StemCell Therapy

Pregnancy for women marks the beginning of a new stage in their lives. Like any other parent, Juhi (namechanged) was excited when she learned about her pregnancy. She had suffered a miscarriage previouslyas her foetus was affected by down syndrome. While consulting with a geneticist, she was advised of a few options that included a non-invasive prenatal test (NIPT) to help screen for down syndrome and a fewother chromosomal disorders. She chose NIPT and waited anxiously for the results. The results arrived soon enough, and it was observed that Juhis baby had a very low or negligible risk ofhaving a serious chromosomal disorder. A few months later she delivered a healthy baby girl. Juhi was elated with the outcome and also understood the value of a genetic test and now advises all herrelatives to undergo a prenatal screening test. A non-invasive prenatal screening test provides expecting parents with reliable information about theirbabys genetic makeup. Such information is vital to expectant parents for thought-through earlypregnancy decisions and to avoid the distress caused by the birth of an abnormal baby unexpectedly.

What are chromosomaldisorders?

The human genetic material consists of 23 pairs of chromosomes. Therefore, any change in this number,wherein extra gain or loss of chromosome can lead to a serious disorder. The most common of thesedisorders are, Trisomy 21, Trisomy 18 and Trisomy 13, in the population.The estimated risk incidence of a baby with a chromosomal disorder is 1:166 births.Therefore, standard pregnancy care involves early screening for serious chromosomal abnormalities.

Genetic screening tests allow for identifying the genetic disorders or potential risks that the unborn babymay carry.NIPT (Non-Invasive Prenatal Test) has brought precision to the practice of diagnosis. With the advancement in technology, tests have been developed that are safe for the foetus and non-invasive. The non-invasive prenatal screening test can screen for common chromosomal abnormalitiessuch as Trisomy 21(Down syndrome), Trisomy 18 (Edward syndrome), Trisomy 13 (Patau syndrome) andcertain other abnormalities like monosomy X (Turners syndrome). There are three main reasons why couples should opt for a test:

It helps identify foetuses at risk of serious chromosomal abnormality.

Leads to better management by providing early information.

Prepares for birth and early intervention wherever possible.

Who needs to get tested?

Non-invasive prenatal testing can be recommended to any pregnant woman but is usually recommendedwhen:

The woman is above 30 years of age. Maternal serum screening provides abnormal results.

Certain abnormalities during the ultrasound are identified.

There is a family history of chromosomal conditions or congenital disabilities.

Couples have had a child with a chromosomal disorder.

A couple has a history of infertility or pregnancy loss.

Genetic testing of the pregnancy remains important as pregnancy is a time-sensitive period. When the general pregnant population is screened, most pregnancies eventually have a low risk of theseconditions. However, about 2-3% of the tested population by NIPT, receive a highrisk result whichrequires follow up confirmatory testing through invasive procedures.

(The author is an expert atreproductive genomics.)

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It's in the genetics - Deccan Herald

Torre, L. A. et al. Global cancer statistics, 2012. CA Cancer J. Clin. 65(2), 87108 (2015).

Article Google Scholar

Finnish Cancer Registry. Cancer Statistics Application (Finnish Cancer Registry, 2020).

Google Scholar

Nagy, R., Sweet, K. & Eng, C. Highly penetrant hereditary cancer syndromes. Oncogene 23(38), 64456470. https://doi.org/10.1038/sj.onc.1207714 (2004).

CAS Article PubMed Google Scholar

Wendt, C. & Margolin, S. Identifying breast cancer susceptibility genesA review of the genetic background in familial breast cancer. Acta Oncol. 58(2), 135146. https://doi.org/10.1080/0284186X.2018.1529428 (2019).

CAS Article PubMed Google Scholar

Melchor, L. & Bentez, J. The complex genetic landscape of familial breast cancer. Hum. Genet. 132(8), 845863. https://doi.org/10.1007/s00439-013-1299-y (2013).

CAS Article PubMed Google Scholar

Vahteristo, P., Eerola, H., Tamminen, A., Blomqvist, C. & Nevanlinna, H. A probability model for predicting BRCA1 and BRCA2 mutations in breast and breast-ovarian cancer families. Br. J. Cancer 84(5), 704708 (2001).

CAS Article Google Scholar

Eerola, H., Aittomki, K. & Nevanlinna, H. Genetic susceptibility to breast cancer. Finnish Med. J. 46, 46954701 (2002).

Google Scholar

Li, J. et al. Prevalence of BRCA1 and BRCA2 pathogenic variants in a large, unselected breast cancer cohort. Int. J. Cancer 144(5), 11951204. https://doi.org/10.1002/ijc.31841 (2019).

CAS Article PubMed Google Scholar

Syrjkoski, K. et al. Population-based study of BRCA1 and BRCA2 mutations in 1035 unselected Finnish breast cancer patients. J. Natl. Cancer Inst. 92(18), 15291531. https://doi.org/10.1093/jnci/92.18.1529 (2000).

Article PubMed Google Scholar

Buys, S. S. et al. A study of over 35,000 women with breast cancer tested with a 25-gene panel of hereditary cancer genes. Cancer 123(10), 17211730. https://doi.org/10.1002/cncr.30498 (2017).

CAS Article PubMed Google Scholar

Kuchenbaecker, K. B. et al. Risks of breast, ovarian, and contralateral breast cancer for BRCA1 and BRCA2 mutation carriers. JAMA 317(23), 24022416. https://doi.org/10.1001/jama.2017.7112 (2017).

CAS Article PubMed Google Scholar

Chen, S. & Parmigiani, G. Meta-analysis of BRCA1 and BRCA2 penetrance. J. Clin. Oncol. 25(11), 13291333. https://doi.org/10.1200/JCO.2006.09.1066 (2007).

Article PubMed Google Scholar

Tai, Y. C., Domchek, S., Parmigiani, G. & Chen, S. Breast cancer risk among male BRCA1 and BRCA2 mutation carriers. J. Natl. Cancer Inst. 99(23), 18111814. https://doi.org/10.1093/jnci/djm203 (2007).

CAS Article PubMed Google Scholar

Mersch, J. et al. Cancers associated with BRCA1 and BRCA2 mutations other than breast and ovarian. Cancer 121(2), 269275. https://doi.org/10.1002/cncr.29041 (2015).

CAS Article PubMed Google Scholar

Rebbeck, T. R. et al. Association of type and location of BRCA1 and BRCA2 mutations with risk of breast and ovarian cancer. JAMA 313(13), 13471361. https://doi.org/10.1001/jama.2014.5985 (2015).

CAS Article PubMed PubMed Central Google Scholar

GeneReviews. BRCA1- and BRCA2-Associated Hereditary Breast and Ovarian Cancer. https://www.ncbi.nlm.nih.gov/books/NBK1247/ (Accessed 20 June 2020).

Metcalfe, K. et al. International trends in the uptake of cancer risk reduction strategies in women with a BRCA1 or BRCA2 mutation. Br. J. Cancer 121(1), 1521. https://doi.org/10.1038/s41416-019-0446-1 (2019).

Article PubMed PubMed Central Google Scholar

Tschernichovsky, R. & Goodman, A. Risk-reducing strategies for ovarian cancer in BRCA mutation carriers: A balancing act. Oncologist 22(4), 450459. https://doi.org/10.1634/theoncologist.2016-0444 (2017).

CAS Article PubMed PubMed Central Google Scholar

Terry, M., Daly, M. & Phillips, K. Y. Risk-reducing oophorectomy and breast cancer risk across the spectrum of familial risk. J. Natl. Cancer Inst. 111(3), 331334 (2019).

Article Google Scholar

Auranen, A. Perinnllisen sypalttiuden tunnistamisella on merkityst mys gynekologisten sypien ehkisyss. Duodecim 134, 12621264 (2018).

Google Scholar

Kotsopoulos, J. BRCA mutations and breast cancer prevention. Cancers (Basel) 10(12), 524. https://doi.org/10.3390/cancers10120524 (2018).

CAS Article Google Scholar

Li, X. et al. Effectiveness of prophylactic surgeries in BRCA1 or BRCA2 mutation carriers: A meta-analysis and systematic review. Clin. Cancer Res. 22(15), 39713981. https://doi.org/10.1158/1078-0432.CCR-15-1465 (2016).

CAS Article PubMed Google Scholar

Pierce, L. J. et al. Ten-year multi-institutional results of breast-conserving surgery and radiotherapy in BRCA1/2-associated stage I/II breast cancer. J. Clin. Oncol. 24(16), 24372443. https://doi.org/10.1200/JCO.2005.02.7888 (2006).

