Normative Reference Values of the Tibial Nerve in Healthy Individuals Using Ultrasonography:A Systematic Review and Meta-Analysis

Background: High-resolution ultrasound of the tibial nerve has been used for screening of several neurologic disorders, but normative reference values of tibial nerve cross-sectional areas (CSA) have not been well established. Thus, the present meta-analysis was performed to generate normative estimates of tibial nerve CSA at various sites of the lower limb based on ultrasonography.Methods: Google Scholar, Scopus and PubMed were searched for potential studies. Studies were required to report tibial nerve CSA in healthy individuals to be included. A random-effect meta-analysis was performed to calculate tibial nerve CSA values. Subgroup and statistical analyses were performed to study covariates.Results: Forty-eight eligible articles consisting of 2695 limbs were included. The average tibial nerve CSA was found to be 10.9 mm2 at the ankle (95% CI: 9.9-11.8) and should not exceed 11.8 mm2 in healthy adults. At the popliteal fossa, the overall CSA was 21.7 mm2 (95% CI: 17.5-25.8) in healthy adults. At both sites, the average tibial nerve CSA was significantly larger in adults than in children, and the differences by geographical region were not statistically significant. At the ankle, tibial nerve CSA increased with age and body mass index, while at the popliteal fossa it increased with age and weight.Conclusions: our findings indicate that the tibial nerve varied not only along its course but also among sub-variables. Establishing normal references values of tibial nerve CSA is helpful to differentiate healthy from diseased tibial nerves such as in diabetic peripheral neuropathy or tarsal tunnel syndrome.</p

Ursolic acid and luteolin-7-glucoside improves rat plasma lipid profile and increases liver glycogen content through glycogen synthase kinase-3

In the present study, two phytochemicals - ursolic acid (UA) and luteolin-7-glucoside (L7G) - were assessed in vivo in healthy rats regarding effects on plasma glucose and lipid profile (total cholesterol, HDL and LDL), as well as liver glycogen content, in view of their importance in the aetiology of diabetes and associated complications. Both UA and L7G significantly decreased plasma glucose concentration. UA also significantly increased liver glycogen levels accompanied by phosphorylation of glycogen synthase kinase-3 (GSK3). The increase in glycogen deposition induced by UA (mediated by GSK3) could have contributed to the lower plasma glucose levels observed. Both compounds significantly lowered total plasma cholesterol and low-density lipoprotein levels, and, in addition, UA increased plasma high-density lipoprotein levels. Our results show that UA particularly may be useful in preventable strategies for people at risk of developing diabetes and associated cardiovascular complications by improving plasma glucose levels and lipid profile, as well as by promoting liver glycogen deposition.MFA and CMS were supported by the Foundation for Science and Technology, Portugal, through the grants SFRH/BD/12527/2003 and SFRH/BD/42566/2007, respectively. This work was supported by the Foundation for Science and Technology, Portugal, research grant POCI/AGR/62040/2004

Prediction of seizure control in non-ketotic hyperglycemic induced seizures

<p>Abstract</p> <p>Background</p> <p>To study the factors predictive for seizure control in non-ketotic hyperglycemic induced seizures (NKHS).</p> <p>Methods</p> <p>We studied 21 patients who were clinically diagnosed as NKHS at Khon Kaen University hospital, Thailand. Multiple linear regression analysis was used to identify the factors predictive for seizure control.</p> <p>Results</p> <p>Most patients had no previous history of diabetes and presented with repetitive partial seizures. The mean number of seizure attacks was 45 times prior to admission. The average duration to terminate seizure was 36 hours and significantly predicted by frequency of seizures (estimate 0.9, p value 0.013).</p> <p>Conclusion</p> <p>Frequency of seizures is the only predictive factor for the success of seizure control in NKHS.</p

Perspectives and Potential Applications of Mitochondria-Targeted Antioxidants in Cardiometabolic Diseases and Type 2 Diabetes

