Resistance training effect on serum insulin-like growth factor 1 in the serum: a meta-analysis.

BACKGROUND: The resistance exercise has drawn considerable attention to the level of insulin-like growth factor 1 in the serum. However, the relationship between resistance exercise and the level of insulin-like growth factor 1 in the serum is conflicting. This meta-analysis was performed to evaluate this relationship. METHODS: A systematic literature search up to May 2020 was performed and 22 studies were detected with 680 subjects. They reported relationships between resistance exercise and the level of insulin-like growth factor 1 in the serum. Odds ratio (OR) with 95% confidence intervals (CIs) was calculated comparing the resistance exercise and the level of insulin-like growth factor 1 in the serum using the continuous method with a random or fixed-effect model. RESULTS: Significantly higher insulin-like growth factor 1 was observed in subjects performing resistance training for less than 16 weeks (OR, 4.03; 95% CI, 2.49-5.57, p<.001); subjects performing resistance training for more than 16 weeks (OR, 11.55; 95% CI, 6.58-16.52, p<.001); subjects older than 60 years (OR, 11.88; 95% CI, 9.84-13.93, p<.001); females (OR, 3.87; 95% CI, 2.26-5.49, p<.001) and males (OR, 16.82; 95% CI, 7.29-26.35, p<.001). However, significantly lower insulin-like growth factor 1 was observed in subjects younger than 60 years (OR, -4.80; 95% CI, -7.74 to -1.86, p=.001). CONCLUSIONS: However, the resistance exercise significantly increases insulin-like growth factor 1 in subjects older than 60 years, both males and females, and subjects performing resistance exercise for all any period. Surprisingly, resistance exercise significantly decreases insulin-like growth factor 1 in subjects younger than 60 years. This relationship forces us to recommend the resistance exercise to improve insulin-like growth factor 1 in serum.

The effect of psyllium consumption on weight, body mass index, lipid profile, and glucose metabolism in diabetic patients: A systematic review and dose-response meta-analysis of randomized controlled trials.

Water-soluble dietary fibers have been shown to improve lipid profile and glucose metabolism in diabetes. The aim of this study was to review the effects of psyllium consumption on weight, body mass index, lipid profiles, and glucose metabolism in diabetic patients in randomized controlled trials. A comprehensive systematic search was performed in PubMed/MEDLINE, Web of Sciences, Cochrane, and Scopus by two independent researchers up to August 2019 without any time and language restrictions. The DerSimonian and Laird random-effects model method performed to calculate the pooled results. Inclusion criteria were randomized controlled trial design, adult subjects, and studies reporting the mean differences with the 95% confidence interval for outcome. Eight studies containing nine arms with 395 participants were identified and included in final analysis. Combined results found a significant reduction in triglycerides, low-density lipoprotein, fasting blood sugar, and hemoglobin A1c following psyllium consumption (weighted mean differences [WMD]: -19.18 mg/dl, 95% CI [-31.76, -6.60], I2 = 98%), (WMD: -8.96 mg/dl, 95% CI [-13.39, -4.52], I2 = 97%), (WMD: -31.71 ml/dl, 95% CI [-50.04, -13.38], I2 = 97%), and (WMD: -0.91%, 95% CI [-1.31, -0.51], I2 = 99%), respectively. There was no significant change in high-density lipoprotein, body mass index, cholesterol, and weight. In conclusion, the results demonstrated a significant reduction in triglycerides, low-density lipoprotein, fasting blood sugar, and hemoglobin A1c by psyllium intervention among diabetic patients.

Antidepressant-like and anxiolytic-like effects of hydrogen sulfide in streptozotocin-induced diabetic rats through inhibition of hippocampal oxidative stress.