Article PubMed Google Scholar

George, A., Kaye, S. & Banerjee, S. Delivering widespread BRCA testing and PARP inhibition to patients with ovarian cancer. Nat. Rev. Clin. Oncol. 14(5), 284296. https://doi.org/10.1038/nrclinonc.2016.191 (2017).

CAS Article PubMed Google Scholar

Robson, M. E. et al. American Society of Clinical Oncology policy statement update: Genetic and genomic testing for cancer susceptibility. J. Clin. Oncol. 33(31), 36603667. https://doi.org/10.1200/JCO.2015.63.0996 (2015).

CAS Article PubMed Google Scholar

Manchanda, R., Sun, S. & Patel, S. Economic evaluation of population-based BRCA1/BRCA2 mutation testing across multiple countries and health. Cancer 12(7), 1929. https://doi.org/10.3390/cancers12071929 (2020).

CAS Article Google Scholar

Yang, X. et al. Cancer risks associated with germline PALB2 pathogenic variants: An international study of 524 families. J. Clin. Oncol. 38(7), 674685. https://doi.org/10.1200/JCO.19.01907 (2020).

CAS Article PubMed Google Scholar

Kankuri-Tammilehto, M., Vihinen, P. & Schleutker, J. Heredity of cancer. Finnish Med. J. 14, 880886 (2019).

Google Scholar

Kiiski, J. I. et al. FANCM mutation c.5791C>T is a risk factor for triple-negative breast cancer in the Finnish population. Breast Cancer Res. Treat. 166(1), 217226. https://doi.org/10.1007/s10549-017-4388-0 (2017).

CAS Article PubMed PubMed Central Google Scholar

Mavaddat, N., Antoniou, A. C., Easton, D. F. & Garcia-Closas, M. Genetic susceptibility to breast cancer. Mol. Oncol. 4(3), 174191. https://doi.org/10.1016/j.molonc.2010.04.011 (2010).

CAS Article PubMed PubMed Central Google Scholar

Barkardottir, R. et al. Haplotype analysis in Icelandic and Finnish BRCA2 999del5 breast cancer families. Eur. J. Hum. Genet. 9(10), 773779 (2001).

CAS Article Google Scholar

Vehmanen, P. et al. Low proportion of BRCA1 and BRCA2 mutations in Finnish breast cancer families: evidence for additional susceptibility genes. Hum. Mol. Genet. 6, 2309 (1997).

CAS Article Google Scholar

Huusko, P. et al. Evidence of founder mutations in Finnish BRCA1 and BRCA2 families. Am. J. Hum. Genet. 62, 1544 (1998).

CAS Article Google Scholar

Sarantaus, L. et al. Multiple founder effects and geographical clustering of BRCA1 and BRCA2 families in Finland. Eur. J. Hum. Genet. 8(10), 757763 (2000).

CAS Article Google Scholar

Thomassen, M. et al. BRCA1 and BRCA2 mutations in Danish families with hereditary breast and/or ovarian cancer. Actancology 47, 772777 (2008).

CAS Google Scholar

Moller, P. et al. Genetic epidemiology of BRCA mutationsFamily history detects less than 50% of the mutation carriers. Eur. J. Cancer 43, 17131717 (2007).

Article Google Scholar

Rebbeck, T. et al. Mutational spectrum in a worldwide study of 29,700 families with BRCA1 or BRCA2 mutations. Hum. Mutat. 35, 593 (2018).

Article Google Scholar

Li, J. et al. Cancer therapy and prevention open access prevalence of BRCA1 and BRCA2 pathogenic variants in a large, unselected breast cancer cohort. Int. J. Cancer 144(5), 11951204 (2019).

CAS Article Google Scholar

Kremeyer, B. et al. The BRCA1 exon 13 duplication in the Swedish population. Fam. Cancer 4, 191194 (2005).

Article Google Scholar

Tonin, P. et al. Frequency of recurrent BRCA1 and BRCA2 mutations in Ashkenazi Jewish breast cancer families. Nat. Med. 2, 11791183 (1996).

CAS Article Google Scholar

Iyevleva, A. G. et al. Non-founder BRCA1 mutations in Russian breast cancer patients. Cancer Lett. 298, 258263 (2010).

CAS Article Google Scholar

Ghadirian, P. et al. The contribution of founder mutations to earlyonset breast cancer in French-Canadian women. Clin. Genet. 76, 421426 (2009).

CAS Article Google Scholar

Daly, M. B. et al. NCCN guidelines insights: Genetic/familial high-risk assessment: Breast and ovarian, version 2.2017. J. Natl. Compr. Cancer Netw. 15(1), 920. https://doi.org/10.6004/jnccn.2017.0003 (2017).

CAS Article Google Scholar

Yang, X. et al. Evaluation of polygenic risk scores for ovarian cancer risk prediction in a prospective cohort study. J. Med. Genet. 55(8), 546554. https://doi.org/10.1136/jmedgenet-2018-105313 (2018).

CAS Article PubMed Google Scholar

Mars, N. et al. The role of polygenic risk and susceptibility genes in breast cancer over the course of life. Nat. Commun. 11(1), 6383. https://doi.org/10.1038/s41467-020-19966-5 (2020).

ADS CAS Article PubMed PubMed Central Google Scholar

Finnish Breast Cancer Group. Rintasyvn valtakunnallinen diagnostiikka- ja hoitosuositus 2019. (Accessed 20 June).

Phi, X. A. et al. Magnetic resonance imaging improves breast screening sensitivity in BRCA mutation carriers age 50 years: Evidence from an individual patient data meta-analysis. J. Clin. Oncol. 33(4), 349356. https://doi.org/10.1200/JCO.2014.56.6232 (2015).

Article PubMed Google Scholar

Paluch-Shimon, S. et al. Prevention and screening in BRCA mutation carriers and other breast/ovarian hereditary cancer syndromes: ESMO Clinical Practice Guidelines for cancer prevention and screening. Ann. Oncol. 27(suppl 5), 103110. https://doi.org/10.1093/annonc/mdw327 (2016).

Article Google Scholar

Boyle, P. Triple-negative breast cancer: Epidemiological considerations and recommendations. Ann. Oncol. 23(Suppl 6), 712. https://doi.org/10.1093/annonc/mds187 (2012).

Article Google Scholar

Foulces, W. D., Smith, I. E. & Reis-Filho, J. S. Triple-negative breast cancer. N. Engl. J. Med. 363, 19381948. https://doi.org/10.1056/NEJMra1001389 (2010).

Article Google Scholar

Schaapveld, M. et al. The impact of adjuvant therapy on contralateral breast cancer risk and the prognostic significance of contralateral breast cancer: A population based study in the Netherlands. Breast Cancer Res. Treat. 110(1), 189197. https://doi.org/10.1007/s10549-007-9709-2 (2008).

CAS Article PubMed Google Scholar

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Genetic, clinic and histopathologic characterization of BRCA-associated hereditary breast and ovarian cancer in southwestern Finland | Scientific...

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If we understand the causes of cancer, then we can start highlighting the known causes, the lifestyle issues that introduce or increase our risk

Environmental and metabolic factors not just genetics are growing considerations in the fight against cancer, concludes a research review by a leading expert at the University of Alberta.

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Cancer as a genetic disease, focusing on the set of genetic instructions every person is born with; it is also an environmental disease, focusing on the exposome, which includes everything a persons body has been exposed to; and cancer is a metabolic disease, focusing on the metabolome, or all the chemical byproducts of the process of metabolism, explains David Wishart, professor in the departments of biological sciences and computing science, in a Thursday news release.

But that metabolic perspective hasnt had much research until now, as more scientists begin to understand the metabolomes role in cancer.

Heritable cancers account for just five to 10 per cent of all cancers, Wishart said, with the other 90 to 95 per cent initiated by factors in the exposome, which in turn trigger genetic mutations.

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Thats an important thing to consider, because it says that cancer isnt inevitable.

As cancer develops and spreads in the body, it creates its own environment and introduces certain metabolites, becoming a self-fuelled disease. And thats where cancer as a metabolic disorder becomes really important.

Considering the genome, exposome and metabolome together when thinking about cancer shows more promise for finding treatments.

Researchers who focus only on the genetic perspective are looking to address particular mutations but there are around 1,000 genes that can become cancerous when mutated, and it typically takes two different mutations within these cells for cancer to grow, notes Wishart, meaning there are a million potential mutation pairs. Then it can become hopeless to narrow down possibilities when seeking new treatments.

