by Seoul National University, under the direction of Beomseok Jeon, MD, PhD and Han-Joon Kim, MD, PhD. The Core G team also plans to coordinate their work with that being done at NIH under the direction of Sonja Scholz, MD, PhD. The group, collectively known as "Core G" (Genetics), will work closely with Vik Khurana, MD, PhD, board member and Scientific Liaison of the Board of Directors of the MSA Coalition and Chief of the Movement Disorders Division at Brigham and Women's Hospital and Harvard Medical School. Dr. Khurana will endeavor to integrate Core G team-member efforts more broadly into the MSA Collaborative Cores Initiative sponsored by the Coalition that will seed fund additional projects over time.

"I am thrilled that after years of planning and deliberation that Core G is funded and ready to go," said Khurana. "This group of terrific researchers, together with their expertise, bring precious patient samples from three continents to establish a foundation upon which other collaborations and initiatives will be built. We are under no illusion that the genetics of MSA will prove challenging, no less than a moonshot. At the same time, genetic insights promise to unlock powerful hypothesis-driven science that can find cures. And so, this moonshot is worth the effort and has been structured to be collaborative, open and sustainable in the long-term."

"We are incredibly proud of assembling this group of world-renowned researchers to collaborate on this project. It has taken almost three years to organize this project and obtain consents from all the institutions involved. Great care has been taken by all contributing institutions to safeguard the privacy of the patients and anonymize the genetic materials, so that patient privacy is protected," said Cynthia Roemer, MSA Coalition board chair. "We are also grateful to our many donors, who have made this project possible, and to the patients we have lost to MSA who generously left bequests to the MSA Coalition to further critical research like this. We quite literally could not do it without them!"

Dana Vuzman, PhD is an Instructor of Medicine at Harvard Medical School and the Director of Genomic Platform Development at DBMI. Dr. Vuzman oversees the implementation of the Clinical Genome Analysis Platform (CGAP) and the Single Cell RNA Platform in the Department. Prior to joining DBMI, she served as Chief Informatics Officer at One Brave Idea, Sr. Director of Biomedical Informatics at KEW, Inc., and Co-Director at Brigham Genomic Medicine. Dr. Vuzman earned her PhD in Computational Biology from the Weizmann Institute of Science in Israel and completed her postdoctoral training in Computational Genetics at Brigham and Women's Hospital and Harvard Medical School.

Matt Farrer, PhD is critically acclaimed for his work in the genetics and neuroscience of Parkinson's disease. His inspiration to apply genetic analysis to complex neurologic disorders came from early work as a care assistant of patients and families with neurologic and psychiatric disorders. Dr. Farrer earned his first degree in Biochemistry with a Doctoral degree in Molecular and Statistical Genetics from St. Mary's Hospital Medical School, UK. He completed a fellowship in Medical Genetics at the Kennedy-Galton Centre, UK and in Neurogenetics at Mayo Clinic. Dr. Farrer became an Assistant Professor of Molecular Neuroscience in 2000 where he opened his first laboratory to predict and prevent Parkinson's disease. Dr. Farrer became a tenured professor in 2006, a Mayo Consultant, and subsequently, a Distinguished Mayo Investigator. In 2010, Dr. Farrer was awarded a Canada Excellence Research Chair to build the Centre for Applied Neurogenetics and Neuroscience at the University of British Columbia, Vancouver, Canada where he became a Professor of Medical Genetics. The Province of British Columbia subsequently awarded him the Don Rix Chair in Precision Medicine, and his team had many notable accomplishments including several new genes and mouse models for Parkinson's disease. The team also implemented high-throughput sequencing in pediatric seizure disorders and neonatology in clinical service. The former was funded through the Medical Services Plan of British Columbia and was a first for Canada.

