Background Infection with the novel severe acute respiratory syndrome coronavirus 2 has been associated with a hypercoagulable state. Emerging data from China and Europe have consistently shown an increased incidence of venous thromboembolism (VTE). We aimed to identify the VTE incidence and early predictors of VTE at our high-volume tertiary care center. Methods We performed a retrospective cohort study of 147 patients who had been admitted to Temple University Hospital with coronavirus disease 2019 (COVID-19) from April 1, 2020 to April 27, 2020. We first identified the VTE (pulmonary embolism [PE] and deep vein thrombosis [DVT]) incidence in our cohort. The VTE and no-VTE groups were compared by univariable analysis for demographics, comorbidities, laboratory data, and treatment outcomes. Subsequently, multivariable logistic regression analysis was performed to identify the early predictors of VTE. Results The 147 patients (20.9% of all admissions) admitted to a designated COVID-19 unit at Temple University Hospital with a high clinical suspicion of acute VTE had undergone testing for VTE using computed tomography pulmonary angiography and/or extremity venous duplex ultrasonography. The overall incidence of VTE was 17% (25 of 147). Of the 25 patients, 16 had had acute PE, 14 had had acute DVT, and 5 had had both PE and DVT. The need for invasive mechanical ventilation (adjusted odds ratio, 3.19; 95% confidence interval, 1.07-9.55) and the admission D-dimer level ≥1500 ng/mL (adjusted odds ratio, 3.55; 95% confidence interval, 1.29-9.78) were independent markers associated with VTE. The all-cause mortality in the VTE group was greater than that in the non-VTE group (48% vs 22%; P = .007). Conclusion Our study represents one of the earliest reported from the United States on the incidence rate of VTE in patients with COVID-19. Patients with a high clinical suspicion and the identified risk factors (invasive mechanical ventilation, admission D-dimer level ≥1500 ng/mL) should be considered for early VTE testing. We did not screen all patients admitted for VTE; therefore, the true incidence of VTE could have been underestimated. Our findings require confirmation in future prospective studies.

Fear-related psychopathologies such as post-traumatic stress disorder are characterized by impaired extinction of fearful memories. Recent behavioral evidence suggests that the neuropeptide tuberoinfundibular peptide of 39 residues (TIP39), via its receptor, the parathyroid hormone 2 receptor (PTH2R), modulates fear memory. Here we examined the anatomical and cellular localization of TIP39 signaling that contributes to the increase in fear memory over time following a traumatic event, called fear memory incubation. Contextual freezing, a behavioral sign of fear memory, was significantly greater in PTH2R knock-out than wild-type male mice 2 and 4 weeks after a 2 s 1.5 mA footshock. PTH2R knock-out mice had significantly reduced c-Fos activation in the medial amygdala (MeA) following both footshock and fear recall, but had normal activation in the hypothalamic paraventricular nucleus and the amygdalar central nucleus compared with wild-type. We therefore investigated the contribution of MeA TIP39 signaling to fear incubation. Similar to the effect of global TIP39 signaling loss, blockade of TIP39 signaling in the MeA by lentivirus-mediated expression of a secreted PTH2R antagonist augmented fear incubation. Ablation of MeA PTH2R-expressing neurons also strengthened the fear incubation effect. Using the designer receptor exclusively activated by designer drug pharmacogenetic approach, transient inhibition of MeA PTH2R-expressing neurons before or immediately after the footshock, but not at the time of fear recall, enhanced fear incubation. Collectively, the findings demonstrate that TIP39 signaling within the MeA at the time of an aversive event regulates the increase over time in fear associated with the event context.

While bacteremia due to Serratia marcescens is not uncommon, it rarely causes infective endocarditis. We report an isolated case of a 53-year-old male with history of intravenous drug abuse who presented with multiple acute pain symptoms and was found to have S. marcescens bacteremia with septic emboli in his spleen, brain, and testes, secondary to a large aortic vegetation, as well as aortic infective endocarditis with severe aortic regurgitation requiring aortic valve replacement. His course of disease was further complicated by epidural and psoas abscesses and a necrotic testicle requiring orchiectomy due to his ongoing intravenous drug abuse. This case is an atypical presentation of S. marcescens infection, as he had no overt signs of infection such as fever or significant leukocytosis that are typical of bacteremia, and it also highlights the severity and complicated nature of S. marcescens-infective endocarditis.

Introduction: Anorectal mucosal melanoma (ARMM) is an uncommon and highly aggressive malignancy. Given its rarity, there is insufficient evidence on the optimal medical management which presents as a clinical challenge to its diagnosis and treatment. Treatment of ARMM typically involves a multimodal approach including surgical resection, chemotherapy, targeted therapy and/or immunotherapy. Case Presentation: Here, we present a case of a 78-year-old female who presented with a four-month history of rectal bleeding and bowel incontinence. Ultimately, colonoscopy revealed a mass at the anal verge, and biopsy of the mass showed malignant cells that stained positive for S100, Melan-A and HMB-45, consistent with the diagnosis of malignant melanoma. Molecular testing revealed no BRAF, KIT or NRAS gene mutations. PD-L1 immunohistochemistry showed tumor proportion score of 1%. She underwent abdominoperineal resection with a plan to initiate immunotherapy with an anti-PD-1 checkpoint inhibitor. This case highlights a rare aggressive malignancy and reviews its treatment option, which are mostly extrapolated from its cutaneous counterpart and some derived from a few case reports. Due to its rarity, there is no consensus guideline for the treatment of ARMM.