Background: Multidrug-resistant Acinetobacter baumannii (MDRAB) has emerged as an important pathogen of nosocomial infections. Even though cefoperazone-sulbactam is frequently used to treat MDRAB infections, this single-drug therapeutic approach often results in antibiotic resistance. Thus, combination therapy is preferred over single-drug therapy, particularly in the case of carbapenemase-producing gram negative bacteria. The aim of this study was to investigate the efficacy of cefoperazone-sulbactam combined with either tigecycline or rifampicin against clinical isolates of MDRAB. Methods: One hundred and three MDRAB bacteria were isolated from patients in two hospitals in China.The Epsilomer test (E test) was used to determine the minimum inhibitory concentration (MIC) values for amikacin, ceftazidime, cefepime, levofloxacin, rifampicin, cefoperazone-sulbactam, meropenem, tigecycline, and gentamicin against MDRAB isolates. In vitro effects of various antibiotic combinations were measured and the fractional inhibitory concentration index (FICI) was calculated for each drug combination.Results: Approximately 17.5% of the isolates were resistant to tigecycline, whereas more than 84.2%isolates were resistant to other antimicrobial agents tested in this study. Cefoperazone-sulbactam revealed remarkable synergistic effects when used in combination with either tigecycline or rifampicin. However, for the isolates with MICs lower than blood peak concentration after combination therapy, the ratio was lower in highly resistant isolates compared to the least resistant bacteria. Conclusions: In vitro cefoperazone-sulbactam in combination with tigecycline or rifampicin showed the highest synergistic or additive activity against MDRAB isolates. However, acquisition of highly antibiotic resistant bacteria may lessen the effectiveness of combination therapy.

Background Tuberculous meningitis (TBM) is the most lethal form of tuberculosis worldwide. Data on critically ill TBM patients in the intensive care unit (ICU) of China are lacking. We tried to identify prognostic factors of adult TBM patients admitted to ICU in China. Methods We conducted a retrospective study on adult TBM in ICU between January 2008 and April 2018. Factors associated with unfavorable outcomes at 28 days were identified by logistic regression. Factors associated with 1-year mortality were studied by Cox proportional hazards modeling. Results Eighty adult patients diagnosed with TBM (age 38.5 (18–79) years, 45 (56 %) males) were included in the study. An unfavorable outcome was observed in 39 (49 %) patients and were independently associated with Acute Physiology and Chronic Health Evaluation (APACHE) II > 23 (adjusted odds ratio (aOR) 5.57, 95 % confidence interval (CI) 1.55–19.97), Sequential Organ Failure Assessment (SOFA) > 8 (aOR 9.74, 95 % CI 1.46–64.88), and mechanical ventilation (aOR 18.33, 95 % CI 3.15–106.80). Multivariate Cox regression analysis identified two factors associated with 1-year mortality: APACHE II > 23 (adjusted hazard ratio (aHR) 4.83; 95 % CI 2.21–10.55), and mechanical ventilation (aHR 9.71; 95 % CI 2.31–40.87). Conclusions For the most severe adult TBM patients of Medical Research Council (MRC) stage III, common clinical factors aren’t effective enough to predict outcomes. Our study demonstrates that the widely used APACHE II and SOFA scores on admission can be used to predict short-term outcomes, while APACHE II could also be used to predict long-term outcomes of adult patients with TBM in ICU.

The aim of the present study was to explore the effects of miR-218-1-3p and miR-149 on the biological function of non-small cell lung cancer (NSCLC) cells A549. Paired NSCLC and adjacent tissues were obtained from 50 NSCLC patients admitted to Shandong Provincial Chest Hospital Affiliated to Shandong University (Jinan, China) from April 2015 to May 2018. The expression levels of miR-218-1-3p and miR-149 were detected by reverse transcription-quantitative PCR (RT-qPCR). The lung adenocarcinoma A549 cells were assigned into the blank group (without transfection), negative control (NC) group (transfected with miRNA NC), and the transfected groups miR-218-1-3p mimic and miR-149 mimic groups. Proliferation and cell growth were determined by CCK-8 assay and cell invasion ability in vitro was assessed by Transwell assay. Flow cytometry was carried out for the detection of cell apoptosis. RT-qPCR results showed that the expression levels of miR-218-1-3p and miR-149 in NSCLC tissues were significantly lower than those in adjacent tissues (P<0.001). At 48 and 72 h, the cell growth of the A549 cells in the miR-218-1-3p mimic and miR-149 mimic groups was significantly lower than that in the NC and blank groups (P<0.05). The number of invasive cells in the miR-218-1-3p mimic and miR-149 mimic groups was significantly lower than that in the NC and blank groups (P<0.05). The apoptotic rate of A549 cells in the miR-218-1-3p mimic and miR-149 mimic groups was significantly higher than that in the NC and blank groups (P<0.05). In conclusion, upregulation of miR-218-1-3p and miR-149 can inhibit the proliferation, invasion and migration of A549 cells in NSCLC, thereby promoting the apoptosis of A549 cells. Thus, miR-218-1-3p and miR-149 can be used as new molecular targets for the diagnosis and treatment of NSCLC.