In 2019, Dr. Farrer accepted an endowed chair at the Norman Fixel Institute for Neurological Diseases (thanks to a generous endowment from the Lauren and Lee Fixel Family Foundation). Dr. Matt Farrer also directs the UF Clinical Genomics Program. As such he currently has appointments and affiliations in the UF College of Medicine's Neurology and Pathology Departments, Clinical and Translational Science Institute, the Evelyn F. and William L. McKnight Brain Institute, the Center for Translational Research in Neurodegenerative Disease, and the Center for Neurogenetic in addition to the Norman Fixel Institute for Neurological Diseases.

Henry Houlden, MBBS, MRCP, PhD: Dr. Houlden is a professor of neurology and neurogenetics in the Department of Neuromuscular Disease, University College, London, Queen Square Institute of Neurology, and undertakes research laboratory works on neurogenetics and movement disorders with a particular interest in rare diseases that are adult or childhood-onset, such as multiple system atrophy (MSA), spinocerebellar ataxia and other movement disorders, inherited neuromuscular conditions, and difficult to diagnose disorders, particularly in diverse and underrepresented populations. He assists with the integration of new gene discovery with exome and genome sequencing identifying disease genes such as CANVAS, NARS1, NKX-6.2, SCA11, SCA15, GRIA2, and GAD1, with functional experimental validation in human tissue and other model systems. Dr. Houlden has clinical expertise in inherited neurological disorders and movement disorders such as multiple system atrophy, ataxia, leukodystrophy, epilepsy and paroxysmal conditions, spastic paraplegia and neuromuscular conditions.

Matt Huentelman, PhD: Dr. Huentelman's research interests center around the investigation of the "-omics" (genomics, transcriptomics, and proteomics) of neurological traits and disease. His laboratory's overarching goal is to leverage findings in these disciplines to better understand, diagnose, and treat human diseases of the nervous system.

Dr. Huentelman joined TGen in July of 2004 after completing his doctoral work at the University of Florida's Department of Physiology and Functional Genomics at the McKnight Brain Institute where he investigated the application of gene therapy in the study and prevention of hypertension. His undergraduate degree is in Biochemistry from Ohio University's Department of Chemistry and Biochemistry at Clippinger Laboratories. Dr. Huentelman's career includes visiting researcher stints in Moscow, Russia at the MV Lomonosov Moscow State University "Biology Faculty" and in the United Kingdom within the University of Bristol's Department of Physiology.

Beomseok Jeon, MD, PhD: Professor Jeon is the medical director of the Movement Disorder Center, Seoul National University Hospital and is interested in genetics of Parkinsonism and medical and surgical treatment of advanced Parkinson's Disease.

Dr. Jeon earned his undergraduate, MD and PhD degrees from Seoul National University. His clinical interests include Parkinson's disease and other movement disorders including tremor, ataxia, dystonia, and chorea. His research focuses on the role of genetics in movement disorders, especially in the Korean population. He has established a DNA bank of thousands of Korean patients with movement disorders and normal controls. He is also involved in treatment of advanced Parkinson disease, and works with neurosurgical colleagues for various surgical treatment.

Han-Joon Kim, MD, PhD: Dr. Kim is a Professor in the Department of Neurology and the Movement Disorder Center at Seoul National University Hospital, Seoul, Korea. After graduation from the Medical College of Seoul National University in 1997, Dr. Kim took an internship and residency in neurology at Seoul National University Hospital (SNUH) where he became a Movement Disorder Specialist.

Clinically, Dr. Kim has experience with patients with various movement disorders including Parkinson's Disease (PD), Multiple System Atrophy (MSA), other atypical Parkinsonisms, and ataxias. Notably, Dr. Kim has set up a large registry of Korean MSA patients, which will serve as a basis for both observational and interventional studies in this rare disease.