There is abundant evidence to suggest that mitochondrial dysfunction is a main cause of insulin resistance and related cardiometabolic comorbidities. On the other hand, insulin resistance is one of the main characteristics of type 2 diabetes, obesity, and metabolic syndrome. Lipid and glucose metabolism require mitochondria to generate energy, and when O2 consumption is low due to inefficient nutrient oxidation, there is an increase in reactive oxygen species, which can impair different types of molecules, including DNA, lipids, proteins, and carbohydrates, thereby inducing proinflammatory processes. Factors which contribute to mitochondrial dysfunction, such as mitochondrial biogenesis and genetics, can also lead to insulin resistance in different insulin-target tissues, and its association with mitochondrial dysfunction can culminate in the development of cardiovascular diseases. In this context, therapies that improve mitochondrial function may also improve insulin resistance. This review explains mechanisms of mitochondrial function related to the pathological effects of insulin resistance in different tissues. The pathogenesis of cardiometabolic diseases will be explained from a mitochondrial perspective and the potential beneficial effects of mitochondria-targeted antioxidants as a therapy for modulating mitochondrial function in cardiometabolic diseases, especially diabetes, will also be considered.Contract grant sponsor: PI10/1195; Contract grant sponsor: PI 12/1984; Contract grant sponsor: CIBERehd CB06/04/0071; Contract grant sponsor: PROMETEO 2010/060; Contract grant sponsor: ACOMP/2012/042; Contract grant sponsor: ACOMP/2012/045; Contract grant sponsor: ACOMP2013/061; Contract grant sponsor: European Regional Development Fund (ERDF)

Insulin resistance, lipotoxicity, type 2 diabetes and atherosclerosis: the missing links. The Claude Bernard Lecture 2009

Insulin resistance is a hallmark of type 2 diabetes mellitus and is associated with a metabolic and cardiovascular cluster of disorders (dyslipidaemia, hypertension, obesity [especially visceral], glucose intolerance, endothelial dysfunction), each of which is an independent risk factor for cardiovascular disease (CVD). Multiple prospective studies have documented an association between insulin resistance and accelerated CVD in patients with type 2 diabetes, as well as in non-diabetic individuals. The molecular causes of insulin resistance, i.e. impaired insulin signalling through the phosphoinositol-3 kinase pathway with intact signalling through the mitogen-activated protein kinase pathway, are responsible for the impairment in insulin-stimulated glucose metabolism and contribute to the accelerated rate of CVD in type 2 diabetes patients. The current epidemic of diabetes is being driven by the obesity epidemic, which represents a state of tissue fat overload. Accumulation of toxic lipid metabolites (fatty acyl CoA, diacylglycerol, ceramide) in muscle, liver, adipocytes, beta cells and arterial tissues contributes to insulin resistance, beta cell dysfunction and accelerated atherosclerosis, respectively, in type 2 diabetes. Treatment with thiazolidinediones mobilises fat out of tissues, leading to enhanced insulin sensitivity, improved beta cell function and decreased atherogenesis. Insulin resistance and lipotoxicity represent the missing links (beyond the classical cardiovascular risk factors) that help explain the accelerated rate of CVD in type 2 diabetic patients

Additional low-pressure pulmonary recruitment for reducing post-laparoscopic shoulder pain in gynecologic laparoscopy: a randomized controlled trial

Objective To evaluate the effectiveness of additional low-pressure pulmonary recruitment in reducing postoperative shoulder pain. Methods A double-blind randomized controlled trial was conducted at Srinagarind Hospital between May 2021 and October 2021. Forty patients who underwent laparoscopic gynecologic surgery were randomized into either an intervention group that received additional low-pressure pulmonary recruitment (30 cmH2O) (n=20) or a control group (n=20). Shoulder pain was evaluated using a numerical rating scale from 0 to 10, 24, and 48 hours after the operation. Results The mean±standard deviation of shoulder pain at 24 hours after the operation of both the intervention and control groups were 2.10±2.27 and 1.45±1.73 points, respectively. The shoulder pain at 48 hours after the operation of the intervention and control groups were 1.15±1.46 and 0.85±1.73 points, respectively. There were no statistical differences in the mean difference between the two groups at 24 and 48 hours after operation (P=0.49; 95% confidence interval [CI], −0.61 to 1.91 and P=1.00; 95% CI, −0.96 to 1.56, respectively). No statistically significant differences were observed in additional analgesic medications used in either group, such as intravenous morphine or oral acetaminophen. Conclusion Additional low-pressure pulmonary recruitment to reduce shoulder pain after laparoscopic surgery for benign gynecologic diseases did not show a significant benefit compared to the control group, especially when administering postoperative around-the-clock analgesia