Furthermore, we identified various alterations regarding the gene expression of explanted lungs with PVR, as compared to controls. Specifically, the dysregulation of microtubule associated serine/threonine kinase 2 and protein-o-mannose kinase SGK196 in all disease groups suggests a key role in pulmonary vasculopathy for the first time. Our findings promise to help develop novel target-specific interventions and innovative approaches to facilitate clinical diagnostics in an elusive group of diseases. Diabetic retinopathy (DR) is a common complication of diabetes and a leading cause of blindness among the working-age population. Diabetic patients often experience functional deficits in dark adaptation, contrast sensitivity and color perception before any microvascular pathologies on the fundus become detectable. Previously, we found that the regeneration of 11-cis-retinal and visual pigment is impaired in a type 1 diabetes animal model, which negatively affects the visual function at the early stage of DR. Here, we demonstrated that the treatment of Akita mice, a type 1 diabetic model, with the visual pigment chromophore, 9-cis-retinal, rescued a- and b-wave amplitudes of scotopic electroretinography (ERG) responses, compared to vehicle-treated Akita mice. Also, the administration of 9-cis-retinal significantly alleviated oxidative stress as demonstrated by reduced 3-nitrotyrosine levels in the retina of Akita mice. Acetosyringone cost Further, the 9-cis-retinal treatment decreased retinal apoptosis as shown by the TdT-mediated dUTP nick-end labeling (TUNEL) and DNA fragment Enzyme-Linked ImmunoSorbent Assay (ELISA). Overall, these findings demonstrated that 9-cis-retinal administration restored visual pigment formation, decreased oxidative stress and retinal degeneration, which resulted in improved visual function in diabetic mice, suggesting that chromophore deficiency plays a causative role in visual defects in the early DR. Zaire ebolavirus (EBOV) causes Ebola virus disease (EVD), which carries a fatality rate between 25-90% in humans. Liver pathology is a hallmark of terminal EVD; however, little is known about temporal disease progression. We utilized multiplexed fluorescent immunohistochemistry (mIHC) and in situ hybridization (mISH) in combination with whole slide imaging (WSI) and image analysis (IA) to quantitatively characterize temporospatial signatures of viral and host factors as related to EBOV pathogenesis. Eighteen rhesus monkeys euthanized between 3-8 days post-infection (DPI) and 3 uninfected controls were enrolled in this study. Compared to semi-quantitative histomorphological ordinal scoring, quantitative IA was able to detect subtle and progressive features of early and terminal EVD that was not feasible with routine approaches. Sinusoidal macrophages were the earliest cells to respond to infection, expressing the pro-inflammatory cytokine gene IL-6. IL-6 expression was subsequently also observed in fibrovascular compartments. Interferon stimulating gene-15 (ISG-15), displayed an early, progressive, and ubiquitous signature with hybridization of both mesenchymal and epithelial compartments. ISG-15 expression was prominent near infected cells, but not in infected cells, supporting that hypothesis that bystander cells produce a robust interferon gene response. This study contributes to our current understanding of early EVD progression and illustrates the value of digital pathology and quantitative IA serve in infectious disease research. Cholestatic liver injury may lead to a series of hepatobiliary syndromes, which can progress to cirrhosis and impaired liver regeneration, eventually resulting in liver-related death. It is known that the mammalian target of rapamycin complex 2 (mTORC2) is a major regulator of liver metabolism and tumor development. However, the role of mTORC2 signaling in cholestatic liver injury has not been characterized to date. In this study, we generated liver specific Rictor knockout mice to block the mTORC2 signaling pathway. Mice were treated with 3,5-diethoxycarbonyl-1,4-dihydrocollidine (DDC) to induce cholestatic liver injury. We found that DDC feeding induced cholestatic liver injury and ductular reaction as well as activation of the mTORC2/Akt signaling pathway in wild-type mice. Loss of mTORC2 led to significantly decreased oval cell expansion after DDC feeding. Mechanistically, we found that this phenotype was independent of mTORC1/Fatty Acid Synthase (Fasn) cascade or Yap signaling. Notch pathway was instead strongly inhibited during DDC induced cholestatic liver injury in liver specific Rictor KO mice. Furthermore, AAV-TBG-Cre mediated mTORC2 deficiency in adult hepatocytes did not inhibit ductular reaction in this cholestatic live injury mouse model. Our results indicated that mTORC2 signaling effectively regulates liver regeneration by inducing oval cell proliferation. Liver progenitor cells or bile duct cells, rather than mature hepatocytes, would be the major source of ductular reaction in DDC-induced cholestatic liver injury. PURPOSE To explore the current status and determine the uniformity of parental leave policies among US radiology residency programs. METHODS An electronic survey was developed and sent to 222 radiology residency program directors (PDs) in June 2019 to assess their policies and attitudes toward parental leave. The survey was administered via the Internet Qualtrics Research Suite (Qualtrics, Provo, Utah) format with four reminders sent over the course of 2 months before closing the data collection. RESULTS In all, 74 PDs responded to the survey. Of those, 88% claimed to have a maternal leave policy (88% explicitly written and 77% paid); 80% had a paternal leave policy (88% explicitly written and 75% paid). The average length of maternal and paternal leaves was 7.4 ± 3.9 and 3.7 ± 3.7 weeks, respectively. Parental leaves were allocated at least every other year in over 70% of programs. Approximately 60% of the PDs required residents to make up call rotations for parental leaves. About 90% of responsive programs adjusted angiography and fluoroscopy rotations for trainees throughout the pregnancy or according to the trainee's request. Policies did not generally address issues of breastfeeding and nontraditional parenthood. CONCLUSION The proportion of radiology programs with explicit maternal leave policies remained constant compared with previous surveys during the last two decades. However, there was a dramatic rise in the adoption of paternal leave policies. Overall, there was a lack of national uniformity in radiology residency programs' policies concerning parental leave, leaving open the possibility of national guidance in addressing the issue.