Sonja W. Scholz, MD, PhD: Dr. Scholz is a Neurologist and Neurogeneticist specialized in movement and cognitive disorders. She received her medical degree from the Medical University Innsbruck, Austria. Following graduation, she was a post-doctoral fellow at the Laboratory of Neurogenetics at the NIH's National Institute on Aging (NIA) under the supervision of Drs. Andrew Singleton and John Hardy. She obtained a Ph.D. in Neurogenomics from the University College London, UK in 2010. She then moved to Baltimore to complete her neurology residency training at Johns Hopkins. In 2015, Dr. Scholz received the McFarland Transition to Independence Award for Neurologist-Scientists. She is a Lasker Clinical Research Tenure Track Investigator within the Neurogenetics Branch at the NIH's National Institute of Neurological Disorders and Stroke (NINDS). Her laboratory focuses on identifying genetic causes of neurodegenerative diseases, such as dementia with Lewy bodies, multiple system atrophy, and frontotemporal dementia.

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Moriah Meeks, MSA Coalition, +1 (312) 270-0171, mmeeks@staff.msacoalition.org

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The Multiple System Atrophy Coalition Announces a Groundbreaking Project to Explore the Genetics of MSA - Johnson City Press (subscription)

Data breaches are scarily common in todays digital world, and even gargantuan businesses can easily be brought to their knees should a wayward phishing attempt (or a disgruntled former employee) succeed in making off with valuable information.

While your small business probably doesnt have all of the same calibre of worries as your more monolithic counterparts, dont make the mistake of thinking that your data cant be stolen to devastating effect, even if you think the data you have is irrelevant and not worthy of being stolen (youre wrong).

Cloud storage and increased collaborative tool use means that things like sensitive documents and files are at increased risk of theft. Small businesses are especially susceptible to this due to a lower likelihood of advanced security usage, so it pays to know what kinds of things you might be at risk of losing.

According to MUO, employees are most likely to steal collaborative documents, consumer databases, and any resources devoted to research and development.

Safeguarding these items can be tricky due to their relatively high-traffic use, so a preventive strategy is your best defense.

It should be noted that trust in your employees is crucial, and treating them like theyre poised to steal from you at any moment is not a particularly effective management strategy.

However, its important to be aware of the following reasons and possible preventive measures for employee theft of data.

Firstly, corporate espionage (as dramatic as it sounds) is still something you have to worry about as a small business owner. It isnt uncommon for competitors to bribe (or even simply persuade) current employees to share data, even if your competitors are relatively small themselves.

Your employees should know that data is sacred (and confidential), but employing things like intrusion systems and holding trainings for recognition of espionage can help prevent this problem.

Those competitors might also try to snag some of your employees, and not just for their work ethic. Employees may save their own copies of documents that they think will be helpful in their new workspace; in doing so, they can unwittingly aid your competitor with much more than their skillset. Again, reminding your employees that all work documents are both confidential and property of your brand can cut down on accidental data theft in this category.

Non-Compete agreements and NDAs can also prevent this kind of theft, intentional or otherwise; if an employee chooses to leave your business, making sure they are aware of their contractual obligations is key. Perhaps the worst competitor you can have is a former employee who launches their own business in your field, though, and this is a situation in which data theft can be intellectual. Once again, Non-Competes and NDAs are helpful in mitigating damage in this context.

Finally, angry employees can find themselves doing a myriad of dumb (and harmful) things, up to and including data theft.

As mentioned earlier, early prevention is the best way to keep your data on your servers and out of your departing employees hands. Restricting employee access to files and folders can limit the number of possible breaches, and the aforementioned Non-Compete and Nondisclosure agreements are absolutely crucial in any business that deals in datajust make sure youre discussing the terms of those agreements with employees as they come and go.

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This startup wants to keep your dog alive longer based on genetic info - The American Genius

The first look at a threatened rattlesnake species recent genetic history suggests that inbreeding necessitated by limited habitat may not be as detrimental as theory would predict it to be.

In fact, scientists speculate that Eastern massasauga rattlesnakes may have pre-adapted to living in small, isolated populations where the most dangerous genetic mutations that arose could be easily exposed and purged.

Researchers sequenced the genomes of 90 Eastern massasauga rattlesnakes, which were listed as threatened under the Endangered Species Act in 2016 because of loss and fragmentation of their wetland habitat. For comparison, the researchers also sequenced 10 genomes of a close relative, the Western massasauga rattlesnake, a common species with no limitations on breeding opportunities and large populations.

