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The prevalence of non-obese nonalcoholic fatty liver disease (NAFLD) is increasing worldwide with unclear etiology and pathogenesis. Here, we show GP73, a Golgi protein upregulated in livers from patients with a variety of liver diseases, exhibits Rab GTPase-activating protein (GAP) activity regulating ApoB export. Upon regular-diet feeding, liver-GP73-high mice display non-obese NAFLD phenotype, characterized by reduced body weight, intrahepatic lipid accumulation, and gradual insulin resistance development, none of which can be recapitulated in liver-GAP inactive GP73-high mice. Common and specific gene expression signatures associated with GP73-induced non-obese NAFLD and high-fat diet (HFD)-induced obese NAFLD are revealed. Notably, metformin inactivates the GAP activity of GP73 and alleviates GP73-induced non-obese NAFLD. GP73 is pathologically elevated in NAFLD individuals without obesity, and GP73 blockade improves whole-body metabolism in non-obese NAFLD mouse model. These findings reveal a pathophysiological role of GP73 in triggering non-obese NAFLD and may offer an opportunity for clinical intervention., Dysregulation of lipid metabolism and transport contribute to the pathogenesis of non-alcoholic fatty liver disease (NAFLD). Here the authors identify GP73 as a TBC-domain Rab GTPase-activating protein that regulates very low-density lipoprotein export and promotes NAFLD development in mice.

Parotid gland tuberculosis constantly results in unnecessary medical examinations and surgery because of its similarities in the presentation to neoplasms of the parotid gland. Although parotid gland involvement is extremely rare even in tuberculosis-endemic countries, accurate diagnosis of this clinical entity is of great significance because tuberculous parotitis can be successfully treated medically without surgical therapy. Fine needle aspiration cytology (FNAC) and molecular identification of the parotid swellings are efficient in making a rapid diagnosis. Herein, we report an early misdiagnosis of malignancy from a renal transplantation patient on long-term immunologic inhibitor therapy, who ultimately proved to have tuberculosis of the parotid gland by FNAC and molecular identification. The aim of this study is to describe and analyze the etiologic characteristics, epidemiology, clinical presentations, diagnostic methods, histopathologic findings, and pathogenic mechanisms of these rare infections.

Background Recently, the rise of syphilitic seroresistance brings great confusion to the clinical diagnosis and treatment of syphilis, and no clear diagnostic marker has been found to distinguish syphilitic seroresistance from other progression of syphilis. This study evaluated the serum chemokines levels of CCL2, CXCL8, CXCL9, and CXCL10 and its correlation with blood routine, coagulation, and biochemical indexes in seroresistant syphilitic patients. Method Serum levels of chemokines were quantitatively determined by Flow Cytometric Bead Array (CBA). The results expressed in pg/ml. Clinical parameters were detected and analyzed according to the clinical laboratory standards. A correlation analysis was subsequently performed. Results The seroresistant syphilitic patients increased significantly serum chemokines levels of CXCL8 (***p, In this study, the concentration of cytokines in blood samples of patients with Treponema pallidum infection in Zhejiang Provincial People's Hospital was detected by flow cytometry. Our data showed that seroresistant syphilitic patients presented significantly increased levels of the serum chemokines CXCL8, CXCL9, and CXCL10 when compared to non‐infected individuals.

Background Nocardia is an opportunistic pathogen, which occurs in patients with autoimmune diseases and immune dysfunction, and can cause bacteremia and other life‐threatening complications. The clinical manifestations of Nocardia pneumonia are similar to tuberculous and other clinical common bacterial pneumonia, but its antibacterial treatments are different and detection methods are unique, which may lead patients to suffer for many years due to clinical misdiagnosis and missed diagnosis. Methods Imaging and laboratory examinations were performed for preliminary diagnosis, and next‐generation sequencing was used to identify the exact species type of Nocardia in the bronchoalveolar lavage fluid (BALF) of the patient. Results Imaging and laboratory parameters preliminarily implied that the patient was infected with Nocardia with Sjogren's syndrome (SS), and NGS showed that the strain was N. terpenica. Conclusions Accurate etiological diagnosis and corresponding antibiotics are key to improve the prognosis of pulmonary nocardiosis in this case. Nocardia pneumonia is rare in clinical practice; it is of great medical significance to improve the understanding of pulmonary nocardiosis.

SummarySevere acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection induces new-onset diabetes and severe metabolic complications of pre-existing diabetes. The pathogenic mechanism underlying this is incompletely understood. Here, we provided evidence linking circulating GP73 with the exaggerated gluconeogenesis triggered by SARS-CoV-2 infection. We found that SARS-CoV-2 infection or glucotoxic condition increased the cellular secretion of GP73. Secreted GP73 trafficked to the liver and kidney to stimulate gluconeogenesis through cAMP/PKA pathway. By using global phosphoproteomics, we found a drastic remodeling of PKA kinase hub exerted by GP73. Notably, COVID-19 patients showed pathologically elevated plasma GP73, and neutralization of the secreted GP73 inhibited enhanced PKA signaling and glucose production associated with SARS-CoV-2 infection. GP73 blockade also reduced gluconeogenesis and lowered hyperglycemia in type 2 (T2D) diabetic mice. Therefore, our findings provide novel insight into the roles of GP73 as a key glucogenic hormone and mechanistic clues underlying the development of SARS-CoV-induced glucose abnormalities.

Introduction Mycoplasma pneumoniae is a common cause of respiratory infections in humans. The aim of this study was to investigate the infection of Mycoplasma pneumoniae (MP) in patients with acute respiratory tract infections in Zhejiang Province from 2008 to 2017, and to provide evidence for the early diagnosis and prevention of MP pneumonia. Methods MP‐DNA was detected in nasopharyngeal swabs of patients with acute respiratory tract infection by real‐time fluorescent PCR (TaqMan probe). Statistical analysis and epidemiological investigation were carried out on the test results. Results There were 10 296 patients with acute respiratory tract infection in Zhejiang Provincial People's Hospital from 2008 to 2017, including 4387 females and 5909 males. A total of 1251 MP‐DNA–positive patients were detected, with a total positive rate of 12.2% (1251/10296). Among 1251 patients with MP infection, 571 were female positive, with an average positive rate of 13.0% (571/4387), and 680 were male positive, with a positive rate of 11.5% (680/5909). From 2008 to 2017, the positive rates were 22.8% (33 cases), 20.9% (211 cases), 20.9% (350 cases), 5.5% (70 cases), 11.7% (136 cases), 15.2% (190 cases), 7.8% (94 cases), 5.9% (62 cases), 7.8% (56 cases), and 6.0% (49 cases), respectively. Of 1251 MP‐DNA–positive patients, 1243 (99.4%) were younger than 18 years old. Conclusions Mycoplasma pneumoniae infection mainly occurs from late summer to autumn and in the age below 18 years, suggesting that early diagnosis and prevention of MP infection in adolescents should be emphasized., Figure 1. Annual, quarter, and monthly cases and positivity of MP from 2008 to 2017