Biochemistry

Postdoctoral Researcher, Seaweed Molecular Biology, Physiology and Genetics, Ryan Institute, School job with NATIONAL UNIVERSITY OF IRELAND, GALWAY |…

Postdoctoral Researcher Seaweed Molecular Biology, Physiology and Genetics, Ryan Institute, School of Natural Sciences.NUIG RES 192-22Applications are invited from suitably qualified candidates for a full time position as a Postdoctoral Researcher (Plant Molecular Biology & Metabolism) in the Plant Systems Biology research group of Dr. Ronan Sulpice at the National University of Ireland, Galway.This 24 months position is funded by the Marine Institute and is available from September 2022 to end date of August 2024.

Job Description:The successful candidate will combine advanced knowledge of molecular genetics research with large-scale metabolic and phenotypic screening of algae. The experiments will consist of large scale metabolic analyses and growth phenotyping screens, whole genome sequencing of Palmaria strains, and data will be aggregated in a built for purpose database. Traits of focus in the project will include identification of genetic markers to identify best performing strains, both for biomass quality and growth performance.Thus experimental approaches employed in the project will include DNAseq, biochemical assays, phenotyping, and extensive field- and lab-level screening.In addition to the experimental aspect of the project, the successful candidate is expected to contribute to the dissemination of the results, help to report the results, and participate in the daily life of the laboratory.

Duties: What the successful candidate will do attached to the specific post (list /bulletpoint)-Sample seaweeds-Extract DNA, and analyse NGS data generated-perform large throughput metabolic and growth analyses-collaborate with the laboratory team technically and scientifically-write papers/reports-interact with stakeholders-participate to report progress to grant agency-participate in dissemination activities-participate in lab management and co-supervision of students-may act as mentor to co-supervisor of students and have limited teaching hours

Qualifications/Skills required:

Essential Requirements:Track record in molecular biology, ideally with a background on micro- or macro-algae.PhD in Plant or seaweed biology and a good research track record that demonstrates strong capabilities and outputs.knowledge of R for analysis of large datasetsStrong proven (via publications, patents and other research outputs) research recordOrganisational, writing and report/paper drafting skills.Driving licenseSkills in biochemistry (metabolic analyses)

Desirable Requirements:Previous experience in a laboratory from the private sectorHave experience in grant writingEvidence for team working (including supervision and/or lab management experience)

Salary: 39,523- 45,609 per annum pro rata for shorter and/or part-time contracts (public sector pay policy rules pertaining to new entrants will apply).Start date: Position is available from 01/09/2022

Continuing Professional Development/Training:Researchers at NUI Galway are encouraged to avail of a range of training and development opportunities designed to support their personal career development plans.

Further information on research and working at NUI Galway is available on Research at NUI Galway

For information on moving to Ireland please see http://www.euraxess.ie

Further information about the laboratory is available at https://sulpice-lab.com/

Informal enquiries concerning the post may be made to Dr. Ronan Sulpice ronan.sulpice@nuigalway.ie

To Apply:Applications to include a covering letter, CV, and the contact details of three referees should be sent, via e-mail (in word or PDF only) to Dr. Ronan Sulpice ronan.sulpice@nuigalway.ie

Please put reference number NUIG RES 192-22 in subject line of e-mail application.

Closing date for receipt of applications is 5.00 pm 15/08/2022

We reserve the right to re-advertise or extend the closing date for this post.

National University of Ireland, Galway is an equal opportunities employer. All positions are recruited in line with Open, Transparent, Merit (OTM) and Competency based recruitment

'NUI Galway provides continuing professional development supports for all researchers seeking to build their own career pathways either within or beyond academia. Researchers are encouraged to engage with our Researcher Development Centre (RDC) upon commencing employment - see http://www.nuigalway.ie/rdc for further information.

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Postdoctoral Researcher, Seaweed Molecular Biology, Physiology and Genetics, Ryan Institute, School job with NATIONAL UNIVERSITY OF IRELAND, GALWAY |...

Genetics

Explained| Genetics and its Mendelian inheritance – The Hindu

Long before genes, genomes and genetics were known, Augustinian monk Gregor Mendel established three principles of inheritance from his experiments on pea plants.

Long before genes, genomes and genetics were known, Augustinian monk Gregor Mendel established three principles of inheritance from his experiments on pea plants.

Its a commonly observed habit in families to draw likenesses between members of the youngest generation and their ancestors. This baby has a smile like her mother, one would say, or, He has exactly the temperament of his grandfather. This project may be extended by some to even saying, X writes so well, she has inherited this from her eldest aunt. If someone should be outstandingly brilliant in math or history, quick follows the comment Its all in the genes.

Now, many of these traits may not be heritable, or little is known about whether they are inherited. So these statements often are mere speculations; however, they are speculations supported by a pervasive and instinctive knowledge of the laws of genetics and the mechanism of genes and heredity. Of course, its one thing to pull out statements like this based on purely anecdotal occurrences and quite another to demonstrate them through years of careful experimentation.

The latter is what Gregor Mendel did. In the 1860s, much before the gene was discovered or the term genetics was coined, Mendel, a monk of the order of St. Augustine, discovered the cornerstone of genetics the laws of Mendelian inheritance using a methodical approach that is the envy of scientists even today. For this, he later came to be celebrated as the father of genetics.

For eight years, starting with 22 pea plants, he and his disciples allowed the plants to self-pollinate and cross-pollinate and came up with around 10,000 descendent plants. By observing them, Mendel came up with three laws. The first of these is the principle of uniformity all the progeny of a cross between plants that differ in only one trait will look alike. This can be understood as follows if the parent plants differ by only one trait say, one has wrinkled seeds and one has round seeds but are alike in all other aspects, the progeny will all have round seeds or all have wrinkled seeds depending on which trait is dominant. It was Gregor Mendel who first introduced the concepts of dominant and recessive traits.

But he believed, and showed experimentally, that the progeny contain the other traits within them and pass them on to subsequent generations. Continuing our previous example, if the four identical-looking plants from generation two, all with round seeds, were cross-fertilized, their offspring would have a mix of round and wrinkled seeds in a 3:1 ratio. This showed that even though they themselves had only round seeds, they carried in them something, let us say particles, that passed on the trait to their offspring.

Based on the above concept, Mendel put forth the second principle of inheritance, which is that the particles which determine these traits are separated during meiosis into gametes, and that meiosis produces an equal number of egg or sperm cells that contain particles carrying each trait.

The third principle he laid down was the principle of independent assortment, which statesthat alleles of one locus segregate into gametes independently of alleles of other loci. This means the choiceof one trait (say round or wrinkled seeds) does not affect the passing on of choices of a different trait (such as white or purple flowers).

With these laws, Mendel established the foundation of genetics even though he did not know anything about genes, genomes and genetics. No wonder, then, that he is known as the father of genetics. He submitted these findings and his observations of eight years in 1865 to the relatively lesser-known journal published by the Natural History Society of Brno (now in the Czech Republic).The paper was not noticed or celebrated much when he was alive. When Mendel died in 1884, all his papers were burnt, making it really difficult to trace out his contributions.

Decades later, in 1900, Mendels paper was independently discovered by three scientists working in the field. Further work has revealed much more complex details of genetics and inheritance, but Mendel has a place that cannot be denied.

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Explained| Genetics and its Mendelian inheritance - The Hindu

Genetics

NIH grant awarded to Marshall researcher for studying genetic mechanisms of cocaine addiction – News-Medical.Net

Price E. Dickson, Ph.D., an assistant professor of biomedical sciences at the Marshall University Joan C. Edwards School of Medicine, has received a $407,000 grant from the National Institutes of Health to study the genetic and genomic mechanisms driving the relationship between social reward and cocaine addiction.

