• Griffin Albright posted an update 6 months ago

    Qualitative interview-based pilot study.

    A traumatic spinal cord injury (TSCI) profoundly disrupts the way individuals experience their body. Awareness of one’s body is an important element in the psychological adjustment process after TSCI. This pilot study aimed to explore the body experience of individuals during post-acute rehabilitation following TSCI.

    Specialized acute care and rehabilitation center in Switzerland.

    Eight semi-structured face-to-face interviews were conducted with patients in the post-acute phase of their TSCI. Body experience was explored in relation to perceptive, cognitive, emotional, and behavioral aspects. The interviews were transcribed verbatim, and a structured content analysis was performed according to the Mayring method.

    The individuals verbalized body experience in all explored aspects. The two participants with tetraplegia described high body-related awareness, including dependence on other persons or aids, whereas individuals with paraplegia focused on their abilicess.The recently discovered lytic polysaccharide monooxygenases (LPMOs), which cleave polysaccharides by oxidation, have been associated with bacterial virulence, but supporting functional data is scarce. Here we show that CbpD, the LPMO of Pseudomonas aeruginosa, is a chitin-oxidizing virulence factor that promotes survival of the bacterium in human blood. The catalytic activity of CbpD was promoted by azurin and pyocyanin, two redox-active virulence factors also secreted by P. aeruginosa. Homology modeling, molecular dynamics simulations, and small angle X-ray scattering indicated that CbpD is a monomeric tri-modular enzyme with flexible linkers. Deletion of cbpD rendered P. aeruginosa unable to establish a lethal systemic infection, associated with enhanced bacterial clearance in vivo. CbpD-dependent survival of the wild-type bacterium was not attributable to dampening of pro-inflammatory responses by CbpD ex vivo or in vivo. Rather, we found that CbpD attenuates the terminal complement cascade in human serum. Studies with an active site mutant of CbpD indicated that catalytic activity is crucial for virulence function. Finally, profiling of the bacterial and splenic proteomes showed that the lack of this single enzyme resulted in substantial re-organization of the bacterial and host proteomes. LPMOs similar to CbpD occur in other pathogens and may have similar immune evasive functions.Mutations in human equilibrative nucleoside transporter 3 (ENT3) encoded by SLC29A3 results in anemia and erythroid hypoplasia, suggesting that ENT3 may regulate erythropoiesis. Here, we demonstrate that lysosomal ENT3 transport of taurine-conjugated bile acids (TBA) facilitates TBA chemical chaperone function and alleviates endoplasmic reticulum (ER) stress in expanding mouse hematopoietic stem and progenitor cells (HSPCs). Slc29a3-/- HSPCs accumulate less TBA despite elevated levels of TBA in Slc29a3-/- mouse plasma and have elevated basal ER stress, reactive oxygen species (ROS), and radiation-induced apoptosis. Reintroduction of ENT3 allows for increased accumulation of TBA into HSPCs, which results in TBA-mediated alleviation of ER stress and erythroid apoptosis. Transplanting TBA-preconditioned HSPCs expressing ENT3 into Slc29a3-/- mice increase bone marrow repopulation capacity and erythroid pool size and prevent early mortalities. Together, these findings suggest a putative role for a facilitative lysosomal transporter in the bile acid regulation of ER stress in mouse HSPCs which may have implications in erythroid biology, the treatment of anemia observed in ENT3-mutated human genetic disorders, and nucleoside analog drug therapy.BACKGROUND Drug reaction with eosinophilia and systemic symptoms (DRESS) syndrome is a drug-induced hypersensitivity reaction that can result in a severe cutaneous adverse drug reaction (SCAR). It is a rare and potentially life-threatening condition that occurs after exposure to sulfonamides, antibiotics, or antiepileptics. Selleckchem H3B-6527 Its incidence in children is not established; however, the mortality rate is documented at approximately 10%. DRESS syndrome is believed to result from an interaction between multiple factors, including genetics, abnormalities of metabolism, and reactivation of certain herpes family viruses including EBV and HHV-6. The classic presentation includes fever, rash, and lymphadenopathy. Symptoms begin approximately 3 to 8 weeks after exposure to the offending agent. CASE REPORT We present a unique case of DRESS syndrome in a 14-year-old girl occurring after the ingestion of minocycline and amoxicillin-clavulanic acid (amoxicillin). Identification of the offending agent was complicated by the patient having been on multiple antibiotics within a short timeframe of the initial presentation of symptoms. In addition to swelling and pruritus, the patient experienced vision problems due to papilledema with bilateral hemorrhage. The treatment course was further complicated by a decrease in kidney function, requiring the patient’s medication regimen to be adjusted accordingly. CONCLUSIONS This is a unique case of DRESS syndrome demonstrating the potential influence of certain viruses on the severity of its presentation. This case also highlights the need to adjust the steroid regimen to reduce the potentially harmful effects on various organ systems.BACKGROUND Hepatocellular carcinoma (HCC) causes a heavy disease burden worldwide. Cell division cycle 45 (Cdc45) and its encoding gene (CDC45) have been studied for a long time, but their expression patterns and roles in liver carcinogenesis and advanced HCC deterioration are still incompletely understood. This study integrated tissue microarray and bioinformatics analyses to explore the expression and clinical value of CDC45 and Cdc45 in HCC. MATERIAL AND METHODS In HCC, the expression and relationships with clinic-pathological parameters of CDC45 and Cdc45 were investigated by integrating the RNA-sequencing data, downloaded from The Cancer Genome Atlas and Oncomine databases, and tissue microarray with immunohistochemistry staining. Co-expressed genes and genetic alterations of CDC45 separately obtained from Oncomine and cBioPortal databases were identified to shed light on the potential mechanisms of CDC45 in HCC. RESULTS CDC45 and Cdc45 were both overexpressed in HCC tissues, and the CDC45 level progressively increased from stage I to III.

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