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This article is brought to you thanks to the collaboration ofThe European Stingwith theWorld Economic Forum.

Author: Habiba Al Alsafar, Associate Professor, Department of Biomedical Engineering, Khalifa University of Science, Technology and Research (KUSTAR) & Elizabeth ODay, Founder and Chief Executive Officer, Olaris Inc

Diagnosing diseases can be complex, because illness is not a fixed state and has to be considered in context. We may be born with factors that predispose us to disease, but our lifestyle dictates if and when undesirable symptoms will manifest themselves.

For example, our middle-eastern forefathers were relatively healthier than us because of a nomadic lifestyle which was considerably more active. Our genes have remained unchanged in our recent history, yet the prevalence of a number of lifestyle diseases such as diabetes and obesity has risen in contemporary middle eastern countries. This is in part due to a shift towards more sedentary lifestyles. The environment and our lifestyles are working in concert with inherent elements (that is, the products of our genome) to contribute to the status of our health.

The intersection of genetics and lifestyle choices is playing an increasingly significant role in managing the health of middle eastern populations. The prevalence of chronic disease, in particular diabetes and its associated complications, is alarmingly high throughout the Gulf States. According to the 2017 report from the International Diabetes Federation, 11% of the population in the Middle East and North Africa (MENA) region has diabetes. Disturbingly, the prevalence is higher in the population of countries like the United Arab Emirates (UAE), where 19.3% of those between the ages of 20 and 79 have type-2 diabetes. A number of major co-morbidities are linked to diabetes and of these, cardiovascular disease is the highest cause of mortality in the UAE, accounting for 40% of mortalities. Non-communicable diseases (NCDs) in total are responsible for 77% of all deaths in the UAE. Both men and women are dying prematurely, resulting in a profound impact on families specifically and the community on the whole. The impact is not only limiting progress and development of the nation, it has a bearing on government spending as treating end-stage disease carries significant costs.

To manage the health of a nation we must shift our attention to examine both genetics and the impact of lifestyle choices.

A recent audit of the worlds genomic data showed that the predominant genomes in public databases belong to Europeans (81%), while only 0.08% of the genome inventory represents ancestries from Arab and Middle Eastern populations. The genomes of people of Asian and African ancestries at 14% and 3% respectively were also relatively low.

A breakdown of non-European genomic data samples

Image: Nature

As alluded to above, the genome is a key part of the puzzle that is required for understanding disease within a population. Efforts are clearly being made to increase our understanding of the genomes of people with middle eastern ancestries and the genomes from efforts in Kuwait, Qatar and the UAE are now available. It comes at a time when sequencing costs have plummeted and are no longer prohibitive. Innovation in genome sequencing technologies does not appear to be slowing, and continued reductions in the cost can be expected.

We have and continue to propose the need to develop collaborative linkages: locally, throughout the region and internationally. Collaboration needs to be encouraged and should involve all sectors of healthcare, including practicing physicians and paramedics, policy-makers and research scientists. It is only through coordinated efforts throughout the region that patients will ultimately be provided with the information that will enable individuals, and their care providers, to make informed decisions about their health and wellbeing. Importantly, strong local leadership is required, because as the Portuguese writer and Nobel laureate Jos Saramago put it: If you dont write your books, nobody else will do it for you. No one else has lived your life.

NCDs account for 77% of all deaths in UAE

Image: WHO

The paradigm shift in healthcare that personalized or precision medicine customizing medical treatment to the individual characteristics, needs and preferences of a patient during all stages of care represents has been made possible through the availability of large datasets compiled by healthcare systems, technological advancements in next-generation genome sequencing and the development of proper analytical tools to identify relationships in vast datasets.

This is a systems biology approach that uses genome, phenome and microbiome data to quantify the wellness of an individual and to provide indicators of their impending disease state. The Pioneer 100 Wellness Project (P100) was a longitudinal study in the US designed to test this approach. It that was conceived on the rationale that as the scale of personal data increases with the convergence of advances in electronic health records sets, big data analysis, individual measurement devices, and consumer-activated social networks, it would be possible to define early warning signs for human diseases. Although the opportunities for observing health transitions in P100 were limited, the results were sufficiently compelling that it has justified refinements for an extended study involving a larger population of more than 100,000 individuals.

Health and healthcareHow is the World Economic Forum bringing data-driven healthcare to life?

The application of precision medicine to save and improve lives relies on good-quality, easily-accessible data on everything from our DNA to lifestyle and environmental factors. The opposite to a one-size-fits-all healthcare system, it has vast, untapped potential to transform the treatment and prediction of rare diseasesand disease in general.

But there is no global governance framework for such data and no common data portal. This is a problem that contributes to the premature deaths of hundreds of millions of rare-disease patients worldwide.

The World Economic Forums Breaking Barriers to Health Data Governance initiative is focused on creating, testing and growing a framework to support effective and responsible access across borders to sensitive health data for the treatment and diagnosis of rare diseases.

The data will be shared via a federated data system: a decentralized approach that allows different institutions to access each others data without that data ever leaving the organization it originated from. This is done via an application programming interface and strikes a balance between simply pooling data (posing security concerns) and limiting access completely.

The project is a collaboration between entities in the UK (Genomics England), Australia (Australian Genomics Health Alliance), Canada (Genomics4RD), and the US (Intermountain Healthcare).

Although currently viewed as a radical shift, preemptive measures have been proposed since the turn of the last century. In 1903, motivated by concerns about the healthcare of his time, Thomas Edison said: The doctor of the future will give no medicine, but will interest his patient in the care of the human frame, in diet and in the cause and prevention of disease. Through the more than 100 years since this statement, preventative strategies have taken hold in some areas of medicine (such as immunization), but there is more to do. In the words of the 11th century Persian physician and polymath Avicenna, There are no incurable diseases only the lack of will. There are no worthless herbs only the lack of knowledge. There is certainly no lack of will, and our knowledge is only expanding.

Therefore, the opportunity to apply personal medicine practices in the UAE to prevent or delay the onset of disease will have substantial social and economic impacts. The American physcian and systems biologist Dr Leroy Hood has predicted that the wellness and prevention market will outgrow the healthcare market, in part due to economic modelling which suggests that the reactive therapeutic route is unsustainable for ageing populations. The time to act is now.

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How studying genetics and lifestyle can shape a healthier MENA region - The European Sting

Disclaimer: Early release articles are not considered as final versions. Any changes will be reflected in the online version in the month the article is officially released.

Author affiliations: Ghent University, Merelbeke, Belgium (E. Vandoorn, A. Parys, K. Van Reeth); Ghent University and Ghent University Hospital, Ghent, Belgium (I. Leroux-Roels, G. Leroux-Roels); National Animal Disease Center, Ames, Iowa, USA (A. Vincent)

Humans and swine are susceptible to influenza A viruses (IAVs) of hemagglutinin (HA) subtypes H1 and H3, which are widespread in both species. Human IAVs frequently are transmitted to swine, after which the HA surface protein generally undergoes slower antigenic evolution (drift) in swine than in humans (13). Therefore, swine can be considered a reservoir for past human IAVs. Because antigenic drift variants of human IAVs replace each other over time, younger persons only have been exposed to more recent strains and human population immunity against older human IAVs gradually decreases (4). Consequently, human-origin swine IAVs (swIAVs) can be reintroduced into the human population after a certain period and cause a pandemic, as illustrated by the influenza A(H1N1)pdm09 virus (pH1N1) (5). The H1 of this swine-origin virus is related to the H1 of human seasonal H1N1 IAVs that circulated in 19181950. In 2009, only persons born before the 1950s had cross-reactive antibodies against H1N1 viruses, so a pandemic was possible (6,7).

The evolution of swIAVs is different from and more complex than that of human IAVs because of multiple introductions of human IAVs into swine and geographic separation of swine populations (8). H1 swIAV colloquial names indicate their origin and region of circulation. An improved classification system subdivides H1 swIAVs into 3 lineages and 28 clades on the basis of H1 nucleotide sequence homology (9). The lineages are 1A, 1B, and 1C, with the number representing the subtype (H1) and the letter representing the lineage. Clades and subclades are indicated with 13 digits. Classical swine lineage 1A contains IAVs with the human 1918 pandemic H1N1 virus as a common ancestor. Most clades are restricted to America and Asia, but pH1N1 viruses (1A.3.3.2) circulate in swine and humans worldwide. Human seasonal lineage 1B contains swIAVs with an H1 derived from human seasonal IAVs. These human-like H1 swIAVs emerged in Europe in the late 1980s and in North America in the early 2000s. Eurasian avian lineage 1C contains swIAVs that originated from avian IAVs. These avian-like swIAVs emerged in Europe in 1979 and spread to Asia in 1993 (1013). Apart from antigenic evolution in the HA, IAVs also can evolve via exchange of gene segments with other IAVs of different subtypes or clades infecting the same cell, called reassortment (14), which frequently occurs in pigs. A reassortant IAV with an antigenically novel HA and the capacity to infect and spread in humans could cause a pandemic.

Since 2010, 35 zoonotic infections with H1 swIAVs were reported in North America and 10 in Europe (1517; Parys et al., unpub. data). Human population immunity is a major factor determining the pandemic risk for swIAVs. Hemagglutination inhibiting (HI) and virus neutralizing (VN) antibodies in serum are accepted correlates of protection (18). Evaluating humans of different age groups for HI and VN antibody titers against a range of antigenically different swIAVs might help clarify the public health risk.

In a previous seroprevalence study for H3 swIAVs in humans from Luxembourg, we demonstrated a correlation with the nature of the swIAV and its relation to human IAVs on the one hand and the persons birth year on the other (19). A large comparative seroprevalence study for H1 swIAVs is lacking. Previous studies examined limited numbers of H1 swIAVs or samples or did not evaluate the relation between birth year and antibody responses (12,13,2025). In addition, most studies were conducted before or during the 2009 pandemic, but the circulation of pH1N1 viruses in humans likely changed the serologic profile against H1 swIAVs. We assessed prevalence and titers of protective antibodies against all major H1 swIAV clades in various age groups in Belgium in 2017. We also examined the relation between antibodies against human-like swIAVs and their presumed human seasonal ancestor IAV. The results will help assess the public health risk for different H1 swIAVs.

During August 2017January 2018, a total of 549 anonymized serum samples were collected from immunocompetent persons with unknown influenza vaccination or infection history born during 19202017 at Ghent University Hospital (Ghent, Belgium). Samples included 6 per birth year with 1:1 ratio between male and female patients. Exclusion criteria included active oncologic disease or hematologic malignancies, immunosuppressive treatment, organ transplantation, admission to intensive care, and end-stage renal disease on dialysis treatment. This study was approved by the Commission for Medical Ethics of the Ghent University Hospital (approval no. 2017/0834).

