A rapid, simple, accurate, and affordable method for the detection of drug-resistant tuberculosis is very critical for the selection of antimicrobial therapy and management of patient treatment. High-resolution melting curve analysis has been used for the detection of rifampin resistance in Mycobacterium tuberculosis and has shown promise. We did a systematic review and metaanalysis of published studies to evaluate the accuracy of high-resolution melting curve analysis for the detection of rifampin resistance in clinical M. tuberculosis isolates. We searched the PubMed, BIOSIS Previews, and Web of Science databases to identify studies and included them according to predetermined criteria. We used the DerSimonian-Laird random-effects model to calculate pooled measures and applied Moses' constant for linear models to fit the summary receiver operating characteristic curve. According to the selection criteria, most of the identified studies were excluded, and only seven studies were included in the final analysis. The overall sensitivity of the high-resolution melting curve analysis was 94% (95% confidence interval [CI], 92% to 96%), and the overall specificity was very high at 99% (95% CI, 98% to 100%). The values for the pooled positive likelihood ratio, negative likelihood ratio, and diagnostic odds ratio were 63.39 (95% CI, 30.21 to 133.00), 0.06 (95% CI, 0.04 to 0.09), and 892.70 (95% CI, 385.50 to 2,067.24), respectively. There was no significant heterogeneity across all included studies for the measurements we evaluated. The summary receiver operating characteristic curve for the same data shows an area of 0.99 and a Q* value of 0.97. High-resolution melting curve analysis has high sensitivity and specificity for the detection of rifampin resistance in clinical M. tuberculosis isolates. This method might be a good alternative to conventional drug susceptibility tests in clinical practice.

Cardiovascular disease is the leading cause of human mortality and morbidity worldwide. Atherosclerosis (AS) is the underlying pathological responsible in most acute and severe cardiovascular diseases including myocardial infarction and stroke. However, current drugs applied to the treatment of AS are not clinically effective, and there is a large residual risk of cardiovascular disease and multiple side effects. Increasing evidence supports a close relationship between microorganisms and the incidence of AS. Recent data have shown that probiotics can improve multiple key factors involved in the development and progression of AS, including cholesterol metabolism imbalance, endothelial dysfunction, proinflammatory factor production, macrophage polarization, intestinal flora disturbance, and infection with pathogenic microorganisms, and therefore probiotics have attracted great interest as a novel potential “medicine”. This review is aimed at summarizing the effects of probiotics on various influencing factors, and providing valuable insights in the search for early prevention and potential therapeutic strategies for AS.

Coronary heart disease (CHD) is caused by coronary atherosclerosis and has a high morbidity and mortality rate worldwide. There are challenges in both early screening and treatment of CHD. The appearance and development of CHD is a complex metabolic disorder process. Therefore, to search for new biomarkers of CHD, we analyzed the peripheral blood metabolome in patients with CHD. In the study, a plasma metabolite, 4′-Phosphopantetheine (4-PPanSH), which was discovered by HPLC-MS/MS, as peripheral blood 4-PPanSH decreases, the degree of coronary blockage gradually aggravates. In addition, the 4-PPanSH supplement limited atherosclerotic plaque formation and endothelial injury in mice. Further, in vascular endothelial cells, 4-PPanSH effectively inhibited ROS generation and ox-LDL accumulation. In summary, 4-PPanSH was associated with the degree of coronary stenosis, and the 4-PPanSH supplement reduced atherosclerotic plaque generation, which could be associated with 4-PPanSH acting as a potent antioxidant that inhibits ROS generation and alleviates vascular endothelial injury.

