Associations of oxytocin with metabolic parameters in obese women of childbearing age

Introduction: The aim of this study was to compare plasma oxytocin levels in obese women of childbearing age with non-obese women of childbearing age, and to investigate the relationship between plasma oxytocin levels and metabolic parameters (including blood glucose, insulin resistance, blood lipid, and blood pressure). Material and methods: A total of 151 obese women of childbearing age and 160 non-obese women of childbearing age were enrolled in this study. Plasma oxytocin levels were measured by electrochemiluminescence immunoassays. Height, body weight, body mass index (BMI), fasting blood glucose (FBG), fasting insulin (FI), homeostasis model assessment for insulin resistance (HOMA-IR), total triglycerides (TG), total cholesterol (TC), low-density lipoprotein-C (LDL-C), high-density lipoprotein-C (HDL-C), systolic blood pressure (SBP), and diastolic blood pressure (DBP) were measured in all subjects. Quantile regression analysis was used to analyse the associations of plasmaoxytocin levels with FBG, FI, HOMA-IR, TG, TC, LDL-C, HDL-C, SBP, and DBP. Results: In obese women of childbearing age, plasma oxytocin levels were lower compared with non-obese controls. After adjusting for age, quantile regression analysis showed that the plasma oxytocin levels were inversely associated with HOMA-IR at the quantile level between 0.27 and 0.79 (i.e. the HOMA-IR level of 2.11 and 3.07, respectively), the plasma oxytocin levels were inversely associated with TC after the quantile level of 0.21 (i.e. the TC level of 3.78 ), and the plasma oxytocin levels were inversely associated with LDL-C at all quantile levels of LDL-C. In addition, the plasma oxytocin levels showed a positive association with HDL-C at all quantile levels of HDL-C.No significant associations were found between the plasma oxytocin levels and FBG, FI, TG, SBP, and DBP. Conclusions: Oxytocin deficiency was common in obese women of childbearing age. Oxytocin showed negative correlation with HOMA-IR, TC, and LDL-C, while it showed positive association with HDL-C. Our findings suggest that oxytocin played an important role in inhibiting metabolic disorders associated with obesity in women of childbearing age.

The Roles of Platelet GPIIb/IIIa and αvβ3 Integrins during HeLa Cells Adhesion, Migration, and Invasion to Monolayer Endothelium under Static and Dynamic Shear Flow

During their passage through the circulatory system, tumor cells undergo extensive interactions with various host cells including endothelial cells and platelets. Mechanisms mediating tumor cell adhesion, migration, and metastasis to vessel wall under flow condition are largely unknown. The aim of this study was to investigate the potential roles of GPIIb/IIIa and αvβ3 integrins underlying the HeLa-endothelium interaction in static and dynamic flow conditions. HeLa cell migration and invasion were studied by using Millicell cell culture insert system. The numbers of transmigrated or invaded HeLa cells significantly increased by thrombin-activated platelets and reduced by eptifibatide, a platelet inhibitor. Meanwhile, RGDWE peptides, a specific inhibitor of αvβ3 integrin, also inhibited HeLa cell transmigration. Interestingly, the presence of endothelial cells had significant effect on HeLa cell migration regardless of static or cocultured flow condition. The adhesion capability of HeLa cells to endothelial monolayer was also significantly affected by GPIIb/IIIa and αvβ3 integrins. The arrested HeLa cells increased nearly 5-fold in the presence of thrombin-activated platelets at shear stress condition (1.84 dyn/cm2 exposure for 1 hour) than the control (static). Our findings showed that GPIIb/IIIa and αvβ3 integrins are important mediators in the pathology of cervical cancer and provide a molecular basis for the future therapy, and the efficient antitumor benefit should target multiple receptors on tumor cells and platelets

Treatment with lamivudine versus lamivudine and thymosin alpha-1 for e antigen-positive chronic hepatitis B patients: a meta-analysis