During the two-year R21 grant, Dickson and his research team will study the genetic and genomic mechanisms driving social reward and the preference for a social reward over a drug reward. Social rewards refer to the reinforcing social stimuli that individuals experience during interactions with others. A strong drive to seek out social interactions rather than drugs of abuse may confer addiction resistance, whereas the absence of this drive may result in addiction vulnerability, Dickson explains.

"Despite the importance of social rewards in addiction, the genetic mechanisms underlying variation in the preference for a social reward over a drug reward have been unexplored," Dickson said. "Because the mouse genome is very similar to the human genome, genetic studies using mice can provide valuable information about the genetics underlying human addiction."

To model the vast genetic diversity in humans, the team will use mice from the Collaborative Cross mouse panel, which contains almost all of the genetic diversity present in both wild and laboratory mice. To identify the genetic mechanisms underlying the preference for social interactions rather than addictive drugs, individual Collaborative Cross mice will have the choice to intravenously self-administer cocaine or to briefly interact with another mouse. Single-cell RNA sequencing will then be used to identify genetic signatures associated with these preferences in the reward circuitry of the brain.

"The successful completion of this project will provide a foundation for future deep characterization of identified genetic mechanisms driving the preference for a social reward over a drug reward in mice and contribute to the development of novel, more effective addiction treatments, Dickson said."

Since joining Marshall's faculty in 2020, Dickson has authored or co-authored four publications in academic journals and four presentations at scientific conferences. He is a recipient of a 2020 K99/R00 program grant from the National Institute on Drug Abuse to further his research on the genetic relationship between stress and addiction. Dickson joined the School of Medicine faculty in June 2020, following seven years of postdoctoral research at the Jackson Laboratory in Bar Harbor, Maine.

The grant (1R21DA054929-01A1) was announced July 12 by U.S. Senators Joe Manchin (D-WV) and Shelley Moore Capito (R-WV).

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NIH grant awarded to Marshall researcher for studying genetic mechanisms of cocaine addiction - News-Medical.Net

Genetics

Population genomics of Group B Streptococcus reveals the genetics of neonatal disease onset and meningeal invasion – Nature.com

Johri, A. K. et al. Group B Streptococcus: global incidence and vaccine development. Nat. Rev. Microbiol. https://doi.org/10.1038/nrmicro1552 (2006).

Nizet, V. I., Ferrieri, P. A. & Rubens, C. E. Molecular pathogenesis of group B streptococcal disease in newborns. Streptococcal Infect. Clin. Asp. Microbiol. Mol. Pathog. 180221 (Oxford Univ. Press, New York, NY, 2000).

Davies, H. G., Carreras-Abad, C., Le Doare, K. & Heath, P. T. Group B Streptococcus: trials and tribulations. Pediatr. Infect. Dis. J. https://doi.org/10.1097/INF.0000000000002328 (2019).

Seale, A. C. et al. Estimates of the burden of Group B Streptococcal disease worldwide for pregnant women, stillbirths, and children. Clin. Infect. Dis. https://doi.org/10.1093/cid/cix664 (2017).

World Health Organisation. Group B Streptococcus Vaccine: Full Value of Vaccine Assessment. Financial Analysis. (World Health Organisation, 2021).

Schuchat, A. Epidemiology of group B streptococcal disease in the United States: Shifting paradigms. Clin. Microbiol. Rev. https://doi.org/10.1128/cmr.11.3.497 (1998).

Bekker, V., Bijlsma, M. W., van de Beek, D., Kuijpers, T. W. & Van der Ende, A. Incidence of invasive group B streptococcal disease and pathogen genotype distribution in newborn babies in the Netherlands over 25 years: a nationwide surveillance study. Lancet Infect. Dis. https://doi.org/10.1016/S1473-3099(14)70919-3 (2014).

Bevan, D., White, A., Marshall, J. & Peckham, C. Modelling the effect of the introduction of antenatal screening for group B Streptococcus (GBS) carriage in the UK. BMJ Open https://doi.org/10.1136/bmjopen-2018-024324 (2019).

Ancona, R. J., Ferrieri, P. & Williams, P. P. Maternal factors that enhance the acquisition of group-B streptococci by newborn infants. J. Med. Microbiol. 13, 273280 (1980).

CAS PubMed Article Google Scholar

Tazi, A. et al. Risk factors for infant colonization by hypervirulent CC17 group B Streptococcus: toward the understanding of late-onset disease. Clin. Infect. Dis. 69, 17401748 (2019).

CAS PubMed Article Google Scholar

Gizachew, M. et al. Proportion of Streptococcus agalactiae vertical transmission and associated risk factors among Ethiopian mother-newborn dyads, Northwest Ethiopia. Sci. Rep. 10, 3477 (2020).

ADS CAS PubMed PubMed Central Article Google Scholar

Hung, L.-C. et al. Risk factors for neonatal early-onset group B streptococcus-related diseases after the implementation of a universal screening program in Taiwan. BMC Public Health 18, 438 (2018).

PubMed PubMed Central Article Google Scholar

Schrag, S. J. et al. A population-based comparison of strategies to prevent early-onset group B Streptococcal disease in neonates. N. Engl. J. Med. 347, 233239 (2002).

PubMed Article Google Scholar

Lawn, J. E. et al. Every country, every family: time to act for group B Streptococcal disease worldwide. Clin. Infect. Dis. ciab859, https://doi.org/10.1093/cid/ciab859 (2021).

Romain, A.-S. et al. Clinical and laboratory features of group B Streptococcus meningitis in infants and newborns: study of 848 cases in France, 20012014. Clin. Infect. Dis. 66, 857864 (2018).

PubMed Article Google Scholar

Alhhazmi, A., Hurteau, D. & Tyrrell, G. J. Epidemiology of invasive group B Streptococcal disease in Alberta, Canada, from 2003 to 2013. J. Clin. Microbiol. 54, 17741781 (2016).

CAS PubMed PubMed Central Article Google Scholar

Moore, M. R., Schrag, S. J. & Schuchat, A. Effects of intrapartum antimicrobial prophylaxis for prevention of group-B-streptococcal disease on the incidence and ecology of early-onset neonatal sepsis. Lancet Infect. Dis. 3, 201213 (2003).

PubMed Article Google Scholar

Ohlsson, A. & Shah, V. S. Intrapartum antibiotics for known maternal Group B streptococcal colonization. Cochrane Database Syst. Rev. https://doi.org/10.1002/14651858.CD007467.pub4 (2014).

Nishihara, Y., Dangor, Z., French, N., Madhi, S. & Heyderman, R. Challenges in reducing group B Streptococcus disease in African settings. Arch. Dis. Child. 102, 72 LP72 77 (2017).

Article Google Scholar

Buurman, E. T. et al. A novel hexavalent capsular polysaccharide conjugate vaccine (GBS6) for the prevention of neonatal group b streptococcal infections by maternal immunization. J. Infect. Dis. https://doi.org/10.1093/infdis/jiz062 (2019).

Madhi, S. A. et al. Safety and immunogenicity of an investigational maternal trivalent group B streptococcus vaccine in healthy women and their infants: a randomised phase 1b/2 trial. Lancet Infect. Dis. https://doi.org/10.1016/S1473-3099(16)00152-3 (2016).

Heyderman, R. S. et al. Group B streptococcus vaccination in pregnant women with or without HIV in Africa: a non-randomised phase 2, open-label, multicentre trial. Lancet Infect. Dis. https://doi.org/10.1016/S1473-3099(15)00484-3 (2016).