Samples were evaluated for antibodies against 11 viruses representing 7 major H1 swIAV clades circulating in Europe, North America, and Asia; 2 human seasonal progenitor IAVs for European and North American human-like swIAVs; and 1 human seasonal IAV that circulated right before the pH1N1 virus (Table 1). We used epidemiologic data (1012) and the H1 classification system (9) to select major H1 swIAV clades. We selected test viruses on the basis of amino acid homology and antigenic relatedness to currently circulating swIAVs of each clade. We selected the human progenitor IAVs based on the literature (26,27).

We downloaded nucleotide sequences of the viruses HA1, the main target of neutralizing antibodies, from Genbank and translated these to amino acids. We used the MUSCLE algorithm for sequence alignment and the Jones-Taylor-Thornton model and nearest-neighbor-interchange heuristic method to construct maximum-likelihood trees in MEGA7 (28). We determined the percent of amino acid homology between test viruses and numbers of identical amino acids in presumed antigenic sites (29) with MEGA7 and R version 3.2.2 (30).

We obtained North American swIAVs and corresponding swine serum from the U.S. Department of Agriculture-Agricultural Research Service. We obtained human seasonal IAVs and corresponding ferret serum from Francis Crick Institute (London, UK), and Asian swIAV from Hong Kong University (Hong Kong). We antigenically characterized test viruses in cross-HI and cross-VN assays with postvaccination swine serum for swIAVs or postinfection ferret serum for human seasonal IAVs. Because serum against A/Brisbane/59/2007 was not available, we used ferret serum against A/Egypt/10/2007 instead; the HA sequence is identical in both. We propagated viruses in MDCK cells; all passages were <6. We calculated antigenic distances from HI and VN titers as described previously (31) and converted these into antigenic dendrograms by using the neighbor-joining method in MEGA7. One antigenic unit represents a 2-fold difference in HI or VN titer.

We tested individual samples in HI assays and pooled samples per birth year in VN assays for antibodies against each test virus. Both assays were performed according to standard procedures (32,33). We expressed antibody titers for HI as the reciprocal of the highest serum dilution showing complete hemagglutination inhibition of 4 hemagglutinating units of virus or, for VN, 50% neutralization of 100 TCID50 (50% tissue culture infective doses) of virus. The starting dilution was 1:20, and we considered a titer of 40 positive.

We calculated geometric mean titers (GMTs) and 95% CIs for HI and VN antibody titers of samples from each birth decade against each test virus by using log2-transformed data. Samples with a titer <20 were assigned a titer of 10. For non-stratified data, we calculated Spearman correlation coefficients (CCs) between HI titers or between VN titers against different viruses. We used Kruskal-Wallis and Mann-Whitney U tests to compare antibody titers between age groups for a certain virus or between viruses for a certain age group. We used Fisher exact test to compare proportions of positive samples. For all statistical tests, we applied Bonferroni adjustment of the p values and we considered corrected p values of <0.05 statistically significant. We performed all analyses by using R version 3.2.2.

Figure 1

Figure 1. Epidemiologic, phylogenetic, and antigenic relationship between influenza A test viruses from classical swine lineage 1A, human seasonal lineage 1B, and Eurasian avian lineage 1C. A) Schematic representation of the H1 IAV...

We tested samples for antibodies against 11 IAVs from the classical swine 1A, human seasonal 1B, or Eurasian avian 1C lineage. HA1 aa sequence homology between viruses of different lineages was <75% with 1935/50 identical amino acids in presumed antigenic sites. Classical swine and avian-like IAVs were phylogenetically most closely related (Figure 1, panel A; Table 2). Within-lineage HA1 aa homology was 82%97%, with 3649 identical amino acids in antigenic sites. Human-like swIAVs and their presumed human seasonal progenitor IAV shared 90%94% aa in the HA1 and 3642 aa in antigenic sites.

Antigenic dendrograms based on cross-HI and cross-VN assays showed similar trends to the phylogenetic tree, except for swOK13 (Tables 35; Figure 1). This North American human-like 1b swIAV (1B.2.2.2) clustered separately from other IAVs of its lineage, including its presumed human ancestor, NC99.

Figure 2

Figure 2. Number of positive human serum samples in the hemagglutination inhibition assay (titer >40) for each test virus compared with the total number of samples tested per birth cohort. Birth cohorts...

Figure 3

Figure 3. Number of positive human serum samples in the virus neutralization assay (titer >40) for each test virus compared with the total number of samples per birth cohort. Birth cohorts are...

We tested human serum samples against human seasonal IAVs related to 1B swIAVs from 1986 (TW86), 1999 (NC99), and 2007 (BR07) to evaluate a persons potential exposure to or vaccination with these IAVs. Overall, 39% were seropositive for TW86, 31% for NC99, and 22% for BR07 in HI and 48% were seropositive for TW86, 51% for NC99, and 29% for BR07 in VN (Figures 2, 3). Seroprevalences and GMTs against TW86 were highest for persons born during 19771986 and lowest for the 2 youngest groups, those born during 19972017 (Tables 6, 7). For NC99 and BR07, HI responses were highest for those born during 19871996, and VN responses were highest for those born during 19371946 (NC99 only) and 19972006. Persons born during 20072017 had minimal responses. Antibody responses against human seasonal IAVs were related to birth year and the year of virus isolation, with peak responses in persons born right before the virus circulated and lowest responses in persons born afterwards.

The major avian-origin swIAV clades are European avian-like 1C.2.1, represented by swG10, and Asian avian-like 1C.2.3, represented by swHK11. For swG10, 10% of all samples tested positive in HI and 7% in VN (Figures 2, 3). Seroprevalence was <20% and GMTs were <20 for all age groups except the oldest, those born during 19201926, with 40% seropositive in HI and GMTs for HI and VN of 24 (Tables 6, 7).

For swHK11, overall seroprevalence was 25% in HI and 34% in VN. Like swG10, responses against swHK11 were highest for those born during 19201926; 52% in HI, 72% in VN, and GMTs 38. Responses were minimal in both HI and VN for persons born during 19471956; 11% in HI, 10% in VN, and GMTs <20.

European human-like swIAV swG12 (1B.1.2.1) represents the human-like H1 swIAV clade circulating in Belgium, and TW86 was selected as its presumed human ancestor virus. At least half of all samples tested positive for swG12, 50% in HI and 59% in VN (Figures 2, 3). We noted statistically significant differences in seroprevalences and GMTs, which were higher (62% in HI and 74% in VN; GMTs 44) in persons born before 1996 than in persons born during 19972017 (5% in HI and in VN; GMTs <20; p<0.001) (Tables 6, 7). GMTs peaked (87) in HI in those born during 19771986 and in VN for those born during 19671976. Results for swG12 were similar to those for its presumed human ancestor virus, TW86.

North American human-like H1 swIAVs (1B.2) result from the introduction of a human IAV in the early 2000s, and we selected NC99 as their presumed human ancestor. For the most prevalent 1 clade (1B.2.2), swAL16 represents subclade 1a (1B.2.2.1), whereas swIL10 and swOK13 represent subclade 1b (1B.2.2.2).

Among samples, 24% tested positive for swAL16 in HI and 39% in VN (Figures 2, 3). Seroprevalences and GMTs were highest in those born during 19871996 in HI (55%; GMT 35) and in those born during 19471956 in VN (70%; GMT 59), but no antibodies against swAL16 were detected in the youngest group, those born during 20072017 (Tables 6, 7). Like for European human-like virus swG12 (1B.1.2.1), antibody responses against North American 1a virus swAL16 (1B.2.2.1) resembled those against its presumed human ancestor virus, NC99.

For the 1b swIAVs (1B.2.2.2), <10% were seropositive (swIL10, 10% in HI and VN; swOK13, 5% in HI and 4% in VN) (Figures 2, 3). We did not see statistically significant differences in seroprevalences between the 2 1b swIAVs or between age groups, with following exceptions. HI-seroprevalence of those born during 19271936 was statistically significantly higher for swIL10 (13%) than for swOK13 (2%; p<0.04). HI seroprevalence for swOK13 of those born during 19771986 was statistically significantly higher (21%) compared with groups born during 19271936 (2%), 19571966 (0), and 20072017 (0; p<0.04). GMTs were <20 in all age groups except those born during 19371956, who had VN GMTs of 2230 against swIL10 (Tables 6, 7). Unlike the other 2 human-like swIAVs tested, responses against 1b swIAVs (1B.2.2.2) did not concur with those against the presumed human ancestor virus NC99. Responses against swIL10 and swOK13 were generally statistically significantly lower than against NC99 (p<0.05).

We used swOH07 as reference virus to evaluate antibody responses against classical swine virus clade (1A.3.3.3) and CA09 as reference virus to evaluate classical swine virus clade pH1N1 (1A.3.3.2), which derived its HA from swIAVs. Overall, 50% of the samples tested positive for swOH07 (50% in HI; 78% in VN) and CA09 (54% in HI; 81% in VN), with high seroprevalences in all age groups (36%100% in HI; 50%100% in VN), except in those born during 19471956 in HI (swOH07, 17%; CA09, 24%) (Figures 2, 3). HI titers peaked in the 2 oldest groups, those born during 19201936; VN titers peaked in the 2 oldest groups and in those born during 19972006 (Tables 6, 7). No statistically significant difference was noted in responses against classical swine (1A.3.3.3) and pH1N1 (1A.3.3.2) IAVs.

Antibody titers against epidemiologically related human and swine IAVs were highly correlated for classical swine viruses swOH07 (1A.3.3.3) and CA09 (1A.3.3.2), European human-like swIAV swG12 (1B.1.2.1) and human ancestor IAV TW86, North American human-like 1a swIAV swAL16 (1B.2.2.1) and human ancestor IAV NC99, and European and Asian avian-like swIAVs swG10 (1C.2.1) and swHK11 (1C.2.3) (CC=0.680.86 in HI; CC=0.630.77 in VN; Table 8). Of note, titers against avian-like and classical swine IAVs also were strongly correlated (CC=0.550.68 in HI; CC=0.490.67 in VN). In contrast, CCs were low between titers against North American human-like 1b viruses swIL10 and swOK13 (1B.2.2.2) and human ancestor virus NC99 (0.420.43 in HI; 0.300.39 in VN [the first value of which is not statistically significant]).