Depression is highly prevalent in individuals with diabetes, and depressive symptoms are less responsive to current antidepressant therapies. Oxidative stress plays a major role both in the pathogenesis of diabetes and in major depression and anxiety disorders. Hydrogen sulfide (H2S), the third gaseous mediator, is a novel signaling molecule in the brain that has both antioxidative activity and antidepressant-like and anxiolytic-like effects. We hypothesized that H2S could produce antidepressant-like and anxiolytic-like effects in diabetic patients through its antioxidative effect. To test this hypothesis, we generated streptozotocin (STZ)-induced diabetic rats. We found that H2S alleviated depressive-like behaviors of STZ-induced diabetic rats in the forced swimming and tail suspension tests and reduced their anxiety-like behaviors in the elevated plus maze test. We also found that H2S significantly reduced levels of malondialdehyde and 4-hydroxynonenal and elevated levels of superoxide dismutase and reduced glutathione in the hippocampus of STZ-induced diabetic rats. The results provide evidence for antidepressant-like and anxiolytic-like effects of H2S in STZ-induced diabetic rats and suggest that the therapeutic effects may result from inhibition of hippocampal oxidative stress. These findings suggest that elevating H2S signaling is a potential target for treatment of depressive and anxiety disorders related to diabetes.

Disturbance of hippocampal H2S generation contributes to CUMS-induced depression-like behavior: involvement in endoplasmic reticulum stress of hippocampus.

The chronic unpredictable mild stress (CUMS) model is a widely used experimental model of depression. Exogenous stress-induced neuronal cell death in the hippocampus is closely associated with the pathogenesis of depression. Excessive and prolonged endoplasmic reticulum (ER) stress triggers cell death. Hydrogen sulfide (H2S), the third endogenous signaling gasotransmitter, plays an important role in brain functions as a neuromodulator and a neuroprotectant. We hypothesized that the disturbance of endogenous H2S generation and ER stress in the hippocampus might be involved in CUMS-induced depression-like behaviors. Thus, the present study focused on whether CUMS disturbs the generation of endogenous H2S and up-regulates ER stress in the hippocampus and whether exogenous H2S prevents CUMS-induced depressive-like behaviors. Results showed that CUMS-treated rats exhibit depression-like behavior and hippocampal ER stress responses including up-regulated levels of glucose-regulated protein 78, CCAAT/enhancer binding protein homologous protein, and cleaved caspase-12 expression, while the endogenous generation of H2S in the hippocampus is suppressed in CUMS-treated rats. Furthermore, exogenous H2S prevents CUMS-induced depression-like behavior. These data indicated that CUMS-induced depression-like behaviors are related to the disturbance of endogenous H2S generation and ER stress in the hippocampus and suggested that endogenous H2S and ER stress are novel treatment targets of depression.

Hemophagocytic lymphohistiocytosis caused by herpes simplex virus type 1 in a young adult: a case report with literature review.

Hemophagocytic lymphohistiocytosis is a severe hyperinflammatory syndrome that can be potentially life-threatening without appropriate treatment. Although viral infection is the most common trigger of hemophagocytic lymphohistiocytosis, cases of herpes simplex virus type 1-induced hemophagocytic lymphohistiocytosis are rare in adults. This study aims to provide a comprehensive overview of the clinical characteristics and treatment outcomes associated with HSV-1-induced HLH. We herein report an adult case of hemophagocytic lymphohistiocytosis caused by herpes simplex virus type 1, diagnosed on the basis of peripheral blood metagenomic next-generation sequencing results. The patient exhibited a favorable response to treatment, involving dexamethasone, intravenous immunoglobulin, and acyclovir. Notably, etoposide administration was deemed unnecessary, and there has been no recurrence of the disease within the year following treatment. Early and sensitive recognition, rapid and precise diagnosis, and timely and appropriate treatment facilitated the successful treatment of this case.

circTLK1 facilitates the proliferation and metastasis of renal cell carcinoma by regulating miR-495-3p/CBL axis.

Renal cell carcinoma (RCC) is a common urological malignancy. Circular RNAs (circRNAs) have been confirmed to play an important regulatory role in various cancers. This study aimed to investigate the role and potential mechanism of circTLK1 (hsa_circ_0004442) in RCC. The levels of circTLK1, Cbl proto-oncogene (CBL), and microRNA-495-3p (miR-495-3p) were detected by quantitative reverse transcription polymerase chain reaction or western blot. Cell proliferation, cycle arrest and apoptosis, migration, and invasion were assessed by colony formation, flow cytometry, scratch, and transwell assays. The levels of E-cadherin and Vimentin were measured by western blot. The targeting relationship between miR-495-3p and miR-495-3p or CBL was verified by dual-luciferase reporter assay. Tumor growth in vivo was evaluated by xenograft assay. The results found that circTLK1 and CBL were up-regulated in RCC tissues and cells. Silencing of circTLK1 or CBL inhibited proliferation and metastasis and accelerated apoptosis in RCC cells. In addition, circTLK1 directly bound to miR-495-3p, and CBL was the target of miR-495-3p. circTLK1 sponged miR-495-3p to increase CBL expression. Moreover, knockdown of circTLK1 suppressed tumor growth in vivo. In conclusion, down-regulation of circTLK1 restrained proliferation and metastasis and promoted apoptosis in RCC cells by modulating miR-495-3p/CBL axis.

