ABSTRACT
Objective: This study sought to determine the mean prognostic usefulness of seleniumphosphate synthase (SEPHS1) by investigating its expression in 33 human malignancies and its relationship to tumor immunity.Methods: The expression of selenophosphate synthase 1 (SEPHS1) in 33 human malignant tumors was examined using the Genotype-Tissue Expression (GTEx), Cancer Genome Atlas (TCGA), and TIMER databases. Furthermore, the TCGA cohort was used to investigate relationships between SEPHS1 and immunological checkpoint genes (ICGs), tumor mutation burden (TMB), microsatellite instability (MSI), and DNA mismatch repair genes (MMRs). To establish independent risk factors and calculate survival probabilities for liver hepatocellular carcinoma (LIHC) and brain lower-grade glioma (LGG), Cox regression models and Kaplan-Meier curves were utilized. Eventually, the Genomics of Cancer Drug Sensitivity (GDSC) database was used to evaluate the drug sensitivity in LGG and LIHC patients with high SEPHS1 expression.Results: Overall, in numerous tumor tissues, SEPHS1 was highly expressed, and it significantly linked with the prognosis of LGG, ACC, and LIHC (P < .05). Furthermore, in numerous cancers, SEPHS1 expression was linked to tumor-infiltrating immune cells (TIICs), TMB, MSI, and MMRs. According to univariate and multivariate Cox analyses, SEPHS1 expression was significant for patients with LGG and LIHC.Conclusion: High SEPHS1 expression has a better prognosis for LGG, while low SEPHS1 expression has a better prognosis for LIHC. Chemotherapy was advised for LGG patients, particularly for those with high SEPHS1 expression because it can predict how responsive patients will be to 5-Fluorouracil and Temozolomide. This interaction between SEPHS1 and chemoradiotherapy has a positive clinical impact and may be used as evidence for chemotherapy for LGG and LIHC patients.
Subject(s)
Carcinoma, Hepatocellular , Glioma , Liver Neoplasms , Selenium , Humans , PhosphatesABSTRACT
Kashin-Beck disease (KBD) is a nutrition-related osteoarthropathy, and selenium (Se) deficiency is an environmental risk factor for KBD. Notch/Hes1 signaling pathway plays a vital role in regulating cartilage, but its exact mechanisms in KBD remain unknown. The Se contents were determined using the hydride atomic fluorescence spectrometry assay technique, and the mRNA levels were detected via quantitative real-time PCR. The chondrocyte injury models were established by Se deficiency and tert-butyl hydroperoxide (tBHP), respectively; apoptosis and necrosis rates were detected using Hoechst 33,342/PI and Annexin V-FITC/PI. The results showed that the Se levels in the flour of KBD areas were lower than that of the non-KBD areas, and the Se levels in the plasma of KBD patients were lower than that of the controls. The expressions of Notch1, Jagged1, and Hes1 were higher in the whole blood of KBD patients than those of the controls, and Notch1 was negatively correlated with the expression of BCL2, while was positively correlated with BAX. In injury, chondrocytes induced by low Se and tBHP, the expression of Notch1, Jagged1, and Hes1 increased, apoptosis and necrosis rates increased in Se deficiency and tBHP groups, while Se supplementation reversed it. Decreased plasma Se in KBD patients may be related to low dietary Se. Se deficiency might be involved in the pathological process of KBD by activating the Notch/Hes1 signaling pathway to induce excessive apoptosis of chondrocytes, the activation of Notch/Hes1 promotes oxidative injury, and Se supplementation could reverse it. The importance of Notch/Hes1 signaling pathway in KBD development will provide a new potential target for KBD.