Our results show that serum antibody responses of immunocompetent persons in Belgium against major H1 swIAV clades depend on the swIAV tested and its relation to human seasonal IAVs and the persons birth year. Overall seroprevalences were high (50%) for classical swine (1A.3.3.2, 1A.3.3.3) and for European human-like (1B.1.2.1) swIAVs, intermediate (24%) for North American human-like 1a (1B.2.2.1) and Asian avian-like (1C.2.3) swIAVs, and low (<10%) for North American human-like 1b (1B.2.2.2) and European avian-like (1C.2.1) swIAVs. Our results are consistent with previous studies that aimed to compare antibody responses in nonswine workers with those in persons with frequent swine contact (7,2025), although those studies examined only a limited number of swIAV clades or samples. Overall, most previous studies showed lower seroprevalences for Asian avian-like (2%10%) and European avian-like (05%) swIAVs in the general population or in nonswine workers (13,20,2224). A 2010 study in the United Kingdom also found a lower seroprevalence of 11% for a European human-like (1B.1.2.1) swIAV (24). The major difference between our study and studies conducted before or during the 2009 pandemic is the lower seroprevalence of 3%15% for classical swine IAVs in previous studies (13,20,2224). The circulation of pH1N1 viruses (1A.3.3.2) likely contributes to increased seroprevalence rates against these related classical swine IAVs. In our study, the oldest group, those born during 19201926 who are 9197 years of age, had the highest antibody responses against H1 swIAVs of classical swine (1A.3.3) and avian-like (1C.2) lineages, for which antibody titers were correlated (13,20,21). Responses against human seasonal IAVs and related European and North American 1a human-like H1 swIAVs (1B) generally were highest in those born during 19771996, who are 2140 years of age, and lowest in those born during 19962017, who are 020 years of age. Responses against North American 1b human-like H1 swIAVs (1B.2.2.2) generally were low across all age cohorts.

Antibody responses against past human seasonal IAVs TW86, NC99, and BR07 generally peaked in persons born near the time during which the respective IAV or similar viruses circulated, whereas responses were low in most persons born after. Within an age group, responses generally were highest against an antigenic representative of the virus encountered first. These findings concur with the theory of antigenic seniority: humans are expected to have antibodies against human seasonal IAVs that circulated after their birth, with highest responses against the virus encountered first. Antigenic seniority likely occurs because of periodic boosting of these antibodies by subsequent exposures to related human seasonal IAVs (4,34,35). Antibody titers against European human-like swIAV swG12 (1B.1.2.1) and North American human-like 1a swIAV swAL16 (1B.2.2.1) concur with those against their respective human ancestor viruses TW86 and NC99 because of close antigenic relationship to their ancestor IAV. Overall high seroprevalences against pH1N1 virus CA09 (1A.3.3.2) and antigenically closely related classical swine virus swOH07 (1A.3.3.3) can be explained by recent exposure to currently circulating pH1N1 viruses. Because the oldest persons were born during 19201936, when human IAVs closely related to the 1918 pandemic virus, the ancestor of classical swine IAVs, circulated, they could have had cross-reactive antibodies against classical swine IAVs before 2009. These antibodies might have been boosted by later exposure to pH1N1 viruses, which might account for the high responses in this group (6,7). Consistent with results for serum samples collected after pH1N1 virus infection in a previous study (21), cross-reactivity was higher against the Asian than against the European avian-like H1 swIAV, which differ by only 1 aa in antigenic sites (Table 2). Whether this single amino acid mutation is the reason for the difference in seroprevalence is still unknown (36,37).

European human-like (1B.1.2.1) and North American human-like 1a (1B.2.2.1) H1 swIAVs are antigenically more closely related to their human ancestor than North American human-like 1b (1B.2.2.2) H1 swIAVs (Figure 1; Tables 3, 4). North American human-like H1 swIAVs (1B.2) have been shown to drift 4 times faster than European human-like H1 swIAVs (1B.1). Increased antigenic diversity of the former since 2008 has led to the emergence of swIAVs that are antigenically distinct from the human precursors, mainly within the 1b subclade (3,27). This evolution can explain the recognition of selected European human-like and North American human-like 1a but not North American human-like 1b H1 swIAVs by human serum samples. Because the human ancestor IAVs no longer circulate in humans, swine can be considered a reservoir for old human IAVs. Seroprevalences for European human-like and North American human-like 1a H1 swIAVs are expected to decrease over time because the youngest age groups were never exposed to these human IAVs. On the basis of our results, we estimate that it could take <80 years for the population to become fully susceptible.

Seroprevalences of immunocompetent persons in Belgium for swIAVs representing major H1 swIAV clades suggest that North American human-like 1b (1B.2.2.2) and European avian-like (1C.2.1) H1 swIAVs currently pose the highest risk to public health. North American human-like 1b (1B.2.2.2) swIAVs rapidly drifted away from its human ancestor, whereas European avian-like (1C.2.1) swIAVs never circulated in humans. Seroprevalences of <10% for these viruses are comparable to 2%19% against the pH1N1 virus right before the pandemic (7). Our results suggest that the risk of reintroduction of these H1 swIAVs in the human population might be higher than for H3 swIAVs, given that 20% of persons 0100 years of age from Luxembourg tested seropositive for representative European and North American cluster IV H3 swIAVs in 2010 (19). Seroprevalences against the other currently circulating human-like H1 swIAV clades were higher than against 1B.2.2.2 and 1C.2.1, but these viruses, along with H3 swIAVs, also keep evolving in swine. As they continue to drift away from their human ancestor and population immunity wanes with lack of exposure, these viruses might also pose a risk to public health soon.

We evaluated human population immunity against H1 swIAVs on the basis of serum HI and VN antibodies, which are directed against the highly variable head region of the HA. We did not measure antibodies or T-cell responses against the HA stalk, the neuraminidase, or internal viral proteins, such as the nucleoprotein. Although these immune mechanisms are much less potent than neutralizing anti-HA antibodies, their targets are more conserved between IAVs of humans and swine (3842). Therefore, persons with minimal antibody titers in our study still might have some degree of immunity and protection against zoonotic infection with swIAVs. Furthermore, population immunity is only one aspect determining the pandemic potential of swIAVs (18). Another factor is their ability to spread in humans, which is difficult to investigate (43). Our results stress the need for continuous surveillance and characterization of circulating swIAVs and frequent monitoring of humans for antibodies against these swIAVs.

Ms. Vandoorn was a PhD student at the Laboratory of Virology, Faculty of Veterinary Medicine, Ghent University, during the study period. Her primary research interests are swine influenza A virus surveillance in Belgium and the Netherlands and broadly protective vaccination strategies for influenza A viruses.

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Suggested citation for this article: Vandoorn E, Leroux-Roels I, Leroux-Roels G, Parys A, Vincent A, Van Reeth K. Detection of H1 swine influenza A virus antibodies in human serum samples by age group. Emerg Infect Dis. 2020 Sep [date cited]. https://doi.org/10.3201/eid2609.191796

The conclusions, findings, and opinions expressed by authors contributing to this journal do not necessarily reflect the official position of the U.S. Department of Health and Human Services, the Public Health Service, the Centers for Disease Control and Prevention, or the authors' affiliated institutions. Use of trade names is for identification only and does not imply endorsement by any of the groups named above.

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Detection of H1 Swine Influenza A Virus Antibodies in Human Serum Samples by Age Group - CDC

Scientists at the University of WisconsinMadison have published a proof-of-concept method to correct an inherited form of macular degeneration that causes blindness, and that is currently untreatable.

Andrew Hellpap608-225-5024ahellpap@uwhealth.org

The researchers were able to correct the disease in stem cells from patients with BEST1 mutations by overwhelming broken copies of the gene with many functional copies of BEST1. This approach worked for most, but not all, of the BEST1 mutations that they tested. As an alternative approach for mutations that did not respond to this gene augmentation method, the team used CRISPR-Cas9 gene editing to target and correct the mutations.

A paper chronicling the research, co-led by David Gamm, MD, PhD, professor of ophthalmology and visual sciences in the School of Medicine and Public Health, was published online July 23 in the American Journal of Human Genetics. The study was also led by Kris Saha, PhD, associate professor of biomedical engineering and Wisconsin Institute for Discovery, and Bikash Pattnaik, PhD, assistant professor of pediatrics.

This BEST1 gene encodes a protein that regulates the movement of chloride across a layer of the retina called the retinal pigment epithelium (RPE). Best disease is dominant, meaning that people who inherit only one faulty copy of the BEST1 gene from either their mother or their father will develop the disorder. Mutations in BEST1 cause the retinal layer to break down, resulting in blurred central vision that progresses to irreversible vision loss.

People with Best disease have a wide range of mutations that can affect different parts of the protein, all of which were thought to require complex, individualized gene therapies to fix them, Gamm said. We found that many of these mutations were actually very sensitive to a broader gene therapy method that is already established for other retinal diseases.

Fixing a dominant genetic disease via gene therapy typically requires precise removal or repair of the nonfunctional gene without causing harm to the functional gene a difficult task that is frequently unsuccessful. In contrast, recessive genetic diseases that arise when a person inherits two nonfunctional genes one from each parent can be corrected by a technique called gene augmentation. This well-established process introduces a functional copy of the gene to fill the void.

To use another analogy, dominant mutations produce workers that actively look to sabotage the efforts of their capable coworkers, whereas recessive mutations produce proteins that never show up for work at all, Gamm said. As it turns out, the latter situation is usually simpler to treat than the former.

A team of researchers at the McPherson Eye Research Institute, which Gamm directs, hypothesized that it may be possible to adequately dilute the influence of the nonfunctional BEST1 protein by counter-balancing it with many functional copies of BEST1 protein through gene augmentation.

In the lab, the approach worked in RPE cells derived from induced pluripotent stem cells of patients with most, but not all, of the BEST1 gene mutations they tested. Where gene augmentation did not succeed, the team was able to correct the dysfunction using CRISPR-Cas9 gene editing.

The research was carried out in large part by Divya Sinha, PhD, an assistant scientist in Gamms lab, Ben Steyer, a former MD-PhD student in Sahas lab, and Pawan Shahi, PhD, postdoctoral research associate in Pattnaiks lab. The research team also included Sushmita Roy, PhD, associate professor of biostatics and medical informatics at the UW School of Medicine and Public Health and Wisconsin Institute for Discovery.

The scientists demonstrated that their two-pronged gene therapy strategy may hold potential to treat all Best disease mutations in a highly effective manner.

We were able to reverse the disease in all the cell lines using one method or the other, Gamm said. We were also able to determine which mutations were likely to respond to the first-line gene augmentation strategy, and which would be better served with the second-line gene editing approach.

An additional benefit came into focus as this research progressed, according to Gamm.

Our findings also could be applicable to some dominant genetic mutations that affect tissues elsewhere in the body, he said. Its very exciting.

This work was supported by the National Eye Institute, Foundation Fighting Blindness, McPherson Eye Research Institute Sandra Lemke Trout Chair in Eye Research, Retina Research Foundation Emmett Humble Chair, Sarah E. Slack Prevention of Blindness Fund (a component Fund of the Muskingum County Community Foundation),Research to Prevent Blindness, National Science Foundation, Burroughs Wellcome Fund, Retina Research Foundation Kathryn and Latimer Murfee Chair and Retina Research Foundation M.D. Mathews Professorship, and VitreoRetinal Surgery Foundation. This study was supported in part by a UW Data Science Initiative grant and the UW2020 Initiative.

