Effects of Baduanjin Exercise on lung function and 6 min walk in COPD patients: a systematic review and meta-analysis.

COPD is a public health problem of global concern, which seriously affects the quality of life of patients and is also the third leading cause of death from non-communicable diseases. To investigate the effect of Ba duan jin exercise on lung function and the results of a 6-min walking trial in patients with stable COPD. Literature databases such as Web of Science, Embase, PubMed, Cochrane Library, Chinese Biomedical Literature (CBM), CNKI, Wanfang Data and VIP were searched by computer, the search period is up to January 2024. Literature screening, quality evaluation and data extraction were carried out independently by two researchers. And use RevMan 5.3 software and StataMP 18 (64-bit) software to process the relevant outcome indicators. A total of 16 RCT studies with 1184 patients were included. The meta-analysis results showed that compared with the control group, Ba Duan Jin exercise could improve FEV1 (MD = 0.29, 95% CI (0.20, 0.37), P < 0.0001), FEV1/FVC (%) (MD = 3.86, 95% CI (2.24, 5.47), P < 0.00001), and 6-min walking distance (MD = 45.41, 95% CI (33.93, 56.89), P < 0.00001) in stable COPD patients. The results of subgroup analysis based on the duration of the intervention cycle, research quality, and intervention frequency showed that periodic Ba Duan Jin exercise can significantly improve the relevant lung function levels to varying degrees. At the same time, the intervention effect of Ba Duan Jin exercise during the implementation process is also affected by the duration of the exercise cycle, exercise frequency, and the completion of the exercise plan. Ba Duan Jin exercise has a positive improvement effect on lung function and 6-min walking distance in stable COPD patients. In the process of exercise implementation, attention should be paid to cultivating exercise habits, stabilizing and improving attendance rates, and strictly implementing training techniques to achieve the best clinical outcomes for these patients.

Retracted: Long Chain Non-Coding RNA (lncRNA) HOTAIR Knockdown Increases miR-454-3p to Suppress Gastric Cancer Growth by Targeting STAT3/Cyclin D1.

This publication has been retracted by the Editor due to the identification of non-original figure images and manuscript content that raise concerns regarding the credibility and originality of the study and the manuscript. Reference: Jiang, He Li, Heping Xiang, Ming Gao, Chunlin Yin, Haiping Wang, Yuansong Sun, Maoming Xiong. Long Chain Non-Coding RNA (lncRNA) HOTAIR Knockdown Increases miR-454-3p to Suppress Gastric Cancer Growth by Targeting STAT3/Cyclin D1. Med Sci Monit, 2019; 25: 1537-1548. DOI: 10.12659/MSM.913087.

Differential expression profile analysis of cisplatin­regulated miRNAs in a human gastric cancer cell line.

Cisplatin, one of the most commonly used drugs in combination chemotherapy, is an effective anti­tumor agent widely used for diverse tumor types. MicroRNAs (miRNAs/miRs) are involved in the occurrence, development, diagnosis and treatment of cancer. Therefore, the aim of the current study was to explore whether cisplatin exerts anticancer effects by causing differential expression of miRNAs in human gastric cancer cells. The human gastric cancer cell line NCI­N87 was cultured with a certain dose of cisplatin and high­throughput sequencing combined with reverse transcription­quantitative polymerase chain reaction (RT­qPCR) was performed to detect cisplatin­regulated miRNAs. miRNAs upregulated and downregulated following cisplatin exposure were analyzed. High­throughput sequencing revealed 33 upregulated and 16 downregulated miRNAs. A total of five significantly upregulated and five significantly downregulated miRNAs were identified by RT­qPCR. The expression levels of hsa­miR­1246 and hsa­miR­892b were consistent with the results obtained from high­throughput sequencing. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway clustering of cisplatin­regulated miRNAs revealed that the miRNAs regulated genes involved in several biological processes and signaling pathways. The results obtained in the current study suggested that cisplatin may exert an important anticancer effect in gastric cancer via complex biological processes and signaling pathways.

