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.

Effects of levothyroxine therapy on bone mineral density and bone turnover markers in premenopausal women with thyroid cancer after thyroidectomy

Introduction: We investigated the impact of long-term levothyroxine (LT4) treatment on bone mineral density (BMD) and bone turnover markers (BTMs) in premenopausal women with differentiated thyroid cancer (DTC) after thyroidectomy. Material and methods: Sixty-five premenopausal women who received LT4 therapy at least one year (range, 1.5–9.0 years) after thyroidectomy for DTC and 50 premenopausal women without thyroid diseases were enrolled in this study. We measured the Z-scores of lumbar and hip BMD, serum free triiodothyronine (FT3), free thyroxine (FT4), thyroid-stimulating hormone (TSH), intact parathyroid hormone (iPTH), N-terminal propeptide of type 1 N procollagen (P1NP), C terminal telopeptide of type 1 collagen (CTX-1), calcium (Ca), phosphorus (P), vitamin D3, and alkaline phosphatase (ALP) in all participants. Results: In DTC subjects, serum TSH levels were lower, and serum FT4, P1NP, CTX-1, and ALP levels were higher compared with controls. The prevalence of low BMD was higher in DTC subjects than in controls. Multivariate logistic regression analysis showed that serum TSH levels were negatively associated with CTX-1 and ALP. Conclusions: We found a high prevalence of low BMD among premenopausal women who received long-term LT4 therapy for DTC after thyroidectomy. Long-term TSH suppression therapy was a significant risk factor for decreased bone strength, mainly by increasing bone turnover.

Evidence for Majorana bound state in an iron-based superconductor

The search for Majorana bound state (MBS) has recently emerged as one of the most active research areas in condensed matter physics, fueled by the prospect of using its non-Abelian statistics for robust quantum computation. A highly sought-after platform for MBS is two-dimensional topological superconductors, where MBS is predicted to exist as a zero-energy mode in the core of a vortex. A clear observation of MBS, however, is often hindered by the presence of additional low-lying bound states inside the vortex core. By using scanning tunneling microscope on the newly discovered superconducting Dirac surface state of iron-based superconductor FeTe1-xSex (x = 0.45, superconducting transition temperature Tc = 14.5 K), we clearly observe a sharp and non-split zero-bias peak inside a vortex core. Systematic studies of its evolution under different magnetic fields, temperatures, and tunneling barriers strongly suggest that this is the case of tunneling to a nearly pure MBS, separated from non-topological bound states which is moved away from the zero energy due to the high ratio between the superconducting gap and the Fermi energy in this material. This observation offers a new, robust platform for realizing and manipulating MBSs at a relatively high temperature.Comment: 27 pages, 11 figures, supplementary information include

Nearly quantized conductance plateau of vortex zero mode in an iron-based superconductor

Majorana zero-modes (MZMs) are spatially-localized zero-energy fractional quasiparticles with non-Abelian braiding statistics that hold a great promise for topological quantum computing. Due to its particle-antiparticle equivalence, an MZM exhibits robust resonant Andreev reflection and 2e2/h quantized conductance at low temperature. By utilizing variable-tunnel-coupled scanning tunneling spectroscopy, we study tunneling conductance of vortex bound states on FeTe0.55Se0.45 superconductors. We report observations of conductance plateaus as a function of tunnel coupling for zero-energy vortex bound states with values close to or even reaching the 2e2/h quantum conductance. In contrast, no such plateau behaviors were observed on either finite energy Caroli-de Genne-Matricon bound states or in the continuum of electronic states outside the superconducting gap. This unique behavior of the zero-mode conductance reaching a plateau strongly supports the existence of MZMs in this iron-based superconductor, which serves as a promising single-material platform for Majorana braiding at a relatively high temperature

Long intergenic non-protein coding RNA 00174 promotes cardiac hypertrophy by targeting miR-150-5p

Purpose: miR-150-5p is associated with several diseases but its relation with cardiac hypertrophy (CH) is yet to be unveiled. However, long intergenic non-protein coding RNA 174 (LINC00174) is implicated in CH. The purpose of this study was to investigate the roles of LINC00174 and miR-150-5p in relation to CH progression.Methods: A mechanical cyclic stretch was applied to create 4 groups of H9 cardiomyocytes: 15 % 7, 15, 24 and 48 hr stretches, as well as unstretched control. Transfection method was used to up-regulate expression levels of LINC00174 and miR-150-5p in H9 cardiomyocytes. RT-qPCR and Western blot were used to determine the effect of LINC00174 on mRNA expression levels of miR-150-5p, proliferation and apoptosis biomarkers. Cell proliferation was determined by CCK-8 assay and the target gene of LINC00174 was detected by luciferase reporter assay. Results: Expression level of LINC00174 was high in H9 stretched cardiomyocytes. When overexpressed, it enhanced the mRNA expression of proliferation biomarkers and down-regulated apoptosis biomarkers. More so, miR-150-5p was down-regulated in H9 stretched cardiomyocytes and it was a direct target of LINC00174. Furthermore, miR-1505p restoration reversed the effects of LINC00174 overexpression on proliferation and apoptosis biomarkers. Conclusion: LINC00174 and miR-150-5p may be novel biomarkers for early diagnosis of CH

Specific alterations of gut microbiota in diabetic microvascular complications: A systematic review and meta-analysis