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UW researchers devise approach to treat rare, incurable form of blindness - University of Wisconsin-Madison

NEW YORK, Aug. 05, 2020 (GLOBE NEWSWIRE) -- Prevail Therapeutics Inc. (Nasdaq: PRVL), a biotechnology company developing potentially disease-modifying AAV-based gene therapies for patients with neurodegenerative diseases, today announced that Asa Abeliovich, M.D., Ph.D., Founder and Chief Executive Officer of Prevail, will present at the virtual 2020 Wedbush PacGrow Healthcare Conference on Tuesday, August 11, 2020 at 1:45 p.m. ET.

The webcast will be available in the Events and Presentations section of the Company's website at ir.prevailtherapeutics.com. The webcast will be archived for 90 days following the presentation.

About Prevail Therapeutics Prevail is a gene therapy company leveraging breakthroughs in human genetics with the goal of developing and commercializing disease-modifying AAV-based gene therapies for patients with neurodegenerative diseases. The Company is developing PR001 for patients with Parkinson’s disease with GBA1 mutations (PD-GBA) and neuronopathic Gaucher disease; PR006 for patients with frontotemporal dementia with GRN mutations (FTD-GRN); and PR004 for patients with certain synucleinopathies.

Prevail was founded by Dr. Asa Abeliovich in 2017, through a collaborative effort with The Silverstein Foundation for Parkinson’s with GBA and OrbiMed, and is headquartered in New York, NY.

Forward-Looking Statements Related to Prevail Statements contained in this press release regarding matters that are not historical facts are forward-looking statements” within the meaning of the Private Securities Litigation Reform Act of 1995, as amended. Examples of these forward-looking statements include statements concerning the potential for Prevail’s gene therapy candidates to transform the treatment of patients with, and slow or halt the progression of, FTD-GRN and other neurodegenerative diseases. Because such statements are subject to risks and uncertainties, actual results may differ materially from those expressed or implied by such forward-looking statements. These risks and uncertainties include, among others: Prevail’s novel approach to gene therapy makes it difficult to predict the time, cost and potential success of product candidate development or regulatory approval; Prevail’s gene therapy programs may not meet safety and efficacy levels needed to support ongoing clinical development or regulatory approval; the regulatory landscape for gene therapy is rigorous, complex, uncertain and subject to change; the fact that gene therapies are novel, complex and difficult to manufacture; and risks relating to the impact on our business of the COVID-19 pandemic or similar public health crises. These and other risks are described more fully in Prevail’s filings with the Securities and Exchange Commission (SEC), including the Risk Factors” section of the Company’s Quarterly Report on Form 10-Q for the period ended March 31, 2020, filed with the SEC on May 14, 2020, and its other documents subsequently filed with or furnished to the SEC. All forward-looking statements contained in this press release speak only as of the date on which they were made. Except to the extent required by law, Prevail undertakes no obligation to update such statements to reflect events that occur or circumstances that exist after the date on which they were made.

Media Contact: Mary Carmichael Ten Bridge Communications mary@tenbridgecommunications.com 617-413-3543

Investor Contact: investors@prevailtherapeutics.com

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Prevail Therapeutics to Present at 2020 Wedbush PacGrow Healthcare Conference - Stockhouse

Human genetics is the study of how genetic, environmental, and behavioral factors, as well as their interactions, influence human traits, health, and disease. Public health genetics applies advances in human genetics and genomics to improve public health and prevent disease in diverse populations. Genetic counselors work as members of a health care team, providing information and support to patients with genetic disorders and those at risk for inherited conditions.

The Department of Human Genetics is dedicated to graduate training in human genetics research (including molecular, statistical, and bioinformatics research), public health genetics, and genetic counseling.

The mission of the department is to

Human genetics research has helped answer fundamental questions about human nature and led to the development of effective treatments for many diseases that greatly impact human health. Faculty in the Department of Human Genetics have developed and used genetic methods to investigate the causes and treatment of hereditary and acquired human illness and to understand and explore the impact of genetics on public health, education, and disease prevention.

Pitt Public Health human genetics faculty and students currently are involved in varied research projects, including...

Graduates of Pitt Public Healths human genetics program typically go on to positions in academia or in industry and usually are employed by their graduation dates. Alumni currently are working in academic, government, health care, and commercial sectors, including...

The Department of Human Genetics offers four masters level programs, and two doctoral programs:

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Human Genetics | Pitt Public Health | University of Pittsburgh

Imagine a coyote, rangy and resilient. Is she ambling through a canyon dotted with sagebrush or loping in an urban alley lined with dumpsters? In recent decades, the latter has become a more common sight. As cities expand, coyotes move right in. Rather than shrinking from the big-city lights, they rummage for opportunities.

But even as individual coyotes thrive, cities' built features are shaping their genomesacross generations, according to a recent study in the Journal of Urban Ecology. A widening genetic gulf separates city coyotes and their country cousins. And as urban space sprawls, coyotes genetic diversity declines. This finding suggests that humans built environment has consequences even for creatures that seem to thrive in our midst.

Scientists already know city coyotes tend to differ from their country counterpartsin behavior: theyre bolder and more exploratory, more likely to eat human-sourced foods and occupy a smaller territory. But the picture of what genetic differences if any might exist between coyotes has been more murky.

About 30 years ago, fewgeneticdifferences existed between coyotes across North America suggesting coyotes moved freely, and so did their genes. Historically, coyotes ranged only across the arid West and Great Plains. Since 1900, they have beenpushing out of their home turf, and today they prowl the continent from coast to coast. Scientists assumed that mobile, adaptable coyotes weren't impeded much by urban sprawl. More recent studies have found coyotes clustering genetically by range or region, but few have honed in on specific urban areas.

Urban coyote

National Park Service

By narrowing their focus to the greater Los Angeles area, scientists from Pepperdine University uncovered a more complex picture lurking in urban coyotes genes. Pulling DNA from 125 samples of muscle, liver, and skin, they examined coyotes living in mountains, farmland, suburbs, and the city. The team mapped coyotes genetic structure alongside the surrounding landscape, accounting for key urban features like freeways and road density.

A clear split between urban and rural coyotes emerged. Rural coyotes living among mountains and natural vegetation formed the largest, most genetically diverse group. Urban coyotes, on the other hand, made up three distinct clusters each with decreased genetic diversity. Researchers could deduce which coyotes roam wide-open spaces and which dodge city traffic.

Rural coyotes shared a similar genetic profile even across long distances, suggesting natural barriers didnt impede their movement or gene flow. Even in coyotes separated by 160 miles, rural coyotes clustered with each other instead of their urban counterparts nearby. The surrounding environment mattered more than the geographic distance.

Why this genetic split between city and country coyotes? It could stem in part from natal-biased habitat dispersal, the researchers suggest. Animals tend to prefer habitats similar to where they grew up. When an urban coyote knows how to avoid the citys hazards and harvest its resources, she is more likely to raise babies with those skills. And when generations of street-smart coyotes stick around the same spot, the genetic gap between them and their country cousins widens.

But this isnt the whole story, the researchers argue. City coyotes werent just genetically distinct from their rural relatives; their DNA also differed from that of other city coyotes. Rather than forming one large group as the rural coyotes did, urban coyotes split into three genetically distinct populations.

The cities built features help explain why. One distinct cluster of city coyotes prowled through downtown Los Angeles, lurked by the Hollywood sign, and roamed near the Long Beach Airport. The coyotes in this clusterhad both DNA and habitat in common hyper-urban areas with high road density.

Scientists found a similar pattern in Orange County. Where major highways and commercial districts sliced through the land, so did a boundary between two distinct coyote populations. Despite roaming a similar urban environment, coyotes on one side of the highway were genetically distinct from their relatives on the other side. Coyotes' genetic structure mirrored the urban terrain.

Coyote

Peter Eades / USFWS

These findings suggest humans built environment shapes coyotes movement, the researchers argue. Major freeways, dense roads, and human development prevent urban coyotes from crossing into other areas. These built barriers keep old residents in, and new migrants out and thus leave a stamp on coyotes DNA across generations.

This is important because when a population becomes isolated, their genetic diversity tends to dwindle. Genetic diversity reflects a populations overall health, as well as an ability to adapt to future changes in the environment. Think of it like a box of tools passed down for a vast, unpredictable, multi-generational home restoration project. If the roof collapses or the plumbing busts, youre going to need more than just a hammer. The more options you have, the better whether theyre hand tools orgenes. Each genetic characteristic represents another option, in a toolbox of past solutions and potential answers.

Even as individual urban coyotes thrive, their collective genetic toolbox shrinks. The citys built features restrict urban coyotes travels more than previously thought, with significant effects on their population genetics. These findings suggest that urbanization even takes a toll on creatures that seem to flourish in human environments.

This result also points to the importance of preserving natural corridors in cities not just for coyotes, but for other urban wildlife, too. Safe passageways allow diverse species to cross between habitats, enabling both physical movement and gene flow. Los Angeles County has made natural corridors a priority by identifying Significant Ecological Areas (SEAs) and planning links between them. In fact, in 2023, Los Angeles is slated to become home to the largest wildlife corridor in the world a highway overpass in the works since 2019.

Coyotes have a reputation as survivors, adaptable and enduring. But urbanization is also here to stay, and scientists are still learning about its genetic implications for our wildlife neighbors. This study highlights the value of better understanding these effects on all creatures in the urban landscape even the most versatile and wily of them all.

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'Hyper urban' coyote genomes are growing apart their from city and rural cousins - Massive Science

CAMBRIDGE, Mass.--(BUSINESS WIRE)--Triplet Therapeutics, Inc., a biotechnology company leveraging insights from the human genetics of repeat expansion disorders (REDs), announced today that co-founder, president, and CEO Nessan Bermingham, Ph.D., will speak at three upcoming virtual events:

Dr. Bermingham will discuss Triplets recent activities, including the companys selection of its first clinical candidate from its proprietary thRED Engine, TTX-3360, an antisense oligonucleotide with the potential to modify the course of REDs by targeting the DNA Damage Response (DDR) pathway, and its initiation of an international natural history study of Huntingtons disease, SHIELD HD.

About TTX-3360

TTX-3360, an antisense oligonucleotide, is the first clinical candidate developed from Triplets proprietary thRED Engine and the first clinical candidate with the potential to modify the course of repeat expansion disorders (REDs) by targeting the DNA Damage Response (DDR) pathway. A significant body of evidence supports the role of the DDR pathway as the primary driver of repeat expansion and subsequent disease onset and progression in many REDs, including Huntingtons disease (HD), myotonic dystrophy (DM1) and fragile X syndrome. Triplet is initially focusing development of TTX-3360 in HD and may also evaluate it in other central nervous system indications such as spinocerebellar ataxias (SCAs), fragile X syndrome, and familial amyotrophic lateral sclerosis (ALS).

