The efficacy of Tai Chi for essential hypertension: A systematic review and meta-analysis.

AIM: We aimed to assess the impact of Tai Chi interventions on individuals with essential hypertension and to compare the effects of Tai Chi versus control in this population. BACKGROUND: Tai Chi has been extensively utilized in the prevention of essential hypertension. Nevertheless, there is a lack of consensus regarding its benefits for treating essential hypertension. DESIGN: A systematic review and meta-analysis was conducted. DATA SOURCES: We conducted a systematic literature search of the Medline, Scholar, Elsevier, Wiley Online Library, Chinese Academic Journal (CNKI) and Wanfang databases from January 2003 to August 2023. REVIEW METHODS: Using the methods of the Cochrane Collaboration Handbook, a meta-analysis was conducted to assess the collective impact of Tai Chi exercise in controlling hypertension. The primary outcomes measured included blood pressure and nitric oxide levels. RESULTS: The participants consisted of adults with an average age of 57.1 years who had hypertension (mean ± standard deviation systolic blood pressure at 148.2 ± 12.1 mmHg and diastolic blood pressure at 89.2 ± 8.3 mmHg). Individuals who practiced Tai Chi experienced reductions in systolic blood pressure of 10.6 mmHg, diastolic blood pressure of 4.7 mmHg and an increase in nitric oxide levels. CONCLUSIONS: Tai Chi can be a viable lifestyle intervention for managing hypertension. Greater promotion of Tai Chi by medical professionals could extend these benefits to a larger patient population.

Elevated methylation of cyclin dependent kinase inhibitor 2B contributes to the risk of coronary heart disease in women.

Cyclin dependent kinase inhibitor 2B (CDKN2B) encodes a cyclin-dependent kinase inhibitor that may enhance the formation of atherosclerotic plaques. The aim of the present study was to investigate the contribution of CDKN2B promoter methylation on the risk of coronary heart disease (CHD). The present results indicated a significant association between increased CDKN2B methylation and the risk of CHD (adjusted P=0.043). A breakdown analysis according to sex demonstrated that CDKN2B methylation was significantly associated with the risk of CHD in women (adjusted P=0.010), but not in men. A further breakdown analysis by age indicated a significant association of CHD in the women >60 years (P=0.024). Luciferase reporter gene assay results indicated that the CDKN2B promoter fragment significantly enhanced luciferase activity (P<0.001). In addition, CDKN2B transcription was significantly enhanced following treatment with 5-aza-2'-deoxycytidine methylation inhibitor in human aortic endothelial cells (HAEC) and human primary coronary artery smooth muscle cells (HPCASMC; P<0.05 and P<0.01), but not in 293 cells. Notably, estrogen treatment reduced CDKN2B methylation of several CpGs and significantly increased CDKN2B gene expression levels in HAEC, HPCASMC and 293 cells (P<0.05 and P<0.01). Additionally, treatment of HAEC and HPCASMC with simvastatin and γ-carboxy-L-glutamic acid reduced CDKN2B promoter methylation and increased CDKN2B transcription concomitantly. The present study suggests that CDKN2B promoter methylation may be associated with sex dimorphism in the pathogenesis of CHD.

Serum expression level of IL-6 at the diagnosis time contributes to the long-term prognosis of SCLC patients.

Cytokines are vital mediators involved in tumor immunity. We aimed to explore whether the expression levels of IL-1ß, TNF-α and IL-6 have impacts on prognosis of SCLC patients. In this study, we concluded 707 non-operable SCLC patients at stage III or IV into this study and analyzed the relationships between interleukins and OS/PFS by cox regression analysis and Kaplan-Meier analysis (log-rank test). As a result, under current standard chemotherapy, SCLC patients with higher IL-6 expression level had a shortened OS compared with those with normal level (HR: 0.381, 95%CI: 0.177-0.822, p=0.014). Furthermore, IL-6 expression level contributed mostly to patients without a smoking history. Non-smoking patients with a high IL-6 level showed a 6 months shortened OS than those with normal IL-6 level (10.50 vs 16.90 months, p=0.003 by Log-Rank test in Kaplan-Meier analysis). IL-6 had no obvious impacts on first-line PFS in these SCLC patients. To conclude, IL-6 acts as an independent factor of long-term prognosis of SCLC patients under current therapy.

ACTN3 genotype and physical function and frailty in an elderly Chinese population: the Rugao Longevity and Ageing Study.