Subject(s)
Kashin-Beck Disease , Selenium , Humans , Cartilage/metabolism , Cartilage/pathology , Kashin-Beck Disease/metabolism , Necrosis , Selenium/deficiency , Selenium/metabolism , Selenium/pharmacology , Signal Transduction , Transcription Factor HES-1/metabolism , Receptors, NotchABSTRACT
BACKGROUND: Selenium (Se) is a vital trace element playing its biological functions through selenoprotein, which has been implicated in various physiological and pathological processes. A growing number of studies indicate that low Se increases the risk of cardiovascular diseases (CVDs). This meta-analysis aimed to compare and analyze differences in Se levels between patients with heart failure (HF), myocardial infarction (MI), coronary heart disease (CHD), and healthy people. This will provide ideas with the potential to improve clinical intervention and prevention of CVDs. METHODS: The PubMed, Embase, Chinese National Knowledge Infrastructure (CNKI) and Chinese Biomedical databases were systematically searched for relevant publications until November 20, 2020. The following combination keywords were used: "(heart failure disease OR myocardial infarction OR coronary heart disease) AND (selenium OR Se)". The identified studies were screened against inclusion and exclusion criteria and extracted data were analyzed using RevMan5.3 and State 16.0 software. RESULTS: A total of 49 eligible studies (including 61 cohorts) were obtained. Results of the meta-analysis showed that there was a significant difference in Se levels between HF, MI, CHD patients and healthy people. The standard mean difference (SMD) level of Se in HF patients [SMD = -0.98, 95 % CI (-1.34, -0.62)], MI patients [MI: SMD = -3.46, 95 % CI (-4.43, -2.85)], and CHD patients [CHD: SMD = -0.47, 95 % CI (-0.64, -0.28)] were all significantly lower compared to healthy controls. Analysis of the correlation between Se level and publication year showed that SMD of Se levels in HF and controls was positively correlated with time. Se level was found to be a good diagnostic marker of MI (AUC = 0.7107, P = 0.0167, Sensitivity = 77.27 %, Specificity = 72.73 %). CONCLUSIONS: This meta-analysis shows that Se levels in patients with HF, MI, and CHD are generally lower compared with healthy controls. However, due to the small number of included studies, further studies are needed to confirm the present results.
Subject(s)
Cardiovascular Diseases , Coronary Disease , Myocardial Infarction , Selenium , Trace Elements , Cardiovascular Diseases/diagnosis , Humans , Myocardial Infarction/prevention & controlABSTRACT
OBJECTIVE: Kashin-Beck disease (KBD) is an endemic osteoarthropathy, in which excessive apoptosis of chondrocytes occurs. O6-methylguanine-DNA methyltransferase (MGMT), a DNA damage repair gene, plays an important role in apoptosis, but the mechanism is unclear in KBD cartilage injury. This study was to investigate the expression and promoter methylation of MGMT in KBD patients and its role in DNA damage and apoptosis of chondrocytes. METHODS: MGMT mRNA and protein level were detected by quantitative real-time PCR and immunohistochemistry. Demethylation of MGMT was carried out using 5-Aza-2'-deoxycytidine, and the methylation level of MGMT promoter was measured by quantitative methylation specific PCR. Next, small hairpin RNA was used to knockdown the expression of MGMT. Cell viability, apoptosis and DNA damage were determined by MTT assay, flow cytometry, Hoechst 33342 staining and alkaline comet assay following T-2 toxin and selenium treatment. RESULTS: MGMT protein expression and mRNA levels were decreased (P = 0.02, P = 0.007) and promoter methylation was increased (P = 0.008) in KBD patients. Meanwhile, MGMT level was upregulated by 5-Aza-2'-deoxycytidine in chondrocytes (P = 0.0002). DNA damage and apoptosis rates were increased in MGMT-silenced chondrocytes (all P < 0.0001). Furthermore, DNA damage and apoptosis were increased in chondrocytes treated with T-2 toxin (all P < 0.0001), but were decreased after selenium treatment (P < 0.0001, P = 0.01). Decreased mRNA level and increased methylation of MGMT were found in the T-2 toxin group (P = 0.005, P = 0.002), while selenium reversed it (P = 0.02, P = 0.004). CONCLUSIONS: MGMT might play a crucial part in the pathogenesis of KBD cartilage injury, which could provide a therapeutic target for KBD.