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But considering cancer from the metabolic perspective, there are just four major metabolic types, said Wishart, so determining the patients cancer type can immediately guide doctors on the best treatment for their specific cancer.

It really doesnt make a difference where the cancer is its something youve got to get rid of. Its how it thrives or grows that matters, said Wishart. It becomes a question of, Whats the fuel that powers this engine?

Wishart cautions that health-care providers still need a mix of therapeutics for cancer, and a deeper understanding of the metabolome and its role in the cancer feedback loop is also critical to preventing cancer.

If we understand the causes of cancer, then we can start highlighting the known causes, the lifestyle issues that introduce or increase our risk, he said.

From the prevention side, changing our metabolism through lifestyle adjustments will make a huge difference in the incidence of cancer.

The research review was funded by Genome Canada, the Canadian Institutes of Health Research and the Canada Foundation for Innovation.

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Treating, preventing cancer beyond genetics: U of A researcher - Edmonton Journal

Photo provided by Lionheart Cannabis

Chris Fanuzzi calls it his genetic library.

Seed descriptions, batch logistics and references to growers and cultivators who supplied some of the seeds are all noted in the heaps of pages of mostly handwritten notes in his trusty binder.

There are more than 400 recipes for Fanuzzis renowned rotating cannabis menu items, including the famous original Montana Silvertip, a hybrid strain. In the cannabis industry, the term strain refers to a variety of the cannabis plant and can include characteristics such as chemical profile, appearance and effects on consumers.

Maintaining the integrity of the original seeds over time is incredibly difficult for any cultivator, said Fanuzzi, owner and founder of Lionheart Cannabis, Montanas leading medical and recreational cannabis provider. Its an art to be able to sustain a particular genetic makeup of any one plant, especially when you consider these plants are growing alongside one another with the ability to pick up characteristics of the plant strains located, literally, right next to them. And that doesnt even take into account trying to maintain a completely stable environment from year to year, all against a backdrop of legislation that is constantly changing.

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But Fanuzzi has made it work. His company is renowned for its focus on quality, top-of-the-line products, compassionate patient care and educational awareness among clients.

Lionheart currently produces myriad oils, edibles and tinctures in a variety of flavors, strengths and price ranges. In addition to its headquarters in Bozeman, the company has five cultivation facilities throughout the state, as well as dispensaries in Billings, Butte, Helena, Great Falls (Herbal Bliss), Kalispell, Livingston andMissoula.

With 50 to 60 strains on the shelves at any one time, Lionheart is set to roll out scrolling digital menus that will provide customers with real-time product availability and pricing. The company is also enhancing its on-site customer experience by redesigning retail space to include more open floor plans and visual product display areas.

We want to encourage our customers to spend as much time as they want with our budtenders when they are onsite, to look at every jar to find that bud that is really going to work for them, he said. The online menu will only complement that experience.

But back to Montana Silvertip. A genetic cross between Purple Urkel (also known as Granddaddy Purple) and Super Silver Haze, the sativa-dominant bud has a THC level anywhere from 20% to 30%, with an earthy pine and blueberry taste.

Its an absolutely beautiful strain with hues of bright lavender and frosty white, Fanuzzi said. We continue to cross-pollinate its seeds with some of our other renowned strains such as Wedding Crasher, Mandarin Cookie, Purple Punch and Meathead, resulting in some really incredibly viable genetics with lots of different properties that are very popular with our customers.

Other favored staff picks include Do Si Dos, Kimbo Kush, Blue Dream, Lucky Charms, Key Lime Pie and Ginger Tea. And while consumers should note the THC potency levels listed on the product packaging, Fanuzzi said other things to consider include terpene profiles, how the buds are stored (glass jars and turkey bags are best), the smell (too much moisture results in a moldy odor) and feel (should feel spongy like a marshmallow when squeezed). If the bud is too dry, it will crumble. Also, buds stored in sunlight lose their potency more quickly.

Fanuzzi said as his recipe library for strains continues to grow, it also includes notations for those strains that have been bred out over time, including one of his most legendary" strains, the Papaya. Unfortunately, I developed it back in 2007 and never cloned it. So once it was gone, it was gone, recalled Fanuzzi.

Strains today represent combinations and cross-breeding of some of the best products and varieties people like. There are only so many families of land-raised genetics out there, so you continue to fine-tune until you achieve what you think is the perfect combination.

At that point, Fanuzzi adds another page to his binder.

Visit lionheartcannabis.com for more information.

Information provided is for educational and informational purposes only and does not supersede any medical advice given by a physician. Cannabis is still considered a schedule 1 controlled substance and is illegal under federal law. Adults who consume cannabis must keep cannabis products away from animals and out of reach of children. Note that the intoxicating effects of cannabis can sometimes be delayed, so do not operate a vehicle or machinery after consumption. Use of cannabis during pregnancy or while breastfeeding may be harmful. By purchasing cannabis from a dispensary, you are assuming the risk of any damage or loss that occurs during its use.

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Lionheart Cannabis' genetic strains stand the test of time - Billings Gazette

About the position

There is a vacancy for one PhD candidate at The Department of Clinical and Molecular Medicine in collaboration with The Department of Medical Genetics at St. Olavs hospital. The PhD candidate will work on different aspects of the Clinical Academic Group for Rare Genetic Diseases (CAG).

One of the main aims of the CAG is to apply state-of-the-art disease-modelling to the rare genetic diseases. The PhD project will address the steps in onset of neurodevelopmental diseases and identify potential points for diagnostic and therapeutic intervention.

We have implemented different human cell culture and organoid models that enable studying of disease development and progression, as well as the analysis of relevant pathomechanisms. The PhD student will be involved in generation and characterization of patient-specific and healthy-individual induced pluripotent stem cells, development of disease models and their characterization through transcriptome and proteome analysis, imaging and functional testing. As such the project includes work with big data sets.

Required selection criteria

The appointment is to be made in accordance with the regulations in force concerningState Employees and Civil ServantsandRegulations concerning the degrees ofPhilosophiaeDoctor (PhD)andPhilosodophiaeDoctor (PhD) in artistic researchnational guidelines for appointment as PhD, post doctor and research assistant

Preferred selection criteria

Personal characteristics

We offer

Salary and conditions

PhD candidates are remunerated in code 1017, and are normally remunerated at gross from NOK 491 200 per annum before tax, depending on qualifications and seniority. From the salary, 2% is deducted as a contribution to the Norwegian Public Service Pension Fund.

The period of employment is 3 years.

Appointment to a PhD position requires that you are admitted to thePhD programme in Medicine and Health Sciences within three months of employment, and that you participate in an organized PhD programme during the employment period.

The engagement is to be made in accordance with the regulations in force concerning State Employees and Civil Servants, and the acts relating to Control of the Export of Strategic Goods, Services and Technology. Candidates who by assessment of the application and attachment are seen to conflict with the criteria in the latter law will be prohibited from recruitment to NTNU. After the appointment you must assume that there may be changes in the area of work.

It is a prerequisite you can be present at and accessible to the institution daily.

About the application

The application and supporting documentation to be used as the basis for the assessment must be in English.

Publications and other scientific work must follow the application. Please note that applications are only evaluated based on the information available on the application deadline. You should ensure that your application shows clearly how your skills and experience meet the criteria which are set out above.

The application must include:

If all,or parts,of your education has been taken abroad, we also ask you to attach documentation of the scope and quality of your entire education, both bachelor's and master's education, in addition to other higher education. Description of the documentation required can befoundhere. If you already have a statement fromNOKUT,pleaseattachthisas well.

Joint works will be considered. If it is difficult to identify your contribution to joint works, you must attach a brief description of your participation.

In the evaluation of which candidate is best qualified, emphasis will be placed on education,experienceand personal and interpersonalqualities.Motivation,ambitions,and potential will also countin the assessment ofthe candidates.

NTNU is committed to following evaluation criteria for research quality according toThe San Francisco Declaration on Research Assessment - DORA.

General information

Working at NTNU

A good work environment is characterized by diversity. We encourage qualified candidates to apply, regardless of their gender, functional capacity or cultural background.

The city of Trondheimis a modern European city with a rich cultural scene. Trondheim is the innovation capital of Norway with a population of 200,000. The Norwegian welfare state, including healthcare, schools, kindergartens and overall equality, is probably the best of its kind in the world. Professional subsidized day-care for children is easily available. Furthermore, Trondheim offers great opportunities for education (including international schools) and possibilities to enjoy nature, culture and family life and has low crime rates and clean air quality.