The Ohio State University team found that the most potentially damaging gene mutations were less abundant in the Eastern than the Western species. This finding suggests the breeding limitations of small, isolated populations might be accompanied by an evolutionary advantage of being able to elbow out genetic variants that get in the way of survival, saidH. Lisle Gibbs, professor of evolution, ecology and organismal biology at Ohio State and senior author of the study.

This is something that has been reported very recently in other endangered species, but its the first time its been shown in a reptile, Gibbs said. We always worry about genetics and the loss of variation and what it means to be in a small population in which theres lots of inbreeding. At least in this species, maybe its not such a big deal.

From a conservation perspective, perhaps we can downplay genetics and say ecology such as habitat restoration is more important.

Gibbs completed the study with Alexander Ochoa, a former postdoctoral researcher at Ohio State who is now a postdoctoral scholar at the University of Central Florida. The research is published in the journal Molecular Ecology.

Eastern massasauga rattlesnakes live in isolated spaces in midwestern and eastern North America, and evolutionary theory posits that the inevitable inbreeding in such populations threatens species with extinction as genetic mutations accumulate. The smallest populations might reach 30 snakes, but Ohios Killdeer Plains Wildlife Area is home to one of the most genetically diverse and largest populations in the country, numbering in the thousands.

Gibbs has studied Eastern massasaugas for over two decades and, as director of the Ohio Biodiversity Conservation Partnership, advises the Ohio Department of Natural Resources on management of the species.

Through years and years of study, we know that most populations are isolated, like little natural zoos scattered throughout the landscape, Gibbs said. Due to habitat degradation, weve known they show little variation but weve never actually looked at variation in genes that code for things that matter to a rattlesnake.

Only recently has it been possible to apply the research techniques perfected with the human genome to work with this species. Gibbs and Ochoa zeroed in on identifying mutations in genes that may affect survival and reproduction to gauge how hazardous inbreeding might be to Eastern massasaugas.

Though a higher overall number of potentially deleterious mutations were found in the common Western massasaugas, that didnt translate to more threats to their survival because most troublesome gene copies were offset by protective copies. That can happen only in heterozygotes, which have two different copies, or alleles, of a particular gene one inherited from each parent. Because of generations of inbreeding, Eastern massasaugas are much more likely to have two copies of the same allele.

Thats why inbreeding has impacts because thats when you get two bad alleles showing up together, with no good allele to compensate, so there is a negative effect, Gibbs said. Theres more inbreeding, so overall you get more mostly bad mutations together, but the really bad ones, because theyre exposed, are also eliminated at a much greater rate.

Through another analytical technique comparing the narrowing of the Eastern and Western massasauga genetic makeup over several hundred years, Gibbs and Ochoa confirmed the impact human activity has had on the Eastern massasaugas swampy habitat. Unlike the Eastern species, Western massasaugas live in grassy and woodland regions of the south-central United States that are less densely populated by humans.

We looked at what has happened in these snakes and their population sizes over the last 300 years, which is when humans have been tromping all over North America, impacting the landscape, Gibbs said. The impacts in terms of reducing population sizes are greater in Eastern than in Western massasaugas over this period.

The findings could influence management decisions. A common conservation practice would involve introducing snakes from a more genetically diverse population into a highly isolated group to counter the effects of inbreeding. But it turns out the Eastern massasauga might benefit more from preservation of its habitat while the genetics takes care of itself.

This counterintuitive result makes us rethink what living in a small population is, and whether genetic problems are as important as we think they are, Gibbs said. This is certainly not to say living in a small population isnt bad it just may be that the genetic effects are not as bad as we thought.

This work was supported by the State Wildlife Grants Program administered jointly by the U.S. Fish and Wildlife Service and the Ohio Division of Wildlife, with funds provided by the Ohio Biodiversity Conservation Partnership between Ohio State and the Ohio Division of Wildlife, as well as the National Science Foundation.