<p>Abstract</p> <p>Background</p> <p>Currently, there is no evidence on the combination of lamivudine and thymosin alpha-1 on chronic hepatitis B patients. The aim of this study was to compare the effect of lamivudine monotherapy with that of lamivudine and thymosin alpha-1 combination therapy for the treatment of hepatitis B e antigen (HBeAg)-positive hepatitis B patients.</p> <p>Results</p> <p>We searched PUBMED (from 1966 onwards), EMBASE (from 1966), CBMdisk (Chinese Biomedical Database, from 1978), CNKI (National Knowledge Infrastructure, from 1980), the Cochrane Central Register of Controlled Trials and the Cochrane Database of Systematic Reviews. Eight trials (583 patients in total) were identified. The lamivudine and thymosin alpha-1 combination treatment was significantly superior to lamivudine treatment in terms of ALT normalization rate (80.2% vs. 68.8%, P = 0.01), virological response rate (84.7% vs. 74.9%, P = 0.002), and HBeAg seroconversion rate (45.1% vs. 15.2%, P < 0.00001).</p> <p>Conclusion</p> <p>Among HBeAg-positive patients, thymosin alpha-1 and lamivudine combination therapy may be more effective than lamivudine monotherapy, providing superior rates of biochemical response, virological response, and HBeAg seroconversion.</p

Effects of Tai Chi on telomerase activity and gerotranscendence in middle aged and elderly adults in Chinese society

AbstractIntroductionTelomeres are DNA protein structures at the end of chromosomes and are linked to the physical aging process. The improvement of quality of life is closely associated with aerobic exercise, and the dynamic effects of exercise on physiology and psychology are evident with aging. Tai Chi is popularly practiced in China. However, findings on the effects of Tai Chi on telomerase activity (TA) in peripheral blood mononuclear cells, and gerotranscendence (GT), as well as the association of TA and GT with Tai Chi, have been inconsistent.PurposeThis study aims to assess TA in peripheral blood mononuclear cells, GT, and the associations between them. The associations among these variables are determined during six months of Tai Chi intervention among Chinese middle aged and elderly adults.MethodsTA assessment was obtained by TE-ELISA (human telomerase–enzyme linked immunosorbent assay), and GT was measured at the baseline level after six months of Tai Chi intervention.ResultsTA increased significantly in the Tai Chi group from 23.75 ± 3.78 u/mmol (pre-intervention) to 26.31 ± 2.93 u/mmol (after 6 months) (p < 0.05). Compared with the TA in the control group, the TA in the intervention group was statistically significant after six months (p < 0.05). Compared with the GT in the control group, the GT in the intervention group improved significantly after six months (p < 0.05). TA and GT had a positive correlation (r = 0.325, p < 0.01).ConclusionOur data illustrated that Tai Chi had a protective effect on TA and might improve the GT in Chinese middle aged and elderly adults. The TA increased with the increasing GT in Chinese middle aged and elderly adults

Deletion of heat shock protein 60 in adult mouse cardiomyocytes perturbs mitochondrial protein homeostasis and causes heart failure.

To maintain healthy mitochondrial enzyme content and function, mitochondria possess a complex protein quality control system, which is composed of different endogenous sets of chaperones and proteases. Heat shock protein 60 (HSP60) is one of these mitochondrial molecular chaperones and has been proposed to play a pivotal role in the regulation of protein folding and the prevention of protein aggregation. However, the physiological function of HSP60 in mammalian tissues is not fully understood. Here we generated an inducible cardiac-specific HSP60 knockout mouse model, and demonstrated that HSP60 deletion in adult mouse hearts altered mitochondrial complex activity, mitochondrial membrane potential, and ROS production, and eventually led to dilated cardiomyopathy, heart failure, and lethality. Proteomic analysis was performed in purified control and mutant mitochondria before mutant hearts developed obvious cardiac abnormalities, and revealed a list of mitochondrial-localized proteins that rely on HSP60 (HSP60-dependent) for correctly folding in mitochondria. We also utilized an in vitro system to assess the effects of HSP60 deletion on mitochondrial protein import and protein stability after import, and found that both HSP60-dependent and HSP60-independent mitochondrial proteins could be normally imported in mutant mitochondria. However, the former underwent degradation in mutant mitochondria after import, suggesting that the protein exhibited low stability in mutant mitochondria. Interestingly, the degradation could be almost fully rescued by a non-specific LONP1 and proteasome inhibitor, MG132, in mutant mitochondria. Therefore, our results demonstrated that HSP60 plays an essential role in maintaining normal cardiac morphology and function by regulating mitochondrial protein homeostasis and mitochondrial function

