Differences in pulmonary nodular consolidation and pulmonary cavity among drug-sensitive, rifampicin-resistant and multi-drug resistant tuberculosis patients: the Guangzhou computerized tomography study.

Background: Pulmonary nodular consolidation (PN) and pulmonary cavity (PC) may represent the two most promising imaging signs in differentiating multidrug-resistant (MDR)-pulmonary tuberculosis (PTB) from drug-sensitive (DS)-PTB. However, there have been concerns that literature described radiological feature differences between DS-PTB and MDR-PTB were confounded by that MDR-PTB cases tend to have a longer history. This study seeks to further clarify this point. Methods: All cases were from the Guangzhou Chest Hospital, Guangzhou, China. We retrieved data of consecutive new MDR cases [n=46, inclusive of rifampicin-resistant (RR) cases] treated during the period of July 2020 and December 2021, and according to the electronic case archiving system records, the main PTB-related symptoms/signs history was ≤3 months till the first computed tomography (CT) scan in Guangzhou Chest Hospital was taken. To pair the MDR-PTB cases with assumed equal disease history length, we additionally retrieved data of 46 cases of DS-PTB patients. Twenty-two of the DS patients and 30 of the MDR patients were from rural communities. The first CT in Guangzhou Chest Hospital was analysed in this study. When the CT was taken, most cases had anti-TB drug treatment for less than 2 weeks, and none had been treated for more than 3 weeks. Results: Apparent CT signs associated with chronicity were noted in 10 cases in the DS group (10/46) and 9 cases in the MDR group (10/46). Thus, the overall disease history would have been longer than the assumed <3 months. Still, the history length difference between DS patients and MDR patients in the current study might not be substantial. The lung volume involvement was 11.3%±8.3% for DS cases and 8.4%±6.6% for MDR cases (P=0.022). There was no statistical difference between DS cases and MDR cases both in PN prevalence and in PC prevalence. For positive cases, MDR cases had more PN number (mean of positive cases: 2.63 vs. 2.28, P=0.38) and PC number (mean of positive cases: 2.14 vs. 1.38, P=0.001) than DS cases. Receiver operating characteristic curve analysis shows, PN ≥4 and PC ≥3 had a specificity of 86% (sensitivity 25%) and 93% (sensitivity 36%), respectively, in suggesting the patient being a MDR cases. Conclusions: A combination of PN and PC features allows statistical separation of DS and MDR cases.

LncRNA LINC00961 regulates endothelial­mesenchymal transition via the PTEN­PI3K­AKT pathway.

The long noncoding RNA LINC00961 plays a crucial role in cancer and cardiovascular diseases. In the present study, the role and underlying mechanism of LINC00961 in endothelial­mesenchymal transition (EndMT) induced by transforming growth factor beta (TGF­ß), was investigated. Human cardiac microvascular endothelial cells were transfected with LV­LINC00961 or short hairpin LINC00961 plasmids to overexpress or knock down LINC00961 in the cells, respectively. The cells were then exposed to TGF­ß in serum­free medium for 48 h to induce EndMT. Flow cytometric analysis, Cell Counting Kit­8 assay and immunofluorescence staining were performed to examine the cell apoptosis rate, assess cell viability, and identify CD31+/α­SMA+ double­positive cells, respectively. Western blotting and reverse transcription­ quantitative polymerase chain reaction were used to evaluate protein and mRNA expression, respectively. Injury to endothelial cells and EndMT was induced by TGF­ß in a time­dependent manner. LINC00961 overexpression promoted injury and EndMT, whereas LINC00961 knockdown had the opposite effects. Knockdown of LINC00961 attenuated EndMT and injury to endothelial cells induced by TGF­ß via the PTEN­PI3K­AKT pathway. Inhibition of LINC00961 expression may prevent the occurrence of EndMT­related cardiovascular diseases, such as myocardial fibrosis and heart failure. Therefore, LINC00961 shows potential as a therapeutic target for cardiovascular diseases.

Hepatitis C virus core protein impairs metabolic disorder of liver cell via HOTAIR-Sirt1 signalling.

