Condom Use Among Deaf College Students

The overarching aim for the current study was to assess the prevalence of condom use among college students who are deaf and determine if it differed from their hearing peers. Prior to this study, the modest information available suggested that deaf adults were likely engaging in significantly more risky sexual practices than hearing adults. To elucidate this topic, a sample of deaf college students was recruited from a predominately deaf university and administered measures that assessed their current sexual behavior and utilization of condoms during vaginal, anal, and oral sex. Of the three types of sexual contact studied, the results indicated that deaf college students engage in significantly more risky sexual behavior (i.e., less consistent condom use) during vaginal intercourse than hearing young adults. The study concluded by suggesting how future research may explore the motivations and barriers for condom use among deaf young adults, a necessary first step for creating prevention and intervention programs precisely tailored to the needs of deaf college students

Case Report: Disposition of Symptomatic Probable COVID-19

Introduction: The novel coronavirus disease 2019 (COVID-19) presents a challenge for healthcare providers in terms of diagnosis, management, and triage of cases requiring admission.Case Report: A 47-year-old male with symptoms suspicious for COVID-19, pulse oximetry of 93% on room air, and multifocal pneumonia was risk stratified and safely discharged from the emergency department (ED) despite having moderate risk of progression to acute respiratory distress syndrome. He had resolution of his symptoms verified by telephone follow-up.Conclusion: Various risk-stratifying tools and techniques can aid clinicians in identifying COVID-19 patients who can be safely discharged from the ED

Joint Task Force Olympics : monitoring potential terrorists behavior via deceptive computer means

The purpose of this thesis is to deploy tactical deception via a public website. The perception is to have the website be a supportive tool for the Joint Task Force Olympics. In actuality, it will be used to collect various data from those who attempt to access the site. The goal is not to implement a secure, impenetrable computer site or to capture hackers. On the contrary, the preference is to entice individuals or groups to enter the site and study its contents in the hope that we may discover why and from where they have accessed this site, and what files or directories allured them. The objective is to implement a successful deception by following the guidelines of the JP 3-58, Joint Doctrine for Military Deception, which contributes to the successful achievement of military objectives. The deception is focused on people researching information on the Internet for potential terrorist use. Although there are many threats to national security, terrorism is currently the most deadly of threats using one of the most trusted monitors: the Internet. There exists a relationship between the Internet and terrorism, and this thesis intends to exploit it with.http://archive.org/details/jointtaskforceol10945594

Gene expression profiles among murine strains segregate with distinct differences in the progression of radiation-induced lung disease.

Molecular mechanisms underlying development of acute pneumonitis and/or late fibrosis following thoracic irradiation remain poorly understood. Here, we hypothesize that heterogeneity in disease progression and phenotypic expression of radiation-induced lung disease (RILD) across murine strains presents an opportunity to better elucidate mechanisms driving tissue response toward pneumonitis and/or fibrosis. Distinct differences in disease progression were observed in age- and sex-matched CBA/J, C57L/J and C57BL/6J mice over 1 year after graded doses of whole-thorax lung irradiation (WTLI). Separately, comparison of gene expression profiles in lung tissue 24 h post-exposure demonstrated \u3e5000 genes to be differentially expressed (P\u3c0.01; \u3etwofold change) between strains with early versus late onset of disease. An immediate divergence in early tissue response between radiation-sensitive and -resistant strains was observed. In pneumonitis-prone C57L/J mice, differentially expressed genes were enriched in proinflammatory pathways, whereas in fibrosis-prone C57BL/6J mice, genes were enriched in pathways involved in purine and pyrimidine synthesis, DNA replication and cell division. At 24 h post-WTLI, different patterns of cellular damage were observed at the ultrastructural level among strains but microscopic damage was not yet evident under light microscopy. These data point toward a fundamental difference in patterns of early pulmonary tissue response to WTLI, consistent with the macroscopic expression of injury manifesting weeks to months after exposure. Understanding the mechanisms underlying development of RILD might lead to more rational selection of therapeutic interventions to mitigate healthy tissue damage

Autonomous metabolic reprogramming and oxidative stress characterize endothelial dysfunction in acute myocardial infarction

Background: Compelling evidence has accumulated on the role of oxidative stress on the endothelial cell (EC) dysfunction underlying acute coronary syndrome. However, unveiling the underlying metabolic determinants has been hampered by the scarcity of appropriate cell models to address cell-autonomous mechanisms of ED dysfunction. Methods: We have generated endothelial cells derived from thrombectomy specimens from patients affected with acute myocardial infarction (AMI) and conducted phenotypical and metabolic characterization, focused on central carbon metabolism. Results: AMI-derived endothelial cells (AMIECs), but not control healthy coronary endothelial cells, display impaired growth, migration and tubulogenesis. Metabolically, AMIECs displayed augmented reactive oxygen species (ROS) and glutathione intracellular content, along with a diminished glucose consumption coupled to high lactate production. Consistent with diminished glycolysis in AMIECs, the protein levels of 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase type 3, PFKFB3, were downregulated. In contrast, PFKFB4 levels were upregulated, suggesting a shunting of glycolysis towards the pentose phosphate pathway (PPP), supported by upregulation in AMIECs of G6PD, the key enzyme in the oxidative branch of the PPP. Further, the glutaminolytic enzyme GLS was upregulated in AMIECs, providing a mechanistic explanation for the observed increase in glutathione content. Finally, AMIECs displayed a significantly higher mitochondrial membrane potential than control ECs, which, together with high ROS levels, suggest a highly coupled mitochondrial activity in patient ECs. Conclusions: We suggest high mitochondrial proton coupling underlies the abnormally high production of ROS, balanced by PPP- and glutaminolysis-driven synthesis of glutathione, as a primary, cell-autonomous abnormality driving EC dysfunction in AMI. Funding: European Commission Horizon 2020; CIBER- Carlos III National Institute of Health, Spain; Ministerio de Economia y Competitividad (MINECO) and Ministerio de Ciencia e Innovación, Spain; Generalitat de Catalunya-AGAUR, Catalonia; Plataforma Temática Interdisciplinar Salud Global (PTI-SG), Spain; British Heart Foundation, UK. </p