About Triplet Therapeutics

Triplet Therapeutics is a biotechnology company developing transformational treatments for patients with repeat expansion disorders (REDs) a group of more than 50 known genetic diseases including myotonic dystrophy type 1 (DM1), Huntingtons disease (HD), spinocerebellar ataxias (SCAs), Fragile X syndrome, and familial amyotrophic lateral sclerosis (ALS) leveraging insights from patient genetics. Triplet designs and develops potential therapeutics for REDs using its proprietary thRED Engine, which enables the Company to develop a single oligonucleotide targeting the DNA Damage Response (DDR) pathway to potentially treat multiple REDs.

Triplet is backed by investments from Atlas Venture, MPM Capital and Pfizer Ventures, along with Invus, Partners Innovation Fund and Alexandria Venture Investments. Triplet is headquartered in Cambridge, Mass. For more information, please visit http://www.triplettx.com.

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Triplet Therapeutics To Present at Upcoming Events - Business Wire

Baylor College of Medicines Human Genome Sequencing Center is a leader in large scale DNA sequencing research, and the Alkek Center for Metagenomics and Microbiome Research is leading research related to how bacteria and viruses impact human health. Since the outbreak of the COVID-19 pandemic, researchers at both centers have come together to serve the need for COVID-19 testing in the Houston area by combining the expertise of each groups laboratories. Now, Baylor is partnering with local public health departments to provide polymerase chain reaction (PCR) testing for tens of thousands of COVID-19 samples.

We are pleased to work with the outstanding local government groups in this critical public health effort, said Dr. Richard Gibbs, director of the Human Genome Sequencing Center and Wofford Cain Chair and Professor of molecular and human genetics at Baylor. We are proud of the tireless determination and expertise of our centers and college staff that enabled the rapid development of this robust testing capacity to serve the greater Houston community.

Baylor is one of the testing providers for Harris County Public Health. Anyone who wants to be tested can complete a pre-screening questionnaire, either online or by phone. If the person qualifies for testing, they will be given a personalized code and directed to one of the mobile testing sites. Harris County Public Health also provides testing services to individuals living in traditionally high-risk congregate settings such as nursing homes.

We are fortunate to have Baylor College of Medicine as a close partner during the COVID-19 pandemic, said Dr. Umair Shah, executive director of Harris County Public Health. This is a challenging time for our community and as the need for increased testing capacity and getting results to residents faster has grown, Baylor has risen to the occasion. There are countless unsung heroes across Harris County who have stepped up to the plate during this pandemic and Baylor College of Medicine is one of them.

Samples collected at testing sites are sent to the Alkek Center for Metagenomics and Microbiome Research to be prepared for testing. After arriving at the lab, each sample is decontaminated and put in a liquid solution that helps isolate the virus. Technicians then extract the genomic material of the virus (RNA) from the sample. That RNA is then sent to the Human Genome Sequencing Center to undergo quantitative reverse transcription PCR (RT-qPCR) testing. This process works by looking for specific sequences that are unique to the viruss genome. If the samples RNA sequence matches that of the virus, the sample is positive. Each sample must test positive three times to be considered a positive case of COVID-19. A trained interpreter will also provide a final review, confirming a positive or negative case. Each report is signed by respiratory virus expert and Medical Director of the Alkek Center for Metagenomics and Microbiome Research lab, Dr. Pedro Piedra.

On average, results are returned to the tested person within 48 hours. Each test kit is equipped with a bar code that allows the test to be tracked digitally, speeding up the process of informing the tested person and county health officials. If a person tests positive, the Harris County Public Health team will follow up with them for contact tracing.

Widespread testing capacity is a critical component for this pandemic response. Whether we are identifying new cases or are performing surveillance, the only way to effectively allocate resources is with a response that includes testing, said Dr. Joseph Petrosino, chair of the department of molecular virology and microbiology and director of the Alkek Center for Metagenomics and Microbiome Research at Baylor.

Since beginning the partnership with the County in May, the group has tested more than 30,000 samples. The lab also provides COVID-19 testing for other groups in the area.

"We knew we had all the pieces to stand up a testing center fast large scale clinical sequencing, experts in virology and molecular biology, and a secure way to return results to patients, said Ginger Metcalf, Human Genome Sequencing Center Director of Project Development. "We are also fortunate to have such great partners at Harris County Public Health, who have done an amazing job of gathering, tracking and delivering samples, especially for the most at-risk members of our community."

The Baylor testing lab currently has a capacity of more than 1,000 samples a day. Leaders hope to hire more staff soon to increase testing capacity.

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Baylor genomics teams partner to provide COVID-19 testing for Houston area - Baylor College of Medicine News

Gaucher Disease Treatment Market 2020

The Gaucher Disease Treatment survey report contains valuable insights into the industry. The Gaucher Disease Treatment report begins with an understanding of the current market scenario, and goes on to describe the products available in the market, along with their different applications. The report also discusses the manufacturing technology used for production processes and how the availability of the same can affect the market. Our Gaucher Disease Treatment survey report details the scope of growth of the industry and also looks into the different emerging trends in the market. Our report covers the forecast period 2020-2026. Our Gaucher Disease Treatment survey also provides a predicted market valuation for the forecast period, as well as a projected valuation by the end of the forecast period.

The report provides and in-depth analysis of the industrys tools, mechanisms, and sales and distribution methods, which significantly influence the scope for growth. With this information, the segmentation of the market is understood in a much clearer way. The global Gaucher Disease Treatment is influenced by a number of factors such as environmental fluctuations, socio-economic changes, new policies and regulations introduced by the government, and much more. The report also seeks to provide the reader with information regarding the key players in the Gaucher Disease Treatment, and how they have maintained their market shares.

The global Gaucher Disease Treatment survey report includes a section that details the segmentation of the industry and the different elements that influence growth. We provide a regional analysis to determine the key players based on geographical area. The report also includes important industry updates and news that can help the reader gather a more relevant understanding of the market, as well as its growth prospects.

The study encompasses profiles of major companies operating in the Capital Lease Market. Key players profiled in the report includes: Acetelion Pharmaceutical (J&J Ltd.), Erad Therapeutic Inc., JCR Pharmaceuticals Co Ltd., Shire Human Genetics Therapies, Inc., Sonafi (Genzyme Corporation), and Pfizer Inc.

The final report will add the analysis of the Impact of Covid-19 in this report Gaucher Disease Treatment industry.

Get a Sample Copy Of Gaucher Disease Treatment Market @ https://www.reportsandmarkets.com/sample-request/global-gaucher-disease-treatment-market-report-2020-by-key-players-types-applications-countries-market-size-forecast-to-2026-based-on-2020-covid-19-worldwide-spread?utm_source=marketresearchposts&utm_medium=36

Latest industry news

The global Gaucher Disease Treatment report survey includes the latest updates and news from the industry. The information provided will include the latest trends in the market, the release of new and innovative technology, arrival of new products, impact of governmental regulations on sales, and much more. The section will also include details of partnerships, acquisitions, mergers, and takeovers amongst the key players in the industry, and how this can alter the growth prospects.

Gaucher Disease Treatment Market continues to evolve and expand in terms of the number of companies, products, and applications that illustrates the growth perspectives. The report also covers the list of Product range and Applications with SWOT analysis, CAGR value, further adding the essential business analytics. Gaucher Disease Treatment Market research analysis identifies the latest trends and primary factors responsible for market growth enabling the Organizations to flourish with much exposure to the markets.

Market Segment by Regions, regional analysis covers

North America (United States, Canada and Mexico)

Europe (Germany, France, UK, Russia and Italy)

Asia-Pacific (China, Japan, Korea, India and Southeast Asia)

South America (Brazil, Argentina, Colombia etc.)

Middle East and Africa (Saudi Arabia, UAE, Egypt, Nigeria and South Africa)

Research objectives:

To study and analyze the global Gaucher Disease Treatment market size by key regions/countries, product type and application, history data from 2013 to 2017, and forecast to 2026.

To understand the structure of Gaucher Disease Treatment market by identifying its various sub segments.

Focuses on the key global Gaucher Disease Treatment players, to define, describe and analyze the value, market share, market competition landscape, SWOT analysis and development plans in next few years.

To analyze the Gaucher Disease Treatment with respect to individual growth trends, future prospects, and their contribution to the total market.

To share detailed information about the key factors influencing the growth of the market (growth potential, opportunities, drivers, industry-specific challenges and risks).

To project the size of Gaucher Disease Treatment submarkets, with respect to key regions (along with their respective key countries).

To analyze competitive developments such as expansions, agreements, new product launches and acquisitions in the market.

To strategically profile the key players and comprehensively analyze their growth strategies.

The Gaucher Disease Treatment Market research report completely covers the vital statistics of the capacity, production, value, cost/profit, supply/demand import/export, further divided by company and country, and by application/type for best possible updated data representation in the figures, tables, pie chart, and graphs. These data representations provide predictive data regarding the future estimations for convincing market growth. The detailed and comprehensive knowledge about our publishers makes us out of the box in case of market analysis.

Key questions answered in this report

What will the market size be in 2026 and what will the growth rate be?

What are the key market trends?

What is driving this market?

What are the challenges to market growth?

Who are the key vendors in this market space?

What are the market opportunities and threats faced by the key vendors?

What are the strengths and weaknesses of the key vendors?

Table of Contents: Gaucher Disease Treatment Market

Chapter 1: Overview of Gaucher Disease Treatment Market

Chapter 2: Global Market Status and Forecast by Regions

Chapter 3: Global Market Status and Forecast by Types

Chapter 4: Global Market Status and Forecast by Downstream Industry

Chapter 5: Market Driving Factor Analysis

Chapter 6: Market Competition Status by Major Manufacturers

Chapter 7: Major Manufacturers Introduction and Market Data

Chapter 8: Upstream and Downstream Market Analysis

Chapter 9: Cost and Gross Margin Analysis

Chapter 10: Marketing Status Analysis

Chapter 11: Market Report Conclusion

Chapter 12: Research Methodology and Reference

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Gaucher Disease Treatment Market (Impact of COVID-19) Top Growing Companies: Acetelion Pharmaceutical (J&J Ltd.), Erad Therapeutic Inc., JCR...

Newswise Rockville, Md. (August 4, 2020)New research in a genetically diverse rat strain finds high-fat diet and genetics together increase anxiety and depression-like behavior in addition to negatively affecting metabolic health. The study is published ahead of print in Physiological Genomics.

Approximately 40% of adults in the U.S. are overweight or obese, making obesity a public health issue. Previous studies have shown strong links between obesity, diet and anxiety or depression, but the underlying reasons for these co-occurring conditions are unclear. Shared genetics may be one factor at play: Some of the chromosomal locations identified in the human genome associated with depression overlap with those associated with obesity and body mass index. Finding an animal model with genetic variability similar to that found in people is ideal to learn more about how these features intersect and influence one another.