Subject(s)
Cartilage, Articular , Kashin-Beck Disease , Selenium , T-2 Toxin , Cartilage, Articular/metabolism , Chondrocytes/metabolism , DNA , DNA Methylation , Decitabine/pharmacology , Down-Regulation , Guanine/analogs & derivatives , Humans , Kashin-Beck Disease/genetics , Kashin-Beck Disease/metabolism , Kashin-Beck Disease/pathology , RNA, Messenger/metabolism , T-2 Toxin/metabolismABSTRACT
BACKGROUND: This updated and comprehensive meta-analysis study sought to explore the changes of seven essential trace elements, including selenium (Se), iron (Fe), zinc (Zn), manganese (Mn), fluorine (F), iodine (I) and copper (Cu) in Kashin-Beck disease (KBD) patients compared with healthy individuals. The findings of the current study will provide a valuable reference for implementation of early clinical intervention and prevention of KBD. METHODS: All related articles included in this review were retrieved from the following databases: Chinese National Knowledge Infrastructure (CNKI), Wan Fang Data, China Biology Medicine disc (CBM disc), PubMed and Web of Science up to April 30, 2020. The following combination keywords were used as the search criteria: "(Kashin-Beck disease OR KBD) AND ((selenium OR iron OR zinc OR manganese OR fluorine OR iodine OR copper) OR (Se OR Fe OR Zn OR Mn OR F OR I OR Cu))". All statistical analyses were performed using RevMan 5.3 and Stata 16.0 software. RESULTS: A total of 55 articles were included in the current study. Meta-analysis showed that the levels of serum Se (SMD = -2.37, 95 % CI: -1.58 to -0.72, P < 0.00001), hair Se (SMD = -2.19, 95 % CI: -3.05 to -1.33, P < 0.00001), urinary Se (SMD = -2.36, 95 % CI: -3.26 to -1.46, P < 0.00001) and erythrocyte Se (SMD = -5.12, 95 % CI: -9.55 to -0.69, P = 0.02) were significantly lower in KBD patients compared with the levels in healthy controls. Then, the findings showed that the levels of serum F (SMD = -0.58, 95 % CI: -1.04 to -0.12, P = 0.01) and hair I (SMD = -0.57, 95 % CI: -1.06 to -0.08, P = 0.02) in patients were substantially lower than that in controls. Analysis showed that the levels of hair Zn (SMD = 0.26, 95 % CI: 0.04 to 0.49, P = 0.02) and hair Mn (SMD = 0.55, 95 % CI: 0.24 to 0.85, P = 0.0005) were markedly higher in patients compared with the levels in healthy controls. Notably, urinary Se (AUC = 0.7851, P = 0.0235, Sensitivity = 81.82 %, Specificity = 81.82 %) showed a good diagnostic value for KBD. CONCLUSIONS: The findings of the current study showed that the levels of Se, serum F and hair I were lower in patients with KBD compared with those in healthy controls, whereas the levels of hair Zn and hair Mn were higher in KBD patients compared with the levels in controls. This outcome would be further validated in our future studies. Of note, these results indicated that Se, F and I deficiencies were associated with the pathogenesis of KBD.