TNF-α enhances vascular cell adhesion molecule-1 expression in human bone marrow mesenchymal stem cells via the NF-κB, ERK and JNK signaling pathways.

The migration of circulating mesenchymal stem cells (MSCs) to injured tissue is an important step in tissue regeneration and requires adhesion to the microvascular endothelium. The current study investigated the underlying mechanism of MSC adhesion to endothelial cells during inflammation. In in vitro MSC culture, tumor necrosis factor­α (TNF­α) increased the level of vascular cell adhesion molecule­1 (VCAM­1) expression in a dose­dependent manner. The nuclear factor-κB (NF-κB), extracellular signal­regulated kinase (ERK) and c­Jun N­terminal kinase (JNK) signaling pathway inhibitors, pyrrolidine dithiocarbamate (PDTC), U0126 and SP600125, respectively, suppressed VCAM­1 expression induced by TNF­α at the mRNA and protein levels (P<0.05). TNF­α augmented the activation of NF­κB, ERK and JNK, and promoted MSC adhesion to human umbilical vein endothelial cells; however, the inhibitors of NF­κB, ERK and JNK did not affect this process in these cells. The results of the current study indicate that adhesion of circulating MSCs to the endothelium is regulated by TNF-α-induced VCAM-1 expression, which is potentially mediated by the NF­κB, ERK and JNK signaling pathways.

Long-term health effects of persistent exposure to low-dose lr192 gamma-rays.

The aim of the present study was to investigate the effect of persistent low-dose iridium-192 (Ir192) exposure on immunological function, chromosome aberration and the telomerase activity of bone marrow mononuclear cells (BMNCs), in order to increase clinical knowledge of the late effects of persistent low-dose Ir192 gamma-ray exposure. Patients (n=54) accidentally exposed to persistent low-dose Ir192 were included in this 10-year follow-up study. Clinical symptoms, peripheral blood, bone marrow, cellular and humoral immune status, chromosome aberrations and the telomerase activity of BMNCs were analyzed in this study. Exposure to low-dose Ir192 resulted in different degrees of clinical symptoms and significantly lowered complement C3 and C4 levels, CD3+, CD4+ and CD8+ T cell levels, the lymphocyte transformation rate and the percentage of natural killer (NK) cells. It also led to increases in peripheral blood and bone marrow abnormality rates, chromosome aberration rate and BMNC telomerase activity. Exposure to persistent low-dose Ir192 radiation resulted in different degrees of immune dysfunction, and abnormalities of blood cells and bone marrow, which recovered within 1-3 years. Chromosome aberrations were observed to take 5-10 years to recover. However, it would take >10 years for the telomerase activity of BMNCs to be reduced to normal levels. A prolonged follow-up time is required in order to monitor clonal proliferative diseases such as leukemia.

[Magnetic-activated cell sorting combined with multiplex ligation-dependent probe amplification for detecting molecular cytogenetic abnormalities in multiple myeloma].

OBJECTIVE: To investigate the reliability of magnetic-activated cell sorting (MACS) combined with multiplex ligation-dependent probe amplification (MLPA) in the detection of the molecular cytogenetic abnormalities in multiple myeloma. METHODS: The bone marrow cells were collected from 29 patients with multiple myeloma. The immuno magnetically sorted and unsorted cells were detected for TP53 and RB1 expressions using MLPA probes and the results were compared with fluorescent in situ hybridization (FISH). RESULTS: The detection success rate was 100% for MLPA, which yielded results with an concordance rate of 99.1% with the FISH results. The positivity rates of MLPA and FISH were both increased after immunomagnetic sorting of the bone marrow cells. CONCLUSION: MLPA can well suit the clinical needs for detecting molecular cytogenetic abnormalities in multiple myeloma, and the samples should be immuno magnetically sorted before the assay.