BackgroundThe role of gut microbiota in diabetes mellitus (DM) and its complications has been widely accepted. However, the alternation of gut microbiota in diabetic microvascular complications (DC) remains to be determined.MethodsPublications (till August 20th, 2022) on gut microbiota in patients with DC were retrieved from PubMed, Web of Science, Embase and Cochrane. Review Manager 5.3 was performed to estimate the standardized mean difference (SMD) and 95% confidence interval (CI) and calculate alpha diversity indices and the relative abundance of gut microbiota between patients in DC v.s. DM and DC v.s. healthy controls (HC).ResultsWe included 13 studies assessing 329 patients with DC, 232 DM patients without DC, and 241 HC. Compared to DM, patients with DC shared a significantly lower Simpson index (SMD = -0.59, 95% CI [-0.82, -0.36], p < 0.00001), but a higher ACE index (SMD = 0.42, 95% CI[0.11, 0.74], p = 0.009). Compared to HC, DC patients held a lower ACE index (SMD = -0.61, 95% CI[-1.20, -0.02], p = 0.04). The relative abundances of phylum Proteobacteria (SMD = 0.03, 95% CI[0.01, 0.04], p = 0.003, v.s. HC) and genus Klebsiella (SMD = 0.00, 95% CI[0.00, 0.00], p < 0.00001, v.s. HC) were enriched, accompanying with depleted abundances of phylum Firmicutes (SMD = -0.06, 95% CI[-0.11, -0.01], p = 0.02, v.s. HC), genera Bifidobacterium (SMD = -0.01, 95% CI[-0.02,-0.01], p < 0.0001, v.s. DM), Faecalibacterium (SMD = -0.01, 95% CI[-0.02, -0.00], p = 0.009, v.s. DM; SMD = -0.02, 95% CI[-0.02, -0.01], p < 0.00001, v.s. HC) and Lactobacillus (SMD = 0.00, 95% CI[-0.00, -0.00], p < 0.00001, v.s. HC) in DC.ConclusionsGut microbiota perturbations with the depletion of alpha diversity and certain short-chain fatty acids (SCFAs)-producing bacteria were associated with the pathology of DC. Therefore, gut microbiota might serve as a promising approach for the diagnosis and treatment of DC. Further investigations are required to study the mechanisms by which gut dysbiosis acts on the onset and progression of DC

Granulocyte colony-stimulating factor increases the therapeutic efficacy of bone marrow mononuclear cell transplantation in cerebral ischemia in mice

<p>Abstract</p> <p>Background</p> <p>Bone marrow mononuclear cell (BMMC) transplantation is a promising therapy for cerebral ischemia; however, little is known if its therapeutic efficacy may be improved by co-administration of potential modulatory factors in vivo. To explore this possibility, the present study examined the effect of BMMCs and G-CSF on cell proliferation, early neuronal development and neurological function recovery in experimental cerebral ischemia relative to controls that received neither treatment.</p> <p>Result</p> <p>Ischemia/infarct area was significantly reduced in BMMCs+G-CSF group relative to animal groups treated with BMMCs only, G-CSF only or saline. Transplanted BMMCs were found to colocalize with the proliferative cell nuclear antigen (PCNA) and the immature neuronal marker doublecortin (DCX). The BMMCs+G-CSF group showed increased numerical density of cells expressing PCNA and DCX, improved performance in adhesive sticker removal test and reduced neurological function severity scores relative to other groups in a time-dependent manner.</p> <p>Conclusion</p> <p>BMMCs and G-CSF co-administration exhibits synergistic beneficial effect over time. This effect could be at least partially related to increased proliferation and differentiation of bone marrow stem cells and enhanced host brain regeneration and functional recovery. The results suggest that G-CSF can increase the therapeutic efficacy of BMMCs transplantation in an experimental mouse model of cerebral ischemia.</p

MicroRNA-1 acts as a tumor suppressor microRNA by inhibiting angiogenesis-related growth factors in human gastric cancer

Background We recently reported that miR-1 was one of the most significantly downregulated microRNAs in gastric cancer (GC) patients from The Cancer Genome Atlas microRNA sequencing data. Here we aim to elucidate the role of miR-1 in gastric carcinogenesis. Methods We measured miR-1 expression in human GC cell lines and 90 paired primary GC samples, and analyzed the association of its status with clinicopathological features. The effect of miR-1 on GC cells was evaluated by proliferation and migration assay. To identify the target genes of miR-1, bioinformatic analysis and protein array analysis were performed. Moreover, the regulation mechanism of miR-1 with regard to these predicted targets was investigated by quantitative PCR (qPCR), Western blot, ELISA, and endothelial cell tube formation. The putative binding site of miR-1 on target genes was assessed by a reporter assay. Results Expression of miR-1 was obviously decreased in GC cell lines and primary tissues. Patients with low miR-1 expression had significantly shorter overall survival compared with those with high miR-1 expression (P = 0.0027). Overexpression of miR-1 in GC cells inhibited proliferation, migration, and tube formation of endothelial cells by suppressing expression of vascular endothelial growth factor A (VEGF-A) and endothelin 1 (EDN1). Conversely, inhibition of miR-1 with use of antago-miR-1 caused an increase in expression of VEGF-A and EDN1 in nonmalignant GC cells or low-malignancy GC cells. Conclusions MiR-1 acts as a tumor suppressor by inhibiting angiogenesis-related growth factors in human gastric cancer. Downregulated miR-1 not only promotes cellular proliferation and migration of GC cells, but may activates proangiogenesis signaling and stimulates the proliferation and migration of endothelial cells, indicating the possibility of new strategies for GC therapy