Subject(s)
Iodine , Kashin-Beck Disease , Selenium , Trace Elements , Copper , Fluorine , Humans , Iron , Manganese , ZincABSTRACT
Kashin-Beck disease (KBD) is a chronic, degenerative osteoarthropathy related to selenium (Se) deficiency. Se participates in the synthesis of selenoprotein in the form of selenocysteine. In total, 25 selenoproteins, encoded by 25 genes, are currently found in humans; however, the effects of selenoprotein genes on chondrocyte apoptosis, particularly in apoptosis-related genes, remain poorly elucidated. Therefore, in the current study, the expression of selenoprotein genes and apoptosis-related genes were determined by RT-qPCR in patients and chondrocytes and the correlations between them were analyzed using Pearson and Spearman's rank correlation, and the chondrocyte apoptosis rate was detected by Annexin V-FITC/PI. The results showed that the mRNA levels of 17 selenoprotein genes were downregulated, whereas two genes were upregulated in patients with KBD. The BAX/BCL2 ratio and the mRNA levels of BAX and P53 were increased, but the mRNA levels of BCL2 and NF-κB p65 were decreased in patients with KBD. The mRNA levels of GPX2, GPX3, DIO1, TXNRD1, TXNRD3, and SPS2 were most closely associated with apoptosis-related genes in patients with KBD. Moreover, in the Se deficiency group, the mRNA levels of GPX3, DIO1, and TXNRD1 were downregulated and GPX activity was decreased, but the late apoptosis rate, the mRNA levels of BAX and P53, and the BAX/BCL2 ratio were increased; the opposite trend was observed in the Se supplement group. Collectively, these results indicate that selenoprotein transcription profile is dysregulated in patients with KBD. Furthermore, the expression of GPX3, DIO1, and TXNRD1 genes might be involved in the development of chondrocyte apoptosis by affecting antioxidant capacity.
Subject(s)
Kashin-Beck Disease , Selenium , Apoptosis/genetics , Chondrocytes/metabolism , Humans , Kashin-Beck Disease/genetics , Kashin-Beck Disease/metabolism , Selenium/pharmacology , Selenoproteins/genetics , Selenoproteins/metabolismABSTRACT
BACKGROUND: The combination of Traditional Chinese medicine and Western medicine (TCM+WM) has been widely used in the treatment of glomerulosclerosis, but the results are still controversial. This study will assess the clinical efficacy of TCM+WM for glomerulosclerosis and provide evidence-based medical data via meta-analysis. METHOD: The MEDLINE, EMBASE, PubMed, Cochrane Central Registry of Controlled Trials, and multiple Chinese databases (Wan Fang, CNKI, and VIP) were searched for randomized controlled trials (RCT) that compared the effects of WM and TCM+WM. Review Manager 5.3 software was used for the meta-analysis of selected studies, and appropriate tests were performed to determine the quality, heterogeneity and sensitivity of these studies. RESULTS: Sixteen RCTs met the inclusion criteria and were selected for the analysis. Compared with the placebo or WM-treated glomerulosclerosis patients, TCM+WM intervention significantly improved renal function indices including 24-hour urine protein quantity (24âh U-Pro), serum creatinine (Scr), blood urea nitrogen (BUN), creatinine clearance (Ccr). In addition, the serum albumin (ALB), triglyceride (TG), and cholesterol (CHOL) levels were also significantly improved (Pâ<â.05) in patients receiving the combination therapy. Finally, the combination of TCM+WM reduced the indices of glomerulosclerosis more effectively compared with WM alone. CONCLUSION: The combination of TCM+WM can significantly improve the renal function and prognosis of patients with glomerulosclerosis.
Subject(s)
Drugs, Chinese Herbal/therapeutic use , Glomerulosclerosis, Focal Segmental/drug therapy , Medicine, Chinese Traditional/methods , Combined Modality Therapy , Humans , Randomized Controlled Trials as TopicABSTRACT
OBJECTIVE: To conduct a meta-analysis evaluating the effect of combining traditional Chinese medicine (TCM) with Western medicine in treating hepatitis C, and to provide an evidence-based medical strategy. METHODS: Randomized controlled trials (RCTs) comparing the effect of pegylated interferon (Peginterferon) combined with ribavirin (PR) alone and its combination with TCM were manually retrieved from the Weipu Information Resources System (VIP), Wan Fang Database, PubMed, and the Chinese Journal Full Text Database (CNKI). Studies meeting the inclusion criteria were selected and analyzed using the Review Manager 5.3 software. Suitable tests were also performed to determine the quality, heterogeneity, and sensitivity of the studies included in the meta-analysis. RESULTS: Twenty-eight RCTs met the inclusion criteria. The combination therapy or intervention group showed significantly greater HCV-RNA negative rate post-treatment compared to the monotherapy or the control group (Pâ<â.05). In addition, the serum levels of the liver function indicators alanine aminotransferase (ALT), aspartate aminotransferase (AST), and albumin (ALB) were significantly improved after the combination therapy compared to PR alone (Pâ<â.05), while total bilirubin (TB) and r-glutamyltransferase (GGT) levels were not affected by TCM (Pâ>â.05). Finally, the parameters of liver fibrosis were also reduced by the combination therapy more effectively than the monotherapy. CONCLUSION: The combination of TCM and PR can improve the Comprehensive Clinical Efficacy of hepatitis C and have a better negative rate of HCV-RNA with a better benefit in the liver function. The effect of TCMâ+âPR is better than that of PR alone in treating hepatitis C.
