Objective To understand the nosocomial infection distribution,drug resistance characteristics and carbapenemases-producing phenotype of Pseudomonas aeruginosa (PAE)and Acinetobacter baumannii (ABA).Methods The nosocomial infection strains of non-repeated PAE and ABA isolated in this hospital and the infected cases from July 2012 to July 2013 were retrospec-tively collected.The antimicrobial susceptibility test was conducted by the disk diffusion method(K-B method).The modified Hodge test was adopted to preliminarily screen carbapenemase and the positive strains of preliminary screening were further detected met-allo-beta-lactamase(MBL)by 2-mercaptopropionic acid synergy test.Results During the study period,250 strains of non-repeated PAE and 132 strains of ABA were included.All of them were primarily isolated from sputum specimens,accounting for 55.5%.The department distribution was dominated by the intensive care units(ICU),accounting for 20.9%.The antimicrobial susceptibility test showed that the sensitivity of PAE to the testing anti-microbial drugs was more than 70%,its resistance rates to IPM and MEM were 8.5% and 9.5% respectively.However,the resistance rates of ABA to the testing anti-microbial drugs were up to 35.2%-77.4%,its resistance rates to IPM and MEM were 35.2%,39.1% respectively.The occurrence rates of multidrug-resist-ant and pandrug-resistant ABA nosocomial infection was higher than that of PAE,which were 44.7% and 24.0% and 9.1% and 2.8%,respectively.Among 40 strains of carbapenem-resistant PAE,11 strains(27.5%)were positive in the preliminary screening and 2 strains(18.2%)were positive of MBL phenotype.Among 49 strains of carbapeneme-resistant ABA,37 strains(75.5%)were positive in the preliminary screening and only 1 strain(2.7%)was positive of MBL phenotype.Conclusion PAE and ABA in our hospital exhibit different resistance to common antibacterial drugs.The monitoring should be strengthened.The production of car-bapenemsa is one the main mechanisms for PAE resistance to carbapenems.The detection rate of MBL-producing PAE and ABA is lower in our hospital.

Objective Saxagliptin regulates the level of blood glucose by selectively inhibiting high-performance dipeptidyl peptidase 4, but its action mechanism is not yet clear .This study was to investigate the effect of the novel hypoglycemic agent Saxaglip -tin on the expression of long non-coding RNA (LncRNA) metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) and its target gene products transforming growth factor-β1 ( TGF-β1 ) in human umbilical vein endothelial cells ( HUVECs) stimulated by high glucose. Methods HUVECs were cultured in with D-glucose (D-GS) at the concentrations of 5.5, 10, 20, and 30 mmol/L and Saxagliptin at 0, 0.01, 0.1, 1, and 10μmol/L.The best concentrations of D-GS and Saxagliptin were determined as 30 mmol/L and 1 μmol/L, respectively.The HUVECs were divided into four groups:control (5.5 mmol/L D-GS), Saxagliptin (5.5 mmol/L D-GS+1 μmol/L Saxagliptin ) , high glucose ( 30 mmol/L D-GS ) , and high glucose +Saxagliptin (30 mmol/L D-GS +1μmol/L Saxaglip-tin), all cultured for 24 hours.Then the expressions of MALAT1 and TGF-β1 mRNA in the cells were detected by qRT-PCR, that of the TGF-β1 protein determined by Western blot , and the level of TGF-β1 in the supernatant measured by ELISA . Results The expressions of LncRNA-MALAT1 and TGF-β1 were significantly increased in the high glucose group as compared with the control ( 8.65 ±0.70 vs1.00 ±0.00 and 1.36 ±0.07 vs 1.00 ±0.00, P<0.01) but markedly inhibited in the high glucose +Saxagliptin group in compari-son with the high glucose group (2.17 ±0.24 vs 8.65 ±0.70 and 1.15 ±0.02 vs 1.36 ±0.07, P<0.05). Conclusion High glu-cose can induce the overexpression of LncRNA-MALAT1 and its target gene products TGF-β1 in HUVECs and cause damage to the cells, while Saxagliptin can significantly suppress this effect .

