ABSTRACT
Objective:To analyze the outcomes of isoniazid (INH) mono-resistant pulmonary tuberculosis, and risk factors associated with adverse treatment outcomes of INH mono-resistant pulmonary tuberculosis.Methods:A total of 114 cases of INH mono-resistant pulmonary tuberculosis in Xi′an Chest Hospital from January 1, 2018 to December 31, 2020 were retrospectively recruited for analysis. The general information, clinical symptoms, and laboratory test results of patients were collected. With treatment success and adverse treatment outcomes as dependent variables, binary logistic regression analysis was used to analyze the risk factors for the adverse treatment outcome of INH mono-resistant pulmonary tuberculosis.Results:Among 114 patients with INH mono-resistant tuberculosis, 46 cases (40.4%) were cured and 41 cases (36.0%) completed treatment with the success rate of 76.3%(87/114), while 11 cases (9.6%) failed treatment, 13 cases (11.4%) lost to follow up, three cases (2.6%) died.The binary logistic regression analysis showed that male (odds ratio ( OR)=7.22, 95% confidence interval ( CI) 1.47 to 35.43)), no fever at onset ( OR=12.97, 95% CI 2.74 to 61.55), not containing amikacin in the regimen ( OR=5.28, 95% CI 1.20 to 23.31), sputum bacteria load >1+ ( OR=5.87, 95% CI 1.76 to 19.60) were the risk factors for adverse treatment outcomes of INH mono-resistant tuberculosis. Conclusions:The treatment success rate of INH mono-resistant pulmonary tuberculosis patients is high. The risk factors for adverse treatment outcome are male, no fever at the onset, not containing amikacin in the regimen, and sputum bacteria load >1+ .
ABSTRACT
BACKGROUND: Role of autophagy in pulpitis, periapical periodontitis and alveolar bone destruction and the underling mechanisms have not been fully elucidated. OBJECTIVE: To investigate the expression of autophagy-related protein light chain 3B in human pulpitis and periapical periodontitis, in order to explore the rule of autophagy. METHODS: The healthy first premolar or surgically removed third premolar was selected from the patients undergoing orthodontics after their consent informs. The dental pulp cells were treated with 1 mg/L lipopolysaccharide for 0, 6, 12, 24 and 48 hours to induce inflammation. The expression of light chain 3B in normal and lipopolysaccharide-stimulated dental pulp cells was detected by western blot assay. The dotted accumulation of light chain 3B was observed by immunofluorescence. The expression level of light chain 3B in specimens of human chronic periapical periodontitis tissues was tested by real-time RT-PCR. RESULTS AND CONCLUSION: The expression of light chain 3B in dental pulp cells stimulated by lipopolysaccharide for 6, 12, 24 and 48 hours was higher than that in normal dental pulp cells. The expression of light chain 3B increased with time, and peaked at 24 hours. Dotted accumulation of light chain 3B increased with lipopolysaccharide simulation time prolonged. The expression level of light chain 3B in specimens of human chronic periapical periodontitis tissues was higher than that in normal periapical tissues. These results indicate that the expression of light chain 3B is increased in human pulpitis and periapical periodontitis, and morphology also shows an increase of autophagy, suggesting that autophagy may be associated with the occurrence and development of pulpitis and periapical periodontitis.
ABSTRACT
AIM: To study the effects of low density lipoproteins (LDLs) on insulin-like growth factor-1 receptor (IGF-1R), phosphorylated extracellular signal-regulated kinase (p-ERK), Bcl-2 and Bax protein expression in mouse peritoneal macrophages (MPMs). METHODS: Using the methods of immunocytochemistry and Western blotting, the expression of IGF-1R, p-ERK, Bcl-2 and Bax protein in MPMs treated with LDLs, anti-IGF-1R antibody (?-IR-3) or ERK inhibitor (PD98059) were detected. RESULTS: oxLDL significantly increased the IGF-1R protein expression in a dose and time-dependent manner. P-ERK protein expression induced by oxLDL peaked at 5 min. Moreover, oxLDL could induced ERK translocation from cytoplasm to nuclear. When given ?-IR-3, p-ERK protein expression was significantly inhibited, and ERK translocation disappeared. oxLDL increased Bcl-2 protein expression and reduced Bax expression in a dose and time-dependent manner. When given PD98059, Bcl-2 and Bax protein expression induced by oxLDL altered significantly. Native LDL had no significant effect on the expression of these four proteins. CONCLUSIONS: oxLDL may promote cultured MPMs survival at least by enhancing IGF-1R expression and ERK phosphorylation, and there may be many pathways involved in MPMs survival induced by oxLDL, Whereas native LDL had no effects on culture MPMs.