Subject(s)
Antiviral Agents/therapeutic use , Hepatitis C/therapy , Medicine, Chinese Traditional , Alanine Transaminase/blood , Aspartate Aminotransferases/blood , Bilirubin/blood , Combined Modality Therapy , Drug Therapy, Combination , Hepacivirus/genetics , Humans , Interferon-alpha/therapeutic use , Liver Cirrhosis/drug therapy , Polyethylene Glycols/therapeutic use , RNA, Viral/blood , Recombinant Proteins/therapeutic use , Ribavirin/therapeutic use , Serum Albumin , gamma-Glutamyltransferase/bloodABSTRACT
OBJECTIVE: To evaluate the differences between traditional Chinese medicine combined with western medicine and western medicine alone for the treatment of secondary tuberculosis and its impact on the evaluation of clinical efficacy and safety of patients in randomized controlled trials. METHODS: A literature search of all major academic databases was conducted (PubMed, CNKI, Wanfang, VIP). Meta-analysis was conducted using RevMan 5.3 and Stata 12.0 software for those studies that satisfied the inclusion criteria. Ethical approval was not necessary because no people or animals were selected as subjects in this meta-analysis. RESULTS: Twenty-three randomized controlled trials were included in this meta-analysis. The following indicators in the treatment group (traditional Chinese medicine decoction combined with western medicine chemotherapy) improved in comparison with those in the control group:focus absorption rate (RR:1.18; 95% CI: 1.15-1.22);sputum smear negative rate (RR: 1.17; 95% CI: 1.09-1.27);comprehensive clinical effective rate (RR: 1.18; 95% CI: 1.14-1.22);cavity closure rate (RR: 1.37; 95% CI: 1.12-1.67).The difference of Immune function indicator likes CD4+ level (SMD: 0.76; 95% CI: -0.25 to 1.76) between the treatment group and the control group was not significant. In addition, safety evaluation indicators like the decrease rate of white blood cell (WBC) and platelets (PLT) and the elevation rate of alanine aminotransferase (ALT) and uric acid (UA) in the treatment group were reduced compared with those in the control group (Pâ<â.05). CONCLUSIONS: The curative effect of combining traditional Chinese and western medicine for the treatment of secondary tuberculosis is better than that of western medicine alone and is conducive to reducing the incidence of adverse reactions.
