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Background:Recent studies have shown that a majority of multiple myeloma (MM) patients (pts) in the United States (US) are triple-class exposed (TCE) after four lines of therapy (LOT), with poor prognosis for TCE patients. As treatment for MM evolves to include more advanced triplet and quadruplet regimens, a growing number of US pts are likely to reach TCE status in earlier lines of treatment. Therefore, we sought to evaluate the frequency of pts reaching TCE status after receiving two or more prior LOT (3L+) and their associated clinical outcomes.

Female androgenetic alopecia or female-pattern hair loss (FPHL) is highly prevalent and has a great impact on the quality of life. The treatment is a routine challenge in dermatological practice, as many therapeutic options have a limited level of evidence and often do not meet patients expectations. Lack of knowledge of the pathogenesis of the hair miniaturization process and the factors that regulate follicular morphogenesis restricts the prospect of innovative therapies. There is also a lack of randomized, controlled studies with longitudinal follow-up, using objective outcomes and exploring the performance of the available treatments and their combinations. Topical minoxidil, which has been used to treat female pattern hair loss since the 1990s, is the only medication that has a high level of evidence and remains the first choice. However, about 40% of patients do not show improvement with this treatment. In this article, the authors critically discuss the main clinical and surgical therapeutic alternatives for FPHL, as well as present camouflage methods that can be used in more extensive or unresponsive cases.

•ECP-treated leukocytes cryopreserved at -80°C or -150°C for 3 months remain viable•These cells also retain apoptotic potential and therefore the ability to suppress GVHD•In vivoGVHD prevention studies are needed using cryopreserved ECP-treated leukocytes

Cardiac manifestations are common in severe Coronavirus disease 2019 (COVID-19) with rates reported from 2% in non-ICU patients to 59% in non-survivors. Recent CDC data show that COVID-19 patients are at 1.7 higher risk of arrhythmia. AF, which is the most common arrhythmia, is a frequent complication of acute and long COVID-19. It has been reported that the SARS-CoV2 receptor, ACE2, is highly expressed in the heart, leading to the prevalent assumption that infectious virus likely underlies cardiac complications. However, the pathophysiology of cardiac disease in severe COVID-19 has yet to be clarified. We therefore compared the histologic and molecular findings in human cardiac tissue from fatal COVID-19 cases and age-matched controls. Hematoxylin and eosin (H&E) stains revealed histologic changes in the COVID-19 samples, most notably multifocal endothelial cell swelling and degeneration plus microvascular thrombi. Distribution of SARS-CoV2 RNA and nucleocapsid protein expression was investigated by qRT-PCR and in situhybridization (ISH). Trace amounts of viral RNA and no nucleocapsid protein were detected in the COVID-19 hearts. However, 7/11 COVID-19 hearts were positive for viral spike protein. Further validation by immunohistochemistry (IHC) showed that viral spike protein was detected in all 11 COVID-19 hearts. Co-expression analysis revealed that viral spike protein localized mostly to the ACE2+ interstitial macrophages/pericytes that were activated as evidenced by increased IL6 and TNFα expression. Previously, we identified a novel arrhythmia mechanism wherein inflammation-induced vascular endothelial dysfunction triggers cardiomyocyte structural remodeling, particularly of intercalated disc (ID) components including connexin-43 (Cx43) gap junctions and NaV1.5 sodium channels, and thereby promotes arrhythmias. We therefore investigated ID structure in our human samples. Both Cx43 and NaV1.5 showed marked lateral migration in myocytes of COVID-19 hearts, consistent with previous experiments with inflammatory insults in murine hearts. These findings suggest that the viral spike protein, and not direct infection by SARS-CoV2, results in the pathophysiology of cardiac dysfunction in fatal COVID-19.