It has been suggested that Hepatitis C virus (HCV) core protein is associated with metabolic disorders of liver cell. However, the precise mechanism is still unclear. The aim of the present study was to explore the impact of HCV core protein on hepatocyte metabolism by HepG2 and the possible involvement of long non-coding (lnc) RNAs in this process. The effect of HCV core protein on lncRNAs expression was examined with quantitative RT-PCR (qRT-PCR). Manipulation of HVC core protein and lncRNA HOTAIR was to evaluate the role of interaction between them on cell metabolism-related gene expression and cellular metabolism. The potential downstream Sirt1 signal was examined by western blotting and qRT-PCR. Our data suggested that suppression of HOTAIR abrogates HCV core protein-induced reduction in Sirt1 and differential expression of glucose- and lipid-metabolism-related genes. Also it benefits for metabolic homoeostasis of hepatocyte indicated by restoration of cellular reactive oxygen species (ROS) level and NAD/NADH ratio. By manipulation of HOTAIR, we concluded that HOTAIR negatively regulates Sirt1 expression through affecting its promotor methylation. Moreover, overexpression of Sirt1 reverses pcDNA-HOTAIR-induced glucose- and lipid-metabolism-related gene expression. Our study suggests that HCV core protein causes dysfunction of glucose and lipid metabolism in liver cells through HOTAIR-Sirt1 signalling pathway.

[Application prospect about bioremediation of polychlorinated biphenyls-contaminated soil with immobilized microorganism technique: a review].

As one type of the persistent organic pollutants, polychlorinated biphenyls (PCBs) are tremendously harmful to organisms. These compounds are easily absorbed onto soil particles and able to accumulate in soil after they are released into the environment. Bioremediation technology of PCBs-contaminated soils has become a research hotspot in recent years, and immobilized microorganism technique has high developing and applying value because of its unique advantages in environmental remediation. This paper reviewed the chief remediation technology of PCBs-contaminated soils and then analyzed the characteristics of immobilized microorganism technique and its research progress in remediation of organic polluted soil. Finally, the feasibility and problems of this technique in remediation of PCBs-contaminated soil were also discussed.

[Association of tumor necrosis factor alpha 308 G/A gene promoter polymorphism with the presence of chronic obstructive pulmonary disease: a meta-analysis].

OBJECTIVE: To investigate the association between the polymorphism of tumor necrosis factor alpha 308 gene (TNF-alpha-308) promoter and the risk of chronic obstructive pulmonary disease (COPD) using the method of meta-analysis. METHOD: The database of Medline and the Chinese biomedicine disc (CBM) were searched for published case-control studies of the association between the polymorphism of TNF-alpha-308 gene promoter and COPD. Data were extracted using a standardized form and the meta-analysis was performed. RESULTS: Eighteen case-control studies, comprising 1606 patients with COPD and 2551 controls (the oriental population: 666 patients with COPD and 898 controls; the Caucasian: 940 patients with COPD and 1653 controls) were included in the meta-analysis. Using a fixed effect model, the pooled result in the oriental population showed that the TNF2 allele was associated with the susceptibility to COPD [odds ratio (OR) = 2.62, 95% confidence interval (95% CI) 2.00 to 3.43]. The OR for COPD susceptibility in TNF1/2 population was significantly increased at 2.44 (95% CI 1.79 to 3.33) compared to the TNF1/1 population. The OR for COPD susceptibility in the TNF1/2 plus TNF2/2 population was significantly increased at 2.78 (95% CI 2.06 to 3.75) compared to the TNF1/1 population. When adjusted for smoking, the result was similar. However, in the Caucasian population, the TNF2 allele was not associated with the susceptibility to COPD (OR = 0.97, 95% CI 0.84 to 1.14). There was no association between the genotype of TNF-alpha-308 and COPD (OR = 0.96, 95% CI 0.79 to 1.16, and OR = 1.03, 95% CI 0.86 to 1.25), compared between the TNF1/2 population, the TNF1/2 plus the TNF2/2 population and the TNF1/1 population respectively. When adjusted for smoking, the result was similar. CONCLUSION: In the oriental population, the TNF2 allele confers a significant risk for developing COPD. There is no association between the polymorphism of TNF-alpha-308 gene promoter and COPD in the Caucasian population.