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Dysfunction of the endothelial lining of lesion-prone areas of the arterial vasculature is an important contributor to the pathobiology of atherosclerotic cardiovascular disease. Recent studies have indicated that UDP-glucose pyrophosphorylase 2(UGP2) is implicated in cell proliferation and survival. Here we investigated the anti-apoptosis and anti-atherogenic effect of UGP2 in vitro and in vivo.Here, we explored the effects and mechanisms of UGP2 on apoptosis in endothelial cells by flow cytometer and Western blot analyses. And we engineered ldlr−/−ugp2+/− double-deficient mice to evaluated the apoptosis levels in atherosclerotic lesion. A microarray analysis showed that the expression of UGP2 was reduced in human atherosclerotic plaques. In vitro experiments revealed that TP53 interacted with the promotor region of the UGP2 gene, which upregulated UGP2 expression. Augmentation of UGP2 expression downregulated ROS levels, the expressions of Cleaved caspase-3 and apoptosis levels in endothelial cells, and this inhibitory effects of UGP2 on cell apoptosis could be significantly abolished by H2O2. In vivo experiments using ldlr−/−ugp2+/− mice fed a Western high-fat diet demonstrated that UGP2 deficiency promoted atherosclerosis, and increased the levels of ROS, expressions of Cleaved caspase-3 and apoptosis cells in atherosclerotic lesions. Thus, our results provide evidence for UGP2 as a novel target gene of TP53 contributes to anti-apoptosis effect linking to ROS homeostasis differ from canonical pathway, and we suggested that UGP2 could act as potential therapeutic targets to ameliorate atherosclerosis-related diseases.

Objective: To analyze the nosocomial infection of carbapenem-resistant Klebsiella pneumoniae (CRKP) and the prognosis of patients in a general hospital in 2021. Methods:Using unified diagnostic criteria, 103 cases of CRKP infection in a general hospital in 2021 were investigated, including the clinical epidemiological data of age, sex, and department, and the characteristics of department distribution, infection site, population and prognosis of CRKP were analyzed. Results:As global bacterial resistance rises and widely distributed multiple drug-resistant bacteria, XDR gradually becomes untreatable, which leads to an increase in the number of hospital infections. Through the investigation of hospital infection in clinical departments and related disease areas of our hospital, it was found that the majority of clinical departments have detected multidrug-resistant bacteria, which makes us pay more attention to this phenomenon: A total of 106 strains of CRKP were detected in the whole year (repeated detection of CRKP in different specimens from the same patient was only recorded for the first time). The detection rate of CRKP in hospitals was 13.77%, and male patients were far higher than female patients. The internal medicine unit was the department with a high incidence of CRKP infection. After CRKP infection, 70 patients improved, while 33 patients did not improve (χ2= 9.936, P < 0.01).The main source of specimens and sites of infection is the respiratory tract and lungs. Conclusion: The high-risk population of hospital CRKP infection is male elderly patients, the high-risk department is internal medicine, and the main infection site is the lung. The majority of CRKP patients improved after treatment. Tigecycline and cephalosporins enzyme inhibitor compound preparations are effective in the treatment and prognosis of clinical patients with CRKP infection.

Dysfunction of the endothelial lining of lesion-prone areas of the arterial vasculature is an important contributor to the pathobiology of atherosclerotic cardiovascular disease. Recent studies have indicated that UDP-glucose pyrophosphorylase 2(UGP2) is implicated in cell proliferation and survival. Here we investigated the anti-apoptosis and anti-atherogenic effect of UGP2 in vitro and in vivo.Here, we explored the effects and mechanisms of UGP2 on apoptosis in endothelial cells by flow cytometer and Western blot analyses. And we engineered ldlr–/–ugp2+/– double-deficient mice to evaluated the apoptosis levels in atherosclerotic lesion. A microarray analysis showed that the expression of UGP2 was reduced in human atherosclerotic plaques. In vitro experiments revealed that TP53 interacted with the promotor region of the UGP2 gene, which upregulated UGP2 expression. Augmentation of UGP2 expression downregulated ROS levels, the expressions of Cleaved caspase-3 and apoptosis levels in endothelial cells, and this inhibitory effects of UGP2 on cell apoptosis could be significantly abolished by H2O2. In vivo experiments using ldlr–/–ugp2+/– mice fed a Western high-fat diet demonstrated that UGP2 deficiency promoted atherosclerosis, and increased the levels of ROS, expressions of Cleaved caspase-3 and apoptosis cells in atherosclerotic lesions. Thus, our results provide evidence for UGP2 as a novel target gene of TP53 contributes to anti-apoptosis effect linking to ROS homeostasis differ from canonical pathway, and we suggested that UGP2 could act as potential therapeutic targets to ameliorate atherosclerosis-related diseases.