Life and death in a corn desert oasis: reproduction, mortality, genetic diversity, and viability of Illinois' last Eastern Massasauga population

Biodiversity is being lost at an unprecedented rate globally, with the primary driver being habitat loss and fragmentation. As natural habitats contract, species are forced into small often fragmented populations at increased risk of extirpation. Reptile species are thought to be experiencing wide-spread declines, the extent of which may be underestimated due to lack of long-term data for most species. Snakes, especially venomous species, are particularly vulnerable because of their life-history characteristics and often specialized habitat requirements. Unfortunately, snakes are also under-studied due in part to a historical lack of interest in the taxa and the difficulty with finding large numbers of individuals. The Eastern Massasauga (Sistrurus catenatus) is a rattlesnake species native to prairie/grassland and bog habitats from Iowa to New York and Ontario, Canada. The Eastern Massasauga is experiencing range-wide declines primarily caused by anthropogenic habitat conversion to agriculture and was recently proposed for listing as threatened under the Federal Endangered Species Act. In Illinois, only one Eastern Massasauga population remains extant, located at Carlyle Lake, Clinton County. Capture-mark-recapture monitoring of the Carlyle Lake population has been ongoing since 1999, and radio-telemetry was conducted from 2001-2003 and 2009-2011, providing a rare long-term data set for use in conservation planning. To evaluate conservation issues in the Illinois Eastern Massasauga population, I used the long-term data set to evaluate three aspects of population biology that are of concern in small populations: population genetics, reproduction, and mortality. I then integrated those data with a population viability and sensitivity analysis to determine the population trajectory, identify which demographic parameters have the greatest impact on population persistence, and make conservation strategy recommendations. Despite being both small and isolated, the Carlyle Lake Eastern Massasauga population exhibits moderate genetic diversity, no inbreeding or evidence of recent genetic bottlenecks, but low effective population size. Thus, conservation planning should consider genetic factors, but immediate intervention specific to genetic concerns is not necessary. Reproductive output in the Eastern Massasauga is not constrained by female body size, and there is no evidence of a trade-off between offspring size and number. Reproductive output, therefore, appears to be resource dependent and has the potential to increase via targeted conservation actions. Mortality of Eastern Massasaugas is caused primarily by automobiles and predation. Seasonal or permanent closure of non-essential roads and reduction of small carnivore numbers could decrease mortality at Carlyle Lake and positively impact population persistence. Finally, the population viability analysis indicated a positive population growth rate, but also a 65% probability of extinction in 50 years. Sensitivity analyses show that reproductive characteristics (proportion of breeding females, litter size, and offspring sex ratio) and carrying capacity have the greatest impact on population trajectory. Thus, conservation strategies for the Eastern Massasauga should focus on restoring additional habitat to increase carrying capacity, and use more manipulative measures only if the population growth rate becomes negative. This study provides an important application of long-term data for the conservation of an imperiled snake species and functions as a surrogate for other Eastern Massasauga populations or species with similar life histories for which detailed data are not available

Early Childhood Supervision: Tensions in the Advancement of Developmentally Appropriate and Social-Justice Oriented Practice

This case examines the complex interactions among university faculty, teacher candidates, and school-based mentor teachers during supervision. In early childhood, among other skills and dispositions, the use of developmentally appropriate practice and an equity focus are important to the overall advancement of teacher candidates’ practice. However, supervisors do not have oversight of the classrooms in which early childhood candidates are placed for field experiences. In some cases, teacher candidates may be expected to conform to or demonstrate practices themselves which are not developmentally appropriate, or which are inequitable. What is the role of the supervising faculty member in these cases, and how can the supervisor navigate the relationship with mentor teacher and host school, while also supporting appropriate and equitable professional growth in the teacher candidate

Bridging Teacher Candidates, School Communities, and the World During a Pandemic

The Covid-19 pandemic caused distance that separated the teacher from the learner as schools and higher education moved to virtual and flexible learning communities. Likewise, at the same time racial tensions were growing further increasing the distance and divide across the country. This positions teacher educators with the responsibility to bridge this distance. The challenges of preparing educators for activism in a post-Covid educational context that considers cultural literacy, ethical leadership, and community engagement is explored with three narratives. These narratives provide the opportunity to think with and through our commitments in early childhood and elementary teacher education. Collectively, these narratives use the conditions of learning and teaching in a pandemic to consider educational challenges of the past and the things we must do to create a more equitable and just future. We conclude this essay with essential commitments as we work to bridge the distance and build community. Classification: Reflective Essa

