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The cover shows a depiction of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Credit: KTSDESIGN/Science Photo Library/Getty. Used with permission.
This study reports laboratory data and disease outcome of 54 severe- and critical-type COVID-19 hospitalized adult patients in Wuhan, China. Decreased peripheral blood lymphocyte count, prolonged PT, increased secondary fibrinolytic activity, and significantly increased inflammatory factors sIL-2R and IL-6 correlated with the severity of the disease.
Lipopolysaccharide (LPS) is a vital promoter of sepsis-related pulmonary fibrosis. This study revealed that in LPS-induced pulmonary fibrosis, LPS mediates lung fibroblast aerobic glycolysis through the activation of the PI3K-Akt-mTOR/PFKFB3 pathway. Targeting the initiation of aerobic glycolysis may be a constructive treatment for pulmonary fibrosis.
The authors show that zyxin (ZYX) correlates with glioma progression and worse prognosis of patients and identified ZYX as a biomarker for diagnosis. This study provided insights on ZYX function and reveals that ZYX plays an important role in the invasion of glioblastoma through regulation of the e expression of STMN1, a cytoskeleton regulating protein.
Epithelial–mesenchymal transition (EMT) plays a critical role in the progression of salivary gland (SG) fibrosis in primary Sjögren’s syndrome. This study demonstrates the IL-17-dependent activation of EMT in human SG epithelial cells that occurs through both the canonical TGF-β1/Smad2/3 and noncanonical TGF-β1/Erk1/2 pathways.
This study demonstrates that ablation of the l-histidine decarboxylase /histamine axis using a genetically modified mouse model ameliorates liver damage and hepatic fibrosis. Further, histamine reactivates the axis via H1/H2 receptors, thus recapitulating the liver damage and fibrosis of primary sclerosing cholangitis. Histamine regulation of TGF-β1 and VEGF-C may be targeted therapies for this disease.
WFS1 is a causative gene for Wolfram syndrome, a rare neurodegenerative disorder characterized by juvenile-onset diabetes mellitus and optic nerve atrophy. Genetic proof of concept studies coupled with RNA-seq reveal that increasing WFS1 confers a survival advantage to cells under ER stress by activating Akt pathways and preserving ER homeostasis. This work reveals essential pathways regulated by WFS1 and therapeutic targets for Wolfram syndrome.
The authors profiled differentially expressed microRNAs between parental adherent breast cancer cells and breast cancer stem cell (BCSC) -mimicking mammospheres, and identified hsa-miR-27a as a negative regulator for survival and chemoresistance of BCSCs by downregulating genes essential for detoxification of ROS and impairing of autophagy. Enhancement of the hsa-miR-27a signaling pathway may be a potential therapeutic modality for breast cancer.
PD-L1 IHC was evaluated in stored tissue with mass spectrometry (MS). Increased humidity and temperature resulted in considerable immunoreactivity loss, particularly among antibodies recognizing extracellular and discontinuous epitopes, which could be partially mitigated with the use of desiccant. However, even in significantly affected tissues MS was able to quantitate PD-L1 expression and assess peptide oxidation. These results suggest MS is suited for biomarker assessments using stored sections—a sample type commonly encountered in oncology research.
Gene δ-sarcoglycan was knocked out in pigs via gene editing and somatic cell cloning. Loss of expression led to α-, β-, and γ-sarcoglycan depletion in the cardiac and skeletal sarcolemma. Pigs exhibiting systolic dysfunction, myocardial tissue degeneration, and sudden death are promising for studying next-generation therapies for human genetic cardiomyopathy.