Long Chain Non-Coding RNA (lncRNA) HOTAIR Knockdown Increases miR-454-3p to Suppress Gastric Cancer Growth by Targeting STAT3/Cyclin D1.

BACKGROUND Gastric cancer is a common gastrointestinal tumor. The incidence and mortality of gastric cancer are very high. Therefore, it is important to study targeted drugs. Recent studies found long chain non-coding RNA (lncRNAs) and microRNAs (miRNAs) were abnormal in gastric cancer. MATERIAL AND METHODS We collected adjacent normal and cancer tissues of gastric cancer patients and measured HOTAIR, miR-454-3p, STAT3, and Cyclin D1 expression and analyzed the correlation with clinical status. We also measured AGS and SGC7901 cells proliferation rate of different groups by MTT assay, and we evaluated AGS and SGC7901 cell apoptosis and cell cycle by flow cytometry. In addition, we assessed the relative proteins expressions by WB assay. Finally, we explored the correlation between miR-454-3p and STAT3 by use of double luciferase reporter. RESULTS lncRNA HOTAIR was negatively correlated with miR-454-3p expression in gastric cancer tissues. lncRNA HOTAIR knockdown suppressed AGS and SGC7901, which are gastric cancer cell lines that promote cell proliferation by increasing cell apoptosis and keeping the cell cycle in G1 phase. In further mechanism research, we found that the STAT3 and Cyclin D1 proteins expressions were suppressed by lncRNA HOTAIR down-regulation in AGS and SGC7901 cells. CONCLUSIONS Our results suggest that lncRNA HOTAIR knockdown stimulates miR-454-3p expression to inhibit gastric cancer growth by depressing STAT3/Cyclin D1 activity.

CD4 + CD25 + CD127 high cells as a negative predictor of multiple organ failure in acute pancreatitis.

BACKGROUND: It has been suggested that severity of the immune response induced by immune cells is associated with morbidity and mortality from acute pancreatitis. The authors investigated and evaluated the relationship between distinct peripheral lymphocyte subsets at admission and clinical outcome prior to hospital discharge so as to find a predictor to the prognosis of acute pancreatitis in lymphocyte profile. METHODS: Lymphocyte subsets in admission peripheral venous blood were tested through flow cytometry on 48 patients with acute pancreatitis. Clinical data was recorded as well. The primary observational outcomes were multiple organ failure (MOF) and infection. RESULTS: There was a significant difference in natural killer cells between two subgroups sorted by the presence or absence of infection (25.5 ± 4.47 [95% CI 14.4, 36.6] vs 14.8 ± 7.62 [95% CI 12.5,1 7.1] p = 0.021). Patients who developed MOF had lower CD4 + CD25 + CD127high (4.49 ± 1.5 (MOF) [95% CI 3.83, 5.16] vs 6.57 ± 2.65 (non-MOF) [95% CI 5.5, 7.64] p = 0.002) and higher CD127low/high cell counts (1.35 ± 0.66 [95% CI 1.06, 1.65] vs 0.97 ± 0.44 [95% CI 0.79, 1.15] p = 0.02). MOF patients were significantly older (55 ± 14.58 [95% CI 48.49,61.42] vs 46 ± 15.59 [95% CI 39.39,51.99] p = 0.04), and had higher Acute Physiology and Chronic Health Evaluation IIscores (7 ± 3.66 [95% CI 5.5,7.64] vs 4 ± 2.89 [95% CI 2.45,4.78] p = 0.001) and C reactive protein (100.53 ± 94.38 [95% CI 58.69,142.48] vs 50.8 ± 59.2 [95% CI 26.88,74.71] p = 0.04). In a multivariate regression model, only CD4 + CD25 + CD127high cell was a significant predictor of non-MOF. For the detection of non-MOF, CD4 + CD25 + CD127high cell generated a receiver operating characteristic (ROC) curve with an area under the curve of 0.74. CONCLUSION: CD4 + CD25 + CD127high cell at early phase of acute pancreatitis yields good specificity in detecting non-MOF at a suggested cutoff value 6.41%. Patients with fewer natural killer cells may be at risk in developing secondary infection.