Nilo, A. et al. Anti-group B Streptococcus glycan-conjugate vaccines using pilus protein GBS80 as carrier and antigen: comparing lysine and tyrosine-directed conjugation. ACS Chem. Biol. https://doi.org/10.1021/acschembio.5b00247 (2015).

Absalon, J. et al. Safety and immunogenicity of a novel hexavalent group B streptococcus conjugate vaccine in healthy, non-pregnant adults: a phase 1/2, randomised, placebo-controlled, observer-blinded, dose-escalation trial. Lancet Infect. Dis. 21, 263274 (2021).

CAS PubMed Article Google Scholar

Martin, T. R., Ruzinski, J. T., Rubens, C. E., Chi, E. Y. & Wilson, C. B. The effect of type-specific polysaccharide capsule on the clearance of group B Streptococci from the lungs of infant and adult rats. J. Infect. Dis. 165, 306314 (1992).

CAS PubMed Article Google Scholar

Marques, M. B., Kasper, D. L., Pangburn, M. K. & Wessels, M. R. Prevention of C3 deposition by capsular polysaccharide is a virulence mechanism of type III group B streptococci. Infect. Immun. https://doi.org/10.1128/iai.60.10.3986-3993.1992 (1992).

Uchiyama, S. et al. Dual actions of group B Streptococcus capsular sialic acid provide resistance to platelet-mediated antimicrobial killing. Proc. Natl. Acad. Sci. USA. https://doi.org/10.1073/pnas.1815572116 (2019).

Herbert, M. A., Beveridge, C. J. E. & Saunders, N. J. Bacterial virulence factors in neonatal sepsis: group B streptococous. Curr. Opin. Infect. Dis. https://doi.org/10.1097/00001432-200406000-00009 (2004).

Lynskey, N. N. et al. Multi-functional mechanisms of immune evasion by the streptococcal complement inhibitor C5a peptidase. PLOS Pathog. 13, e1006493 (2017).

PubMed PubMed Central Article CAS Google Scholar

Bryan, J. D. & Shelver, D. W. Streptococcus agalactiae CspA is a serine protease that inactivates chemokines. J. Bacteriol. 191, 18471854 (2009).

CAS PubMed Article Google Scholar

Poyart, C. et al. Contribution of Mn-cofactored superoxide dismutase (SodA) to the virulence of Streptococcus agalactiae. Infect. Immun. 69, 50985106 (2001).

CAS PubMed PubMed Central Article Google Scholar

Gibson, R. L., Nizet, V. & Rubens, C. E. Group B Streptococcal -hemolysin promotes injury of lung microvascular endothelial cells. Pediatr. Res. 45, 626634 (1999).

CAS PubMed Article Google Scholar

Zhu, L. et al. Genetic basis underlying the hyperhemolytic phenotype of Streptococcus agalactiae strain CNCTC10/84. J. Bacteriol. 202, e00504e00520 (2020).

CAS PubMed PubMed Central Google Scholar

Deng, L. et al. Characterization of a two-component system transcriptional regulator, LtdR, that impacts group B Streptococcal colonization and disease. Infect. Immun. 86, e0082217 (2018).

CAS PubMed PubMed Central Article Google Scholar

Wang, N.-Y. et al. Group B streptococcal serine-rich repeat proteins promote interaction with fibrinogen and vaginal colonization. J. Infect. Dis. 210, 982991 (2014).

CAS PubMed PubMed Central Article Google Scholar

Buscetta, M. et al. FbsC, a novel fibrinogen-binding protein, promotes Streptococcus agalactiae-host cell interactions. J. Biol. Chem. 289, 2100321015 (2014).

CAS PubMed PubMed Central Article Google Scholar

Doran, K. S. et al. Blood-brain barrier invasion by group B Streptococcus depends upon proper cell-surface anchoring of lipoteichoic acid. J. Clin. Invest. 115, 24992507 (2005).

CAS PubMed PubMed Central Article Google Scholar

Almeida, A. et al. Whole-genome comparison uncovers genomic mutations between group B Streptococci sampled from infected newborns and their mothers. J. Bacteriol. 197, 33543366 (2015).

CAS PubMed PubMed Central Article Google Scholar

Andrea, G. et al. Pan-GWAS of Streptococcus agalactiae highlights lineage-specific genes associated with virulence and niche adaptation. MBio 11, e0072820 (2021).

Google Scholar

Read, T. D. & Massey, R. C. Characterizing the genetic basis of bacterial phenotypes using genome-wide association studies: a new direction for bacteriology. Genome Med. 6, 109 (2014).

PubMed PubMed Central Article CAS Google Scholar

Power, R. A., Parkhill, J. & De Oliveira, T. Microbial genome-wide association studies: lessons from human GWAS. Nat. Rev. Genet. https://doi.org/10.1038/nrg.2016.132 (2016).

Lees, J. A. et al. Large scale genomic analysis shows no evidence for pathogen adaptation between the blood and cerebrospinal fluid niches during bacterial meningitis. Microb. Genomics 3, e000103e000103 (2017).

Google Scholar

Lilje, B. et al. Whole-genome sequencing of bloodstream Staphylococcus aureus isolates does not distinguish bacteraemia from endocarditis. Microb. Genomics 3, e000138 (2017).

Google Scholar

Lees, J. A. et al. Joint sequencing of human and pathogen genomes reveals the genetics of pneumococcal meningitis. Nat. Commun. https://doi.org/10.1038/s41467-019-09976-3 (2019).

Li, Y. et al. Genome-wide association analyses of invasive pneumococcal isolates identify a missense bacterial mutation associated with meningitis. Nat. Commun. 10, 178 (2019).

ADS PubMed PubMed Central Article CAS Google Scholar

Young, B. C. et al. Panton-valentine leucocidin is the key determinant of staphylococcus aureus pyomyositis in a bacterial GWAS. Elife https://doi.org/10.7554/eLife.42486 (2019).

Kulohoma, B. W. et al. Comparative genomic analysis of meningitis- and bacteremia-causing pneumococci identifies a common core genome. Infect. Immun. 83, 41654173 (2015).

Davies, M. R. et al. Atlas of group A streptococcal vaccine candidates compiled using large-scale comparative genomics. Nat. Genet. 51, 10351043 (2019).

CAS PubMed PubMed Central Article Google Scholar

Chaguza, C. et al. Bacterial genome-wide association study of hyper-virulent pneumococcal serotype 1 identifies genetic variation associated with neurotropism. Commun. Biol. 3, 559 (2020).

CAS PubMed PubMed Central Article Google Scholar

Laabei, M. et al. Predicting the virulence of MRSA from its genome sequence. Genome Res. https://doi.org/10.1101/gr.165415.113 (2014).

Coll, F. et al. Genome-wide analysis of multi- and extensively drug-resistant Mycobacterium tuberculosis. Nat. Genet. https://doi.org/10.1038/s41588-017-0029-0 (2018).

Chewapreecha, C. et al. Comprehensive identification of single nucleotide polymorphisms associated with beta-lactam resistance within pneumococcal mosaic genes. PLoS Genet. 10, e1004547e1004547 (2014).

PubMed PubMed Central Article CAS Google Scholar

Farhat, M. R. et al. Genomic analysis identifies targets of convergent positive selection in drug-resistant Mycobacterium tuberculosis. Nat. Genet. 45, 11831189 (2013).

CAS PubMed PubMed Central Article Google Scholar

Suzuki, M., Shibayama, K. & Yahara, K. A genome-wide association study identifies a horizontally transferred bacterial surface adhesin gene associated with antimicrobial resistant strains. Sci. Rep. 6, 37811 (2016).

