Expressions 1981

Expressions contains selected work from the 1981 Creative Writing Contest entrants, Campus Chronicle Photography Contest entrants, and Commercial Art students at Des Moines Area Community College. Design , typography and the layout was done by Journalism students .https://openspace.dmacc.edu/expressions/1003/thumbnail.jp

Genetic Diversity and Population Parameters of Sea Otters, Enhydra lutris, before Fur Trade Extirpation from 1741–1911

All existing sea otter, Enhydra lutris, populations have suffered at least one historic population bottleneck stemming from the fur trade extirpations of the eighteenth and nineteenth centuries. We examined genetic variation, gene flow, and population structure at five microsatellite loci in samples from five pre-fur trade populations throughout the sea otter's historical range: California, Oregon, Washington, Alaska, and Russia. We then compared those values to genetic diversity and population structure found within five modern sea otter populations throughout their current range: California, Prince William Sound, Amchitka Island, Southeast Alaska and Washington. We found twice the genetic diversity in the pre-fur trade populations when compared to modern sea otters, a level of diversity that was similar to levels that are found in other mammal populations that have not experienced population bottlenecks. Even with the significant loss in genetic diversity modern sea otters have retained historical structure. There was greater gene flow before extirpation than that found among modern sea otter populations but the difference was not statistically significant. The most dramatic effect of pre fur trade population extirpation was the loss of genetic diversity. For long term conservation of these populations increasing gene flow and the maintenance of remnant genetic diversity should be encouraged

Prospective role of thyroid disorders in monitoring COVID-19 pandemic

COVID-19 pandemic has affected more than 200 countries and 1.3 million individuals have deceased within eleven months. Intense research on COVID-19 occurrence and prevalence enable us to understand that comorbidities play a crucial role in spread and severity of SARS-CoV-2 infection. Chronic kidney disease, diabetes,respiratory diseases and hypertension are among the various morbidities that are prevalent in symptomatic COVID-19 patients. However, the effect of altered thyroid-driven disorders cannot be ignored. Since thyroid hormone critically coordinate and regulate the major metabolism and biochemical pathways, this review is on the potential role of prevailing thyroid disorders in SARS-CoV-2 infection. Direct link of thyroid hormone with several disorders such as diabetes, vitamin D deficiency, obesity, kidney and liver disorders etc. suggests that the prevailing thyroid conditions may affect SARS-CoV-2 infection. Further, we discuss the oxidative stress-induced aging is associated with the degree of SARS-CoV-2 infection. Importantly, ACE2 protein which facilitates the host-cell entry of SARS-CoV-2 using the spike protein, are highly expressed in individuals with abnormal level of thyroid hormone. Altogether, we report that the malfunction of thyroid hormone synthesis may aggravate SARS-CoV-2 infection and thus monitoring the thyroid hormone may help in understanding the pathogenesis of COVID-19

De Novo SOX6 Variants Cause a Neurodevelopmental Syndrome Associated with ADHD, Craniosynostosis, and Osteochondromas.

SOX6 belongs to a family of 20 SRY-related HMG-box-containing (SOX) genes that encode transcription factors controlling cell fate and differentiation in many developmental and adult processes. For SOX6, these processes include, but are not limited to, neurogenesis and skeletogenesis. Variants in half of the SOX genes have been shown to cause severe developmental and adult syndromes, referred to as SOXopathies. We here provide evidence that SOX6 variants also cause a SOXopathy. Using clinical and genetic data, we identify 19 individuals harboring various types of SOX6 alterations and exhibiting developmental delay and/or intellectual disability; the individuals are from 17 unrelated families. Additional, inconstant features include attention-deficit/hyperactivity disorder (ADHD), autism, mild facial dysmorphism, craniosynostosis, and multiple osteochondromas. All variants are heterozygous. Fourteen are de novo, one is inherited from a mosaic father, and four offspring from two families have a paternally inherited variant. Intragenic microdeletions, balanced structural rearrangements, frameshifts, and nonsense variants are predicted to inactivate the SOX6 variant allele. Four missense variants occur in residues and protein regions highly conserved evolutionarily. These variants are not detected in the gnomAD control cohort, and the amino acid substitutions are predicted to be damaging. Two of these variants are located in the HMG domain and abolish SOX6 transcriptional activity in vitro. No clear genotype-phenotype correlations are found. Taken together, these findings concur that SOX6 haploinsufficiency leads to a neurodevelopmental SOXopathy that often includes ADHD and abnormal skeletal and other features