Subject(s)
Antitubercular Agents/therapeutic use , Drugs, Chinese Herbal/therapeutic use , Tuberculosis, Pulmonary/drug therapy , Alanine Transaminase/blood , Antitubercular Agents/adverse effects , CD4 Lymphocyte Count , Drug Therapy, Combination , Drugs, Chinese Herbal/adverse effects , Humans , Phytotherapy , Platelet Count , Randomized Controlled Trials as Topic , Sputum/microbiology , Treatment Outcome , Tuberculosis, Pulmonary/diagnostic imaging , Tuberculosis, Pulmonary/immunology , Uric Acid/bloodABSTRACT
The aim of the study was to investigate the association between rs5859 in Sep15, rs1139793 in TrxR2 polymorphisms with the risks of KBD and to detect the expression of AP-1 pathway in KBD subjects and in vitro. 208 KBD and 206 control subjects were included. PCR-Restriction Fragment Length Polymorphism (RFLP), Amplification Refractory Mutation Specific-PCR (ARMS-PCR) and Western Blotting were conducted. The results showed the minor A-allele frequency of rs5859 in KBD was statistically significantly higher than that in the control group (Pâ¯<â¯0.05). The cases carrying A-allele had a 2-fold (95%CI: 1.064-3.956) increased risk of developing KBD compared with the G-allele carriers. There was no significant difference in genotype and allele distribution of rs1139793 between KBD patients and controls (Pâ¯>â¯0.05). The frequency of the minor A allele of rs5859 was significantly different in Chinese healthy population compared with European, African and American. The frequency of the minor A allele of rs1139793 showed significant difference when compared with African and American. The levels of JunB, JunD, P65 proteins in KBD group were higher than those in control group (Pâ¯<â¯0.0001). The expression of JunB, JunD, P65 proteins all increased in tBHP-induced C28/I2 oxidative damage model compared with control group (Pâ¯<â¯0.05) and decreased after Se supplementation. Our finding indicated Sep15 is a possible candidate susceptibility gene for KBD. Combined with the in vitro study, our studies reveal novel insights into the mechanism of Se supplementation as an antioxidant via inhibiting the AP-1 signaling pathway in patients with KBD.
Subject(s)
Genetic Predisposition to Disease , Kashin-Beck Disease/genetics , Polymorphism, Single Nucleotide/genetics , Selenoproteins/genetics , Signal Transduction , Thioredoxin Reductase 2/genetics , Transcription Factor AP-1/metabolism , Apoptosis/drug effects , Case-Control Studies , Cell Line , Chondrocytes/drug effects , Chondrocytes/metabolism , Ethnicity/genetics , Female , Gene Frequency , Humans , Male , Middle Aged , Selenium/pharmacologyABSTRACT
OBJECTIVE: Selenium deficiency is a risk factor for Kashin-Beck Disease (KBD), an endemic osteoarthropathy. Although promoter hypermethylation of glutathione peroxidase 3 (GPX3) (a selenoprotein) has been identified in several cancers, little is known about promoter methylation and expression of GPX3 and their relation to selenium in KBD. The present study was thus conducted to investigate this research question. METHODS: Methylation and expressions of GPX3 in whole blood drawn from 288 KBD patients and 362 healthy controls and in chondrocyte cell line were evaluated using methylation-specific PCR and qRT-PCR, respectively. The protein levels of PI3K/Akt/c-fos signaling in the whole blood and chondrocyte cell line were determined with Western blotting. Chondrocytes apoptosis were detected by Hoechst 33342 and Annexin V-FITC/PI staining. RESULTS: GPX3 methylation was increased, GPX3 mRNA was decreased, and protein levels in the PI3K/Akt/c-fos signaling pathway were up-regulated in the whole blood collected from KBD patients as compared with healthy controls. Similar results were obtained for chondrocytes injured by oxidative stress. There was a significant, decreasing trend in GPX3 expression across groups of unmethylation, partial methylation, and complete methylation for GPX3, in sequence. Compared with unmethylation group, protein levels in PI3K/Akt/c-fos pathway were enhanced in partial and complete methylation groups. Treatment of chondrocytes with sodium selenite resulted in reduced methylation and increased expression of GPX3 as well as down-regulated level of PI3K/Akt/c-fos proteins. CONCLUSIONS: The methylation and expression of GPX3 and expression of PI3K/Akt/c-fos pathway are altered in KBD and these changes are reversible by selenium supplementation.
