A Novel Method of Making Hinges Using a Newly Designed Sharp Rongeur to Enhance Radiological and Clinical Outcomes in French-Door Cervical Expansive Laminoplasty.

OBJECTIVE: Although the lamina open angle of making hinges is closely related to the outcomes of French-door laminoplasty (FDL) for treatment of cervical spondylosis, there have been no methods to predict the lamina open angle preoperatively as yet. The aim of this study was to investigate the accuracy of predicting the laminal open angle using our newly designed sharp rongeur, and to compare the postoperative outcomes and complications between the methods of making hinges using the newly designed sharp rongeur and the traditional high-speed micro-drill during the FDL. METHODS: This was a single-center retrospective study. Following the approval of the institutional ethics committee, a total of 39 patients (Male: 28; Female: 11) diagnosed with cervical spondylos who underwent FDL in our institution between January 2018 and May 2019 were enrolled. Patients were divided into two groups based on the method of making hinges (sharp rongeur: 22 cases; high-speed micro-drill: 17 cases). The average age at surgery was 59.1 years (range: 16-85 years). The radiological parameters, clinical outcomes, modified Japanese Orthopaedic Association (mJOA) scale score, and the recovery rate of mJOA were recorded and compared between the groups, respectively. The radiological parameters and clinical measurements at pre- and post-operation stages were compared using the paired-sample t-test, the Wilcoxon signed-rank test, and the Friedman's test, and variables in the two groups were analyzed using an unpaired Student's t-test or a Mann-Whitney U test. RESULTS: The average follow-up period was 20.4 months (range: 14.0-25.9 months), the postoperative open angle was 60.13° ± 3.69° in the rongeur group with 22.78° ± 4.34° of angular enlargement, which was significantly lower than that of 68.96° ± 1.00° in the micro-drill group with 32.75° ± 4.22° of angular enlargement (U = 19.000, p < 0.001). The rongeur group showed a higher fusion rate (34.1% vs 14.7%, χ2  = 11.340, p = 0.001), and a lower fracture rate of the lamina (7.8% vs 25.5%, χ2  = 14.185, p < 0.001) at 1-month post-surgery, compared to the micro-drill group. There were no significant differences in the clinical outcomes and postoperative complications between the two groups (p > 0.05), except in the recovery rate of mJOA scores (0.836 ± 0.138 vs 0.724 ± 0.180, U = 115.000, p = 0.042) and neck disability index (NDI) at the final follow-up (7.55 ± 10.65 vs 14.71 ± 8.72, U = 94.000, p = 0.008). CONCLUSIONS: The special sharp rongeur with a tip angle of 20° could be a preferred method to make hinges during FDL, which can predict the laminal open angle accurately and enlarge it to about 23°, thus reducing the fracture rate and accelerating the bony fusion of hinges compared with the outcomes of the traditional micro-drill method.

Oxidative Stress and Intervertebral Disc Degeneration: Pathophysiology, Signaling Pathway, and Therapy.

Intervertebral disc degeneration (IDD), characterized as decreased proteoglycan content, ossification of endplate, and decreased intervertebral height, is one of the major reasons of low back pain, which seriously affects the quality of life and also brings heavy economic burden. However, the mechanisms leading to IDD and its therapeutic targets have not been fully elucidated. Oxidative stress refers to the imbalance between oxidation and antioxidant systems, between too many products of reactive oxygen species (ROS) and the insufficient scavenging function. Excessive ROS can damage cell lipids, nucleic acids and proteins, which has been proved to be related to the development of a variety of diseases. In recent years, an increasing number of studies have reported that oxidative stress is involved in the pathological process of IDD. Excessive ROS can accelerate the IDD process via inducing the pathological activities, such as inflammation, apoptosis, and senescence. In this review, we focused on pathophysiology and molecular mechanisms of oxidative stress-induced IDD. Moreover, the present review also summarized the possible ideas for the future therapy strategies of oxidative stress-related IDD.

The effects of bariatric surgery on dyslipidemia and insulin resistance in overweight patients with or without type 2 diabetes: a systematic review and network meta-analysis.

