Clinical Features of Nontuberculous Mycobacterial Pulmonary Disease in the Yangtze River Delta of China: A Single-Center, Retrospective, Observational Study.

With increased focus on nontuberculous mycobacterial pulmonary disease (NTM-PD), and the improvement in detection methods, the global incidence continues to increase every year, but the diagnosis and treatment are difficult with a high misdiagnosis rate and poor curative effect. This study aimed to analyze the clinical indicators of different pathogenic NTM in the Yangtze River Delta. The study retrospectively analyzed the medical records of patients with NTM-PD, who resided in the Yangtze River Delta and were diagnosed using sputum or bronchial lavage fluid and hospitalized in Shanghai Pulmonary Hospital from March 2017 to February 2019. The clinical data of confirmed patients were collected. Among the 513 cases of NTM-PD, 482 cases were infected by four common bacteria: Mycobacterium intracellulare (224, 46.5%), M. abscessus (138, 28.6%), M. kansasii (84, 17.4%), and M. avium (36, 7.5%). The analysis found that different NTM strains have their corresponding positive and negative correlation factors (p < 0.05). M. intracellulare, M. abscessus, M. kansasii, and M. avium were the main pathogenic bacteria isolated from patients with NTM-PD in the Yangtze River Delta were. Different strains resulted in different clinical features, assisting in the early diagnosis and treatment of NTM-PD.

Hepatoprotective effects of licochalcone B on carbon tetrachloride-induced liver toxicity in mice.

OBJECTIVES: The objective of this study was to investigate the hepatoprotective effect of licochalcone B (LCB) in a mice model of carbon tetrachloride (CCl4)-induced liver toxicity. MATERIALS AND METHODS: Hepatotoxicity was induced in mice by a single subcutaneous injection (SC) of CCl4. The LCB was administered orally once a day for seven days (PO) as pretreatment at three doses of 1, 5, and 25 mg/kg/day. The levels of superoxide dismutase (SOD), malondialdehyde (MDA), glutathione (GSH), glutathione disulfide (GSSG), C-reactive protein (CRP), tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were analyzed by ELISA. The protein expression degrees of p38 mitogen activated protein kinases (p38) and nuclear factor-k-gene binding (NF-κB) were assayed by western blotting. RESULTS: CCl4-induced hepatotoxicity was manifested by an increase in the levels of ALT, AST, MDA, IL-6, CRP, and TNF-ɑ, and a decrease in the SOD level and GSH/GSSG ratio in the serum. The histopathological examination of the liver sections revealed necrosis and inflammatory reactions. Pretreatment with LCB decreased the levels of ALT, AST, MDA, GSSG, IL-6, CRP, TNF-ɑ, and the protein expression of p38 and NF-κB, increased the level of SOD and GSH, and normalized the hepatic histo-architecture. CONCLUSION: LCB protected the liver from CCl4-induced injury. Protection may be due to inhibition of p38 and NFκB signaling, which subsequently reduced inflammation in the liver.