Subject(s)
Apoptosis/genetics , Chondrocytes/metabolism , Chondrocytes/pathology , DNA Methylation/genetics , Glutathione Peroxidase/genetics , Kashin-Beck Disease/genetics , Apoptosis/drug effects , Case-Control Studies , Cell Line , Chondrocytes/drug effects , DNA Methylation/drug effects , Female , Glutathione Peroxidase/blood , Humans , Kashin-Beck Disease/blood , Male , Middle Aged , Oxidative Stress/drug effects , Phosphatidylinositol 3-Kinases/metabolism , Proto-Oncogene Proteins c-akt/metabolism , Proto-Oncogene Proteins c-fos/metabolism , RNA, Messenger/genetics , RNA, Messenger/metabolism , Selenium/pharmacology , Signal TransductionABSTRACT
OBJECTIVE: Meta-analysis was used to assess the clinical efficacy of acupuncture treatment for simple obesity and to provide evidence-based medical data for treating obesity with acupuncture. METHODS: A comprehensive search of studies on MEDLINE, EMBASE, the Cochrane Central Register of Controlled Trials and Chinese databases (Wan Fang,CNKI and VIP) from 1 January 1915 through 30 November 2015 (MEDLINE search updated through 31 December 2015) was performed. We included only randomised controlled trials (RCTs) that used acupuncture and sham acupuncture to treat simple obesity. The effect of acupuncture on simple obesity was measured using body mass index (BMI), body fat mass (BFM), waist circumference (WC), hip circumference (HC), and body weight (BW). The Jadad scale was used to assess methodological quality. The random effects model was used in the pooled analysis to adjust for the heterogeneity of the included studies, and funnel plots were used to examine publication bias. The differences between treatment groups were reported as mean differences (MD). RESULTS: Eleven RCTs were selected after all relevant literature from the electronic databases had been screened. There were 338 and 305 participants in the acupuncture and sham acupuncture groups, respectively. Auricular and electro acupuncture were both able to reduce BMI in obese patients (MD 0.47 kg/m2, 95% CI 0.35 to 0.58, p<0.001; MD 0.50 kg/m2, 95% CI 0.38 to 0.62, p<0.001). BFM change after acupuncture treatment compared with sham treatment was statistically significant (MD 0.66 kg, 95% CI 0.51 to 0.80, p<0.001). There were also significant differences in WC and HC between the acupuncture and sham acupuncture groups (MDwc2.02 cm, 95% CI 0.21 to 3.83, p=0.03; MDHC2.74 cm, 95% CI 1.21 to 4.27, p=0.0004). BW was not statistically significantly different between the acupuncture and sham acupuncture groups (MD 0.60 kg, 95% CI -0.20 to 1.39, p=0.14). Begg's test and funnel plots showed that the potential publication bias of the included studies was very slight (p>0.05). CONCLUSION: Acupuncture for simple obesity appeared to be an effective treatment, but more studies on the safety of acupuncture used to treat simple obesity are required.
Subject(s)
Acupuncture Therapy , Obesity/therapy , Adult , Evidence-Based Medicine , HumansABSTRACT
The c-Jun N-terminal kinases (JNK) are members of the mitogen-activated protein kinase family and are activated by environmental stress. Se plays an important role in the biological pathways by forming selenoprotein. Selenoproteins have been shown to exhibit a variety of biological functions including antioxidant functions and maintaining cellular redox balance, and compromise of such important proteins would lead to oxidative stress and apoptosis. We examined the expression levels of JNK in Kashin-Beck disease (KBD) patients, tested the potential protective effects of sodium selenite on tert-butyl hydroperoxide (tBHP)-induced oxidative injury and apoptosis in human chondrocytes as well as its underlying mechanism in this study. We produced an oxidative damage model induced by tBHP in C28/I2 human chondrocytes to test the essential anti-apoptosis effects of Se in vitro. The results indicated that the expression level of phosphorylated JNK was significantly increased in KBD patients. Cell apoptosis was increased and molecule expressions of the JNK signalling pathway were activated in the tBHP-injured chondrocytes. Na2SeO3 protected against tBHP-induced oxidative stress and apoptosis in cells by increasing cell viability, reducing reactive oxygen species generation, increasing Glutathione peroxidase (GPx) activity and down-regulating the JNK pathway. These results demonstrate that apoptosis induced by tBHP in chondrocytes might be mediated via up-regulation of the JNK pathway; Na2SeO3 has an effect of anti-apoptosis by down-regulating the JNK signalling pathway.
