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We evaluated the incidence of cardiac events after chemoradiotherapy in patients with stage III non-small cell lung cancer (NSCLC) based on baseline cardiovascular risk and the heart substructures' radiation dose.<br /><br /> From 2008 to 2018, the cardiac events of 258 patients with stage III NSCLC who received definitive chemoradiotherapy were reviewed. The 10-year cardiovascular risk was calculated using the Atherosclerotic Cardiovascular Disease (ASCVD) scoring system. Dose-volume histograms were estimated for each cardiac chamber. A multivariate competing-risk regression analysis was conducted to assess each cardiac event's subhazard function (SHR).<br /><br /> The median follow-up was 27.5months overall and 38.9months for survivors. Among the 179 deaths, none was definitely related to cardiac conditions. Altogether, 32 cardiovascular events affected 27 patients (10.5%) after chemoradiotherapy. Ten were major cardiac adverse events, including heart failure (N=6) and acute coronary syndrome (ACS, N=4). Most cardiovascular events were related to well-known risk factors. However, the volume percentage of the left ventricle (LV) receiving 60Gy (LV V60)&gt;0 was significantly associated with ACS (SHR=9.49, 95% CI=1.28-70.53, P=0.028). In patients with high cardiovascular risk (ASCVD score&gt;7.5%), LV V60&gt;0% remained a negative ACS prognostic factor (P=0.003). Meanwhile, in patients with low cardiovascular risk, the LV radiation dose was not associated with ACS events (P=0.242).<br /><br /> A high LV radiation dose could increase ACS events in patients with stage III NSCLC and high cardiovascular risk. Pre-treatment cardiac risk evaluation and individualized surveillance may help prevent cardiac events after chemoradiotherapy.<br /><br />A high LV radiation dose could increase ACS events in patients with stage III NSCLC and high cardiovascular risk. Pre-treatment cardiac risk evaluation and individualized surveillance may help prevent cardiac events after chemoradiotherapy.The adrenal cortex functions to produce steroid hormones necessary for life. To maintain its functional capacity throughout life, the adrenal cortex must be continually replenished and rapidly repaired following injury. Moreover, the adrenal responds to endocrine-mediated organismal needs, which are highly dynamic and necessitate a precise steroidogenic response. To meet these diverse needs, the adrenal employs multiple cell populations with stem cell function. Here, we discuss the literature on adrenocortical stem cells using hematopoietic stem cells as a benchmark to examine the functional capacity of particular cell populations, including those located in the capsule and peripheral cortex. These populations are coordinately regulated by paracrine and endocrine signaling mechanisms, and display remarkable plasticity to adapt to different physiological and pathological conditions. Some populations also exhibit sex-specific activity, which contributes to highly divergent proliferation rates between sexes. Understanding mechanisms that govern adrenocortical renewal has broad implications for both regenerative medicine and cancer.Complete resection of adrenal cortical carcinoma (ACC) with or without adjuvant therapy offers the best outcome. Recurrence is common, and in individual cases, the long-term outcome is difficult to predict, making it challenging to personalize treatment options. Current risk stratification approaches are based on clinical and conventional surgical pathology assessment. Rigorous and uniform pathological assessment may improve care for individual patients and facilitate multi-institutional collaborative studies. The International Collaboration on Cancer Reporting (ICCR) convened an expert panel to review ACC pathology reporting. Consensus recommendations were made based on the most recent literature and expert opinion. The data set comprises 23 core (required) items. The core pathological features include the following diagnosis as per the current World Health Organization classification, specimen integrity, greatest dimension, weight, extent of invasion, architecture, percentage of lipid-rich cells, capsular invasion, lymphatic invasion, vascular invasion, atypical mitotic figures, coagulative necrosis, nuclear grade, mitotic count, Ki-67 proliferative index, margin status, lymph node status, and pathological stage. Tumors were dichotomized into low-grade (20 mitoses per 10 mm2) ones. Additional noncore elements that may be useful in individual cases included several multifactorial risk assessment systems (Weiss, modified Weiss, Lin-Weiss-Bisceglia, reticulin, Helsinki, and Armed Forces Institute of Pathology scores/algorithms). This data set is now available through the ICCR website with the hope of better standardizing pathological assessment of these relatively rare but important malignancies.The purpose of this study was to examine the deltoid skin biopsy in twenty-three patients with coronavirus disease 2019 (COVID-19), most severely ill, for vascular complement deposition and correlate this with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) viral RNA and protein localization and ACE2 expression. [https://www.selleckchem.com/products/sivelestat-sodium.html Sivelestat] Deltoid skin microvascular complement screening has been applied to patients with various systemic complement-mediated microvascular syndromes, best exemplified by atypical hemolytic uremic syndrome. In 21 of 23 cases, substantial microvascular deposition of complement components was identified. The two patients without significant complement deposition included one patient with moderate disease and a severely ill patient who although on a ventilator for a day was discharged after 3 days. The dominant microvascular complement immunoreactant identified was the terminal membranolytic attack complex C5b-9. Microvascular complement deposition strongly colocalized in situ with the SARS-CoV-2 viral proteins including spike glycoproteins in the endothelial cells as well as the viral receptor ACE2 in lesional and nonlesional skin; viral RNA was not evident. Microvascular SARS-CoV-2 viral protein, complement, and ACE2 expression was most conspicuous in the subcutaneous fat. Although the samples from severely ill patients with COVID-19 were from grossly normal skin, light microscopically focal microvascular abnormalities were evident that included endothelial cell denudement, basement membrane zone reduplication, and small thrombi. It is concluded that complement activation is common in grossly normal skin, especially in the subcutaneous fat which may provide a link between severe disease and obesity, in people with severe COVID-19, and the strong colocalization with the ACE2 receptor and viral capsid proteins without viral RNA suggests that circulating viral proteins (ie, pseudovirions) may dock onto the endothelial of these microvessels and induce complement activation.