Objective To investigate the effect of atorvastatin on the expressions of long non-coding RNA (LncRNA) metastasis-associated lung adenocarcinoma transcript 1 (MALAT1)and inflammation factors in human umbilical vein endothelial cells (HUVECs) stimulated by high glucose. Methods The expression of MALAT1 in HUVECs incubated with high glucose(30 mmol/L) for different time periods were detected by real-time PCR. Under high glucose condition, the expressions of MALAT1, interleukin-6(IL-6), and interleukin-8 (IL-8) in HUVECs were detected after MALAT1 was silenced by siRNA or atorvastatin was added. Results (1) After HUVECs were incubated with high glucose for different time periods, the expressions of MALAT1 were increased to some extent(P<0.05), with the peak at 12h (P<0.01). The levels of IL-6 and IL-8 expression and secretion were increased after HUVECs were stimulated by high glucose for 12h (P<0.05). (2)The silence of MALAT1 markedly suppressed high glucose-stimulated expression and secretion of IL-6 and IL-8 (P<0.05). (3) Atorvastatin significantly inhibited high glucose-stimulated expressions of MALAT1, IL-6, and IL-8(all P<0.05). Conclusions High glucose induces the secretion of inflammatory factors by stimulating MALAT1 expression in endothelial cells. Atorvastatin significantly inhibits high glucose-stimulated MALAT1 expression and decreases inflammatory reaction.

Objective:To explore the influencing factors and guiding significance of troponin I (TnI) increased in patients with renal transplantation.Methods:The clinical data of 195 patients with renal transplantation from December 2019 to June 2021 in Xuanwu Hospital, Capital Medical University were retrospectively analyzed. TnI was routinely detected after surgery, and TnI>0.02 μg/L was abnormal. The incidence of acute coronary syndrome during hospitalization was recorded. Multivariate Logistic regression analysis was used to analyze the independent risk factors of TnI increased after renal transplantation.Results:Among 195 patients with renal transplantation, postoperative TnI increased in 55 cases (28.2%). The age, diabetes complication rate and dialysis time before first renal transplantation in patients with TnI increased were significantly higher than those in patients with TnI normal: (49.2±9.0) years old vs. (41.6±10.6) years old, 27.3% (15/55) vs. 14.3% (20/140) and 24.0 (11.0, 60.0) months vs. 11.0 (4.0, 24.0) months, and there were statistical differences ( P<0.01 or<0.05); there was no statistical difference in hospitalization length of stays ( P>0.05). During hospitalization, acute coronary syndrome occurred in 8 patients (4.1%, 8/195), and 2 patients died. Multivariate Logistic regression analysis result showed that age>50 years old was the independent risk factor of TnI increased after renal transplantation ( OR = 5.11, 95% CI 2.47 to 10.59, P<0.01). Conclusions:The incidence of TnI increased after renal transplantation is high, but the incidence of acute coronary syndrome is not high. The age increases the risk of postoperative TnI increased, but TnI increased does not prolong the hospital stay.

Toll-like receptors (TLRs) is a type of pattern recognition receptors (PRRs), which are singular, non-catalytic and highly homologous. TLRs not only play significant roles in natural immunity, but also act as a bridge between innate immunity and adaptive immunity. Recent studies have revealed that TLRs play critical roles in the development of non-resolving inflammation-related cancer,including the formation of tumor microenvironment, invasion and metastasis, immune escape, etc. Further investigation into the mechanisms responsible for the function of TLRs will be of great value in tumor prevention, early diagnosis and therapy.
Humans ; Inflammation ; Neoplasm Invasiveness ; Neoplasm Metastasis ; Neoplasms ; Toll-Like Receptors ; Tumor Microenvironment