Signing While Driving: An Investigation of Divided Attention Resources Among Deaf Drivers

Safely operating vehicles require significant visual attention. While attention can be divided, cognitive resources are not limitless. Deaf and hearing participants engaged in a simulated driving task while simultaneously engaging in a conversation in their preferred language. Results indicated that hearing drivers may have a performance advantage over deaf drivers, though it is so minor that it will not likely be seen outside of the laboratory setting. The results also indicated differing cognitive processing among hearing and deaf drivers. The results may inform policy, reduce stigma, and serve as the base for future research on deaf-specific cognitive factors of driving

Differentially Expressed Proteins in Primary Endothelial Cells Derived From Patients With Acute Myocardial Infarction

Endothelial dysfunction is one of the primary factors in the onset and progression of atherothrombosis resulting in acute myocardial infarction (AMI). However, the pathological and cellular mechanisms of endothelial dysfunction in AMI have not been systematically studied. Protein expression profiling in combination with a protein network analysis was used by the mass spectrometry-based label-free quantification approach. This identified and quantified 2246 proteins, of which 335 were differentially regulated in coronary arterial endothelial cells from patients with AMI compared with controls. The differentially regulated protein profiles reveal the alteration of (1) metabolism of RNA, (2) platelet activation, signaling, and aggregation, (3) neutrophil degranulation, (4) metabolism of amino acids and derivatives, (5) cellular responses to stress, and (6) response to elevated platelet cytosolic Ca2+ pathways. Increased production of oxidants and decreased production of antioxidant biomarkers as well as downregulation of proteins with antioxidant properties suggests a role for oxidative stress in mediating endothelial dysfunction during AMI. In conclusion, this is the first quantitative proteomics study to evaluate the cellular mechanisms of endothelial dysfunction in patients with AMI. A better understanding of the endothelial proteome and pathophysiology of AMI may lead to the identification of new drug targets

Hyperacusis in children with attention deficit hyperactivity disorder: a preliminary study

The association between hyperacusis and developmental disorders such as autism spectrum disorders has been extensively reported in the literature; however, the specific prevalence of hyperacusis in attention deficit hyperactivity disorder (ADHD) has never been investigated. In this preliminary study, we evaluated the presence of hyperacusis in a small sample of children affected by ADHD compared to a control group of healthy children. Thirty normal hearing children with a diagnosis of ADHD and 30 children matched for sex and age were enrolled in the study. All children underwent audiological and multidisciplinary neuropsychiatric evaluation. Hearing was assessed using pure tone audiometry and immittance test; ADHD was diagnosed following the Diagnostic and Statistical Manual of Mental Disorder criteria. Hyperacusis was assessed through the administration of a questionnaire to parents and an interview with children. Hyperacusis was diagnosed in 11 children (36.7%) in the study group and in four children (13.3%) in the control group; this difference was statistically significant (p = 0.03). The preliminary results of this study suggest a higher presence of hyperacusis in children with attention deficit hyperactivity disorder compared to control children. More studies on larger samples are necessary to confirm these results

Metabolic Alterations in Cardiopulmonary Vascular Dysfunction

Cardiovascular diseases (CVD) are the leading cause of death worldwide. CVD comprise a range of diseases affecting the functionality of the heart and blood vessels, including acute myocardial infarction (AMI) and pulmonary hypertension (PH). Despite their different causative mechanisms, both AMI and PH involve narrowed or blocked blood vessels, hypoxia, and tissue infarction. The endothelium plays a pivotal role in the development of CVD. Disruption of the normal homeostasis of endothelia, alterations in the blood vessel structure, and abnormal functionality are essential factors in the onset and progression of both AMI and PH. An emerging theory proposes that pathological blood vessel responses and endothelial dysfunction develop as a result of an abnormal endothelial metabolism. It has been suggested that, in CVD, endothelial cell metabolism switches to higher glycolysis, rather than oxidative phosphorylation, as the main source of ATP, a process designated as the Warburg effect. The evidence of these alterations suggests that understanding endothelial metabolism and mitochondrial function may be central to unveiling fundamental mechanisms underlying cardiovascular pathogenesis and to identifying novel critical metabolic biomarkers and therapeutic targets. Here, we review the role of the endothelium in the regulation of vascular homeostasis and we detail key aspects of endothelial cell metabolism. We also describe recent findings concerning metabolic endothelial cell alterations in acute myocardial infarction and pulmonary hypertension, their relationship with disease pathogenesis and we discuss the future potential of pharmacological modulation of cellular metabolism in the treatment of cardiopulmonary vascular dysfunction. Although targeting endothelial cell metabolism is still in its infancy, it is a promising strategy to restore normal endothelial functions and thus forestall or revert the development of CVD in personalized multi-hit interventions at the metabolic level