This article was originally published here

Epilepsia. 2021 Nov 6. doi: 10.1111/epi.17115. Online ahead of print.

ABSTRACT

Autism spectrum disorder (ASD) is frequently associated with infants with epileptic encephalopathy, and early interventions targeting social and cognitive deficits can have positive effects on developmental outcome. However, early diagnosis of ASD among infants with epilepsy is complicated by variability in clinical phenotypes. Commonality in both biological and molecular mechanisms have been suggested between ASD and epilepsy, such as occurs with tuberous sclerosis complex. This review summarizes the current understanding of causal mechanisms between epilepsy and ASD, with a particularly genetic focus. Hypothetical explanations to support the conjugation of the two conditions include abnormalities in synaptic growth, imbalance in neuronal excitation/inhibition, and abnormal synaptic plasticity. Investigation of the probable genetic basis has implemented many genes, although the main risk supports existing hypotheses in that these cluster to abnormalities in ion channels, synaptic function and structure, and transcription regulators, with the mammalian target of rapamycin (mTOR) pathway and mTORpathies having been a notable research focus. Experimental models not only have a crucial role in determining gene functions but are also useful instruments for tracing disease trajectory. Precision medicine from gene therapy remains a theoretical possibility, but more contemporary developments continue in molecular tests to aid earlier diagnoses and better therapeutic targeting.

PMID:34741464 | DOI:10.1111/epi.17115

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The epilepsy-autism spectrum disorder phenotype in the era of molecular genetics and precision therapy - DocWire News

A California condor.

It was just an ordinary day of analysing biological samples from California condors in the San Diego Zoo Wildlife Alliance for Leona Chemnick, a researcher in the alliance's conservation genetics labthat was until she came across something that was not quite ordinary. Leona found that two California condor chicks were genetically related to their mother but didn't seem to be related to any male.

Puzzled and likely bewildered, Leona discussed the situation with Oliver Ryder, the Director of Conservation Genetics at San Diego Zoo Wildlife Alliance. It dawned on them, or as Oliver put it, "hit them in the face," that the discovery that neither bird was genetically related to a male implied that both chicks were biologically fatherless. Which meant parthenogenesis, or asexual reproduction, had been at play.

Parthenogenesis is a natural form of asexual reproduction in which an embryo that hasn't been fertilised by sperm continues to develop with only the mother's genetic materials. This is the first time parthenogenesis that researchers have documented in condors. It is also the first time it has been discovered using molecular genetic testing and in any avian species where the female bird has access to a mate.

This phenomenon, although rare, has been observed in fishes and lizards before. So you might wonder why this is such a huge deal. Well, not long ago, California condors had teetered over the edge of extinction, and it was only through extensive and dedicated conservative methods that conservationists were able to save the species from total extinction. Even then, California condors continue to remain critically endangered. It's thus a big deal that condors can reproduce asexually, potentially increasing the species' chances of producing offspring.

Scientists have previously documented parthenogenesis in isolated domesticated birds such as turkeys and chickens, but this is the first time a "virgin birth" has produced viable chicks in a wild condor population.

The California condor parthenotes were produced by two different dams, each of which was housed with a fertile male continuously. Both of these females had a large number of offspring with their partnersone had 11 chicks, while the other had 23 chicks after being paired with a male for over 20 years. Following parthenogenesis, the latter pair reproduced twice more.

"We only confirmed it because of the normal genetic studies we do to prove parentage. Our results showed that both eggs possessed the expected male ZZ sex chromosomes, but all markers were only inherited from their dams, verifying our findings," said Oliver.

Unfortunately, one parthenogenic offspring died in 2003 at the age of 3, and another died in 2017 at 8.

Luckily, the San Diego Zoo Wildlife Alliance researchers could confirm this groundbreaking discovery by analysing data gathered during the successful and collaborative California Condor Recovery Program.

