Background: As of 2016, ≈1.4 million people in the United States identify as transgender. Despite their growing number and increasing specific medical needs, there has been a lack of research on cardiovascular disease (CVD) and CVD risk factors in this population. Recent studies have reported that the transgender population had a significantly higher rate of CVD risk factors without a significant increase in overall CVD morbidity and mortality. These studies are limited by their small sample sizes and their predominant focus on younger transgender populations. With a larger sample size and inclusion of broader age range, our study aims to provide insight into the association between being transgender and cardiovascular risk factors, as well as myocardial infarction. Methods and Results: The Behavioral Risk Factor Surveillance System data from 2014 to 2017 were used to evaluate the cross-sectional association between being transgender and the reported history of myocardial infarction and CVD risk factors. A logistic regression model was constructed to study the association between being transgender and myocardial infarction after adjusting for CVD risk factors including age, diabetes mellitus, hypertension, hypercholesterolemia, chronic kidney disease, smoking, and exercise. Multivariable analysis revealed that transgender men had a >2-fold and 4-fold increase in the rate of myocardial infarction compared with cisgender men (odds ratio, 2.53; 95% CI, 1.14–5.63; P =0.02) and cisgender women (odds ratio, 4.90; 95% CI, 2.21–10.90; P <0.01), respectively. Conversely, transgender women had >2-fold increase in the rate of myocardial infarction compared with cisgender women (odds ratio, 2.56; 95% CI, 1.78–3.68; P <0.01) but did not have a significant increase in the rate of myocardial infarction compared with cisgender men. Conclusions: The transgender population had a higher reported history of myocardial infarction in comparison to the cisgender population, except for transgender women compared with cisgender men, even after adjusting for cardiovascular risk factors.

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Background Bedside ultrasonography in the diagnosis of pneumothorax has been well described in emergency and trauma medicine literature. Its role in detection of iatrogenic pneumothoraces has not been studied. We describe the performance of bedside ultrasonography in detection of procedure related pneumothoraces and highlight some limitations. Methods 185 patients underwent thoracentesis (n=60), transbronchial biopsy (n=48), CT-guided lung biopsy (n=76), and CT-guided cryoablation of a lung mass (n=1). Bedside transthoracic ultrasound examination and post-procedure chest radiograph were performed in all patients. Patients in whom pleural surface was not well imaged with ultrasound were said to have a limited exam. Chest x-ray was the standard for diagnosing pneumothorax. Results Chest x-ray detected pneumothorax in 8/185 patients (4.0%). Ultrasound diagnosed pneumothorax in seven of these patients. Sensitivity, specificity and diagnostic accuracy were 88%, 97% and 97%, respectively. Limited quality ultrasound examinations due to pre-existing lung disease was seen in 43/185 patients. The positive and negative likelihood ratios for patients with adequate scans were 55 and 0.17, respectively. Likelihood ratio for patients with limited quality scan was 1.08. Conclusions Bedside chest ultrasonography, in the presence of good quality scan, is a valuable tool in the evaluation of post procedure pneumothorax. Patients with preexisting lung disease in whom the quality of ultrasound examination is limited should be studied with a chest x-ray.

Background: Third-stage infective larvae (L3) of hookworms are in an obligatory state of developmental arrest that ends upon entering the definitive host, where they receive a signal that re-activates development. Recovery from the developmentally arrested dauer stage of Caenorhabditis elegans is analogous to the resumption of development during hookworm infection. Insulin-like signaling (ILS) mediates recovery from arrest in C. elegans and activation of hookworm dauer L3. In C. elegans, phosphorylation of the forkhead transcription factor DAF-16 in response to ILS creates binding cites for the 14-3-3 protein Ce-FTT-2, which translocates DAF-16 out of the nucleus, resulting in resumption of reproductive development.

CP LVH is a strong predictor of DD, even after adjustment for other potential risk factors and ECG variables.

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When hookworm infective L3s infect their mammalian host, they undergo a temperature shift from that of the ambient environment to that of their endothermic host. Additionally, L3s living in the environment can be exposed to temperature extremes associated with weather fluctuations. The heat shock response (HSR) is a conserved response to heat shock and other stress that involves the expression of protective heat shock proteins (HSPs). The HSR is controlled by heat shock factor 1 (HSF-1), a conserved transcription factor that binds to a heat shock element in the promoter of HSPs, causing their expression. HSF-1 is negatively regulated in part by a HSF binding protein (HSB-1) that binds to and removes HSF-1 trimers bound to HSP gene promoters, resulting in attenuation of the HSR. Herein we describe an HSB-1 ortholog, Ac-HSB-1, from the hookworm Ancylostoma caninum. The Ac-hsb-1 cDNA encodes a 79 amino acid protein that is 71% identical to the Caenorhabditis elegans HSB-1, and is predicted to share the characteristic coiled-coil structural motif comprised of two interacting alpha helices. Recombinant Ac-HSB-1 immunoprecipitated Ce-HSF-1 expressed in mammalian cells that had been heat shocked for 1 h at 42°C, but not from cells incubated at 37°C, indicating that HSB-1 only bound to the active DNA binding form of HSF-1. Expression of Ac-hsb-1 transcripts decreased following 1 h of heat shock, but increased when L3s were incubated at 37°C for 1 h. Activation of hookworm L3s induces an five-to six-fold increase in Ac-hsb-1 expression that peaks at 12 h, coincident with L3 feeding, but that subsequently decreases to two-to three-fold above control at 24 h. Recombinant Ac-HSB-1 immunoprecipitates greater amounts of 70 and 40 kDa proteins from extracts of activated L3s than from non-activated L3s. We propose that an increase in Ac-hsb-1 levels early in activation allows feeding to resume, but that a subsequent decrease in expression permits a HSR that protects nondeveloping L3s at host-like temperatures. Further investigations of the HSR will clarify the role of HSB-1 and HSF-1 in hookworm infection.

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