As an employeeatNTNU, you must at all times adhere to the changes that the development in the subject entails and the organizational changes that are adopted.

In accordance with The Public Information Act (Offentleglova), your name, age, position and municipality may be made public even if you have requested not to have your name entered on the list of applicants.

If you have any questions about the position, please contact Professor Barbara van Loon, telephone +47 73 59 84 23, emailbarbara.v.loon@ntnu.no; Senior consultant clinical geneticist Rune stern, emailRune.Ostern@stolav.no. If you have any questions about the recruitment process, please contact Vebjrn F. Andreassen, e-mail:vebjorn.andreassen@ntnu.no

Please submit your application electronically via jobbnorge.no with your CV, diplomas and certificates. Applications submitted elsewhere will not be considered. Diploma Supplement is required to attach for European Master Diplomas outside Norway. Chinese applicants are required to provide confirmation of Master Diploma fromChina Credentials Verification (CHSI).

Application deadline: 16.05.22

NTNU - knowledge for a better world

The Norwegian University of Science and Technology (NTNU) creates knowledge for a better world and solutions that can change everyday life.

The Department of Clinical and Molecular Medicine (IKOM):

The Department of Clinical and Molecular Medicine (IKOM) is NTNUs largest department, with 450 employees. Our research and teaching help to improve treatment and health.

IKOM has expertise in basic, clinical and translational research within broad disciplinary areas. We study childrens and womens health, cancers, blood disorders and infectious diseases, gastroenterology, inflammation, metabolic disorders, laboratory sciences and medical ethics. The Department offers teaching in medicine at masters and PhD level. We also offer continuing education for employees in the health services.

Deadline16th May 2022EmployerNTNU - Norwegian University of Science and TechnologyMunicipalityTrondheimScopeFulltimeDurationProjectPlace of service

Excerpt from:
PhD Candidate in Rare Genetic Diseases job with NORWEGIAN UNIVERSITY OF SCIENCE & TECHNOLOGY - NTNU | 291220 - Times Higher Education

Is it possible to breed low-emissioncattle and sheep?

A group of Australian researchers and industry leaders think so and they are putting $19 million towards making it happen.

The University of New England, Armidale (UNE) is collaborating with Angus Australia, Meat and Livestock Australia and the NSW Department of Primary Industry to develop genetics to breed livestock that emits less methane.

The project is in line with the beef industry's goal to reach zero carbon emissions by 2030.

"We have always been keen to look at measuring the traits related to methane emissions on our cattle so in the future we can select Angus bulls that will produce lower methane but still be productive," Angus Australia's general manager for genetic improvementChristian Duffsaid.

Mr Duff said the organisation's involvement in the project was driven by the consumer.

"There is no doubt there is a trend towards people wanting to be aware of where their product comes from and its impact on the environment.

"The way we can have an impact is by making sure we're recording those methane traits on cattle ... and then in the future having information to select bulls."

UNE researchersare confident that, through the project, they can achieve a steady and permanent reduction in methane emissions from livestock.

Two UNEprofessors will investigate how to improve the genetic make-up of sheep and cattle.

Over the next five years, they will measure the methane output of 8,000 cattle and 10,000 sheep living in both feedlot and grazing conditions.

The variation between different animals will be analysed and data used to predict which of those animals have genetics that may lower the emissions they produce.

Associate Professor Sam Clark willresearchthe beef component, and saidboth projects could result in a 25 per cent reduction in methane emissions in livestock by 2050.

"A plausible amount to expect from genetic technologies is about 1 per cent methane reduction per year,"he said.

"The key point about that 1 per cent per year is that, when we use breeding to make that change, it's cumulative and permanent.

"It's a bit like your interest rate for the bank, it just keeps accumulating on top of itself."

The project is scheduled to start laterthis month.

See more here:
Armidale researchers hope genetic selection will be key to raising steaks with lower emissions - ABC News

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.

Media Contact

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

Lon Cardon, Ph.D., FMedSci

The Jackson Laboratory, an independent, nonprofit biomedical research institution, today announced the appointment of Lon Cardon, Ph.D., FMedSci, a pioneer in human genetics and drug discovery, as its next president and chief executive officer.

Bar Harbor, Maine, Oct. 04, 2021 (GLOBE NEWSWIRE) -- The Jackson Laboratory, an independent, nonprofit biomedical research institution, today announced the appointment of Lon Cardon, Ph.D., FMedSci, a pioneer in human genetics and drug discovery, as its next president and chief executive officer. Effective on November 29, Cardon will succeed current President and CEO Edison Liu, M.D., who will step down after a decade of leadership. Liu will continue to serve as a JAX professor studying the functional genomics of cancer with a focus on breast cancer.

After ten years of steering JAX through impressive expansion, dramatic change and remarkable achievements, Ed has made an indelible impact at JAX as a leader, researcher, and oncologist in our local communities and within the global biomedical research field, said David Roux, chairman of The Jackson Laboratory Board of Trustees. We are now thrilled to appoint Lon as the next president and CEO of JAX. Under his leadership, Lon will guide the Laboratory as it propels into its next intense period of growth.

Timothy Dattels, vice chairman of The Jackson Laboratory Board of Trustees and chair of the Presidential Search Committee added, As both an accomplished academic researcher as well as a demonstrated successful leader in both pharma and biotech, Lon is extremely well-suited to shape the vision, impact and strategic direction of The Jackson Laboratory over the next decade.

In his new role, Cardon will develop and drive a clear, integrated strategy for the Laboratorys continued long-term success, leveraging the unique and powerful interplay of JAXs deep expertise in mammalian genetics and human genomics combined with the latest advances in digital technologies such as artificial intelligence, machine learning and new computation platforms as well as its research, educational and business strengths.

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For many years there has been immense promise to translate human genetics and genomics discoveries into new diagnostics, prognostics and treatments for both common and rare diseases, said Cardon. Many of the foundational pieces are finally coming into place. The next step is to put them together to begin to realize this promise.

The Jackson Laboratory has a unique combination of critical components to finally approach the long-awaited potential of genetics for translation, coupling deep understanding of mouse models of human disease with extensive genetic and genomics expertise, large-scale research capacity, and computational and data analytics to bring it all together. I am excited to lead the organization to help shape a new era for human health where understanding all of our unique genomes will help to predict, treat and modify the course of disease.

Cardon joined BioMarin in September 2017 as chief scientific officer and senior vice president and was promoted in 2019 to chief scientific strategy officer to enrich BioMarins pipeline. Before joining BioMarin, he was a senior vice president at GlaxoSmithKline, leading departments and divisions spanning genetics, molecular biology, computational biology, statistics and epidemiology, and ultimately leading an early-to-late pipeline division called Alternative Discovery and Development. Prior to Cardons 14-year tenure in industry, he spent the first half of his career as a senior academic in the United Kingdom and United States, initially as professor of Bioinformatics at the University of Oxford and then as professor of Biostatistics at the University of Washington and co-chair of the Herbold Bioinformatics Program at the Fred Hutchinson Cancer Research Center.

Cardon received his Ph.D. from the University of Colorado and conducted his postdoctoral research in the Department of Mathematics at Stanford University. He has been awarded a Wellcome Trust Principal Fellowship and is an elected Fellow of the U.K.s Academy of Medical Sciences and the American Association for the Advancement of Science.

Cardon has authored more than 225 scientific publications and 15 books and chapters, mainly focused on genetics methodology, applications and discoveries for rare and common diseases, ranging from Huntingtons disease to dyslexia. He is an elected Fellow of the UKs Academy of Medical Sciences and the American Association for the Advancement of Science.

About The Jackson Laboratory

The Jackson Laboratory is an independent, nonprofit biomedical research institution with more than 2,400 employees. Headquartered in Bar Harbor, Maine, it has a National Cancer Institute-designated Cancer Center, a genomic medicine institute in Farmington, Conn., and facilities in Ellsworth and Augusta, Maine, in Sacramento, Calif., and Shanghai, China and a joint venture in Beijing. Its mission is to discover precise genomic solutions for disease and empower the global biomedical community in the shared quest to improve human health.

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The Jackson Laboratory appoints Dr. Lon Cardon as its next president and chief executive officer - Yahoo Finance

Theres growing concern about genetic discrimination in New Zealand and the lack of Government intervention in this fast-moving field.

As genetictesting becomes more accessible than ever before, there are calls for a line in the sand to be drawn and a final answer toaquestionnot yet canvassed: should insurers be able to use our geneticinformation?