Objective: To examine the associations of the actinin alpha 3 gene (ACTN3) R577X polymorphism with physical performance and frailty in an older Chinese population. Methods: Data from 1,463 individuals (57.8% female) aged 70-87 years from the Rugao Longevity and Ageing Study were used. The associations between R577X and timed 5-m walk, grip strength, timed Up and Go test, and frailty index (FI) based on deficits of 23 laboratory tests (FI-Lab) were examined. Analysis of variance and linear regression models were used to evaluate the genetic effects of ACTN3 R577X on physical performance and FI-Lab. Results: The XX and RX genotypes of the ACTN3 R557X polymorphism accounted for 17.1 and 46.9%, respectively. Multivariate regression analysis revealed that in men aged 70-79 years, the ACTN3 577X allele was significantly associated with physical performance (5-m walk time, regression coefficient (ß) = 0.258, P = 0.006; grip strength, ß = -1.062, P = 0.012; Up and Go test time ß = 0.368, P = 0.019). In women aged 70-79 years, a significant association between the ACTN3 577X allele and the FI-Lab score was observed, with a regression coefficient of ß = 0.019 (P = 0.003). These findings suggest an age- and gender-specific X-additive model of R577X for 5-m walk time, grip strength, Up and Go Test time, and FI-Lab score. Conclusion: The ACTN3 577X allele is associated with an age- and sex-specific decrease in physical performance and an increase in frailty in an older population.

CPNE1 silencing inhibits the proliferation, invasion and migration of human osteosarcoma cells.

Osteosarcoma (OS) is the most common primary malignancy of the bone affecting children and adolescents. Copine 1 (CPNE1) is a highly conserved calcium-dependent phospholipid-binding protein and may function in regulating signal transduction and membrane trafficking. In the present study, we investigated CPNE1 expression in osteosarcoma tissues and cells, and studied the effects of small interfering RNA (siRNA)-targeting CPNE1 on proliferation, metastasis and chemosensitivity of the osteosarcoma cells. The results demonstrated that CPNE1 was highly expressed in the osteosarcoma tissues and cell lines. Moreover, functional investigations confirmed that CPNE1 knockdown significantly inhibited cell proliferation, colony formation, invasion and metastasis in Saos-2 and HOS cells. Western blot analysis indicated that CPNE1 silencing downregulated the expression of many proteins associated with tumorigenesis and development, including Ras, MEK-1/2, WNT1, ß-catenin, cyclin A1, IRAK2 and cIAP2. In addition, CPNE1 downregulation enhanced the sensitivity of Saos-2 cells towards cisplatin and adriamycin. The present study provides deep insight into the clinical use of lentiviral-mediated CPNE1 silencing for osteosarcoma therapy.

Expression of Carbonic Anhydrase I in Motor Neurons and Alterations in ALS.

Carbonic anhydrase I (CA1) is the cytosolic isoform of mammalian α-CA family members which are responsible for maintaining pH homeostasis in the physiology and pathology of organisms. A subset of CA isoforms are known to be expressed and function in the central nervous system (CNS). CA1 has not been extensively characterized in the CNS. In this study, we demonstrate that CA1 is expressed in the motor neurons in human spinal cord. Unexpectedly, a subpopulation of CA1 appears to be associated with endoplasmic reticulum (ER) membranes. In addition, the membrane-associated CA1s are preferentially upregulated in amyotrophic lateral sclerosis (ALS) and exhibit altered distribution in motor neurons. Furthermore, long-term expression of CA1 in mammalian cells activates apoptosis. Our results suggest a previously unknown role for CA1 function in the CNS and its potential involvement in motor neuron degeneration in ALS.

RTN4 3'-UTR insertion/deletion polymorphism and susceptibility to non-small cell lung cancer in Chinese Han population.

Nogo protein, encoded by gene reticulon-4 (RTN4), includes three major isoforms by different splicing, named Nogo-A Nogo-B and Nogo-C. Nogo proteins play an important role in the apoptosis of cells, especially in tumor cells. RTN4 single nucleotide polymorphisms (SNPs) can influence the efficiency of transcription and translation thus being related with an individual's predisposition to cancer. The CAA insertion/deletion polymorphism (rs34917480) within RTN4 3'-UTR has been reported to be associated with many cancer types. In order to investigate the relationship between this polymorphism and susceptibility to non-small cell lung cancer (NSCLC) in the Chinese population, we conducted the present case-control study including 411 NSCLC patients and 471 unrelated healthy controls. The genotype distributions were significantly different between cases and controls (p=0.014). We found that the del allele could significantly increase NSCLC risk (ins/ins vs ins/del: p=0.007, OR 1.46, 95%CI=1.11-1.93; dominant model: p=0.004, OR 1.47, 95%CI=1.13-1.92 and allele model: p=0.008, OR 1.35, 95%CI=1.08-1.67). This association was stronger in participants over 60 years old, males and smokers. We therefore conclude that the CAA insertion/deletion polymorphism (rs34917480) contributes to non-small cell lung cancer risk in Chinese population. Age, sex and environmental exposure are also related to carcinogenic effects of rs34917480.