HSP90 and SIRT3 expression in hepatocellular carcinoma and their effect on invasive capability of human hepatocellular carcinoma cells.

OBJECTIVE: To vexplore expression of HSP90, SIRT3 in liver cancer tissue and its effect on liver cancer cell invasion ability. METHODS: Moderate expression of HSP90 in SMMC-7721, HepG2, LO2 and Hep-3B cell lines were screened, which was validated by RT-PCR. Over-expression of HSP90 cell line and lentivirus packaging HSP90-RNAi were established, which was validated by RT-PCR and western blot. The level of epithelial-mesenchymal transition (EMT) related gene was detected by western blot. The percentage of cancer stem cells was assayed by flow cytometry. RESULTS: RT-PCR demonstrated the highest expression of HSP90 mRNA in SMMC-7721 cells, the lowest expression of HSP90 mRNA in Hep3B and LO2 and the moderate expression of HSP90 mRNA in Hep-G2. Therefore, HepG2 was selected as a follow-up experiment cell lines. Compared with the blank control group, expression of HSP90 in HSP overexpression group was increased obviously, and expression of HSP90 in HSP90 shRNA group was significantly decreased, which indicated successful establishment of HSP overexpression and shRNA group. The apoptotic cell in hsp-siRNA group was higher than the blank control group, while the HSP overexpression group showed opposite results. Western blot results showed transfection HSP promoted cells EMT transformation, up-regulated the level of E-cadherin, and down-regulated the level of Vimentin; meanwhile, shRNA group showed opposite results. CONCLUSIONS: Carcinoma HepG2 cell transfected high expression of HSP can promote the transformation of EMT, improve the expression of Vimentin, reduce the expression of E-cadherin, and inhibit apoptosis of cancer stem cells, which improve the invasive ability of cancer of the liver cells. While hsp-siRNA group presents opposite results. In summary, the expression of HSP is closely related to the occurrence, development and invasion of cancer of the liver tissue.

Expression and functional perspectives of miR-184 in pancreatic ductal adenocarcinoma.

Pancreatic ductal adenocarcinoma (PDAC) is one of the most aggressive malignant tumors, with its 5-year survival rate lower than 5%. MicroRNAs (miR) have been known as important regulators for the tumorigenesis, progression, invasion and metastasis of various cancers. MiR-184 was found to be abnormally expressed in various cancers including glioma and oral carcinoma. The expression and functional role of miR-184 in PDAC, however, remains unclear. PDAC cell line PANC-1 was transfected with miR-184 inhibitor. Real-time PCR was used to detect the expression of miR-184 in untreated PANC-1, miR-184 inhibitor transfected PANC-1 and controlled normal pancreatic ductal epithelial cell line HPDE6c7. MTT assay was used to detect the effect of miR-184 on the proliferation of PANC-1 cells, while invasion assay and Western blotting were employed to describe the effect on cell invasion ability and expression of caspase-3, respectively. In PANC-1 cells, miR-184 was abundantly expressed. The transfection of inhibitor effectively suppressed the expression of miR-184, and further inhibited both cell proliferation and invasion abilities, in addition to the up-regulation of pro-apoptotic protein caspase 3 expression. The up-regulation of miR-184 in PDAC may facilitate the proliferation and invasion ability, and inhibit apoptosis of tumor cells, thus potentiating the occurrence and development of PDAC. MiR-184, therefore, is a potential molecular target for therapy.

Lack of association of IGFBP-3 gene polymorphisms with colorectal cancer: evidence from 17,380 subjects.