ADS CAS PubMed PubMed Central Article Google Scholar

Hicks, N. D., Carey, A. F., Yang, J., Zhao, Y. & Fortune, S. M. Bacterial genome-wide association identifies novel factors that contribute to ethionamide and prothionamide susceptibility in Mycobacterium tuberculosis. MBio 10, e00616e00619 (2019).

CAS PubMed PubMed Central Article Google Scholar

Sieber, R. N. et al. Genome investigations show host adaptation and transmission of LA-MRSA CC398 from pigs into Danish healthcare institutions. Sci. Rep. 9, 18655 (2019).

ADS CAS PubMed PubMed Central Article Google Scholar

Ma, K. C. et al. Adaptation to the cervical environment is associated with increased antibiotic susceptibility in Neisseria gonorrhoeae. Nat. Commun. 11, 4126 (2020).

ADS CAS PubMed PubMed Central Article Google Scholar

Chewapreecha, C. et al. Genetic variation associated with infection and the environment in the accidental pathogen Burkholderia pseudomallei. Commun. Biol. 2, 428 (2019).

CAS PubMed PubMed Central Article Google Scholar

Jamrozy, D. et al. Increasing incidence of group B streptococcus neonatal infections in the Netherlands is associated with clonal expansion of CC17 and CC23. Sci. Rep. 10, 9539 (2020).

ADS PubMed PubMed Central Article CAS Google Scholar

Bianchi-Jassir, F. et al. Systematic review of Group B Streptococcal capsular types, sequence types and surface proteins as potential vaccine candidates. Vaccine https://doi.org/10.1016/j.vaccine.2020.08.052 (2020).

Nicola, J. et al. Multilocus sequence typing system for group B Streptococcus. J. Clin. Microbiol. 41, 25302536 (2003).

Article CAS Google Scholar

Cheng, L., Connor, T. R., Sirn, J., Aanensen, D. M. & Corander, J. Hierarchical and spatially explicit clustering of DNA sequences with BAPS software. Mol. Biol. Evol. 30, 12241228 (2013).

CAS PubMed PubMed Central Article Google Scholar

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Population genomics of Group B Streptococcus reveals the genetics of neonatal disease onset and meningeal invasion - Nature.com

Genetics

Is alcoholism genetic? Everything you need to know as Vicky Pattinson opens up about her battles – Evening Standard

V

icky Pattison has opened up about her struggle with alcohol and said she was scared to have kids who felt broken like her.

The former Geordie Shore star, 34, has been working with Channel 4 on a documentary about her father, who is an alcoholic and her own relationship with alcohol.

During an interview with Skys Beth Rigby, Vicky admitted to having an addictive personality, adding that she was scared of history repeating itself, as her father is an alcoholic.

Vicky explained that she was unable to live a balanced life and was often self-sabotaging. The media personality said: I always worried because Im like him in a lot of ways and I was aware that I had an addictive personality.

Speaking about her fears around having children, Vicky said: I was also just really scared that I was going to have children who felt in some way broken like me.

But the documentary has brought us a lot of peace and clarity.

But, what is alcoholism, and is it genetic? Heres everything you need to know.

What is alcoholism?

The National Institute on Alcohol Abuse and Alcoholism (NIAAA) defines alcohol dependency as a form of problem drinking that has become severe, with compulsive behaviors and physical dependence associated with the condition.

What causes alcoholism?

Typically, alcohol addiction is considered to involve several complex risk factors:

Stress in ones work or home life may trigger an addiction. When the person drinks alcohol, for example, they may feel relaxed and happy compared to the stress they feel when they are sober. This reinforces the desire to use alcohol as a coping mechanism for stress.

Those who have mental illnesses, especially anxiety, depression, bipolar disorder, and schizophrenia are very likely to struggle with co-occurring alcohol use disorder.

Women are at risk of developing alcoholism faster than men due to differences in body mass, hormones, and metabolism.

Is alcohol dependecy genetic?

Genetics and family history are the most correlated with risk of alcohol dependency, in fact, genetic risk is about half of the problem, while family history is the other half.

Certainly, genetics are passed down through families, but family history also includes the environment in which one was raised. Childhood abuse, parental struggles, and mental illness in close family members all contribute to the risk of developing an addiction to drugs or alcohol.

These are numerous genes found to be associated with substance abuse, including alcoholism. Some genes can help a person regulate their alcohol consumption or avoid the substance altogether; others increase the persons risk of abusing alcohol.

Gene expression is also affected by environment. If a person grows up in a house with a parent who abuses drugs, struggles with mental illness, suffers a major financial setback or similar stress, and the child has a gene linked to alcohol use disorder, they are very likely to develop this condition later in life.

Prevention and education programs can address this risk as part of regular medical checkups. Genetics are understood to be a component of AUD, but not the sole cause.

If youre struggling with alcohol abuse, there are some useful tips on the NHS website for support.

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Is alcoholism genetic? Everything you need to know as Vicky Pattinson opens up about her battles - Evening Standard

Genetics

Cruchaga named Morriss Professor Washington University School of Medicine in St. Louis – Washington University School of Medicine in St. Louis

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Studies genetic architecture of neurodegenerative diseases

Carlos Cruchaga, PhD, has been named the Barbara Burton and Reuben M. Morriss III Professor at Washington University School of Medicine in St. Louis. Shown at his installation ceremony are (from left) David H. Perlmutter, MD, executive vice chancellor for medical affairs and dean of the School of Medicine; Cruchaga; and Chancellor Andrew D. Martin.

Carlos Cruchaga, PhD, a pioneer in the use of human genomic data to understand and elucidate the biology of neurodegenerative diseases such as Alzheimers disease, has been named an inaugural Barbara Burton and Reuben M. Morriss III Professor at Washington University School of Medicine in St. Louis.

Cruchaga was installed by Chancellor Andrew D. Martin and David H. Perlmutter, MD, executive vice chancellor for medical affairs, the George and Carol Bauer Dean of the School of Medicine and the Spencer T. and Ann W. Olin Distinguished Professor.

The professorship was created through a bequest from the late Reuben M. Morriss III and Barbara Burton Morriss to Washington University, to advance Alzheimers disease research.

The Morrisses were devoted members of the St. Louis community, and their investment in Washington University and specifically in Alzheimers research has created three endowed professorships bearing their names, Martin said. Through their generous gift to the university, they will continue to have a powerful impact on research and teaching at the university in perpetuity.

Added Perlmutter: We are deeply grateful to Barbara and Reuben Morriss for investing in Washington University and in our work to advance the understanding and treatment of Alzheimers disease. We look forward to future discoveries from the Cruchaga lab as Carlos combines complex technologies to identify genetic variants that may contribute to Alzheimers, Parkinsons disease and other devastating disorders.

Cruchagas research focuses on leveraging data from genetics, genomics and other omics and integrating that information with findings from neuroimaging and neuropathology to identify novel genes, biological pathways, molecular biomarkers and drug targets that may generate new approaches to diagnosing and treating neurodegenerative illnesses.

Carlos came to Washington University as a postdoc to study the genetics of neurodegenerative illnesses, said Charles F. Zorumski, MD, the Samuel Guze Professor and head of the Department of Psychiatry. In 2014, Carlos became the leader of the genetics group at the Knight Alzheimer Disease Research Center (ADRC) and at the Hope Center for Neurological Disorders in the Department of Neurology. And last year he became the founding director of the Neurogenomics and Informatics Center, pioneering approaches to improve the understanding of causes and potential treatments for these devastating illnesses.