Using blood, eggshell membranes, tissues, and feathers to gather genetic data from 911 individual condors, conservationists have been conducting extensive genetics and genomics research for over 30 years. Before confirming the outcome of this unique case of parthenogenesis, they were able to cross-reference historical genetic records.

The study is expected to have a profound effect on wildlife genetics and conservation science.

The study was published in the Journal of Heredity last week and can be accessed here.

**

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New data show the therapy led to minimal changes in renal function, even after more than 8 years.

New long-term data show that patients with Fabry disease who are treated with migalastat (Galafold) experienced stable renal function after 2 years or more on the drug.

The report offers some of the first data regarding the long-term data regarding the medication, which was approved by the FDA in 2018. The study was published in the journal Molecular Genetics and Metabolism Reports.

Fabry disease is a rare lysosomal storage disease caused by a mutation of the GLA gene. The mutation leads to buildup of globotriaosylceramide (Gb3) throughout the body, including in the kidneys. Renal manifestations of the diseaseas well as likely associated cardiac eventsare a significant cause of mortality and morbidity in patients with Fabry, noted corresponding author Daniel G. Bichet, MD of the University of Montreal, and colleagues.

Enzyme replacement therapy (ERT), in combination with the oral chaperone migalastat, has become the standard treatment for people with Fabry disease. The investigators explained that migalastat works by targeting the lysosomal enzyme lysosomal enzyme -galactosidase A (-Gal A), which is functionally deficient in patients with Fabry.

As a small molecule pharmacological chaperone, migalastat binds to and stabilizes amenable mutant forms of -Gal A in the endoplasmic reticulum, facilitating trafficking of -Gal A to lysosomes and restoring endogenous enzyme activity, Bichet and colleagues wrote.

Previous reports, including the phase 3 clinical trials for migalastat, showed that patients on the medication had stable renal function. However, those studies were based on shorter time frames of 24 months or less.

In the new study, the authors conducted a post-hoc analysis to look at the long-term renal-function changes in patients with amenable GLA variants who were given migalastat for 2 or more years as part of the phase 3 trials and/or long-term open-label extension studies.

A total of 78 patients were included in the analysis. Of those, 36 were ERT-naive, and 42 were ERT-experienced. The 2 groups had average ages of 45 years and 50 years, respectively. The ERT-naive group had a mean baseline estimated glomerular filtration rate (eGFR) of 91.4 mL/min/mL/1.73 m2, while the ERT-experienced group had a mean baseline eGFR of 89.2 mL/min/1.73 m2.

All of the patients were prescribed migalastat at a dose of 123 mg every other day. The patients all took the drug for at least 2 years, and up to 8.6 years. Investigators then calculated an annualized rate of change for the patients, using the Chronic Kidney Disease Epidemiology Collaboration equation.

In the ERT-naive cohort, the mean annualized rates of change from baseline were -1.6 mL/min/1.73 m2 overall. Stratified by gender, male patients had a mean annualized change rate of -1.8 mL/min/1.73 m2 and females had a change rate of -1.4 mL/min/1.73 m2.

In the RT-experienced cohort, the overall mean annualized rate of change was -1.6 mL/min/1.73 m2, -2.6 mL/min/1.73 m2for male patients, and -0.8 mL/min/1.73 m2for female patients.

This translated to a minimal annualized change in renal function from baseline.

Bichet and colleagues said the data show migalastat led to preserved renal function across a broad range of patients.

In conclusion, patients with Fabry disease and amenable GLA variants receiving long-term migalastat treatment (8.6 years) maintained renal function irrespective of treatment status, sex, or phenotype, they wrote.