Genetic discrimination is using someones genetic information to discriminate against them to treat them in a way thats different to someone else because we know something about their genetics.

Currently,lifeand health insurance companies in New Zealand are allowed to use thisdatain determining coverand premiumsfor applicants something experts sayanecdotalevidence suggest hasledto increased premiums, or no cover at all.

While insurers may argue it's their right to know a person's medical history researchers say genetics is, in fact, not a part of one's history, but a part of their future.

There are a lot of complexities in determining someone's genetic makeup and whether they are prone to getting a disease later in life.

There are also ways to mitigate and change the outcome of a patient's health once becoming privy to this information. For example, getting a mastectomywill drastically limit the chances of getting breast cancer, but there are fears an insurer may refuse cover based on a positive BRCA gene test regardless.

University ofOtago law and bioethics lecturerDr Jeanne Snellingsaysif people do have the test,and its positive, they can do things tominimisedevelopment of the disease.

They can undergo surveillance, get prophylactic preventative treatment and their risk could be quite similar to someone elses in the end. But, the insurance company is taking this absolutist approach saying that a positive test disqualifies you from obtaining life insurance cover.

There aredoubts about whether an insurance company would have staff with the expertise on hand to dissect someones genetic information.

University of Aucklands Faculty of Medical and Health Sciences Professor Andrew Shelling says it usually takes acastofspecialists to trawl through the data of an entire persons genome.

Good luck to the insurance company if they can find something, let us know. Because we have an entire team of experts from the clinicians to thebioinformaticiansto the geneticists who sit in a multi-disciplinary clinic each week trying to discuss the outcomes of what theyre looking at.

Based on the increased complexity of genetic testing nowadays, there is also a risk of getting it wrong if you dont have the right expertise. Hesaid.

There'salsoconcernpeople will not opt for undergoing genetic testing purely based on the fact it could be used by insurers -- and thus, miss out on the opportunity to decreasefuturehealth risks.

Despite the life-saving prevention available through genetic testing, experts say people avoiditand research because they are afraid of insurance discrimination.

This not only limits what a person can do to better their health in future -- but stunts medical research, particularly in minority groups like Mori and Pasifika, whose genetics are an even greater enigma to researchers than Pakeha.

Professor Shelling says we know that Mori have been discriminated against for years and this may be another form of it.

We base a lot of our genetics on European DNA, so for our Mori and Pasific people we dont always know what their results mean in a clinical setting.

We have an extra responsibility as genomic scientists to support Mori and Pasific getting genetic testing and make sure they dont get further discriminated against.

In a lot of our research studies around New Zealand, we are trying to increase the number of Mori and Pasific participants.

He fears if they have any concerns about insurance, theyllturn away from being part of these studies.

It's a conflict Jane Tiller anethical, legal and social advisor for Public Health Genomics at Melbournes Monash University --has battled for five years in Australia where a moratorium's been put in place to try and curb the issue.

Now, in Australia, you can get life insurance up to $500,000. If you try and take out more, you have to then disclose your genetic test results. she said.

She says the moratoriums a good step towards consumer protection but its a fraught approach.

"It goes up to certain financial limits and is only five years. So, we dont know what will happen in 2024 when it ends.

We are still gathering data about how its [the moratorium]working. Were remaining concerned about the lack of Government regulations on this issue.We would like to see a complete ban, like in Canada.

The moratorium isalso self-regulated by the insurance industry.

Self-regulation has been shown to be conflicted and problematic, both in Australia and New Zealand.

Theres very little transparency on how insurance companies use this data.Because this is self-regulated, theres a lot of questions around how decisions are made and what data is relied on.

The newly formed AGenDA (Against Genomic Discrimination Aotearoa) group, is lobbying for Government attention on this issue.

AGenDasmessage is that genetic discrimination is not only aconsumer protection issue, but a human rights issue.

Theysay itsnot just about making sure insurers get the information they need todiscriminate; its about stopping them from discriminatingaltogether. Its about ensuring consumers can make decisions about healthcare and learn empowering information without fear of discrimination for themselves or their family members.

They say thesectorhas come to presume divulgence -- an expectation thats been born of our insurance industry over many years.

The Financial Services Councils Richard Kiplin says its not something companies will ask for but if a client has information, it's only fair that they disclose it.

Within the New Zealand sector organisation by organisation will make their own calls. he said.

Whats important for New Zealand consumers to understand is that this is a complex area, and life companies need to assess risk and theyll do that in an appropriate way.

Genetic testing,at this point of time, is not a standard part of that -- but thats obviously evolving and moving very fast.

I think if people have had a genetic test and have information then they know information that a life and health company would want to understand. And so thats a part of the disclosure process.

Kiplin says hes open to working with researchers and other parties in future to solidify guidelines around genetic testing.

We have a robust committee structure thats been looking at some of these issues and reviewing guidelines.

The sector is never static, theres always stuff you can change and this is one of the big areas of the future.Hesaid.

AGenDAis alsoconcerned at the lack of Government intervention.

The Minister of Commerce and Consumer Affairs David Clark points towards the Ministry of Business, Innovation and Employment's Insurance Law Review.

"Insurer use of genetic testing results is one of many issues raised with MBIE during the course of the review, but it was not highlighted as a significant issue in the submissions (it was mentioned in two out of around 500 submissions received). Hesaid.

Clark mirrors the industrys openness to work with experts to understand the situation better.

Im told, the industryhavepreviously told my officials they are not seeing high levels of genetic testing, but I am open to further briefings on the matter.

The MBIEreview was promptedto ensure New Zealands insurance contract law is facilitating insurance markets that work well and enable individuals and businesses to effectively protect themselves against risk.

In November 2019 the Government agreed tothereform which includesmaking sure insurers ask consumers the right questions, the requirement for policies to be written and presented clearly, strengthening protection for consumers against unfair terms and extending powers to the Financial Markets Authority to monitor and enforce compliance.

Next steps for the review include release of an exposure draft Bill for consultation in late-2021.

Genetic testing has been described asa quantum leap for healthcare. A new kind ofapparatuswe can use to decode our future health.

In July 2021,the World Health Organization (WHO) provided the first global recommendations to help establish human genome editing as a tool for public health, with an emphasis on safety, effectiveness and ethics.

While their concerns are mainly based around the use of genetics to edit our DNA --WHO Director-General,Dr Tedros Adhanom Ghebreyesus, recognisedgenome editing and testing as a potential to advance our ability to treat and cure disease.

"But the full impact will only be realized if we deploy it for the benefit of all people, instead of fueling more health inequity between and within countries,Hesaid.

In September, the WHOrecommended DNA testing as a first-choice screening method for cervical cancer prevention.

It recognised DNA-based testing for human papillomavirus (HPV) has been shown to be more effective than todays commonly used screening methods aimed at detecting and preventing cervical cancer, a major cause of death among women worldwide.

Asgenetictestingbecomesmore mainstream,as the technologies mature,and as testsbecome moreprecise and affordable-- it evolves from being aniche offering tobecomingilluminatedon healthcarescentrestage.

And whilegenetictesting is applauded for its potential to become a part of our everyday health toolbox one question remains:should insurers be able to use our genetic information?

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Genetic discrimination: The next great health battle likely to wash up on NZ shores - Newstalk ZB

Sareptas Genetic Therapies Center of Excellence Building Exterior

The new, state-of-the-art research facility encompasses 85,000 square feet and significantly expands Sareptas global research and development capabilities.

Sareptas Chief Scientific Officer Louise Rodino-Klapac and CEO Doug Ingram were joined by distinguished guests including The Honorable JON HUSTED, Lieutenant Governor, State of Ohio; EDDIE PAULINE, President & CEO, BioOhio; JESSICA EVANS, Psy.D., Assistant Director, Speak Foundation; PAT FURLONG, President & CEO, Parent Project Muscular Dystrophy; and representatives from state and local government.

Center dedicated to research and development activities to advance Sareptas industry-leading, multi-platform pipeline

The Center encompasses 85,000 square feet of space, tripling Sareptas footprint in Ohio

CAMBRIDGE, Mass., Oct. 04, 2021 (GLOBE NEWSWIRE) -- Sarepta Therapeutics, Inc. (NASDAQ:SRPT), the leader in precision genetic medicine for rare diseases, today celebrated the grand opening of the Genetic Therapies Center of Excellence (GTCOE), its new research facility in Columbus, Ohio.