Changes in liver and spleen volumes after living liver donation: A report from the adult‐to‐adult living donor liver transplantation cohort study (A2ALL)

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/110585/1/lt24062.pd

The impact of job-demand-control-support on leptin and ghrelin as biomarkers of stress in emergency healthcare workers

Despite the available literature on the consequences of night shiftwork on stress and food intake, its impact on leptin and ghrelin has never been studied. We previously demonstrated that leptin and ghrelin were biomarkers related to stress, and acute stress-induced a decrease in leptin levels and an increase in ghrelin levels. We performed a prospective observational study to assess the influence of night work, nutrition, and stress on the levels of ghrelin and leptin among emergency healthcare workers (HCWs). We took salivary samples at the beginning of a day shift and/or at the end of a night shift. We also monitored stress using the job demand-control-support model of Karasek. We recorded 24-h food intake during the day shift and the consecutive night shift and during night work and the day before. We included 161 emergency HCWs. Emergency HCWs had a tendency for decreased levels of leptin following the night shift compared to before the dayshift (p = 0.067). Furthermore, the main factors explaining the decrease in leptin levels were an increase in job-demand (coefficient −54.1, 95 CI −99.0 to −0.92) and a decrease in job control (−24.9, −49.5 to −0.29). Despite no significant changes in ghrelin levels between shifts, social support was the main factor explaining the increase in ghrelin (6.12, 0.74 to 11.5). Food intake (kcal) also had a negative impact on leptin levels, in addition to age. Ghrelin levels also decreased with body mass index, while age had the opposite effect. In conclusion, we confirmed that ghrelin and leptin as biomarkers of stress were directly linked to the job demand-control-support model of Karasek, when the main cofounders were considered

Wildfire activity enhanced during phases of maximum orbital eccentricity and precessional forcing in the Early Jurassic

Fire regimes are changing due to both anthropogenic climatic drivers and vegetation management challenges, making it difficult to determine how climate alone might influence wildfire activity. Earth has been subject to natural-background climate variability throughout its past due to variations in Earth’s orbital parameters (Milkankovitch cycles), which provides an opportunity to assess climate-only driven variations in wildfire. Here we present a 350,000 yr long record of fossil charcoal from mid-latitude (~35°N) Jurassic sedimentary rocks. These results are coupled to estimates of variations in the hydrological cycle using clay mineral, palynofacies and elemental analyses, and lithological and biogeochemical signatures. We show that fire activity strongly increased during extreme seasonal contrast (monsoonal climate), which has been linked to maximal precessional forcing (boreal summer in perihelion) (21,000 yr cycles), and we hypothesize that long eccentricity modulation further enhances precession-forced fire activity

International meta-analysis of PTSD genome-wide association studies identifies sex- and ancestry-specific genetic risk loci.

The risk of posttraumatic stress disorder (PTSD) following trauma is heritable, but robust common variants have yet to be identified. In a multi-ethnic cohort including over 30,000 PTSD cases and 170,000 controls we conduct a genome-wide association study of PTSD. We demonstrate SNP-based heritability estimates of 5-20%, varying by sex. Three genome-wide significant loci are identified, 2 in European and 1 in African-ancestry analyses. Analyses stratified by sex implicate 3 additional loci in men. Along with other novel genes and non-coding RNAs, a Parkinson's disease gene involved in dopamine regulation, PARK2, is associated with PTSD. Finally, we demonstrate that polygenic risk for PTSD is significantly predictive of re-experiencing symptoms in the Million Veteran Program dataset, although specific loci did not replicate. These results demonstrate the role of genetic variation in the biology of risk for PTSD and highlight the necessity of conducting sex-stratified analyses and expanding GWAS beyond European ancestry populations

Effects of antiplatelet therapy on stroke risk by brain imaging features of intracerebral haemorrhage and cerebral small vessel diseases: subgroup analyses of the RESTART randomised, open-label trial