Published data on the association of IGFBP-3 gene polymorphisms with colorectal cancer (CRC) are inconclusive. We conducted a meta-analysis to derive a precise estimation of the association. A literature search that included PubMed, EMBASE, Elsevier Science Direct and China National Knowledge Infrastructure was conducted to identify studies up to October 15, 2013. Summary odds ratios (ORs) and 95 % confidence intervals (95 % CIs) for IGFBP-3 gene polymorphisms and CRC were calculated in a fixed effect model or a random effect model. We identified 10 separate studies including 7,000 cases and 10,380 controls using search. Meta-analysis was performed for two IGFBP-3 gene polymorphisms (rs2854744 and rs2854746). We found no association between IGFBP-3 gene rs2854744 polymorphism and CRC (P > 0.05). Similar result was observed between rs2854746 polymorphism and CRC (P > 0.05). This meta-analysis demonstrates that there is no association of IGFBP-3 gene rs2854744 and rs2854746 polymorphisms with CRC risk.

Association of CDKN1B gene polymorphisms with susceptibility to breast cancer: a meta-analysis.

A number of case­control studies have been conducted to investigate the association of CDKN1B gene polymorphisms with breast cancer. However, these studies reported conflicting results. The aim of our study was to quantitatively summarize the association of CDKN1B gene polymorphisms with breast cancer. Systemic searches of the PubMed, Excerpta Medica Database, and Chinese Biomedical Literature Database databases were performed, with the last report up to Oct 2012. Odds ratios (ORs) with 95 % confidence intervals (CIs) were used to assess the strength of the association. Seven studies including 6,822 cases and 7,186 controls were involved in this meta-analysis, which was performed for two CDKN1B gene polymorphisms (rs2066827 and rs34330). Significant association was found for rs34330 polymorphism (T versus C: OR = 1.10, 95 % CI = 1.03­1.18, P = 0.003; CT + TT versus CC: OR = 1.38, 95 % CI = 0.98­1.93, P = 0.07; TT versus CC + CT: OR = 1.06, 95 % CI = 0.93­1.21, P = 0.38; TT versus CC: OR = 1.23, 95 % CI = 1.04­1.45, P = 0.02; CT versus CC: OR = 1.42, 95 % CI = 0.97­2.09, P = 0.07), but not for rs2066827 polymorphism (G versus T: OR = 0.99, 95 % CI = 0.91­1.08, P = 0.84; TG + GG versus TT: OR = 0.98, 95 % CI = 0.89­1.08, P = 0.69; GG versus TT + TG: OR = 1.04, 95 % CI = 0.83­1.30, P = 0.75; GG versus TT: OR = 1.03, 95 % CI = 0.82­1.30, P = 0.77; TG versus TT: OR = 0.97, 95 % CI = 0.88­1.08, P = 0.58). This meta-analysis suggests that breast cancer may be associated with CDKN1B gene rs34330 polymorphism, but not rs2066827 polymorphism.

Meta-analysis of CHEK2 1100delC variant and colorectal cancer susceptibility.

Cell cycle checkpoint kinase 2 (CHEK2) gene has been inconsistently associated with colorectal cancer (CRC), particularly the 1100delC variant. To generate large-scale evidence on whether the CHEK2 1100delC variant is associated with CRC susceptibility we have conducted a meta-analysis. Data were collected from the following electronic databases: PubMed, Excerpta Medica Database and Chinese Biomedical Literature Database, with the last report up to November 2010. The odds ratio (OR) and its 95% confidence interval (95% CI) were used to assess the strength of association. We evaluated the contrast of carriers versus non-carriers. Meta-analysis was performed in a fixed/random effect model by using the software Review Manager 4.2. A total of six studies including 4194 cases and 10,010 controls based on the search criteria were involved in this meta-analysis. A significant association of the CHEK2 1100delC variant with unselected CRC was found (OR=2.11, 95% CI=1.41-3.16, P=0.0003). We also found an association of the CHEK2 1100delC variant with familial CRC (OR=2.80, 95% CI=1.74-4.51, P<0.0001). However, the association was not established for sporadic CRC (OR=1.45, 95% CI=0.49-4.30, P=0.50). This meta-analysis demonstrates that the CHEK2 1100delC variant may be an important CRC-predisposing gene, which increases CRC risk.