Maybrady8091

Lower respiratory tract (LRT) disease induced by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) can deteriorate to acute respiratory distress syndrome (ARDS). Because the release of neutrophil extracellular traps (NETs) is implicated in ARDS pathogenesis, we investigated the presence of NETs and correlates of pathogenesis in blood and LRT samples of critically ill patients with COVID-19. Plasma NET levels peaked early after intensive care unit admission and were correlated with the SARS-CoV-2 RNA load in sputum and levels of neutrophil-recruiting chemokines and inflammatory markers in plasma samples. The baseline plasma NET quantity was correlated with disease severity but was not associated with soluble markers of thrombosis or with development of thrombosis. High NET levels were present in LRT samples and persisted during the course of COVID-19, consistent with the detection of NETs in bronchi and alveolar spaces in lung tissue from deceased patient with COVID-19. Thus, NETs are produced and retained in the LRT of critically ill patients with COVID-19 and could contribute to SARS-CoV-2-induced ARDS disease.

The global COVID-19 pandemic has the potential to indirectly impact transmission dynamics and prevention of HIV and other sexually transmitted infections (STI). It is unknown what combined impact reductions in sexual activity and interruptions in HIV/STI services will have on HIV/STI epidemic trajectories.

We adapted a model of HIV, gonorrhea, and chlamydia for a population of approximately 103 000 men who have sex with men (MSM) in the Atlanta area. Model scenarios varied the timing, overlap, and relative extent of COVID-19-related sexual distancing and service interruption within 4 service categories (HIV screening, preexposure prophylaxis, antiretroviral therapy, and STI treatment).

A 50% relative decrease in sexual partnerships and interruption of all clinical services, both lasting 18 months, would generally offset each other for HIV (total 5-year population impact for Atlanta MSM, -227 cases), but have net protective effect for STIs (-23 800 cases). If distancing lasted only 3 months but service interruption lasted 18 months, the total 5-year population impact would be an additional 890 HIV cases and 57 500 STI cases.

Immediate action to limit the impact of service interruptions is needed to address the indirect effects of the global COVID-19 pandemic on the HIV/STI epidemic.

Immediate action to limit the impact of service interruptions is needed to address the indirect effects of the global COVID-19 pandemic on the HIV/STI epidemic.

Current clinical guidelines suggest that adrenal venous sampling (AVS) may not be mandatory in young patients with primary aldosteronism (PA) and a solitary adrenal adenoma on imaging.

The aim of this study was to further elucidate whether conventional imaging alone is sufficient to distinguish unilateral from bilateral PA among patients aged 40 years or younger.

This was a retrospective study where data from 45 patients with PA, aged between 26 and 40 years, who underwent successful AVS between 2005 and 2019, were analyzed. Results concerning laterality on imaging studies and AVS were recorded. Outcome in surgically treated patients was assessed according to the Primary Aldosteronism Surgical Outcomes criteria.

In 4 of 25 patients with unilateral aldosterone production according to AVS, computed tomography inaccurately suggested bilateral disease. Following unilateral adrenalectomy, all 4 patients showed complete clinical success. Five of 20 patients with bilateral aldosterone production according to AVS had a solitary adrenal nodule (8-19 mm) on imaging. ALK assay Two of these 5 patients were treated with unilateral adrenalectomy, neither having complete biochemical and/or clinical success postoperatively. Two of 16 patients younger than 35 years had discordant results, 1 with unilateral and 1 with bilateral aldosterone production, according to AVS.

Imaging studies inaccurately predicted laterality in a significant number of young patients with PA. In contrast to current clinical guidelines, our results support AVS for subtype evaluation in young adults with PA, including patients 35 years or younger.

Imaging studies inaccurately predicted laterality in a significant number of young patients with PA. In contrast to current clinical guidelines, our results support AVS for subtype evaluation in young adults with PA, including patients 35 years or younger.Endoplasmic reticulum (ER) stress serves as a key modulator of the inflammatory response by controlling nuclear factor-kappaB (NF-κB) signaling. Previous studies from our laboratory have reported an abnormal induction of ER stress linked to progesterone resistance in human endometriotic cells. Therefore, an aberrant ER stress response to progesterone might contribute to the altered inflammatory response observed in endometriotic tissues. To evaluate this hypothesis, we investigated whether ER stress is involved in regulation of NF-κB in endometrial stromal cells and whether induction of aberrant ER stress in endometriotic stromal cells affects pro-inflammatory cytokine production. We found that tunicamycin-induced ER stress inhibited NF-κB activation and pro-inflammatory cytokine (IL-6 and COX2) production in TNF-α- or IL-1β-treated normal endometrial stromal cells (NECSs). Tunicamycin increased the expression of A20 and C/EBPβ, which are negative regulators of NF-κB, and this increase inhibited NF-κB activity in NESCs incubated with TNF-α or IL-1β. Similarly, progesterone increased A20 and C/EBPβ expression through upregulation of ER stress in NESCs, resulting in inhibition of NF-κB activity and IL-6 and COX2 production. However, progesterone had no significant effects on induction of ER stress, A20 or C/EBPβ expression, NF-κB activity or IL-6 or COX2 production in ovarian endometriotic cyst stromal cells (ECSCs). In contrast, upregulation of ER stress by tunicamycin significantly reduced IL-6 and COX2 production by inhibiting NF-κB activity in ECSCs. In conclusion, our results suggest that NF-κB activity in endometriotic stromal cells was not inhibited because of an aberrant ER stress response to progesterone, resulting in an increase in pro-inflammatory cytokine production.