Reference

Bichet DG, Torra R, Wallace E, et al. Long-term follow-up of renal function in patients treated with migalastat for Fabry disease. Mol Genet Metab Rep. Published online August 4, 2021. doi:10.1016/j.ymgmr.2021.100786

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The gene, named LZTFL1, is found in 60 per cent of people belonging to South Asian ancestry (Representative image)

Researchers at the Medical Research Council Weatherall Institute of Molecular Medicine, University of Oxford, have identified the gene responsible for doubling the risk of respiratory failures from COVID-19. University of Oxfords Medical Research Council Weatherall Institute of Molecular Medicine researchers have identified the gene that doubles the risk of respiratory failures in those suffering from COVID-19.

The gene, named LZTFL1, is found in 60 per cent of people belonging to South Asian ancestry, suggests study. The researchers also say that this could explain why there have been excess deaths seen in some of the UK communities and how badly India got impacted during the second wave of covid.

Despite finding the gene in 60 per cent of the people, it is too early to say that just one factor had led to these severe repercussions. Socio economic factors play an equal role when it comes to communities being severely impacted by the disease.

Like we said, 60 per cent of South Asian ancestry has this gene in them, 15 per cent of those with European ancestry also inhibits this gene. Also, Afro-Caribbean ancestry also carries the gene (2 per cent ). And hence, this gene does not explain why there were higher covid led deaths in black people and some other minority ethnic communities.

What does the study reveal?

The study which was released in the journal Nature Genetics this week, researchers used cutting edge technology to figure out which gene is responsible for the deaths in 65 year old from covid-19 and whats the role of this gene to this outcome. An artificial intelligence algorithm was used by researchers to analyse huge quantities of genetic data from different types of cells present from all parts of the body. This analysis showed that this genetic signal will affect cells found in the lung.

The study found that there is a possibility that a risky gene present in the body of the human prevents the cells lining the airways and eventually stops the lung from responding to the virus in a proper way. You can also say that the absence of genes can substantially change how a persons lungs respond to covid-19 virus. While the gene may impact the response system of the lungs, it does not impact the immune system of the human body. Researchers thereby believe that even though some people may have this gene, they should respond to the vaccines normally.

Professor Prof James Davies, co author of the study said in the statement that while genetics cannot be changed, the results of the study has shown that people with this particular higher risk gene can be benefited more with the vaccination. The genetic signal in our body affects the lung and not the immune system. Meaning, the increased risk should be cancelled out by the vaccine.

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The pathology, phylogeny, and epidemiology of Echinococcus ortleppi (G5 genotype): a new case report of echinococcosis in China - Infectious Diseases...

ITEM 2.02 Results of Operations and Financial Condition.On November 2, 2021, Myriad Genetics, Inc. (the "Company") announced itsfinancial results for the three months ended September 30, 2021. The earningsrelease is attached hereto as Exhibit 99.1 to this Current Report on Form 8-Kand incorporated herein by reference.