Researchers measured the effects of high-fat diet on the metabolic health and emotional behavior in a type of rodent called the heterogenous stock rat. Because this animal strain is not inbred, it has a wide genetic diversity that more closely mimics the range of traits and characteristics found in humans relative to inbred models. One group of rats was fed a high-fat diet, while a control group consumed a low-fat diet. The research team measured the animals body weight, fat accumulation around the body (fat pad) and blood sugar levels. After 11 weeks, the researchers assessed coping response to stress or despair-like behavior using a swim test where immobility is typically associated with despair-like behavior.

The research team conducted a second study, with a separate group of high-fatfed rats and low-fat controls, to look at additional behavioral tests. The tests were used to determine factors causing the increased immobility. An increase in fat pad size may cause physical limitations resulting in immobility, but the chronic high-fat diet could also contribute to despair-like behavior. In this study, both groups participated in weekly tests starting at week eighta maze and an open field test used to measure anxiety, a test that prompts grooming habits and the previously described swim test used to measure despair-like behavior.

Unsurprisingly the high-fatfed rats had more weight gain and fat accumulation, higher blood sugar levels and reduced glucose tolerance than the low-fat groups. Compared with the controls, the high-fat diet groups showed longer duration of immobility in the swim test, increased anxiety in the maze test and anxious hyperactivity in the open field test. These results suggest that diet, as well as increased fat pad size, plays a role in these emotional behaviors. Contrary to hypothesis, the high-fatfed group did not show disinterest in grooming. In fact, they spent more time grooming than the low-fatfed group. Whether this behavior was anxiety-induced is unclear.

These results lay the groundwork for future investigation to identify genes and variants that predispose individuals to increased [obesity] and worsened metabolic and behavioral health specifically under high-fat diet conditions, the research team wrote. Given the high levels of obesity, the preponderance of high-fat diets worldwide and the complex interplay between obesity and behavioral health, having a model to study the underlying genetics of these traits is of extreme importance.

Read the full article, High fat diet negatively impacts both metabolic and behavioral health in an outbred rat model, published ahead of print in Physiological Genomics.

NOTE TO JOURNALISTS:To schedule an interview with a member of the research team, please contact theAPS Communications Officeor call 301.634.7314. Find more research highlights in our News Room.

Physiology is a broad area of scientific inquiry that focuses on how molecules, cells, tissues and organs function in health and disease. The American Physiological Society connects a global, multidisciplinary community of more than 10,000 biomedical scientists and educators as part of its mission to advance scientific discovery, understand life and improve health. The Society drives collaboration and spotlights scientific discoveries through its 16 scholarly journals and programming that support researchers and educators in their work.

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High-fat Diet and Genetics Lead to Anxiety and Depression in Rats - Newswise

A type of herpes virus, one that causes mono, can in rare cases raise the risk of developing certain types of cancer. And now researchers know how: The Epstein-Barr virus (EBV) can directly latch onto bundles of genetic material in infected cells, and switch "on" nearby genes that turn healthy cells cancerous, according to a new study in human cells.

Not all people who become infected with EBV go on to develop cancer; but in rare instances, the virus can raise people's risk of developing nasopharyngeal cancer, Burkitt's lymphoma and certain stomach cancers, according to the American Cancer Society. While more than 90% of people catch the virus worldwide, only about 1.5% of cancer cases are linked to the infection, according to a 2019 report in the journal Annual Review of Pathology. Other viruses that drive cancer growth, such as hepatitis B and human papillomavirus (HPV), do so by worming their way into the genomes of their infected host but EBV takes a different approach, researchers just found.

Rather than intertwining with host DNA, EBV DNA binds to the surface of the host DNA in a way that makes the molecule change shape, and that turns on cancer-related genes nearby, study author Patrick Tan, executive director of the Genome Institute of Singapore and a professor at the Duke-NUS Medical School, told Live Science in an email. The research, published July 27 in the journal Nature Genetics, pinpoints where on the host genome the viral DNA grabs hold.

Related: 7 odd things that raise your risk of cancer (and 1 that doesn't)

Understanding this process could allow scientists to develop drugs and gene therapies to undo the virus's harmful modifications, Rona Scott, an associate professor of microbiology and immunology at Louisiana State University Health Shreveport, who was not involved in the study, told Live Science in an email.

In addition, "identifying footprints [or telltale marks] of EBV infection in cancer may help us determine if EBV, which infects over 95% of adults worldwide, contributes to other cancers not yet associated with this virus," she said.

While some of the details remain fuzzy, "the link between EBV and certain types of cancer has been known for many years," Tan said. For example, the virus has been linked to about 8% to 10% of stomach cancers, which collectively stand as the third leading cause of cancer death globally, according to a statement from Duke-NUS Medical School.

Past research explained one way EBV fuels cancer: The virus triggers chemical reactions that stick molecular tags known as methyl groups onto genes, switching them "on" or "off," according to a 2007 report in the journal Cancer Science. One theory was that these so-called epigenetic modifications, meaning modifications "on top of" the genome, disabled genes that would normally suppress tumor growth.

But Tan wondered whether EBV was also changing the 3D structure of the host genome in ways that up the risk of cancer.

Cells package DNA in organized bundles called "chromatin," with some genes tucked inside the bundle, unreachable by cellular machinery that translates those genes into protein. Chromatin's structure therefore determines which genes can be turned on or off, and at what time. While this is a helpful control mechanism in healthy cells, certain changes to the chromatin's structure can spur cancer development, according to a 2016 report in the journal Science Tan and his colleagues thought EBV might warp host chromatin in this way.

To find out, the team examined healthy stomach cells and cancerous stomach cells grown in culture, as well as cells sampled from patients with EBV-related stomach cancers, to compare the structure of their genetic material.

Related: The 12 deadliest viruses on Earth

They found that EBV DNA, also packaged into chromatin bundles, bound directly to specific spots within the chromatin of infected stomach cells. Namely, the viral DNA latched onto regions of the host genome known as genetic enhancers, which help to activate specific genes. Although switched off in the healthy cells sampled, these enhancers turned on in response to EBV infection and boosted the activation of cancer-related genes, specifically ones that stimulate cell growth and proliferation, the authors found. When dysregulated, these genes can spur tumor growth.

"We were definitely very surprised by the results," as we did not expect the viral genome to directly participate in rewiring the host cell, and controlling which proteins it builds, Tan said.

Even when the authors removed EBV from infected cells, the structural changes the virus made to host DNA stayed put. The finding supports prior evidence that EBV may contribute to cancer in a "hit-and-run" manner, meaning that even if you eliminate the virus itself, the cell's DNA remains altered and continues to drive tumor growth, Scott said.

But that theory must be confirmed in future studies, Tan added. The team also aims to study if genes that are modified by this process can serve as new drug targets to treat EBV-related cancers, he said.

Perhaps other factors, such as the innate defenses the cells use against viruses, determine which genes EBV can manipulate and in which people, though that must also be confirmed, Scott added.

In many EBV infections, the virus carries out its life cycle tucked away in immune cells called B cells and epithelial cells, which line surfaces of the body, "without much consequence" to the infected person's health, Scott noted. However, in the instances when the virus does contribute to cancer, undermining its ability to reshape the host DNA may be a critical route of treatment, she said.

Originally published on Live Science.

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'Mono' virus turns on cancer-related genes. Here's how. - Live Science

Human challenge trials (HCT) to test Covid-19 vaccines are not necessary at this time as randomised controlled trials are quite feasible owing to the high incidence of the infectious disease, said Dr Anthony Fauci, director of the National Institute of Allergy and Infectious Diseases (NIAID) in the US.

HCTs involve intentionally injecting a human trial participant with an infectious disease organism. Faucis comments come in the backdrop of the Oxford Universitys plans to consider using HCT to speed up the vaccine trials.

The recently published results of their Phase I trial showed that the vaccine did not lead to major adverse reactions and also produced neutralising antibodies in some measure.

Fauci said that an expert consultation was carried out on this issue in the US and it was concluded that such studies were not necessary at this time. The full impact of SARS-CoV-2 infection is not yet fully understood and we dont have highly effective therapies that are available to cure individuals who are infected in the challenge studies. These factors have led us to conclude that human challenge trials are not essential nor are they ethically justified at the present time, Fauci said.

The veteran infectious disease expert who is leading the fight against Covid-19 pandemic in the United States spoke on the issue at a special online symposium organised by the Indian Council of Medical Research (ICMR) on Science and Ethics of vaccine.

Fauci said that the continuing high incidence of the infectious disease, though concerning from a public health standpoint, has made randomised control trials feasible.

The World Health Organization (WHO) has said that this organism may be close wild-type and pathogenic, adapted and/or attenuated from wild-type with less or no pathogenicity, or genetically modified on some manner.

Phase-III clinical trials of the Oxford vaccine candidate had begun late May, and besides testing it on 10,000 people in the United Kingdom, the Universitys team has also tied up with organisations in Brazil and South Africa for Phase-IIII trials.

Dr Adrial Hill, director of the Jenner Institute and professor of human genetics at the University of Oxford made a case for using HCTs in a complementary role and raised a question on the reluctance to use it at ICMRs symposium.

They (HCTs) are not sufficient unto themselves; they need the safety data before you can license it. Given that there are 19 infectious diseases where people in modern era in recent years have been infecting others safely, and the track of all those diseases we see, there have been no issues. Then why are we so reluctant to do this in Covid-19? Hill said.

The most controversial is if we can treat these people, is there a pre-emptive therapy. Now you have Remdemsivir; you have Interferon-Beta, convalescent plasma. I would recommend people consider both approaches in parallel. The second one is massively quicker and less expensive than the first and will add information to your vaccine, Hill added.

Historically, HCTs have been used for small pox, cholera, influenza and typhoid. However, critics have argued that unlike Covid-19, many of these diseases had an alternative therapy available to save people from dying.

Earlier in his brief talk, Fauci said that NIAID, National Institute of Health, ICMR and Department of Biotechnology have partnered for more than 30 years on the Indo-US vaccine action plan (VAP).

Three weeks ago the VAP convened an expert advisory committee to review Covid-19 vaccine research and development in India. Eleven vaccines were reviewed by a panel of experts who provided recommendations for how these candidates might be further developed and assessed. We look forward to continue this involvement and supporting these vaccines R&D efforts, Fauci said.

Hill, too, highlighted that India is among nine countries where the Oxford University has engaged with vaccine manufacturers. The University has tied up with Pune-based Serum Institute of India to produce millions of doses of its prospective vaccine. However, the Indian government clarified on Thursday that it has not entered into agreements with any vaccine manufacturers yet.