The 85,000 square foot state-of-the-art facility expands Sareptas research and development capabilities and footprint, which includes sites in Cambridge, Andover and Burlington, Mass. With more than 70 employees today and plans to double the number of employees by the end of 2022, the Center is focused on discovery, pre-clinical and clinical development supporting Sareptas pipeline of genetic medicines which includes RNA, gene therapy and gene editing programs. The Center also supports process development and optimization work that enables the transition from clinical-scale to commercial-scale manufacturing, a critical task facing companies developing gene therapies.

Advances in the science of genetic medicine are creating incredible opportunities to develop medicines with the potential to transform the lives of people with rare diseases. Sareptas Genetic Therapies Center of Excellence complements and enhances our existing research and development expertise and will play a central and strategic role in our future as the leader in precision genetic medicine, said Doug Ingram, president and chief executive officer, Sarepta.

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Among the guests joining the Sarepta team today for a dedication, ribbon-cutting ceremony and facility tours: The Honorable Jon Husted, Ohios Lieutenant Governor; Pat Furlong, president and chief executive officer, Parent Project Muscular Dystrophy (PPMD); Jessica Evans, assistant director, The Speak Foundation; local officials; and luminaries from Columbus growing biotechnology sector. At the event, Sarepta also announced a $20,000 donation to the Ronald McDonald House Charities of Central Ohio, with Dee Anders, chief executive officer and executive director, Ronald McDonald House Charities of Central Ohio, present to accept.

Sarepta has operated in Columbus since 2018 and were proud to be at the forefront of Columbus emergence as a leading hub for biotechnology committed to the local community and the patients and families we serve, said Louise Rodino-Klapac, Ph.D., Sareptas Columbus-based executive vice president and chief scientific officer. Our growing presence in Ohio will help us strengthen our close working relationships with long-standing local partners such as Nationwide Childrens Hospital, while we work with the greatest urgency to advance our pipeline, further the science of genetic medicine and create an environment where future generations of scientific talent will thrive.

Sarepta Therapeutics decision to expand in Ohio is the latest example that Ohio is a great state to grow a business, said Lt. Governor Jon Husted. When we created the Columbus Innovation District last year, we were focused on cultivating the right environment in central Ohio to attract new investments and jobs in gene and cell therapy. This new facility is a victory, as it builds on our strategy, creating jobs and producing some of the most advanced research and development of precision genetic medicine, further solidifying Ohio as a leader in gene therapy.

About Sarepta TherapeuticsSarepta is on an urgent mission: engineer precision genetic medicine for rare diseases that devastate lives and cut futures short. We hold leadership positions in Duchenne muscular dystrophy (DMD) and limb-girdle muscular dystrophies (LGMDs), and we currently have more than 40 programs in various stages of development. Our vast pipeline is driven by our multi-platform Precision Genetic Medicine Engine in gene therapy, RNA and gene editing. For more information, please visit http://www.sarepta.com or follow us on Twitter, LinkedIn, Instagram and Facebook.

Internet Posting of InformationWe routinely post information that may be important to investors in the 'For Investors' section of our website at http://www.sarepta.com. We encourage investors and potential investors to consult our website regularly for important information about us.

Forward-Looking StatementsThis press release contains "forward-looking statements." Any statements contained in this press release that are not statements of historical fact may be deemed to be forward-looking statements. Words such as "believes," "anticipates," "plans," "expects," "will," "intends," "potential," "possible" and similar expressions are intended to identify forward-looking statements. These forward-looking statements include statements regarding potential opportunities in the rare disease space; the potential transformative benefits of medicines in the rare disease space; our plans to double the number of employees in Columbus, Ohio by the end of 2022; and the potential for our growing presence in Ohio to help strengthen our close working relationships with long-standing local partners while we work with the greatest urgency to advance our pipeline, further the science of genetic medicine and create an environment where future generations of scientific talent will thrive.

These forward-looking statements involve risks and uncertainties that may cause actual results to differ materially from those expressed or implied in the forward-looking statements. Many of these risks and uncertainties are beyond our control. Known risk factors include, among others: we may not be able to execute on our business plans and goals, including meeting our expected or planned regulatory milestones and timelines, clinical development plans, and bringing our product candidates to market, due to a variety of reasons, many of which are outside of our control, including possible limitations on company financial and other resources, manufacturing limitations that may not be anticipated or resolved for in a timely manner, regulatory, court or agency decisions, such as decisions by the United States Patent and Trademark Office with respect to patents that cover our product candidates; the impact of the COVID-19 pandemic; and those risks identified under the heading Risk Factors in our most recent Annual Report on Form 10-K for the year ended December 31, 2020, and most recent Quarterly Report on Form 10-Q filed with the Securities and Exchange Commission (SEC) as well as other SEC filings we make, which you are encouraged to review.

Any of the foregoing risks could materially and adversely affect the Companys business, results of operations and the trading price of Sareptas common stock. For a detailed description of risks and uncertainties we face, we encourage you to review our SEC filings. We caution investors not to place considerable reliance on the forward-looking statements contained in this press release. We undertake no obligation to update forward-looking statements based on events or circumstances after the date of this press release, except as required by law.

Source: Sarepta Therapeutics, Inc.

Investor Contact: Ian Estepan, 617-274-4052iestepan@sarepta.com

Media Contact: Tracy Sorrentino, 617-301-8566tsorrentino@sarepta.com

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Sarepta Therapeutics Opens Genetic Therapies Center of Excellence in Columbus, Ohio - Yahoo Finance

Forester Bradley W. Antill will be a guest speaker at Weldon Baptist Church on Wednesday to discuss the subject Forest Genetics and the Tree of Life.

Born in Norton, Ohio, Antill said he moved to Shallotte to take up a forestry job with the Federal Paperboard. He then moved to Henrico in 1997 for a job with the Coastal Lumber Company in Weldon, which has since changed its name in 2004 to Coastal Timberlands Company.

According to a press release, Antill will discuss how trees are the lifeblood of the local forest industries.

Actually, our very life depends on a specific tree and what we do with it, Antill wrote as an excerpt in the press release. The forest industry has always been at the forefront of genetic research, including cloning; trying to get the best tree to grow. But only one specific tree can claim to be the source of eternal life, the Tree of Life.

The Rev. Francis Kyle, the new pastor at Weldon Baptist, said they are excited to hear Antill speak on the interlaced topics he is knowledgeable and passionate about.

Those intertwining topics are land, trees, people and the God of the Bible who created the land and trees on the third day of creation by merely speaking them into existence Genesis 1:9-13, and created male and female in His image on the sixth day Genesis 1:26-27, Kyle said. And, of course, the Lord Jesus Christ, the financially poor Jewish carpenter from Nazareth yet who simultaneously and supernaturally was also the unselfish and sinless Son of God who lovingly sacrificed Himself for us selfish sinners on an old rugged wooden cross at Calvary in Jerusalem. Brad is a shining and inspiring example of intentionally living to the glory of God in ones workplace.

When asked if his discussion will combine science and religion, Antill disagreed.

I use Creation, the things I see every day in the outdoors, to relate to the Creator, he said. Romans Chapter 1, clearly states that Gods creation is one of the ways God reveals himself, to teach us about who he is. The Bible is his guidebook.

Many in the modern world may prefer to separate science from religion, while others consider creation science instead, which is the teaching and research based upon the belief that biblical accounts of the creation of the world and universe are scientific facts.

Antill also disagreed that science and faith are polar opposites since science only exists because God created the universe and placed physical laws upon which science rests.

What I do is take various elements of forestry, trapping, hunting, fishing and history to illustrate a biblical truth, he said. Man has been searching for a special tree since he was kicked out of the Garden of Eden. So, maybe we can understand that search better by seeing how it is done in forestry.

When asked what people can expect to hear on Wednesday, Antill said his devotions and talks show that the words of the Bible can be understood by seeing the fingerprints left by God surrounding everybody.

Often it involves illustrations parables, similar to what Jesus used when he taught, he said. These everyday examples illustrate a spiritual truth or application found in the Bible. My audience may learn a little bit about forestry, but I hope they learn more about the Creator and his love for us.

Antill said he is passionate about this topic because the Creator desires everyone to understand that their lives have meaning and they were not accidents.

The first decision of consequence man had to make involved a tree, he said. The last decision of consequence a man will make will involve a tree. Lets get together and talk about both.

According to the press release, the presentation is part of Weldon Baptists new Uncommon Christian Speaker Series with a free lunch provided by the churchs Hospitality Committee. Antills outdoor-themed Christian devotional books will also be for sale at a discounted price of $7.

The event will be held from 11:30 a.m. to 1 p.m. inside the Daniel Fellowship Hall at Weldon Baptist Church, 609 Washington Ave. A question and answer session will follow at the presentation.