Cruchaga has published more than 270 manuscripts and is the principal investigator on six grants funded by the National Institutes of Health (NIH). He is a core leader for the biobank and genetics core of the international Dystonia Coalition; the Aging Adult Brain Connectome project; the Alzheimers Biomarkers Consortium-Down Syndrome; the Knight ADRC genetics core; and the Dominantly Inherited Alzheimer Network (DIAN) genetics core.

Cruchaga earned his doctorate in biochemistry and molecular biology in 2005 at the University of Navarra in Pamplona, Spain. As a postdoc, he trained in quantitative human genomics in the laboratory of Alison Goate, DPhil, at Washington University. He established his own laboratory in 2011. His key aim has been to leverage genetics, multi-omics and functional genomics studies in neurodegeneration and diseases of the central nervous system and to translate those into improvements in human health by better understanding the molecular underpinnings of disease.

It is quite an honor to have our work recognized in this way, Cruchaga said. We have been attempting to leverage a great deal of information to identify treatments that might make a big difference in the lives of millions of people affected by Alzheimers disease and other neurodegenerative disorders. This endowment allows us to advance that work, help patients and provide hope for those affected by some very distressing diseases.

A graduate of Saint Louis Country Day School in Ladue, Mo., and Princeton University in New Jersey, Reuben Morriss III earned a law degree from Washington University in 1964. He joined Boatmens Bank, beginning a long career as a leader of the St. Louis financial sector. He eventually became chairman and president of Boatmens Trust Co., a position he held until his retirement in 1995. He was a board chair of Mary Institute and Saint Louis Country Day School and of William Woods University in Fulton, Mo. He also served on the boards of St. Lukes Hospital in Chesterfield, Mo., and the St. Louis Bi-State American Red Cross.

Barbara Burton Morris was a graduate of John Burroughs School in Ladue, and Briarcliff College in Westchester County, N.Y. She was a board member of the Alzheimers Association and the Central Institute for the Deaf, and she donated time and resources to many other local charitable and cultural institutions.

The couple was married for 48 years and had two children, Burton Douglass Morriss and Barbara Dulany Morriss; and five grandchildren. Reuben Morriss III died in 2006, and Barbara Burton Morriss died in 2018.

Washington University School of Medicines 1,700 faculty physicians also are the medical staff of Barnes-Jewish and St. Louis Childrens hospitals. The School of Medicine is a leader in medical research, teaching and patient care, and currently is No. 4 in research funding from the National Institutes of Health (NIH). Through its affiliations with Barnes-Jewish and St. Louis Childrens hospitals, the School of Medicine is linked to BJC HealthCare.

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Cruchaga named Morriss Professor Washington University School of Medicine in St. Louis - Washington University School of Medicine in St. Louis

Genetics

Lifestyle or Genetics: Which is More Important for Heart Health? – One Green Planet

It has been a busy day in the Emergency Department. Doctors, nurses, and other staff are bustling about, doing their best to provide excellent care for every patient. Dialogue fills the nursing stations with background noise. I am walking from room to room, tending to several patients, performing my initial evaluation on some, and providing test results to others. As I finally take a few moments to sit down in front of my computer and do some charting, the nurse in charge hands me the EMS phone.

The paramedic at the other end of the line informs me that they are en route with a 54-year-old male having severe chest pain and difficulty breathing. They have obtained an EKG that is concerning and have given him medications to treat his pain. Their estimated arrival time at our hospital will be in approximately ten minutes.

Upon receiving this report, I spring into action. I notify the nurses, and we begin preparing a room to care for our next patient, setting up monitors, IV start kits, and other resuscitative equipment. The ambulance pulls into the garage, and within another moment, the doors slowly swing open, and the crew rolls in. A dark-haired man is sitting up and leaning forward on the stretcher. Beads of sweat roll down his forehead, and he appears moderately distressed as he clutches his chest.

I greet my patient, Hi, Im Dr. Piriano. When did your symptoms begin?

He looks at me with fear in his eyes. Im so scared.

I know. I place my hand on his shoulder. Dont worry. Were going to help you.

I started to feel pressure in my chest about an hour ago. I feel nauseous, and Im having trouble breathing.

OK, got it. Were going to be doing a lot of things really quickly to take care of you. As I utter these words, a technician has already connected the patient to an EKG machine and is printing out the electrical tracing of his heartbeats. Once complete, she tears the paper from the machine and hands it to me. The pattern on the pink sheet is unmistakablethis man is indeed having a heart attack.

I explain the EKG findings to my patient and tell him that he will need a cardiac catheterization to find the blocked artery and place a stent to open it and restore blood flow to his heart. He is given heart-protective medications, the cardiologist is called, and he is soon whisked off to the catheterization suiteall within thirty minutes from the time he entered the Emergency Department. It is rewarding to know that this gentleman will receive a new lease on life. Modern medicine is undoubtedly incredible, and I am in awe knowing how much progress humans have made. It is truly miraculous to witness the coordinated efforts of a team of people acting so swiftly to save another persons life.

However, I still have one critical questiondid this persons heart attack have to happen at all? The answer to this question is where the story changes from one of suffering to one of hope.

My fictional patient, like millions of real people, has heart disease. Coronary artery disease (CAD) is the most common type of heart disease. It is caused by plaque build-up in the arteries supplying the heart with life-giving oxygen and nutrients, causing these blood vessels to narrow. The most recent statistic from February of 2022 reveals that about 18.2 million adults in the United States age 20 and older have CAD. Although this is certainly a harrowing fact, it can be drastically changed.

How so?

To answer this question, we have to look at the causes of CAD. Without getting into the details of the mechanisms of plaque build-up, suffice it to say that the major players in the development of CAD are cholesterol and inflammation. Thus, if we can lower these two things, we can also reduce our chances of plaque formation. Sounds greatbut how can we do this? The answer is that it all comes down to lifestyle, as levels of cholesterol and inflammation are intimately connected to how we live and what we eat.

Some people may object, citing bad genetics and stating that they have a strong family history of heart disease. They may note multiple relatives who suffered heart attacks at fairly young ages. It doesnt matter what I do. Im doomed to have a heart attack, they may state. On the surface, it may seem as though they have a valid point. However, digging deeper will reveal an entire realm of evidence and knowledge that refutes this belief.

Does lifestyle play a more important role in the health of our hearts than our genes do? Lets take a brief look at some of the research. One of the most prominent figures in this area of study is Dr. Dean Ornish. For more than three decades, Dr. Ornish and his colleagues, in collaboration with major academic institutions, have been conducting research studies investigating the effects of lifestyle on well-being. The participants in their studies made lifestyle changes that consisted of a low-fat vegetarian diet, aerobic exercise, stress management, smoking cessation, and group psychosocial support. Their results were nothing short of remarkable. Thus far, I have been speaking about the prevention of heart disease. These studies demonstrated that a healthy lifestyle could reverse heart disease that has already developed. Amazing! Two of these research papers have been published in the Journal of the American Medical Association and The Lancet. Another study also showed that lifestyle changes, such as those mentioned, improved many of the risk factors that lead to heart disease, such as body weight, blood pressure, and cholesterol.

Even more exciting is the fact that such lifestyle changes not only reduce the risk factors for heart disease but also affect our DNA. A field of science called epigenetics explores how our environments affect our genes. Moreover, it appears that genes have switches and can be activated and inactivated by environmental cues, such as our lifestyles. In other words, live an unhealthy lifestyle, and disease-preventing genes may be deactivated while disease-promoting genes may be activated. Conversely, live a healthy lifestyle, and the opposite may occur. One study examining prostate cancer found that lifestyle changes affected the expression of over 500 genes.