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Human Challenge Trial Neither Essential Nor Ethically Justified at This Time, Says US Expert Anthony Fauci - Yahoo India News

tech2 News StaffJul 30, 2020 11:05:47 IST

The Indian Council of Medical Research (ICMR)has planned to hostan online, multi-country symposium on 'Novel Ideas in Science and Ethics of Vaccines Against Covid-19 Pandemic' on 30 July.

The web symposium willsee leading medical experts and scientists as speakersandpanellists on different themes in the science and ethics around a vaccine for the coronavirus pandemic.

The event would be conducted from 4.30 pm to 6.45 pm today, and livestreamed on ICMR's website.

A vaccination against the coronavirus disease (COVID-19) from German biotechnology company CureVac is administered to a volunteer at the start of a clinical test series at a university clinic in Tuebingen, Germany. Reuters

The first session byDr Anthony S Fauci, Director, National Institute of Allergy and Infectious Diseases, USAis a talkon'Confronting the pandemic'.

This will be followed by remarks from experts on 'Timely & Safe Towards a Covid-19 vaccine - Role of vaccines in ending epidemics'.

Two panel discussions on 'Novel Ideas in Vaccine Development, rollout, and adopting emerging evidence in pandemic situations', and 'Ethics of different development approaches, equity of participation in development & community engagement'areexpected to follow,where many world-leading expertsare expected to share their views.

The 25+ speakersat thesymposium includeProf (Dr) Balram Bhargava, Director General of ICMR; Prof Nir Eyal, Director, Center for Population-level Bioethics (CPLB) at Rutgers School of Public Health; Prof (Dr) Randeep Guleria, Director of AIIMS, New Delhi; Prof Adrian Hill, Director, Jenner Institute & Professor of Human Genetics at the University of Oxford;Prof Adam Kamradt-Scott, Director, Global Health Security Network;Prof Gagandeep Kang, Director, Translational Health Science & Technology Institute;Prof Heidi Larson, Director of the Vaccine Confidence Project (VCP) and Professor, London School of Hygiene and Tropical Medicine, among several others.

Findthe detailed agenda for the symposiumhere.

Find latest and upcoming tech gadgets online on Tech2 Gadgets. Get technology news, gadgets reviews & ratings. Popular gadgets including laptop, tablet and mobile specifications, features, prices, comparison.

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ICMR to host global web conference on science, ethics of COVID-19 vaccine starting 4.30 pm today - Firstpost

Health and medicine | Honors and awards | UW and the community | UW Notebook

July 28, 2020

Recent honors to University of Washington faculty and staff members have come from the Women in Engineering ProActive Network, Association Media & Publishing and The American Society of Human Genetics.

Sociologist Elizabeth Litzler honored by national network promoting women in engineering

Elizabeth Litzler

The Women in Engineering ProActive Network, or WEPAN, has given its 2020 Founders Award to Elizabeth Litzler, UW affiliate assistant professor of sociology and director of the UW Center for Evaluation & Research for STEM Equity.

The award, one of several given annually, is given to a network member who exemplifies the spirit of the WEPAN founders through her extraordinary long-term service to the organization.

The network is a national professional society that uses research and best practices to promote the inclusion of women in the field of engineering. Its members work to connect advocates across North America to increase the participation, retention and success of women and other under-represented groups in engineering from college to executive leadership.

Litzlers and other 2020 WEPAN awards will be presented at the networks next annual conference, planned for January 2021.

* * * Article by Joseph Wartman, Will Pollock of civil and environmental engineering wins award from media group

Joseph Wartman

Professor Joseph Wartman and doctoral student Will Pollock of the UW Department of Civil & Environmental Engineering have won a silver EXCEL Award from Association Media & Publishing for a feature magazine article they co-wrote on geologic hazard risks toSyrian and other refugees.

Their non-technical article was titled No Place to Flee and was published in November 2019 in the American Geophysical Unions journal EOS. Wartman is the H.R. Berg Professor of Civil & Environmental Engineering.

Association Media & Publishing AM&P for short gives out annual bronze, silver and gold EXCEL Awards for books, digital media, journals, magazines, newsletters, newspapers and promotional content. The awards recognize excellence and leadership in association media, publishing, marketing and communications.

* * *

UW Medicines Mary-Claire King, Peter Byers honored by American Society of Human Genetics

The American Society of Human Genetics has honored two UW Medicine faculty members Dr. Mary-Claire King and Dr. Peter Byers with 2020 awards.

Mary-Claire King

King was chosen to receive the societys 2020 William Allan Award, which recognizes substantial and far-reaching scientific contributions to human genetics. The award is named for one of the first American physicians to extensively research human genetics and hereditary diseases. The award comes with a $25,000 prize.

King is the American Cancer Society Professor of Medicine and Genome Sciences, and an affiliate member of the Fred Hutchinson Cancer Research Network.

The societys president, Anthony Wynshaw-Boris of Case Western University, praised King for providing insight into the existence of the gene she named BRCA1, and changed our understanding of cancer prevention and treatment. Read more from the UW Division of Medical Genetics.

Peter Byers

The genetics society, also called ASHG, chose Byers for its 2020 Victor A. McKusick Leadership Award, which is given annually for exemplary leadership and vision by promoting genetics and genomics knowledge in the broader scientific community.

The award, which comes with a $10,000 prize, recognizes the importance of Byers research on the molecular pathogenesis of inherited disorders of connective tissue, and for his leadership in nearly all facets of the societys work. Byers has served as the societys president and editor of its American Journal of Human Genetics. Read more on the UW Division of Medical Genetics website.

The society was founded in 1948 and its 8,000 members include researchers, academics, clinicians, laboratory practice professionals, genetic counselors and nurses. The awards will be presented at the next annual meeting, to be held virtually and not yet scheduled.

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Faculty/staff honors: Women in engineering network nod, winning magazine article on geologic hazards and refugees and two national genetics society...

Scientists around the world have access to a rich trove of information through the Encyclopedia of DNA Elements (ENCODE)--annotated versions of the human and mouse genomes that are vital for interpreting their genetic codes. In the July 29, 2020 issue of the journal Nature, an international consortium of approximately 500 scientists reports on the completion of Phase 3 of an ongoing project, an achievement 20 years in the making that will help reveal how genetic variation shapes human health and disease.

[Watch "ENCODE: Encyclopedia Of DNA Elements": https://www.youtube.com/watch?v=Y3V2thsJ1Wc%5D

Funded by the National Human Genome Research Institute, ENCODE launched in 2003, soon after the human genome was first sequenced. Its researchers are developing a comprehensive catalog of the human and mouse genomes' functional elements--dense arrays of protein-coding genes, non-coding genes, and regulatory elements. Thousands of researchers worldwide have taken advantage of ENCODE data, using it to shed light on cancer biology, cardiovascular disease, human genetics, and other topics.

"When the first draft of the human genome was completed . . . it became immediately clear that while we had the primary sequence of the genome, or we had a draft of it . . . we needed to have an annotation for the genome," says Cold Spring Harbor Laboratory Professor Thomas Gingeras, whose team has been contributing to the ENCODE project since its inception. "We knew where the genes were located. Where the regulatory mechanisms and loci were located was significantly underdeveloped."

In Phase 3, researchers took advantage of the latest genetic technologies to glean data from biological specimens and deeply investigate the regulatory regions outside of genes, where most of the genome's person-to-person variation lies. Their data identifies some 900,000 candidate regulatory elements from the human genome and more than 300,000 from the mouse, which can be explored through ENCODE's new online browser.

Gingeras's team is investigating genome elements that instruct cells about how and when to transcribe DNA sequences into RNA. In a companion publication to the ENCODE report, a team led by Gingeras and collaborator Roderic Guig at the Centre for Genomic Regulation detail work identifying molecular fingerprints that can be used to identify five groups of human cells. "Our work redefines, based on gene expression, the basic histological types in which tissues have been traditionally classified," Guig says.

Those findings are now available through the ENCODE database. Meanwhile, the project has begun its fourth phase, employing new technologies and investigating additional cell types. Gingeras notes:

"This encyclopedia is a living resource. It has a beginning but really no end. It will continue to be improved, and grown, as time goes on."

Originally posted here:

ENCODE3: Interpreting the human and mouse genomes - Science Codex

The Encyclopedia of DNA Elements (ENCODE) Consortium is a universal coordinated effort of research groups funded by the National Human Genome Research Institute (NHGRI). The objective of ENCODE is to make a comprehensive parts list of functional elements in the human genome, including elements that work at the protein and RNA levels, and regulatory elements that control the cells and conditions where a gene is active.

The project will detail how the human genome functions. Recently, the project completed its latest phase- scientists have added millions of candidate DNA switches from the human and mouse genomes. These genomes appear to control when and where genes are turned on, and a new registry that assigns a portion of these DNA switches to useful biological categories.

It also provides the latest visualization tools to help in the use of ENCODEs large datasets.

NHGRI Director Eric Green, M.D., Ph.D. said,A major priority of ENCODE 3 was to develop means to share data from the thousands of ENCODE experiments with the broader research community to help expand our understanding of genome function. ENCODE 3 search and visualization tools make these data accessible, thereby advancing efforts in open science.

To evaluate the potential functions of various DNA locales, ENCODE specialists considered biochemical procedures that are normally connected with the switches that regulate genes. This biochemical methodology is an effective method to investigate the whole genome wholly and quickly.

This strategy assists with finding regions in the DNA that are candidate functional elements DNA regions that are anticipated to be practical components dependent on these biochemical properties. Candidates would then be able to be tested in further experiments to distinguish and portray their useful roles in gene regulation.

Elise Feingold, Ph.D., scientific advisor for strategic implementation in the Division of Genome Sciences at NHGRI and a lead on ENCODE for the institute, said,A key challenge in ENCODE is that different genes and functional regions are active in different cell types. This means that we need to test a large and diverse number of biological samples to work towards a catalog of candidate functional elements in the genome.

During the recently completed third phase of ENCODE, scientists performed almost 6000 experiments in several biological contexts- 4,834 in humans and 1,158 in mice- to enlight details of the genes and their potential regulators in their respective genomes.

Scientists studied developing embryonic mouse tissues to comprehend the timeline of various genomic and biochemical changes that occur during mouse development.

Scientists analyzed how chemical modifications of DNA, proteins that bind to DNA, and RNA (a sister molecule to DNA) interact to regulate genes. Results from ENCODE 3 also help explain how variations in DNA sequences outside of protein-coding regions can influence the expression of genes, even genes located far away from a specific variant itself.

Brenton Graveley, Ph.D., professor and chair of the Department of Genetics and Genome Sciences at UCONN Health, said,The data generated in ENCODE 3 dramatically increase our understanding of the human genome. The project has added tremendous resolution and clarity for previous data types, such as DNA-binding proteins and chromatin marks, and new data types, such as long-range DNA interactions and protein-RNA interactions.