Obesity has become an epidemic in several regions globally; it may lead to cardiovascular diseases, diabetes, and dyslipidemia. Despite many therapies, all bariatric procedures fail in some patients. There is a lack of literature comparing treatment effects on specific metabolic indexes. PubMed, Embase, and Cochrane Central Register of Controlled Trials were searched for relevant articles. GeMTC and R software were used to perform a network meta-analysis, draw forest plots, investigate the possibility of statistical heterogeneity, generate I2 statistics, rank probabilities, and evaluate relative effects of surgical procedures. All analyses were based on a Bayesian consistency model. We included 35 randomized controlled trials, comprising 2198 individuals and 13 interventions. For patients with high insulin resistance, single-anastomosis (mini-) gastric bypass (SAGB) and sleeve gastrectomy (SG) may be effective options, with mean differences (95% confidence intervals [CIs]) of -4.45 (-9.04 to -.34) and -4.23 (-6.74 to -2.22), respectively, compared with control groups. For patients with severe dyslipidemia, in addition to SAGB and SG, duodenal switch (DS) may be an effective surgery, with mean differences (95% CIs) of -.97 (-1.39 to -.55), -1.98 (-3.76 to -.19), .53 (.04 to 1.04), and -.94 (-1.66 to -.16) compared with control groups in terms of triglycerides, total cholesterol, high-density lipoprotein cholesterol (HDL-C), and low-density lipoprotein cholesterol (LDL-C) concentrations, respectively. In adult overweight patients with or without diabetes, SAGB and SG are most effective at ameliorating insulin resistance. SAGB, Roux-en-Y gastric bypass + omentectomy, and DS are useful for reducing triglycerides, total cholesterol, and LDL-C. SG + omentectomy elevates HDL-C concentrations best. Adjustable gastric band and biliopancreatic diversion may not control insulin resistance or dyslipidemia well.

Association Between Serum Insulin and C-Peptide Levels and Breast Cancer: An Updated Systematic Review and Meta-Analysis.

BACKGROUND: Several studies have reported that hyperinsulinemia plays a part in the etiology of breast cancer. However, no consensus has been reached. Therefore, we conducted a meta-analysis to explore the role of insulin and C-peptide in breast cancer. METHODS: A systematic search in PubMed, Embase, and The Cochrane Library was conducted up to September, 2020. Standardized mean differences (SMDs) with 95% confidence intervals (CIs) were used to measure effect sizes. Publication bias was assessed using the Egger test. Stability of these results was evaluated using sensitivity analyses. RESULTS: Fourteen articles including 27,084 cases and five articles including 2,513 cases were extracted for serum insulin levels and C-peptide levels. We found that C-peptide levels were positively associated with breast cancer with overall SMD = 0.37 (95% CI = 0.09-0.65, I2 = 89.1%). Subgroup analysis by control source illustrated a positive relationship between breast cancer and C-peptide levels in population-based control. Subgroup analysis by C-peptide level indicated a positive correlation between breast cancer and C-peptide levels no matter C-peptide levels in case group is ≤3 ng/ml or >3 ng/ml. Subgroup analysis by age showed that C-peptide level positively correlated to breast cancer in women between the ages of 50 and 60. However, we did not identify any relationship between breast cancer and insulin levels (SMD = 0.22, 95% CI = -0.06-0.50, I2 = 97.3%). CONCLUSION: This meta-analysis demonstrated that C-peptide levels were positively related to breast cancer in women, and no relationship between insulin levels and breast cancer was found.

Ghrelin system is involved in improvements in glucose metabolism mediated by hyperbaric oxygen treatment in a streptozotocin­induced type 1 diabetes mouse model.

Type 1 diabetes mellitus (T1DM) is an autoimmune disorder for which the only effective therapy is insulin replacement. Hyperbaric oxygen (HBO) therapy has demonstrated potential in improving hyperglycemia and as a treatment option for T1DM. Ghrelin and HBO have been previously reported to exert proliferative, anti­apoptotic and anti­inflammatory effects in pancreatic cells. The present study investigated the mechanism underlying HBO­ and ghrelin system­mediated regulation of glucose metabolism. Male C57BL/6 mice were intraperitoneally injected with streptozotocin (STZ; 150 mg/kg) to induce T1DM before the diabetic mice were randomly assigned into the T1DM and T1DM + HBO groups. Mice in the T1DM + HBO group received HBO (1 h; 100% oxygen; 2 atmospheres absolute) daily for 2 weeks. Significantly lower blood glucose levels and food intake were observed in mice in the T1DM + HBO group. Following HBO treatment, islet ß­cell area were increased whereas those of α­cell were decreased in the pancreas. In addition, greater hepatic glycogen storage in liver was observed, which coincided with higher pancreatic glucose transporter 2 (GLUT2) expression levels and reduced hepatic GLUT2 membrane trafficking. There were also substantially higher total plasma ghrelin concentrations and gastric ghrelin­O­acyl transferase (GOAT) expression levels in mice in the T1DM + HBO group. HBO treatment also abolished reductions in pancreatic GOAT expression levels in T1DM mice. Additionally, hepatic growth hormone secretagogue receptor­1a levels were found to be lower in mice in the T1DM + HBO group compared with those in the T1DM group. These results suggest that HBO administration improved glucose metabolism in a STZ­induced T1DM mouse model. The underlying mechanism involves improved insulin­release, glucose­sensing and regulation of hepatic glycogen storage, an observation that was also likely dependent on the ghrelin signalling system.

L-Carnitine Is Involved in Hyperbaric Oxygen-Mediated Therapeutic Effects in High Fat Diet-Induced Lipid Metabolism Dysfunction.