Polymorphism in PHD1 gene and risk of non-small cell lung cancer in a Chinese population.

Hypoxia is a common phenomenon in the development of solid tumors, and hypoxia inducible factor 1 (HIF-1) plays a central role in coordinating the cellular response to hypoxia and in oxygen homeostasis. The prolyl hydrolase 1 (PHD1) is a key adjustment factor that mediates the HIF-1 degradation and relates with the process of tumorigenesis. Thus, polymorphism in PHD1 may affect cellular response to hypoxic conditions and associate with cancer susceptibility. We conducted a case-control study with 406 non-small cell lung cancer cases and 812 healthy controls matched on age and sex to examine the effect of rs10680577 polymorphism within the PHD1 promoter on non-small cell lung cancer (NSCLC) risk in a Chinese population. The genotype of rs10680577 polymorphism was detected by non-denaturing polyacrylamide gel electrophoresis. The ins/del genotype of rs10680577 was associated with significantly increased non-small cell lung cancer risk (ins/del vs. ins/ins: OR = 1.35, 95 % confidence interval (CI) 1.05-1.74, P = 0.020; ins/del vs. ins/ins + del/del: OR = 1.34, 95 % CI = 1.04-1.72, P = 0.022). In addition, the association was more pronounced in the group of >60 years of age. rs10680577 polymorphism is associated with the risk of non-small cell lung cancer in a Chinese population. This is the first time to show that PHD1 rs10680577 is associated NSCLC risk.

Analysis of SEMA3B methylation and expression patterns in gastric cancer tissue and cell lines.

The family of semaphorins has been demonstrated to possess tumor suppressor activity, in which semaphorin 3B (SEMA3B) is differentially expressed in several types of tumors. The relationship between SEMA3B expression and its clinical significance in gastric cancer (GC) is currently unclear. In the present study, the expression and methylation status of the SEMA3B gene were detected by quantitative PCR and bisulfite sequencing PCR (BSP). Data indicated that the levels of SEMA3B mRNA decreased in gastric tumor tissues and the methylation status of SEMA3B in the tumor group was higher than the paired normal tissues. By BSP, the SEMA3B gene showed high methylated status which was detected in all 4 cell lines (AGS, BGC-823, MGC-803 and SGC-7901). Treatment of the cells with 5-Aza-2'-deoxycytidine revealed clearly elevated mRNA levels of SEMA3B. These results were further confirmed by western blot analysis of Sema3b protein expression. At the same time, increased expression of p53 mRNA in BGC-823, MGC-803 was detected and indicated that p53 may be involved in the regulation of SEMA3B expression in specific genetic background. Downregulation of SEMA3B was negatively correlated with tumor size and N staging in GC (p<0.05). In conclusion, CpG methylation of SEMA3B epigenetically regulates SEMA3B expression during development of GC. Furthermore, 5-Aza-2'-deoxycytidine could reverse the hypermethylation status of SEMA3B, which may benefit future studies exploring the application of demethylating agents in clinical usage of GC.

A unique reaction pathway of fluorine-substituted ethyl groups on Cu(111): successive alpha,alpha-fluoride elimination.

Fluorine-substituted ethyl groups on Cu(111) were generated by thermal scission of the C-I bond in the adsorbed C2F5I. Temperature-programmed reaction spectrometry observed a novel pathway resulting in the evolution of C4F6 above 400 K. Among the various isomers, this product was identified as hexafluro-2-butyne. Although abstraction of two fluorine atoms from the starting Cu-CF2CF3 was required, Cu-CCF3 (trifluoroethylidyne) was favored over Cu-CF=CF2 (trifluorovinyl) as the intermediate because this ethyl-ethylidyne-butyne pathway was suppressed on a Cu(100) surface devoid of the key threefold hollow binding sites for ethylidyne. Once formed, perfluoroethylidyne readily coupled to afford a tightly surface-bound hexafluoro-2-butyne up to 400 K. Therefore, the C-F bonds adjacent to the metal were found to be more susceptible to the bond activation, leading the chemisorbed perfluoroethyl to eliminate two F atoms successively from the alpha-carbon. This preference for alpha-elimination rather than beta-elimination (the most favorable route in hydrocarbons) may be quite general for metal surface-mediated reactions involving fluorinated alkyl groups.