Exhibit 99.1 contains "forward-looking statements" within the meaning of thePrivate Securities Litigation Reform Act of 1995, including statements relatingto our business, goals, strategy and financial and operational outlook. These"forward-looking statements" are management's present expectations of futureevents and are subject to a number of risks and uncertainties that could causeactual results to differ materially and adversely from those described in theforward-looking statements. These risks include, but are not limited to:uncertainties associated with COVID-19, including its possible effects on theCompany's operations and the demand for its products and services; risks relatedto the Company's ability to efficiently and flexibly manage its business amiduncertainties associated with COVID-19; the risk that sales and profit marginsof the Company's existing molecular diagnostic tests may decline or that theCompany may not be able to operate its business on a profitable basis; risksrelated to the Company's ability to generate sufficient revenue from itsexisting product portfolio or in launching and commercializing new tests; risksrelated to changes in governmental or private insurers' coverage andreimbursement levels for the Company's tests or the Company's ability to obtainreimbursement for its new tests at comparable levels to its existing tests;risks related to increased competition and the development of new competingtests and services; the risk that the Company may be unable to develop orachieve commercial success for additional molecular diagnostic tests in a timelymanner, or at all; the risk that the Company may not successfully develop newmarkets for its molecular diagnostic tests, including the Company's ability tosuccessfully generate revenue outside the United States; the risk that licensesto the technology underlying the Company's molecular diagnostic tests and anyfuture tests are terminated or cannot be maintained on satisfactory terms; risksrelated to delays or other problems with operating the Company's laboratorytesting facilities; risks related to public concern over genetic testing ingeneral or the Company's tests in particular; risks related to regulatoryrequirements or enforcement in the United States and foreign countries andchanges in the structure of the healthcare system or healthcare payment systems;risks related to the Company's ability to obtain new corporate collaborations orlicenses and acquire new technologies or businesses on satisfactory terms, if atall; risks related to the Company's ability to successfully integrate and derivebenefits from any technologies or businesses that it licenses or acquires; risksrelated to the Company's projections about the potential market opportunity forthe Company's products; the risk that the Company or its licensors may be unableto protect or that third parties will infringe the proprietary technologiesunderlying the Company's tests; the risk of patent-infringement claims orchallenges to the validity of the Company's patents; risks related to changes inintellectual property laws covering the Company's molecular diagnostic tests, orpatents or enforcement, in the United States and foreign countries; risksrelated to security breaches, loss of data and other disruptions, including fromcyberattacks; risks of new, changing and competitive technologies andregulations in the United States and internationally; the risk that the Companymay be unable to comply with financial operating covenants under the Company'scredit or lending agreements; and other factors discussed under the heading"Risk Factors" contained in Item 1A of the Company's Transition Report on Form10-K filed with the Securities and Exchange Commission on March 16, 2021, aswell as any updates to those risk factors filed from time to time in theCompany's Quarterly Reports on Form 10-Q or Current Reports on Form 8-K.

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The exhibit(s) may contain hypertext links to information on our website orother parties' websites. The information on our website and other parties'websites is not incorporated by reference into this Current Report on Form 8-Kand does not constitute a part of this Form 8-K.In accordance with General Instruction B-2 of Form 8-K, the information setforth in Item 2.02 and in Exhibit 99.1 shall not be deemed to be "filed" forpurposes of Section 18 of the Securities Exchange Act of 1934, as amended (the"Exchange Act"), or otherwise subject to the liability of that section, andshall not be incorporated by reference into any registration statement or otherdocument filed under the Securities Act of 1933, as amended or the Exchange Act,except as shall be expressly set forth by specific reference in such filing.

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image:Dr. Manel Esteller view more

Credit: Josep Carreras Leukaemia Research Institute

Manel Esteller, Director of the Josep Carreras Leukemia Research Institute (IJC), ICREA Researcher and Professor of Genetics at the University of Barcelona is recognized by the prestigious Stanford University in the United States among the top 0.1% of researchers with the most impact on world level in all areas of Science.

This is reflected in a study recently published by the Data Center for Biomedical Sciences, Statistics, Meta-Analysis and Innovation (METRICS) of Stanford University. Considering more than 100,000 researchers in 22 scientific disciplines worldwide in terms of the citations of their discoveries, their main authorship and their transcendence for other researchers, the authors conclude that Dr Esteller occupies position 127 of the ranking, being the first biomedical researcher considered for those who work in Spain.

Dr Manel Esteller's research focuses on the epigenetic mechanisms involved in the onset and progression of human diseases, mainly cancer. The results derived from their studies have allowed, in addition to knowing the molecular bases of various pathologies, the development of novel diagnostic tools and new therapies for human diseases.

Reference article:

Baas, Jeroen; Boyack, Kevin; Ioannidis, John P.A. (2021), August 2021 data-update for Updated science-wide author databases of standardized citation indicators, Mendeley Data, V3, doi: 10.17632/btchxktzyw.3

Disclaimer: AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert system.

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Dr. Manel Esteller, director of the Josep Carreras Leukaemia Research Institute, recognized among the researchers with the most scientific impact...