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Threatened rattlesnakes' inbreeding makes species more resistant to bad mutations - The Ohio State University News

Dublin, Sept. 30, 2021 (GLOBE NEWSWIRE) -- The "Global Animal Genetics Market Research Report: Forecast (2021-2026)" report has been added to ResearchAndMarkets.com's offering.

The global animal genetics market is likely to grow at a CAGR of 6.4% in the forecast period of 2021-26 due to the surging advancements in continuous genetic alteration practices resulting in the growing production of animals with modified breeds and massive investments by numerous end-user industries. Animal producers are gaining huge milk & meat production by leveraging the technology of animal genetic alterations. With the help of strategic breeding, farmers can yield more substantial gains, which shall expand the end-user base and the overall market growth.

Based on the Animal Type, the Poultry segment registered the fastest market growth. It accounted for higher than USD 1.4 billion in recent years and is likely to continue the pace. The prominent factors for the market growth are the rise in the requirement for better quality food products, like meat, eggs & milk, and the flooding population & urbanization across regions. Hence, it shall continue to propel the demand and attain the fastest market growth in the forecast period.

Based on the Animal Type, the Canine segment in the animal genetics market shall attain the largest market share in the forecast years. It owes to the rapidly increasing research for high-quality breeding among dogs. Furthermore, the genetic research on canines is expanding the discovery of diverse genes implicating in the size, personality traits, and fur color. These factors are leading to the exponential demand for animal genetics to enhance the overall market share., states the author in their research report, "Global Animal Genetics Market Analysis, 2021."

Various microeconomic and macroeconomic characters are burgeoning exponential extensions for the APAC market. Factors like high population density and urban sprawl are enduring the demands of food producers to satisfy nutritional needs by increasing livestock production. Moreover, the animal healthcare ecosystem has been on a constant development path and is creating several opportunities for market leaders to bring effective testing procedures.

The Global Animal Genetics Market has a vast opportunity due to the constant launches and developments of new products and strategies. Various companies adopt these practices to extend their brand and product globally in the animal genetics industry.

With the swiftly surging population, their main objective is to meet the growing demands of different people. Moreover, producers operating in the market adopted different approaches of product innovation to cater to the rapidly changing customer demands.

Key Questions Answered in the Market Research Report:1. What are the overall market statistics or market estimates (Market Overview, Market Size- By Value, Forecast Numbers, Market Segmentation, Market Shares) of the Global Animal Genetics Market?2. What is the region-wise industry size, growth drivers, and challenges?3. What are the key innovations, opportunities, current & future trends, and regulations in the Global Animal Genetics Market?4. Who are the key competitors, their key strengths & weaknesses, and how do they perform in the Global Animal Genetics Market based on the competitive benchmarking matrix?5. What are the key results derived from the market surveys conducted during the Global Animal Genetics Market study?

Key Topics Covered:

1. Introduction

2. Preface

3. Executive Summary

4. Impact of COVID-19 on Global Animal Genetics Market

5. Global Animal Genetics Market Trends & Insights

6. Global Animal Genetics Market Dynamics

7. Global Animal Genetics Market Hotspots & Opportunities

8. Global Animal Genetics Market Regulations & Policy

9. Global Animal Genetics Market Outlook, 2016- 2026F

10. North America Animal Genetics Market Outlook, 2016-2026F

11. South America Animal Genetics Market Outlook, 2016-2026F

12. Europe Animal Genetics Market Outlook, 2016-2026F

13. Middle East & Africa Animal Genetics Market Outlook, 2016-2026F

14. Asia Pacific Animal Genetics Market Outlook, 2016-2026F

15. Key Strategic Imperatives for Success and Growth

16. Competition Outlook

Companies Mentioned

For more information about this report visit https://www.researchandmarkets.com/r/sjxkme

About ResearchAndMarkets.comResearchAndMarkets.com is the world's leading source for international market research reports and market data. We provide you with the latest data on international and regional markets, key industries, the top companies, new products and the latest trends.

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Opportunities in the Animal Genetics Market to 2026: Asia Pacific Set to Witness Rapid Growth in - GlobeNewswire