Read the rest here:
'Forest Genetics and the Tree of Life': Local forester to speak at Weldon Baptist about God, living things - The Daily Herald

The Supreme Court on Friday sought a response from the government on a plea challenging a notification for NEET-Super Specialities (NEET-SS) 2021 in August allowing postgraduates from a broad spectrum of medical disciplines to apply for Doctorate of Medicine (Medical Genetics) and Doctorate of National Board in Medical Genetics courses.

A Bench of Justices D.Y. Chandrachud and B.V. Nagarathna issued notice and listed the case for hearing after two weeks.

The order was passed on a petition filed by the Society of Indian Academy of Medical Genetics, which challenged the validity of the information bulletin published by the National Board of Examinations on August 31.

The society argued that the bulletin contradicted the guidelines prescribed by the National Medical Commission that only aspirants from Medicine, Paediatrics and Obstetrics could apply for the Medical Genetics courses concerned.

The petition noted that elite medical institutes such as the AIIMS restricted admissions to the Medical Genetics courses to these three streams.

Excerpt from:
Supreme Court issues notice to government on admission to Medical Genetics courses - The Hindu

My grandfather was convinced that his mothers depression began with his fathers stroke. Up to that point, my mother could handle life, he said. Suddenly, she couldnt, because she couldnt do anything about my dad. But I cant help but wonder if its more complicated than that. I think about what Austin told me about the genetic vulnerabilities we all inherit, and I find it hard to believe that Elfriedes depression suddenly appeared in her 60s.

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In recent years, research has been conducted into the idea of inherited family trauma, especially in relation to descendants of survivors of the Holocaust or Indian residential schools. While these are extreme examples of a traumatic event that can affect generations, further research also suggests that inherited trauma can affect anyone.Many of us walk around with trauma symptoms we cant explain, said Mark Wolynn, author of It Didnt Start with You: How Inherited Family Trauma Shapes Who We Are and How to End the Cycle, in an interview with Psychology Today. We might have a life-long depression that feels like ours but isnt ours.

According to Wolynn, mental illness symptoms could be the result of trauma that has been inherited. One of the most obvious signs is that we can experience a sudden onset of anxiety or fear when we hit a certain age or reach a certain milestone, he says. Its as though theres an ancestral alarm clock inside us that starts ringing.

To explore my own history, I wanted to learn more about Elfriede. So I visited my grandfather in his 24th-floor apartment in the middle of the pandemic summer. We sat a couple of metres apart; I wore a mask, and I sanitized my equipment before pushing record. My grandfathers apartment overlooked Winnipegs sprawling urban elm forest. It all seemed so far removed from the stories he was telling me.

During the war, Elfriede and her sons moved out of the city to avoid the bombings and lived with their relatives on a farm. She worked as a seamstress, trading her labour for food and other necessities. Despite the challenges, my grandfather said his mother was a joyful person during this time. We were always singing when we did the dishes, he said, adding that Elfriede was always whistling and full of vigour.

However, just because Elfriede sang and whistled doesnt mean there wasnt sadness or worry around their house. There were sad times, he admitted. In his family, it was acknowledged that this was a part of life, and he recalled his mother joking to enjoy being sad. You dont have to be strong when youre sad, she would tell him. If you need to cry, just go ahead and cry.

Talking with my grandfather about mental illness, I sometimes felt as though we were communicating across a great divide. He spoke in terms of clear causes and effects. I asked him if he had ever felt depressed or anxious, and he described a time in his early 30s, when he and my grandmother were living in Whitehorse with four children under the age of six. He hesitated to use the word anxiety but told me that there were times at the end of the month when the young couple could barely afford groceries. There was a reason for me being anxious, and I think if youre anxious for a reason, you should be.

One of the most obvious signs is that we can experience a sudden onset of anxiety or fear when we hit a certain age or reach a certain milestone. Its as though theres an ancestral alarm clock inside us that starts ringing.

But its not always that cut and dried for me. Often, I have a hard time determining what is causing my anxiety, or why some days I wake up feeling depressed and others I wake up feeling fine. I think about my unexplained anxieties or depression and I wonder if these could somehow be connected to a trauma experienced by Elfriede or one of my other ancestors whose experience of mental illness I know less about.

Of course, one of the main reasons for learning about these family histories is to also figure out ways to make mental illness a less disruptive part of ones life. Although our genetics or inherited trauma may predispose us to have a full mental illness jar, as Austin puts it, she also emphasizes that there are ways to manage its contents. Strategies such as exercise, routines, healthy eating habits, a good nights sleep or the right medication can help people avoid reaching the point where their jar is overflowing.

Just a couple of years ago, my mother began cross-stitching to help increase the size of her own jar. Most of the pieces shes stitched have a minimalist style colourful text on a plain background. Shes referred to it as a form of meditation, a way to ruminate on a particular word or phrase as she pierces the fabric with the needle and draws the thread through, over and over, until its finished. Shes stitched simple words, such as love or peace, as well as profanity-laced slogans such as fuck the patriarchy.

She stitched a series of pieces at the beginning of the pandemic, the ones that I described at the start of this essay. In the weeks after we stapled the messages to the utility poles around our neighbourhood, we watched as people shared their discoveries of the cross-stitches on local Facebook pages, describing how they had brightened their day or reminded them of the good in the world.

Its been more than a year since then, and, on the whole, I think I can confidently say that my mental health has improved. My mother and I still talk about the ways we experience our mental illness and the coping mechanisms that we have developed, but these days our conversations are less about managing mental health crises and more about whether we are feeling well enough to slowly wean ourselves off our medications. At the same time, I am now aware of the family history of mental illness that will shadow me throughout my life, possibly stitched into my very DNA, and how Im more prepared than ever to take it on.

***

Isaac Wurmann is a writer based in Berlin.

This story first appeared in Broadviews Oct/Nov 2021 issue with the title My fathers nose, my mothers anxiety.

We hope you found this Broadview article engaging.

Our team is working hard to bring you more independent, award-winning journalism. But Broadview is a nonprofit and these are tough times for magazines. Please consider supporting our work. There are a number of ways to do so:

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My mother and I have the same mental health disorders. But is it genetic? - Broadview Magazine

An international research team led bythe University of California, San Diego (UCSD) has identified a genetic cause for a syndrome that has stumped clinicians for many years. And thescientists saythey might be able toprevent the disease-causing mutation during pregnancy based on promising mouse studies.

The researchers identified the condition,dubbed Zaki syndrome,after doctors from around the world compared clinical notes that showed children born with it had DNA mutations in the Wnt-less, or WLS, gene. By boosting Wnt signaling with a drug in mouse models, they were able to reverse developmental disabilities caused by the disease, they reported in The New England Journal of Medicine.

Zaki is a rarecondition that hampers prenatal development ofthe eyes, brain, hands, kidneys and heart and that causes lifelong disabilities.The syndrome is named after Maha Zaki, M.D., Ph.D., at the National Research Center in Cairo, who was the first to spot it.

RELATED:Haisco to pay $140M to get the ball rolling on Biosplice's phase 3 osteoarthritis drug in China

The UCSD team, working withRady Childrens Institute for Genomic Medicine and researchers around the world,started by scouring databases of20,248 families who had children with neurodevelopmental disorders. They zeroed in on mutations in the WLS gene, which controls signaling levels for Wnt, a hormonelike protein that's involved in embryonic development. The scientists then created stem cells and mouse models of Zaki syndrome and used them to test a drug that boosts Wnt signaling.

The drug, CHIR99021, amped up Wnt signalingand restored development in the models. The mouse embryos grew body parts that had failed to develop, and their organs resumed normal growth, the scientists said.

The Wnt signaling pathway, discovered in the 1980s, has caught investor interest and is core to the missions of biotechs Surrozenand Biosplice Therapeutics, formerly known as Samumed. Biosplice's Wnt-modulating kinase inhibitor is in multiple phase 3 trials and has garnered licensing agreements in China and Korea in recent months. Meanwhile, Surrozen is targeting Wnt in designing regenerative medicines for diseases in the eye, lung, kidney and a host of other areas. Phase 1 studies are slatedfor next year, and the biotech hit the Nasdaq last month.

The UCSD-led team was surprised to discover that Zaki syndrome could could be prevented in preclinical models with a drug,said author Guoliang Chai, Ph.D., a former postdoctoral fellow at UCSD's School of Medicine, in a statement. Now the researchers are thinking about how to transform Zaki into an entirely preventable condition.We can see this drug, or drugs like it, eventually being used to prevent birth defects, if the babies can be diagnosed early enough.