Lipid metabolism dysfunction and obesity are serious health issues to human beings. The current study investigated the effects of hyperbaric oxygen (HBO) against high fat diet (HFD)-induced lipid metabolism dysfunction and the roles of L-carnitine. C57/B6 mice were fed with HFD or normal chew diet, with or without HBO treatment. Histopathological methods were used to assess the adipose tissues, serum free fatty acid (FFA) levels were assessed with enzymatic methods, and the endogenous circulation and skeletal muscle L-carnitine levels were assessed with liquid chromatography-tandem mass spectrometry (LC-MS/MS). Additionally, western blotting was used to assess the expression levels of PPARα, CPT1b, pHSL/HSL, and UCP1. HFD treatment increased body/adipose tissue weight, serum FFA levels, circulation L-carnitines and decreased skeletal muscle L-carnitine levels, while HBO treatment alleviated such changes. Moreover, HFD treatment increased fatty acid deposition in adipose tissues and decreased the expression of HSL, while HBO treatment alleviated such changes. Additionally, HFD treatment decreased the expression levels of PPARα and increased those of CPT1b in skeletal muscle, while HBO treatment effectively reverted such changes as well. In brown adipose tissues, HFD increased the expression of UCP1 and the phosphorylation of HSL, which was abolished by HBO treatment as well. In summary, HBO treatment may alleviate HFD-induced fatty acid metabolism dysfunction in C57/B6 mice, which seems to be associated with circulation and skeletal muscle L-carnitine levels and PPARα expression.

Central nesfatin-1 activates lipid mobilization in adipose tissue and fatty acid oxidation in muscle via the sympathetic nervous system.

Little is known about the influence of central nesfatin-1 on lipid metabolism under diabetic conditions. The main objective of this study was to characterize the mechanisms by which central nesfatin-1 regulates lipid metabolism in streptozotocin (STZ)-induced type 2 diabetes mellitus (T2DM) and whether the sympathetic nervous system is involved. Male Kunming mice were fed high-fat diets (HFDs) and were treated twice with low-dose STZ (100 mg/kg, intraperitoneal [IP]) to generate the T2DM model. Pharmacological adrenergic blockage (phentolamine 10 mg/kg, propranolol 0.017 mmol) and surgical denervation of sympathetic nervous system of the hindlimb and inguinal fat were used to block nerve conduction to determine whether the effect of central nesfatin-1 required the hypothalamic-sympathetic nervous system axis. Plasma free fatty acid (FFA) and insulin levels were measured. AMP-activated protein kinase (AMPK) levels in skeletal muscle and hormone-sensitive lipase and adipose triglycerides lipase (HSL/ATGL) levels in white adipose tissue (WAT) were measured using western blot. mRNA expression of AMPK was measured. We found that there were significantly fewer NUCB2/nesfatin-1 immunoreactive neurons in the paraventricular nucleus (PVN) and supraoptic nucleus (SON) in T2DM mice. Central nesfatin-1 administration decreased levels of plasma FFA significantly and activated AMPK to enhance fatty-acid oxidation in skeletal muscle in T2DM mice. In addition, HSL and ATGL were significantly activated during triglyceride mobilization in WAT triggered by central nesfatin-1 administration. Adrenergic blockade and morphological denervation of the sciatic and femoral nerves reduced these changes. Taken together, these data suggest that central nesfatin-1 regulates peripheral lipid metabolism in type 2 diabetes via the sympathetic nervous system.

Relation of Circulating Resistin to Insulin Resistance in Type 2 Diabetes and Obesity: A Systematic Review and Meta-Analysis.

Background: Resistin, a cysteine-rich polypeptide encoded by the RETN gene, which plays an important role in many mechanisms in rodent studies, including lipid metabolism, inflammation and insulin resistance. Nevertheless, the relationship between resistin and insulin resistance in humans is under debate. The present study was designed to clarify the correlation between resistin and insulin resistance. Methods: A systematic literature search was performed using PubMed, Embase and Cochrane Library until March 3, 2019 with the keywords "resistin" and "insulin resistance." Funnel plots and Egger's test were used to detect publication bias. A random-effects model was used to calculate the pooled effect size. Subgroup analysis and meta regression was performed to identify the sources of heterogeneity. Results: Fifteen studies were included in our systematic review. Among them, 10 studies with Pearson coefficients were used for meta-analysis. We found resistin levels were weakly correlated with insulin resistance in those with T2DM and obesity (r = 0.21, 95% CI: 0.06-0.35, I 2 = 59.7%, P = 0.003). Nevertheless, subgroup analysis suggested that circulating resistin levels were significantly positively correlated with insulin resistance in individuals with hyperresistinemia (≥14.8 ng/ml) (r = 0.52, 95% CI: 0.35-0.68, I 2 = 0.0%, P = 0.513). And there was no relationship between circulating resistin and insulin resistance in those with normal circulating resistin levels (<14.8 ng/ml) (r = 0.08, 95% CI: -0.01-0.18, I 2 = 0.0%, P = 0.455). Publication bias was insignificant (Egger's test P = 0.592). Conclusion: In T2DM and obese individuals, resistin levels were positively correlated with insulin resistance in those with hyperresistinemia, but not in those with normal circulating resistin levels.