This information is truly powerful and inspiring. It provides evidence that we are not victims of our genes. An individual is not doomed to have a heart attack solely because many family members have already suffered through one. By changing our lifestyles, we can prevent disaster. We can control our destinies and our lives. We have that capability, and there is extraordinary hope in that.

Reducing your meat intake and eating more plant-based foods is known to help withchronic inflammation,heart health,mental wellbeing,fitness goals,nutritional needs,allergies,gut health,andmore! Unfortunately, dairy consumption also has been linked to many health problems, includingacne,hormonal imbalance,cancer, and prostate cancer,and has manyside effects.

For those interested in eating more plant-based, we highly recommend purchasing one of our manyplant-based cookbooksor downloading theFood Monster Appwhich has thousands of delicious recipes making it the largest vegan recipe resource to help reduce your environmental footprint, save animals and get healthy! And, while you are at it, we encourage you to also learn about theenvironmentalandhealth benefitsof aplant-based diet.

Here are some resources to get you started:

For more Animal, Earth, Life, Vegan Food, Health, and Recipe content published daily, subscribe to theOne Green Planet Newsletter! Lastly, being publicly-funded gives us a greater chance to continue providing you with high-quality content. Please consider supporting us by donating!

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Lifestyle or Genetics: Which is More Important for Heart Health? - One Green Planet

Genetics

mLOY: The genetic defect that explains why men have shorter lives than women – EL PAS USA

We have long been baffled as to why men live around five years less than women, on average. But now a new study suggests that, beyond the age of 60, the main culprit is a genetic defect: the loss of the Y chromosome, which determines sex at birth.

Its clear that men are more fragile, the question is why, explains Lars Forsberg, a researcher at Uppsala University in Sweden.

For decades it was thought that the male Y chromosomes only function was to generate sperm that determine the sex of a newborn. A boy carries one X chromosome from the mother and one Y from the father, while a girl carries two Xs, one from each parent.

In 1963, a team of scientists discovered that as men age, their blood cells lose the Y chromosome due to a copying error that happens when the mother cell divides to produce a daughter cell. In 2014, Forsberg analyzed the life expectancy of older men based on whether their blood cells had lost the Y chromosome, a mutation called mLOY. The effect recorded was mindblowing, the researcher recalls.

Men with fewer Y chromosomes had a higher risk of cancer and lived five and a half years less than those who retained this part of the genome. Three years later, Forsberg discovered that this mutation makes getting Alzheimers three times as likely. What is most worrying is the enormous prevalence of this defect. Twenty percent of men over the age of 60 have the mutation. The rate rises to 40% in those over 70 and 57% in those over 90, according to Forsbergs previous studies. It is undoubtedly the most common mutation in humans, he says.

Until now, nobody knew whether the gradual disappearance of the Y chromosome in the blood played a pivotal role in diseases associated with aging. In a study just published in the journal Science, Forsberg and scientists from Japan and the US demonstrate for the first time that this mutation increases the risk of heart problems, immune system failure and premature death.

The researchers have created the first animal model without a Y chromosome in their blood stem cells: namely, mice modified with the gene-editing tool CRISPR. The study showed that these rodents develop scarring of the heart in the form of fibrosis, one of the most common cardiovascular ailments in humans, and die earlier than normal mice. The authors then analyzed the life expectancy recorded in nearly 15,700 patients with cardiovascular disease whose data are stored in the UK public biobank. The analysis shows that loss of the Y chromosome in the blood is associated with a 30% increased risk of dying from cardiovascular disease.

This genetic factor can explain more than 75% of the difference in life expectancy between men and women over the age of 60, explains biochemist Kenneth Walsh, a researcher at the University of Virginia in the US and co-author of the study. In other words, this mutation would explain four of the five years lower life expectancy in men. Walshs estimate links to a previous study in which men with a high mLOY load live about four years less than those without it.

It is well known that men die earlier than women because they smoke and drink more and are more prone to recklessness. But, beyond the age of 60, genetics becomes the main culprit in the deterioration of their health: It seems as if men age earlier than women, Walsh points out.

The study reveals the molecular keys to the damage associated with the mLOY mutation. Within the large group of blood cells can be found the immune systems white blood cells responsible for defending the body against viruses and other pathogens. The loss of the Y chromosome triggers aberrant behavior in macrophages, a type of white blood cell, causing them to scar heart tissue, which in turn increases the risk of heart failure. Researchers have shown that the damage can be reversed if they give mice pirfenidone, a drug approved to treat humans with idiopathic pulmonary fibrosis, a condition in which the lungs become scarred and breathing becomes increasingly difficult.

There are three factors that increase the risk of Y chromosome loss. The first is the inevitable ageing process. The longer one lives, the more cell divisions occur in the body and the greater the likelihood of mutations occurring in the genome copying process. The second is smoking. Smoking causes you to lose the Y chromosome in your blood at an accelerated rate; if you stop smoking, healthy cells once again become the majority, says Walsh. But the third is also inevitable: other inherited genetic mutations can increase the gradual loss of the Y chromosome in the blood by a factor of five, explains Forsberg.

Both Forsberg and Walsh believe that this study opens up an enormous field of research. Still to be studied is whether men with this mutation also have cardiac fibrosis and whether this is behind their heart attacks and other cardiac ailments. We also need to better understand why losing the Y chromosome damages health. For now, we have shown that the Y chromosome is not just there for reproduction, but is is also important for our health, says Forsberg. The next step is to identify which genes are responsible for the phenomenon.

The loss of this chromosome has been detected in all organs and tissues of the body and at all ages, although it is more evident after 60. It is abundant in the blood because this is a tissue that produces millions of new cells every day from blood stem cells. Healthy stem cells produce healthy daughter cells and mutated ones produce daughter cells with mLOY.

A previous study showed that this mutation of the Y chromosome disrupts the function of up to 500 genes located elsewhere in the genome. It has also been shown to damage lymphocytes and natural killer cells, evident in men with prostate cancer and Alzheimers disease, respectively.

There are hardly any tests for mLOY at present. But Forsberg and his colleagues have designed a PCR test that measures the level of this mutation in the blood and could serve to determine which levels of this mutation are harmful to health. Right now, we see people in their 80s with 80% of their blood cells mutated, but we dont know what impact this has on their health, says Walsh.

Another unanswered question is why men lose the genetic mark of the male with age. The evolutionary logic, argue the authors of the paper, is that men are biologically designed to have offspring as soon as possible and to live 40 to 50 years at most. The spectacular increase in life expectancy in the last century has meant that men and women live to an advanced age 80 and 86 years in Spain, respectively which makes the effect of these mutations more evident. Another fact which possibly has some bearing on the issue: the vast majority of people who reach 100 are women.

To transform all these discoveries into treatments, we first need to better understand this phenomenon, says Forsberg. We men are not designed to live forever, but perhaps we can increase our life expectancy by a few more years.

Biochemist Jos Javier Fuster, who studies pathological mutations in blood cells at the National Center for Cardiovascular Research, stresses the importance of the work. Until now it was not clear whether the loss of Y was the cause of cancer, Alzheimers disease and heart failure, he explains. This is the first demonstration in animals that it has a causal role. The human Y chromosome is different from the mouse chromosome, so the priority now is to accumulate more data in humans. This is a great first step in understanding this new mechanism behind aging-linked diseases, he adds.