Subject(s)
Chondrocytes/drug effects , JNK Mitogen-Activated Protein Kinases/metabolism , Kashin-Beck Disease/metabolism , MAP Kinase Signaling System , Osteoarthritis/metabolism , Oxidative Stress/drug effects , Sodium Selenite/pharmacology , Antioxidants/metabolism , Antioxidants/pharmacology , Apoptosis/drug effects , Cell Survival/drug effects , Chondrocytes/metabolism , Down-Regulation , Glutathione Peroxidase/metabolism , Humans , Phosphorylation , Reactive Oxygen Species/metabolism , Selenium/pharmacology , Signal Transduction , Up-Regulation , tert-ButylhydroperoxideABSTRACT
Kashin-Beck disease (KBD) is an endemic, degenerative osteoarthropathy, and particularly seen in China. A deficiency of selenium and iodine is implicated as the main etiological factor for KBD. This meta-analysis aimed to evaluate the differences in the selenium and iodine levels between patients with KBD and healthy individuals. Eligible articles published before March 6, 2015 were searched from four electronic databases. Data extraction and quality assessment of included studies were performed by two independent reviewers. Results were summarized as standardized mean difference (SMD) with 95 % confidence intervals (CIs). Cohen's d test was used to estimate the difference of the effect size between patients with KBD and healthy controls. A total of 26 cross-sectional studies were included in the meta-analysis. The pooled SMD showed that the whole blood selenium (Cohen's d = 4.39, P < 0.001), serum selenium (Cohen's d = 2.42, P = 0.015), hair selenium (Cohen's d = 5.46, P < 0.001), and urinary selenium (Cohen's d = 4.16, P < 0.001) levels were significantly lower in patients with KBD than that in healthy controls. There was no significant difference of plasma selenium (Cohen's d = 0.08, P = 0.936) and urinary iodine (Cohen's d = 0.33, P = 0.744) levels between subjects with KBD and healthy controls. In conclusion, the levels of selenium, but not iodine were significantly lower in subjects with KBD than that in healthy controls. Selenium deficiency might be associated with the risk of KBD.
Subject(s)
Iodine/blood , Kashin-Beck Disease/blood , Selenium/blood , Case-Control Studies , Cross-Sectional Studies , HumansABSTRACT
OBJECTIVE: To investigate the impact of family members and health care providers on the use of folic acid supplements in pregnant women, and to provide basic data for improving the effectiveness of folic acid intervention. METHODS: A cross-sectional study was conducted in hospitals and households from June to September in 2009. Face-to-face anonymous questionnaires were distributed to 2094 women, who were pregnant at least three months or postpartum in one year, in two counties of Gansu Province. RESULTS: The awareness rate of folic acid was in 62.2% of 2094 pregnant women, and 25.4% of them have taken folic acid. Higher knowledge about folic acid of family members (OR = 0.268, 95% CI 0.208 - 0.346), agreed with taking folic acid by family members (OR = 0.103, 95% CI 0.031 -0.338), and urging pregnant women to take folic acid by family members (OR = 0.147, 95% CI 0.115 - 0.190) were significant predictors for having folic acid taken by pregnant women. Propagating knowledge related to folic acid (OR = 0.252, 95% CI 0.197 - 0.323) and directing pregnant women to use folic acid (OR = 0.168, 95% CI 0.096 - 0.296) by health care providers were also the important predictors for folic acid intake. CONCLUSION: Family members and health care providers play an important role in affecting the use of folic acid among pregnant women. In order to improve the effectiveness of intervention with folic acid, family members of pregnant women and health care providers should be included into the target population to receive an intensive propaganda campaign on folic acid education to improve the use of folic acid in pregnant women extensively.