Read this article:
Researchers unravel the genetic cause of a childhood disorder and a potential way to prevent it with drugs - FierceBiotech

"Cancer is a disease of genetics, yet clinical practice has struggled to keep pace with rapid advancements in research, particularly with respect to the role of germline genetics. Testing guidelines and medical policy often codify barriers, further lengthening the path to adoption of widespread testing and in some cases restricting access to precision therapies and clinical treatment trials," said Ed Esplin, M.D., Ph.D., FACMG, FACP, clinical geneticist at Invitae. "Research presented at ASCO shows that cancer-linked genetic changes are common across cancer types and when patients do receive germline testing, over two thirds of those with positive results are eligible for changes to their treatment plans. It's clear that incorporating germline testing alongside tumor profiling can help oncologists better tailor treatment for each patient."

Data from 250 pancreatic cancer patients from the landmark INTERCEPT study conducted at the Mayo Clinic found that nearly one in six patients with pancreatic cancer (n=38) showed cancer-linked genetic changes and, importantly, receiving germline testing was associated with improved survival.

A separate study of prostate cancer patients confirmed similar findings in other cancer types that limiting testing deprives patients and clinicians of actionable information. In the first-ever presentation of the PROCLAIM study, which was conducted primarily in community urology clinics, of patients diagnosed with prostate cancer, a significant number of cancer-linked variants were missed if testing was done based on NCCN guidelines. Of the 532 patients with clinician-reported data, nearly half, 45% (n=239), did not meet NCCN criteria. Overall, 59 patients had a cancer-linked variant; one in 10 of them did not meet the criteria (9.6%, n=23), and 12.3% (n=36) of patients met the criteria. When a 12-gene panel was used, only 29 patients were found to have a cancer-linked variant and one third of these patients were missed by guidelines.

A third study showed simply changing medical policy is not enough to drive changes in clinician adoption. In a review of two independent datasets, including commercially insured and Medicare Advantage enrollees, only 3% (n=1,675) of the 55,595 colorectal cancer patients received germline genetic testing, despite medical policy recommending germline genetic testing for all colorectal cancer patients (consistent with the INTERCEPT colorectal cancer study). Of the patients who received testing, 18% (n=143) had a cancer-linked variant and two thirds, or 67% (n=96), of those patients were potentially eligible for precision therapy and/or clinical trials.

"The data have been available for years that show knowing what changes patients have in their genes is beneficial to treating their cancer. Yet the oncology community has been slower to adopt germline testing than tumor profiling, for reasons that are not entirely clear. These data presented at ASCO highlight the need for oncologists to embrace germline genetic testing as routine practice for all cancer patients," said Robert Nussbaum, M.D., chief medical officer at Invitae. "A positive germline genetic result may enable patients to enroll in clinical trials or gain access to new precision medicines. And equally important, the discovery of an inherited variant can alert relatives to seek out earlier cancer screening, helping avoid later-stage diagnoses and offering a treatment benefit if cancer develops."

Invitae aims to help overcome obstacles to the adoption of genetic testing by providing physicians with clinical consults to help interpret results and reducing cost as a barrier to genetic information. Invitae also provides patients direct access to genetic counselors, helping to integrate routine genetic testing into patient care with GIA, a HIPAA-compliant chatbot. Family members are also able to receive no-charge genetic testing if a positive result is found.

Details of the 2021 ASCO presentations:

Oral Abstract Session: Prevention, Risk Reduction, and Hereditary Cancer

Poster Discussion Session: Prevention, Risk Reduction, and Hereditary Cancer

Poster Session: Prevention, Risk Reduction, and Hereditary Cancer

Poster Session: Gastrointestinal Cancer--GastroesophageaI, Pancreatic, and Hepatobiliary

About InvitaeInvitae Corporation(NYSE: NVTA) is a leading medical genetics company whose mission is to bring comprehensive genetic information into mainstream medicine to improve healthcare for billions of people. Invitae's goal is to aggregate the world's genetic tests into a single service with higher quality, faster turnaround time, and lower prices. For more information, visit the company's website atinvitae.com.

Safe Harbor StatementThis press release contains forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995, including statements relating to the benefits of germline testing and genetic information; and that the data presented at ASCO highlight the need for increased germline testing in all cancer patients regardless of medical policy. Forward-looking statements are subject to risks and uncertainties that could cause actual results to differ materially, and reported results should not be considered as an indication of future performance. These risks and uncertainties include, but are not limited to: the company's history of losses; the company's ability to compete; the company's failure to manage growth effectively; the company's need to scale its infrastructure in advance of demand for its tests and to increase demand for its tests; the company's ability to use rapidly changing genetic data to interpret test results accurately and consistently; security breaches, loss of data and other disruptions; laws and regulations applicable to the company's business; and the other risks set forth in the company's filings with the Securities and Exchange Commission, including the risks set forth in the company's Quarterly Report on Form 10-Q for the quarter ended March 31, 2021. These forward-looking statements speak only as of the date hereof, and Invitae Corporation disclaims any obligation to update these forward-looking statements.

Contact:Laura D'Angelo[emailprotected](628) 213-3283

SOURCE Invitae Corporation

http://www.invitae.com

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Germline genetic testing can benefit all cancer patients as a routine practice in cancer care - PRNewswire

The loss of diversity in fields and gardens has real consequences, according to Tommy Carter, USDA professor, soybean breeding and genetics emeritus faculty, North Carolina State University. Carter explains the importance of increasing genetic diversity in crops in this Sustainable, Secure Food blog.

Modern crop varieties are often too uniform genetically speaking for good agricultural health, Carter writes. Thats because many new varieties are too closely related like cousins or siblings. This uniformity makes them less useful as breeding stock in current breeding efforts because they have lost useful genes which are still present in the landraces.

Soybean provides a good example regarding the insufficient diversity in modern varieties. Farmers domesticated soybean perhaps five thousand years ago in central China. These seeds spread through most of Asia via caravans with population migration. Adapting soybean to local conditions as soybean spread slowly over Asia, ancient farmers selected out more than 10,000 diverse varieties from domestication to the present. Many of these are now preserved by USDA and China in seed banks.

Although the thousands of old Asian soybean landraces are genetically diverse, modern U.S varieties are not. In the process of developing modern soybean varieties for U.S. farmers, the first generations of U.S. soybean breeders (~1930-1990) essentially ignored genetic diversity. They instead focused on adapting soybean for mechanical farming. Hundreds of new varieties were released to U.S. farmers in a successful endeavor to improve productivity, but these varieties were not very diverse, genetically speaking.

Today, U.S. soybean breeding programs are widely recognized as limited by insufficient genetic diversity. Breeding progress slowed, and the reasons are twofold:

Two landmark soybean USDA cultivars, Lee and Forrest, in the southern U.S. offer prime examples of this problem. They were released in the 1950s and 1970s. Their superior agronomics and popularity on the farm led to their heavy use as parental stocks for breeding during the following decades.

The result was a new generation of progeny (soybean children) that were highly related not only to the landmark varieties Lee and Forrest, but to each other as well. Although they performed well in the field, these brother and sister soybeans were not good mating stock for producing new varieties. The term inbreeding is often used to describe this effect in animal breeding, and the term applies here as well.

Short-term gains made in developing Lee and Forrest, thus, came at the expense of long-term progress. Diversity, the basis for new progress, was lost. But a new plan from the USDA-ARS, known as the 301 Plan, has the goal to restore diversity to applied breeding programs. Science in the 301 Plan results in new, unique breeding lines which have diverse pedigrees and genetics.

A new release of soybean USDA-N6004 is part of that effort. When new varieties of plants are certified by the USDA, they receive an official registration number. Some breeders then choose to name their variety with a more common name, such as Lee and Forrest soybean mentioned. Breeders created USDA-N6004 soybean by hybridizing of USDA cultivar NC-Roy and Japanese cultivar Blue Side. Blue Side is a vegetable (edamame) soybean that comes from outside the U.S.s genetic base. Japanese germplasm generally is not well represented as parental stock in U.S. breeding. Thus, Japan appears to be a rich untapped source of diverse genes for future U.S. soybean breeding.

Source: Sustainable, Secure Food blog written by members of the American Society of Agronomy and Crop Science Society of America, which is solely responsible for the information provided and is wholly owned by the source. Informa Business Media and all its subsidiaries are not responsible for any of the content contained in this information asset.

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Increasing genetic diversity in crops is important - Farm Progress