The Distribution, Drug Susceptibility, and Dynamic Trends of Pseudomonas aeruginosa Infection in a Tertiary Hospital in China During 2016‒2022.

Background: Drug-resistant Pseudomonas aeruginosa infections rapidly increased and contributed to life-threatening nosocomial infections; however, the distribution, species, drug susceptibility and dynamic trends of P. aeruginosa infection in China remained unclear. This study was conducted to better understand the epidemiological data of increased P. aeruginosa infections from 2016 to 2022 in a hospital in China. Methods: This study involved 3301 patients infected with P. aeruginosa, diagnosed using a nosocomial infection surveillance system in a tertiary hospital between 2016 and 2022. The P. aeruginosa infections from 2016 to 2022 were assessed according to the hospital department and species, and the drug susceptibility was evaluated using 16 antimicrobial agents. Results: The P. aeruginosa infection prevalence in the hospital department was: Neurosurgery (14.30%), Emergency (13.30%), and Critical Care Medicine (11.69%). Samples for P. aeruginosa infection identification were from sputum (72.52%) and other secreta (9.91%). The P. aeruginosa infections demonstrated a greater sensitivity to amikacin (AMK, 91.82%), tobramycin (TOB, 82.79%), and gentamycin (GEN, 82.01%); however, P. aeruginosa infection demonstrated greater resistance to ticarcillin (22.57%), levofloxacin (21.63%), and ciprofloxacin (18.00%). Conclusion: The P. aeruginosa infections were commonly observed in the Neurosurgery, Emergency, and Critical Care Medicine departments and demonstrated greater sensitivity to AMK, TOB, and GEN than the other drugs.

Investigation of the material basis of Xiexin Tang to alleviate type 2 diabetes mellitus based on spectrum-effect analysis by UPLC-Q-TOF/MS.

Xiexin Tang (XXT) is a classic prescription for treating diabetes in clinical practices for thousands of years in China, which has been also proved by a large number of modern pharmacological studies. However, due to its complex composition, the bioactive ingredients of XXT is still unclear. In present researches, spectrum-effect relationship analysis is widely used to explore the material basis of traditional medical herbs, so this method was adopted in this study. Firstly, the extract of XXT was separated and enriched into 5 fractions by macroporous adsorption resin. Then, UPLC-Q-TOF/MS method was used for qualitative identification of components in each eluting part, and efficacy of each fraction was assessed by the T2DM rat model. Based on grey relational analysis and pearson bivariate correlation analysis, it was found that the components such as berberine, gallic acid, catechin, epicatechin, acteoside, berberastine and 1-O-galloyl-ß-D-glucose might be the main effective basis of XXT to improve T2DM.

MicroRNA-212 promotes the recovery function and vascular regeneration of endothelial progenitor cells in mice with ischemic stroke through inactivation of the notch signaling pathway via downregulating MMP9 expression.

Ischemic stroke is a refractory disease caused by cerebral ischemic injury, which results in brain dysfunction. This study intends to investigate the effects of microRNA-212 (miR-212) on the recovery function and vascular regeneration of endothelial progenitor cells (EPCs) by inactivation of the Notch signaling pathway by binding to matrix metallopeptidase 9 (MMP9) in mice with ischemic stroke. According to the results of database retrieval systems and data analysis, MMP9 was predicted as a gene related to ischemic stroke and miR-212 is a potential regulating mRNA of MMP9. All 72 healthy adult C57BL6 mice were selected for middle cerebral artery occlusion (MCAO) establishment. Cerebral infarction was observed under triphenyltetrazolium chloride staining. A series of inhibitors, activators, and siRNAs were introduced to the verified regulatory functions for miR-212 governing MMP9 in ischemic stroke. Cell proliferation was detected by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay and tube-forming ability by tubule formation test. Reverse transcription quantitative polymerase chain reaction and Western blot analysis were used to detect the expressions of miR-212, MMP9, Hes-1, and Notch-1. The corresponding results demonstrated that the area of cerebral infarction and the number of neuronal necrosis increased in the MCAO group in contrast to the sham group. Meanwhile, upregulation of miR-212 or downregulation of MMP9 decreases the expressions of MMP9, Hes-1 Notch-1, increases cell proliferation and tube-forming ability and improves the pathological conditions of EPCs. Our study suggests that miR-212 promotes recovery function and vascular regeneration of EPCs through negative regulation of the Notch signaling pathway via downregulating expression of MMP9, thus provides a clinical theoretical basis for ischemic stroke therapy.

MicroRNA-410 inhibition of the TIMP2-dependent MAPK pathway confers neuroprotection against oxidative stress-induced apoptosis after ischemic stroke in mice.

Ischemic stroke (IS) is an acute cerebral event characterized by a high incidence rate, high disability rate as well as a high mortality. More recently, accumulative literature has provided evidence highlighting the role played by microRNAs (miRs) in the development of neurons. Hence, the aim of the present study was to investigate the neuroprotective role of miR-410 in IS. Microarray-based gene expression profiling of AMI was conducted in order to identify differentially expressed genes (DEGs) and the corresponding miRs regulating these genes. IS models were established to assess neurology on a scoring basis. Superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) activity and malondialdehyde (MDA) were all subsequently assessed. The functional role of miR-410 in IS was determined based on ectopic expression, knockdown and reporter assay experiments in hippocampal neurons. The expressions of microRNA-410, TIMP2, ERK, p38MAPK, JNK were all examined accordingly. The survival rate was assessed by MTT assay, and cell cycle and apoptosis by flow cytometry. After the loss of hippocampal neurons, infarct size as well as oxidative stress injury had been detected, microarray technology revealed that TIMP2 was differentially expressed in IS and that miR-410 regulated TIMP2. Initial observations revealed elevated levels of TIMP2 expression and MDA activity, in addition to evidence obtained indicated that the MAPK pathway had been activated along with decreased SOD, GSH-Px activity and miR-410 expression in IS mice. Ectopic expression of miR-410 was observed to inactivate the MAPK pathway, TIMP2 expression and hippocampal neuron apoptosis, while elevated hippocampal neuron survival rates and cell cycle entry were detected. Furthermore, TIMP2 as a direct target gene of miR-410, was determined to be negatively regulated by miR-410, while the MAPK pathway was found to be inhibited following TIMP2 knockdown. Our results revealed that the overexpression of miR-410 could ameliorate hippocampal neuron loss, reduce infarct size and oxidative stress injury in IS mice. Taken together, the key evidence of the current study elucidated the distinct nature of the inhibitory effect on IS as a result of overexpressed miR-410 whereby the conferral of neuroprotection was observed in oxidative stress-induced apoptosis post IS through the TIMP2-dependent repression of the MAPK pathway in mice.

Impact of acute and chronic stress hormone on male albino rat brain.

The present investigation aimed to evaluate the acute and chronic effect of stress (stress hormone) in male albino rat brain. Nor-epinephrine was used for the treatment and saline used for the control. Nor-epinephrine was dissolved in the saline and administered orally to the rats. Following nor-epinephrine administration, the brain was removed surgically at 6 h, 12 h and 45 days. Alanine tansaminase (ALT), aspartate transaminase (AST) and alkaline phosphatase (ALP) were significantly altered in the rats. Lipid peroxidation was measured as malondialdehyde (MDA), showed altered lipid peroxidation. Hematological markers such as packed cell volume (PCV), white blood cells (WBC), neutrophil, lymphocytes and hemoglobin were significantly altered compared to controls. Altered serum biochemical and hematological markers, lipid peroxidation and enzyme activities leads to adverse effect in the cellular metabolism and physiological activities of rats.