Background Findings from the RESTART trial suggest that starting antiplatelet therapy might reduce the risk of recurrent symptomatic intracerebral haemorrhage compared with avoiding antiplatelet therapy. Brain imaging features of intracerebral haemorrhage and cerebral small vessel diseases (such as cerebral microbleeds) are associated with greater risks of recurrent intracerebral haemorrhage. We did subgroup analyses of the RESTART trial to explore whether these brain imaging features modify the effects of antiplatelet therapy

Recessive mutations in SPTBN2 implicate β-III spectrin in both cognitive and motor development

β-III spectrin is present in the brain and is known to be important in the function of the cerebellum. Heterozygous mutations in SPTBN2, the gene encoding β-III spectrin, cause Spinocerebellar Ataxia Type 5 (SCA5), an adult-onset, slowly progressive, autosomal-dominant pure cerebellar ataxia. SCA5 is sometimes known as "Lincoln ataxia," because the largest known family is descended from relatives of the United States President Abraham Lincoln. Using targeted capture and next-generation sequencing, we identified a homozygous stop codon in SPTBN2 in a consanguineous family in which childhood developmental ataxia co-segregates with cognitive impairment. The cognitive impairment could result from mutations in a second gene, but further analysis using whole-genome sequencing combined with SNP array analysis did not reveal any evidence of other mutations. We also examined a mouse knockout of β-III spectrin in which ataxia and progressive degeneration of cerebellar Purkinje cells has been previously reported and found morphological abnormalities in neurons from prefrontal cortex and deficits in object recognition tasks, consistent with the human cognitive phenotype. These data provide the first evidence that β-III spectrin plays an important role in cortical brain development and cognition, in addition to its function in the cerebellum; and we conclude that cognitive impairment is an integral part of this novel recessive ataxic syndrome, Spectrin-associated Autosomal Recessive Cerebellar Ataxia type 1 (SPARCA1). In addition, the identification of SPARCA1 and normal heterozygous carriers of the stop codon in SPTBN2 provides insights into the mechanism of molecular dominance in SCA5 and demonstrates that the cell-specific repertoire of spectrin subunits underlies a novel group of disorders, the neuronal spectrinopathies, which includes SCA5, SPARCA1, and a form of West syndrome

The Human-Specific and Smooth Muscle Cell-Enriched LncRNA SMILR Promotes Proliferation by Regulating Mitotic CENPF mRNA and Drives Cell-Cycle Progression Which Can Be Targeted to Limit Vascular Remodeling.

RATIONALE: In response to blood vessel wall injury, aberrant proliferation of vascular smooth muscle cells (SMCs) causes pathological remodeling. However, the controlling mechanisms are not completely understood. OBJECTIVE: We recently showed that the human long noncoding RNA, SMILR, promotes vascular SMCs proliferation by a hitherto unknown mechanism. Here, we assess the therapeutic potential of SMILR inhibition and detail the molecular mechanism of action. METHODS AND RESULTS: We used deep RNA-sequencing of human saphenous vein SMCs stimulated with IL (interleukin)-1α and PDGF (platelet-derived growth factor)-BB with SMILR knockdown (siRNA) or overexpression (lentivirus), to identify SMILR-regulated genes. This revealed a SMILR-dependent network essential for cell cycle progression. In particular, we found using the fluorescent ubiquitination-based cell cycle indicator viral system that SMILR regulates the late mitotic phase of the cell cycle and cytokinesis with SMILR knockdown resulting in ≈10% increase in binucleated cells. SMILR pulldowns further revealed its potential molecular mechanism, which involves an interaction with the mRNA of the late mitotic protein CENPF (centromere protein F) and the regulatory Staufen1 RNA-binding protein. SMILR and this downstream axis were also found to be activated in the human ex vivo vein graft pathological model and in primary human coronary artery SMCs and atherosclerotic plaques obtained at carotid endarterectomy. Finally, to assess the therapeutic potential of SMILR, we used a novel siRNA approach in the ex vivo vein graft model (within the 30 minutes clinical time frame that would occur between harvest and implant) to assess the reduction of proliferation by EdU incorporation. SMILR knockdown led to a marked decrease in proliferation from ≈29% in controls to ≈5% with SMILR depletion. CONCLUSIONS: Collectively, we demonstrate that SMILR is a critical mediator of vascular SMC proliferation via direct regulation of mitotic progression. Our data further reveal a potential SMILR-targeting intervention to limit atherogenesis and adverse vascular remodeling