As a new feature, ENCODE 3 scientists created a resource detailing different kinds of DNA regions and their corresponding candidate functions. A web-based tool called SCREEN(link is external) allows users to visualize the data supporting these interpretations.

The projects latest results were published in Nature, accompanied by 13 additional in-depth studies published in other major journals.

Read more from the original source:

Revealing the intrinsic functioning of human and mouse genomes - Tech Explorist

Schizophrenia is a complex neuropsychiatric disorder, influenced by a combined action of genes and environmental factors. The neurodevelopmental origin is one of the most widely recognized etiological models of this heterogeneous disorder. Environmental factors, especially infections during gestation, appear to be a major risk determinant of neurodevelopmental basis of schizophrenia. Prenatal infection may cause maternal immune activation (MIA) and enhance risk of schizophrenia in the offspring. However, the precise mechanistic basis through which MIA causes long-lasting schizophrenia-like behavioral deficits in offspring remains inadequately understood. Herein, we aimed to delineate whether prenatal infection-induced MIA causes schizophrenia-like behaviors through its long-lasting effects on immune-inflammatory and apoptotic pathways, oxidative stress toxicity, and antioxidant defenses in the brain of offspring. Sprague-Dawley rats were divided into three groups (n=15/group) and were injected with poly (I:C), LPS, and saline at gestational day (GD)-12. ExceptIL-1, plasma levels ofIL-6, TNF-, and IL-17A assessed after 24h were significantly elevated in both thepoly (I:C)- and LPS-treated pregnant rats, indicating MIA. The rats born to dams treated with poly (I:C) and LPS displayed increased anxiety-like behaviors and significant deficits in social behaviors. Furthermore, the hippocampus of the offspring rats of both the poly (I:C)- and LPS-treated groups showed increased signs of lipid peroxidation, diminished total antioxidant content, and differentiallyupregulated expression of inflammatory (TNF, IL6, and IL1), and apoptotic (Bax, Cas3, and Cas9) genes but decreased expression of neuroprotective (BDNF and Bcl2) genes. The results suggest long-standing effects of prenatal infections on schizophrenia-like behavioral deficits, which are mediated by immune-inflammatory and apoptotic pathways, increased oxidative stress toxicity, and lowered antioxidant and neuroprotective defenses. The findings suggest that prenatal infections may underpin neurodevelopmental aberrations and neuroprogression and subsequently schizophrenia-like symptoms.

PubMed

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Maternal Immune Activation Causes Schizophrenia-like Behaviors in the Offspring through Activation of Immune-Inflammatory, Oxidative and Apoptotic...

Geneticist Dr Kat Arney takes a look at the ancient war between our genes and the pathogens that infect us, looking back thousands of years to the Black Death and before, all the way through to our very latest foe.

One of the most curious things about COVID-19 the disease caused by the novel SARS-CoV-2 coronavirus thats causing so much trouble is the wide variation in how it affects different people, from being a very serious or even fatal illness, through a range of strange symptoms like skin rashes or diarrhea as well as the cough, fever and loss of smell, which vary in their severity. And there are some lucky people who seem to catch the virus but have no symptoms at all. So, do these differences lie in our genetics? Or are their other factors at play?

To find out, Kat speaks with consultant geriatrician Dr Claire Steves from Kings College London. Shes part of a team of researchers analysing data from the COVID Symptom Study app, originally built by health science company ZOE to survey some of the thousands of identical and non-identical twins involved in the TwinsUK cohort study. The app now has more than 4 million users in the UK, US and Sweden, and is providing valuable insights into the key symptoms of COVID-19 and how they affect different people.

COVID-19 is just the latest in a long string of outbreaks, epidemics and pandemics that have ravaged humanity over the years. Christiana Scheib, head of the ancient DNA research facility at the University of Tartu, Estonia, is looking at much older plagues including the Black Death to discover how underlying genetic variations may have contributed to susceptibility to disease. By studying ancient remains from many burial sites in the Cambridge area, shes piecing together a picture of the past to understand how these people lived and died.

Finally, Kat talks to Lucy Van Dorp from University College London, who is studying how the human genome has co-evolved over millennia alongside the pathogens that infect us. Although it may seem strange to be studying ancient diseases in todays modern era, particularly when weve got a brand new pandemic to worry about, her work to trace the spread, movement and migration of humans and their pathogens is essential for understanding the spread of outbreaks today, including COVID-19.

Full transcript, links and references available online at GeneticsUnzipped.com

Genetics Unzipped is the podcast from the UK Genetics Society, presented by award-winning science communicator and biologist Kat Arney and produced by First Create the Media. Follow Kat on Twitter @Kat_Arney, Genetics Unzipped @geneticsunzip, and the Genetics Society at @GenSocUK

Listen to Genetics Unzipped on Apple Podcasts (iTunes) Google Play, Spotify, or wherever you get your podcasts

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Podcast: The ancient war between genes and disease - Genetic Literacy Project

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With uncertainty hanging over the campus during the pandemic, the University of Pittsburgh Graduate School of Public Health was kicking around socially distanced ideas of how to welcome students back.

Thats when the school hit upon the notion that a screening of a modern opera about the father of sanitation in medicine would be a perfect midsummer event.

On Wednesday evening, Pitt is holding a virtual watch party featuring a performance of a music-theater opera called Semmelweis. Its about an outspoken 19th-century Hungarian obstetrician, Ignaz Semmelweis, who said doctors could prevent the spread of germs by washing their hands. While it would seem like an obvious idea, Semmelweis was attacked for it.

The work, which was produced by the Budapest Operetta Theatre and Bartok Plusz Opera Festival, was created by American composer Raymond J. Lustig, Irish-American librettist Matthew Doherty and Hungarian director Martin Boross.

The presentation of the recorded performance begins at 6:30 p.m. followed by a live question-and-answer session with Lustig and Matt Gray, director of American Opera Projects.

The School of Public Health has new students scheduled to start in the fall and we decided that we needed to interact with them with some actual programming in the summer in light of whats going on, said Cindy Bryce, a Pitt associate professor of health policy and management and associate dean for student affairs at the School of Public Health. We thought the Semmelweis performance would be perfect for a virtual get-together.

In true operatic tradition, Semmelweis life story is both inspiring and tragic. Much like his contemporaries, English physician John Snow and French biologist Louis Pasteur, Semmelweis was known as an early pioneer of antiseptic procedures.

During the mid-19th century, childbed fever was common in hospitals, including Vienna General Hospital where Semmelweis worked in the obstetrical clinic. The clinics doctors wards had a 10% mortality rate, three times the mortality rate of midwives wards.

Realizing that doctors hands were infected as they came straight to the delivery room from other work such as autopsies, Semmelweis urged the practice of hand washing with chlorinated lime solutions in 1847.

Semmelweis published a book about his findings and hand washing reduced the mortality rate to below 1%. But some doctors were offended by the idea that they should have to wash their hands and rejected it.

Prior to Semmelweis, if you were a cultured, educated physician in all the major centers of Europe, you did whatever you wanted when it came to child birth, said Dr. David N. Finegold, the Pitt professor of human genetics who proposed the Semmelweis opera showing. You could come from a post-mortem examination and without washing your hands, deliver a baby. With the institution of hand-washing, the mortality rate dropped dramatically. But Semmelweis was ridiculed for that.

Semmelweis died in 1865 after being institutionalized for a nervous breakdown.

You can imagine the urgency he must have felt, pushing extra hard to get people to listen to him and getting extra frustrated when people didnt, said Lustig, the composer.

Lustig explained that the incentive for denial was very strong among 19th-century doctors.

Semmelweis was directly pointing to the doctors hands as the cause of many hundreds of thousands of deaths over the years. I empathize with Semmelweis but I also empathize with those who must have found it incredibly hard to accept what he was trying to tell people, that their own hands had been the cause of deaths, Lustig said.

And Lustig sees parallels between what happened in Semmelweis time and what American society is going through during the current pandemic.

We see it today, all the time people sort of wanting to continue a certain behavior because if they can continue it, it must never have been the cause. Therefore they have nothing to worry about.

Finegold said some comparisons can even be made between Semmelweis and infectious diseases expert Dr. Anthony Fauci.

Fauci is politically correct, Finegold said. Semmelweis stood up for whats right and didnt have to be as politically correct to retain his position. He recognized the problem and was able to implement things that might make it better and they did. Fauci knows what will make it better and says it but he doesnt have the power (to implement things).

Lustig said he was inspired to compose Semmelweis by imagining what he must have gone through.

Thats really what went into our work is trying to understand what its like to be that person thats got this piece of news that nobody wants to hear, this very negative light bulb that went off in his head, and dealing with trying to convince people and at the same time to turn the ship as quickly as possible before many more women and their babies die on his watch, Lustig said.

He must have been haunted and every day that went by that he couldnt convince people must have been torture for him.

Tonights event is open to anyone who is interested. To register for the Semmelweis watch party, go to publichealth.pitt.edu/semmelweis.

Paul Guggenheimer is a Tribune-Review staff writer. You can contact Paul at 724-226-7706 or pguggenheimer@triblive.com.

Categories:Coronavirus | Editor's Picks | Education | Health | Local | Allegheny

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Pitt's School of Public Health welcomes students with opera about obstetrician who championed hand-washing - TribLIVE

NASDAQ:BNGO fell on Monday, despite more news that should keep investors bullish on the healthcare company. The stock price dropped8.64% to finish the trading session at $0.8131 per share, nearly wiping out the 14% rise from Friday of last week. BioNano briefly touched a low of $0.78before finishing out strong, climbing back above $0.80 to end the day. Surprisingly, there was a higher than average volume trading throughout the day, which is another relatively positive sign for investors who have remained loyal to the company.

The micro-cap healthcare sector produced another mixed day of results, even as the Nasdaq rebounded from the mini correction to end last week. BioNano Genomics Inc. rivals Pacific Biosciences of California (NASDAQ: PACB) rose on Monday, despite a Zacks Consensus Estimate report that Wall Street is expecting a 43.8% year over year decline in revenues. Other industry companies like Progenity Inc. (NASDAQ:PROG), Predictive Oncology Inc. (NASDAQ:POAI)and Precipio (NASDAQ:PRPO) all remained relatively flat.

Earlier on Monday, a report from Oppenheimer stated that 5-Star healthcare analyst Kevin DeGeeter doubled down on his stock price upgrade, giving BioNano an 'Outperform' rating and a new price target of $1.50 per share. While this is lower from his price target earlier in the year of $1.83, investors should still feel optimistic that there is quite a bit of sentiment on Wall Street that Bionano Genomics Inc. has a bright future on coronavirus vaccine development. Along with their usual work in human genetics, BioNano has been in the news recently for its work in discovering commonalities in the genetic variants of young male patients who had severe cases of COVID-19.

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BNGO Stock Price: BioNano Genomics Inc. retreats, starts week in the red - FXStreet