The cells of the human body group their DNA into 23 pairs of chromosomes that pair up one by one when a cell copies its genome to generate a daughter cell. The Y is the only one that does not have a symmetrical partner to pair up with: instead, it does so with an X chromosome; and the entire Y chromosome is often lost, explains Luis Alberto Prez Jurado from Pompeu Fabra University in Barcelona. For now, six genes have been identified within the Y chromosome that would be responsible for an impact on health, he says. All of them are related to the proper functioning of the immune system. In part, this would also explain the greater vulnerability of males to viral infections, including Covid-19.

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mLOY: The genetic defect that explains why men have shorter lives than women - EL PAS USA

Genetics

CUHK Business School Research Reveals the Genetic Makeup of a Leader – NewsPatrolling

HONG KONG SAR Media OutReach 21 July 2022 Is there such a thing as a natural-born leader? A new study sheds light on the genetic influences on leadership and found a surprising connection with bipolar disorder and alcohol consumption.

Individuals in leadership positions are more likely to have certain genes and not all of them are good. An increased tendency to drink alcohol which has been shown to cause cancer and an increased risk of bipolar disorder are among the negative health indicators associated with leaders, according to findings from a new study.Identifying these specific genes helps us understand how our biology influences occupational health and well-being, and specifically, how that plays out among people in leadership positions.Our findings provide insights into the heredity of leadership positions and also the shared genetic underpinnings between the leadership position itself and ones general health, saysLi Wendong, Associate Professor at Department of Management at The Chinese University of Hong Kong (CUHK) Business School, and a co-author of the study.Our research continues the biological story of leadership. Since the late 1980s, studies using twins have shown that differences in peoples genetic make-up account for 30 percent of differences in whether they hold leadership roles. Now we have gone a step further in and conducted genomic studies using a vast database to identify genes related to leadership, adds Prof Li, who notes that the study has implications for leaders and prospective leaders in managing their health and well-being for their long-term career development.A significant reason why our findings matter is that leaders well-being affects their behaviours, which may influence the performance and well-being of their subordinates, teams, and organisations. The implications arising from a leaders health can be vast, he says.Diving Deeper Beyond Twin StudiesThe research team, which were led by of Prof. Li, Prof. Song Zhaoli at the National University of Singapore and Prof. Fan Qiao at Duke-NUS Medical School, conducted the study using data from the U.K. Biobank, the largest public genetic and health database in the world. Researchers extracted genetic and occupational information of over 240,000 individuals of European ancestry. They also tapped on the U.K. Standard Occupation Classification and U.S. Occupational Information Network for information related to leadership roles and managing demands.Leadership has been an important and classic topic in genetic research since the early 19th century, when modern human genetics was first formed as a scientific field.Modern genetics research on leadership appeared much later using the classic twin approach. Twin studies are studies conducted on identical or fraternal twins. They aim to reveal the relative importance of environmental and genetic influences. Twin research is considered a key tool in behavioural genetics and in content fields, from biology to psychology.The new study, titledGenetics, leadership position, and well-being: An Investigation with a large-scale GWAS, furthered previous areas of inquiry by providing results from a whole-genome exploration of leadership. It unraveled genetic correlations between leadership and known measures of well-being and health. The study also considered other socioeconomic measures such as income and education so that what was revealed was a truer picture of leaders genetic profiles.Watch Out at the TopThe study brought to light possible unique genetic associations between well-being and leadership. It found that genetic influences associated with leadership position may be detrimental to well-being. This is in contrast to previous research that showed a positive correlation between leadership and general health and well-being indicators and revealed a fundamental reason why holding a leadership position is not always beneficial to ones health and well-being.After adjusting for the effects of income and education, holding leadership positions was genetically linked to a higher Body Mass Index, an increased risk for cardiovascular disease, and further reduced longevity.The high psychological demands embedded in holding leadership positions chronic stressors might play a role because they stimulate psycho-biological stress responses, including changes in fat metabolism and cardiovascular function, which are detrimental to health in the long run. says Prof. Li.In other words, leaders may be genetically pre-disposed to develop the above stress-induced diseases and conditions, but the stress involved in being a leader can trigger or exacerbate such an impact.One of the most relevant and surprising genetic markers this study found to be associated with leadership is the genetic variant linked to an increased risk of bipolar disorder and schizophrenia.While those with bipolar disorder or schizophrenia may have some advantages to become leaders, we are the first to find genetic variants linked to both leadership and bipolar disorder and schizophrenia, says Prof. Li.Bipolar disorder, formerly called manic depression, is a mental health condition that can cause mood swings of various severity, ranging from emotional highs (mania or hypomania) and lows (depression). While most people diagnosed with bipolar disorder will experience some emotional symptoms between episodes, some may not experience any.Prior research on bipolar disorder concludes that it is a mixed blessing in leaders. On the one hand, leadership studies found bipolar disorder to be linked to positive traits of high intelligence, creativity, and entrepreneurship. Other research shows it can negatively affect ones job performance.Also observed in the study is a genetic connection between leadership and an increase in alcohol consumption an unhealthy behaviour that has been shown to cause cancer.Personal Traits CountAside from strictly genetic considerations, the research team tested genetic correlations between leadership position and a set of observable personal traits that are traditionally related to leadership: intelligence, risk tolerance, and height. The results suggested that the genes that are believed to drive leadership may also be related to these traits. In finding links between the traits and underlying genes in leaders, researchers think it is possible that these genes may carry genetic influences on leadership through many of these personal traits.While genetic research into the role of leadership is in its infancy, the new study is an important step forward and is likely to shed light on the direction and scope of future studies in the field. While certain genes can play a role in whether an individual turns out to be a leader or not, they may not end up expressing themselves. At the very least, they are not a determining factor in shaping the well-being of a leader. Behaviour and lifestyle can influence the expression of genes and improve the chances of good health in leaders. And good health is always an important asset to any organisation, no matter where leadership resides, Prof. Li adds.Reference:Zhaoli Song, Wen-Dong Li, Xuye Jin, Junbiao Ying, Xin Zhang, Ying Song, Hengtong Li, and Qiao Fan,Genetics, leadership position, and well-being: An investigation with a large-scale GWAS (March 14, 2022). Available athttps://doi.org/10.1073/pnas.2114271119.This article was first published in the China Business Knowledge (CBK) website by CUHK Business School:https://bit.ly/3PsquqYHashtag: #CUHKBusinessSchool

The issuer is solely responsible for the content of this announcement.

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CUHK Business School Research Reveals the Genetic Makeup of a Leader - NewsPatrolling

Genetics

Global Immunoassay Market Strategies, Trends, Forecasts 2022-2027: The Genetic Blizzard and the Move to Point of Care Drive Dramatic Change for…

DUBLIN, July 22, 2022 /PRNewswire/ -- The "Immunoassay Market: Strategies and Trends, Forecasts by Application, Technology, Product, User and by Country, with Multiplex and Point of Care Market Analysis, Executive Guides, Customized Forecasting and Analysis" report has been added to ResearchAndMarkets.com's offering.

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The workhorse of the diagnostic industry is finding new legs. The pandemic has created a new demand for rapid easily available diagnostics. Immunoassay is stepping up.

Advances in genetic knowledge are creating new markets for immunoassay. Rapid diagnostics, point of care, biomarkers and consumer markets are all areas of expansion while traditional immunoassay maintains a strong position in the growing market for clinical diagnostics.

The report profiles 58 companies, large and small, working in this area. This research makes you the expert in your organization.