Diaqua­bis­(1-methyl-1H-imidazole-κN 3)bis­[2-(naphthalen-1-yl)acetato-κO]cobalt(II)

In the title compound, [Co(C12H9O2)2(C4H6N2)2(H2O)2], the CoII ion is located on an inversion centre and displays a distorted octa­hedral coordination geometry. Two O atoms from two water mol­ecules and two carboxyl­ate O atoms from two 2-(naphthalen-1-yl)acetate ligands are in the equatorial plane and two N atoms from two 1-methyl-1H-imidazole ligands are in the axial positions. The structure is stabilized by intra­molecular O—H⋯O hydrogen bonds. Inter­molecular O—H⋯O hydrogen bonds link the complex mol­ecules into chains along [100]

Bardoxolone methyl induces apoptosis and autophagy and inhibits epithelial-to-mesenchymal transition and stemness in esophageal squamous cancer cells

Natural and synthetic triterpenoids have been shown to kill cancer cells via multiple mechanisms. The therapeutic effect and underlying mechanism of the synthetic triterpenoid bardoxolone methyl (C-28 methyl ester of 2-cyano-3,12-dioxoolean-1,9-dien-28-oic acid; CDDO-Me) on esophageal cancer are unclear. Herein, we aimed to investigate the anticancer effects and underlying mechanisms of CDDO-Me in human esophageal squamous cell carcinoma (ESCC) cells. Our study showed that CDDO-Me suppressed the proliferation and arrested cells in G2/M phase, and induced apoptosis in human ESCC Ec109 and KYSE70 cells. The G2/M arrest was accompanied with upregulated p21Waf1/Cip1 and p53 expression. CDDO-Me significantly decreased B-cell lymphoma-extra large (Bcl-xl), B-cell lymphoma 2 (Bcl-2), cleaved caspase-9, and cleaved poly ADP ribose polymerase (PARP) levels but increased the expression level of Bcl-2-associated X (Bax). Furthermore, CDDO-Me induced autophagy in both Ec109 and KYSE70 cells via suppression of the phosphoinositide 3-kinase/protein kinase B/mammalian target of rapamycin (PI3K/Akt/mTOR) signaling pathway. There were interactions between the autophagic and apoptotic pathways in Ec109 and KYSE70 cells subject to CDDO-Me treatment. CDDO-Me also scavenged reactive oxygen species through activation of the nuclear factor (erythroid-derived 2)-related factor 2 (Nrf2) pathway in Ec109 and KYSE70 cells. CDDO-Me inhibited cell invasion, epithelial-mesenchymal transition, and stemness in Ec109 and KYSE70 cells. CDDO-Me significantly downregulated E-cadherin but upregulated Snail, Slug, and zinc finger E-box-binding homeobox 1 (TCF-8/ZEB1) in Ec109 and KYSE70 cells. CDDO-Me significantly decreased the expression of octamer-4, sex determining region Y-box 2 (Sox-2), Nanog, and B lymphoma Mo-MLV insertion region 1 homolog (Bmi-1), all markers of cancer cell stemness, in Ec109 and KYSE70 cells. Taken together, these results indicate that CDDO-Me is a promising anticancer agent against ESCC. Further studies are warranted to explore the molecular targets, efficacy and safety of CDDO-Me in the treatment of ESCC