Study on Correlation between Type 2 Diabetes and No-Reflow after PCI.

Diabetes, a serious chronic disease globally, is often complicated with cardiovascular diseases for which percutaneous coronary intervention (PCI) is the mainstay. The no-reflow rate of diabetic patients after PCI is 2-4 times higher than that of nondiabetic patients, yet the specific mechanism is still unclear. This study was designed to investigate the correlation between the duration of diabetes, preoperative blood glucose level, coronary angiographic blood flow, coronary artery stenosis level, and no-reflow after PCI. A total of 131 patients with type 2 diabetes who underwent PCI in our hospital from 2019 to 2020 were divided into control group and observation group. The disease duration, preoperative blood glucose level, coronary angiographic blood flow, and coronary artery stenosis level of the two groups were calculated. There were differences in the duration of diabetes between the two groups; the blood glucose level of the control group was about 3.8%, which was lower than 5.8% of the observation group; the thrombolysis in myocardial infarction (TIMI) value of the control group was 18.46 ± 4.6, which was lower than 20.67 ± 3.9 of the observation group; The degree of coronary stenosis in the control was 63% ± 2%, which was lower than 76% + 3% in the observation group. Binary logistic stepwise regression analysis was performed on these indicators and no-reflow after PCI to explore the correlation between these indicators and no-reflow after PCI in diabetic patients. The study found that the diabetes duration, higher preoperative blood glucose level, coronary angiography blood flow, and coronary artery were positively associated with no-reflow after PCI.

Association of tumor necrosis factor-α gene polymorphisms and coronary artery disease susceptibility: a systematic review and meta-analysis.

BACKGROUND: The goal of this study was to review relevant case-control studies to determine the association of tumor necrosis factor-α (TNF-α) gene polymorphisms and coronary artery disease (CAD) susceptibility. METHODS: Using appropriate keywords, we identified relevant studies using PubMed, Cochrane, Embase, CNKI, VANFUN, and VIP. Key pertinent sources in the literature were also reviewed, and all articles published through April 2019 were considered for inclusion. Based on eligible studies, we performed a meta-analysis of association between 308G/A, 238G/A, 857C/T, 863C/A and 1031 T/C polymorphisms in TNF-α and risk of CAD. RESULTS: We found 25 studies that were consistent with this meta-analysis, including 7697 patients in the CAD group and 9655 control patients. TNF-α 308G/A locus A showed no significant association with CAD susceptibility by the five models in the analysis of the overall population, European, African, South Asian, and North Asian patients. TNF-α 863C/A locus A and 1031 T/C locus C exhibited no significant association with CAD susceptibility. TNF-α 238G/A locus A had no significant association with CAD susceptibility in the overall population. However, TNF-α 238G/A locus A showed significant association with higher CAD susceptibility in the subgroup of Europeans and north Asians. TNF-α 857C/T locus T had no significant association with CAD susceptibility in the analysis of the overall population and Europeans. In the north Asian population, TNF-α 857C/T locus T was associated with lower CAD susceptibility by the heterozygote model. CONCLUSION: TNF-α 308G/A, 857C/T, 863C/A, and 1031 T/C has no significant association with CAD susceptibility. TNF-α 238G/A locus A has significant association with CAD susceptibility in Europeans and north Asians, but has no significant association in the overall population. Studies with a larger sample size are required to confirm the association between TNF-α 238G/A and CAD susceptibility.

Drug-resistant genes carried by Acinetobacter baumanii isolated from patients with lower respiratory tract infection.

BACKGROUND: Acinetobacter baumanii (A. baumanii ) remains an important microbial pathogen resulting in nosocomial acquired infections with significant morbidity and mortality. The mechanism by which nosocomial bacteria, like A. baumanii, attain multidrug resistance to antibiotics is of considerable interest. The aim in this study was to investigate the spread status of antibiotic resistance genes, such as multiple ß-lactamase genes and aminoglycoside-modifying enzyme genes, from A. baumanii strains isolated from patients with lower respiratory tract infections (LRTIs). METHODS: Two thousand six hundred and ninety-eight sputum or the bronchoalveolar lavage samples from inpatients with LRTIs were collected in 21 hospitals in the mainland of China from November 2007 to February 2009. All samples were routinely inoculated. The isolated bacterial strains and their susceptibility were analyzed via VITEK-2 expert system. Several kinds of antibiotic resistant genes were further differentiated via polymerase chain reaction and sequencing methods. RESULTS: Totally, 39 A. baumanii strains were isolated from 2698 sputum or bronchoalveolar lavage samples. There was not only a high resistant rate of the isolated A. baumanii strains to ampicillin and first- and second-generation cephalosporins (94.87%, 100% and 97.44%, respectively), but also to the third-generation cephalosporins (ceftriaxone at 92.31%, ceftazidine at 51.28%) and imipenem (43.59%) as well. The lowest antibiotic resistance rate of 20.51% was found to amikacin. The OXA-23 gene was identified in 17 strains of A. baumanii, and the AmpC gene in 23 strains. The TEM-1 gene was carried in 15 strains. PER-1 and SHV-2 genes were detected in two different strains. Aminoglycoside-modifying enzyme gene aac-3-Ia was found in 23 strains, and the aac-6'-Ib gene in 19 strains. aac-3-Ia and aac-6'-Ib genes hibernated in three A. baumanii strains that showed no drug-resistant phenotype. CONCLUSIONS: A. baumanii can carry multiple drug-resistant genes at the same time and result in multi-drug resistance. Aminoglycoside-modifying enzyme genes could be hibernating in aminoglycoside sensitive strains without expressing their phenotype.