Key Topics Covered:

1 Market Guides1.1 Immunoassay Market - Strategic Situation Analysis & COVID Impact1.2 Guide for Executives, Marketing, Sales and Business Development Staff1.3 Guide for Management Consultants and Investment Advisors

2 Introduction and Market Definition2.1 Immunoassay Markets Definition In This Report2.1.1 Enzyme Based2.1.2 Immunofluorescence2.1.3 Chemiluminescence2.1.4 DNA/NAT2.1.5 RIA & Other2.1.6 Reagents/Kits, Analyzers, Software & Services2.1.7 Infectious Disease2.1.8 Auto-Immune2.1.9 Endocrinology2.1.10 Oncology2.1.11 Cardiology2.1.12 Other Specialty2.2 Market Definition2.2.1 Market Sizes2.2.2 Currency2.2.3 Years2.3 Methodology2.3.1 Authors2.3.2 Sources2.4 Perspective: Healthcare, the IVD Industry, and the COVID-19 Pandemic2.4.1 Global Healthcare Spending2.4.2 Spending on Diagnostics2.4.3 Important Role of Insurance for Diagnostics

3 Industry Overview3.1 Industry Participants3.1.1 IVD Supplier3.1.2 Independent lab specialized/esoteric3.1.3 Independent lab national/regional3.1.4 Independent lab analytical3.1.5 Public National/regional lab3.1.6 Hospital lab3.1.7 Physician lab3.1.8 Audit body3.2 The Clinical Laboratory Market Segments3.2.1 Traditional Market Segmentation3.2.2 Laboratory Focus and Segmentation3.2.3 Hospital Testing Share3.2.4 Economies of Scale3.2.5 Hospital vs. Central Lab3.2.6 Physician Office Lab's3.2.7 Physician's and POCT3.3 Immunoassay -Markets and Discussion3.3.1 Instruments - Genetics changes the picture3.3.1.1 RIA - A Technology Shows its Age3.3.1.2 Immunoassay vs. PCR vs. Sequencing - A See-Saw Battle3.3.1.3 The Smart Shrinking Instrument - Serious Implications3.3.1.4 Research Funding and Capital Expense - Instrument Pooling3.3.1.5 Multiplex vs. POC - A Tradeoff Analysis3.3.2 Reagents and Kits - Genetics changes the picture3.3.2.1 Bigger Test Menus a Boon for Kit Market3.3.2.2 Physician Office Labs - A New Frontier3.3.3 Rapid and POCT to Threaten Instrument Markets3.3.4 OTC and DTC - Huge Market Potential3.3.5 Economies of Scale. Going Away?3.3.6 Lower Barriers to Entry for Instruments/Analyzers3.3.7 Miniaturization and Technology Drive Acquisition

Story continues

4 Market Trends4.1 Factors Driving Growth4.1.1 Diagnostic Factors4.1.2 Changing Technologies Spur Early Instrument Retirement4.1.3 Consumer Channels Open Wider4.1.4 Immunity Technology Comes of Age4.2 Factors Limiting Growth4.2.1 Increased Competition Lowers Price4.2.2 Threat from PCR Based Instruments4.2.3 Lower Barriers to Entry4.2.4 Wellness has a downside4.3 Immunoassay Instrumentation4.3.1 Instrumentation Tenacity4.3.2 Declining Cost of Instruments Changes Industry Structure4.3.3 Listing of Instrument Specifications4.3.4 Immunoassay - CRISPR Diagnostics

5 Immunoassay Recent Developments5.1 Recent Developments - Importance and How to Use This Section5.1.1 Importance of These Developments5.1.2 How to Use This Section5.2 FDA Grants EUA to Xtrava Health COVID Point-of-Care Antigen Test5.3 Alamar Biosciences Raises $80M for Immuno-Sandwich Assay Platform5.4 FDA grants breakthrough device to multiplex immunoassay5.5 Quidel, Beckman Settle Cardiac Immunoassay Dispute5.6 BGI Americas, Advaite Form SARS-CoV-2 Testing Partnership5.7 BioMerieux Gets CE Mark for Three Dengue Immunoassays5.8 COVID-19 Portfolio to Accelerate At-Home Infectious Disease Testing5.9 Roche Diagnostics Expanding Testing Portfolio in 20215.10 PerkinElmer Long-Term Outlook5.11 Quidel Updates Outlook for C19 Testing5.12 Dx Companies Look at Multiplex Tests for SARS-CoV-2, Influenza5.13 Becton Dickinson and NAT Diagnostics Acquisition5.14 New test diagnoses Lyme disease within 15 minutes5.15 Multiplexed Immunoassay System Differentiates Malaria Species5.16 ERBA Mannheim Unveils Next-Generation Nexus unit5.17 Uman Diagnostics And Bio-Techne Announce Agreement For Neurofilament Light Assay5.18 Software reduces variability in ELISA biomarker tests5.19 Arrayit Corporation Allergy Testing Network Doubles

6 Profiles of Key Companies6.1 Abbott Diagnostics6.2 Abcam6.3 Arlington Scientific6.4 Arrayit Corporation6.5 Autobio Diagnostics6.6 Awareness Technology6.7 Beckman Coulter Diagnostics6.8 Becton, Dickinson and Company6.9 Biocartis6.10 Biomatik6.11 bioMerieux Diagnostics6.12 Bioneer Corporation6.13 Bio-Rad Laboratories, Inc.6.14 BioTek Instruments6.15 Boditech Med, Inc6.16 Boster Biological Technology6.17 Diamedix (Erba Diagnostics)6.18 Diasorin S.p.A.6.19 Dynex Technologies6.20 Enzo Biochem6.21 Eurofins Scientific6.22 FUJIFILM Wako Diagnostics6.23 Fujirebio6.24 Gold Standard Diagnostics6.25 Grifols6.26 Hycor Biomedical6.27 Immunodiagnostic Systems (IDS)6.28 Immunodiagnostik AG6.29 Inova Diagnostics6.30 JR Biomedical6.31 Luminex Corp6.32 Maxim Biomedical6.33 Mbio Diagnostics6.34 Meso Scale Discovery6.35 Millipore Sigma6.36 Mindray6.37 Molecular Devices6.38 MP Biomedical6.39 MyCartis6.40 Operon6.41 Ortho Clinical Diagnostics6.42 Perkin Elmer6.43 Qiagen Gmbh6.44 Quidel6.45 R&D Systems6.46 Randox Toxicology6.47 Roche Molecular Diagnostics6.48 SD Biosensor6.49 Serametrix6.50 Siemens Healthineers6.51 Sysmex6.52 Tecan6.53 Thermo Fisher Scientific Inc.6.54 TOSOH Bioscience6.55 Veredus Laboratories6.56 Vircell6.57 YD Diagnostics6.58 Zhejiang Orient Gene Biotech

7 The Global Market7.1 Global Market by Country7.2 Global Market by Application7.3 Global Market by Technology7.4 Global Market by Product7.5 Global Market by User

8 Global Market by Application8.1 Endocrinology Applications8.2 Immune Applications8.3 Oncology Applications8.4 Infectious Disease Applications8.5 Cardiology Applications8.6 Other Applications

9 Immunoassay by Technology9.1 Enzyme9.2 Fluorescence9.3 Chemiluminescence9.4 Nucleic Acid9.5 Rapid/POC9.6 Other Technology

10 Immunoassay by Product10.1 Instrument10.2 Reagents10.3 Services

11 Immunoassay by User11.1 Hospital11.2 Outpatient Lab11.3 POC/Other

12 Vision of the Future of Immunoassay

13 Appendices13.1 United States Medicare System: 2021 laboratory Fees Schedule

For more information about this report visit https://www.researchandmarkets.com/r/wnx0xr

Media Contact:

Research and MarketsLaura Wood, Senior Managerpress@researchandmarkets.com

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Global Immunoassay Market Strategies, Trends, Forecasts 2022-2027: The Genetic Blizzard and the Move to Point of Care Drive Dramatic Change for...