We hypothesized that a part of therapeutic effects of endurance training on insulin resistance is mediated by increase in cardiac and skeletal muscle mitochondrial lactate transporter, monocarboxylate transporter 1 (MCT1). Therefore, we examined the effect of 7 weeks endurance training on the mRNA and protein expression of MCT1 and MCT4 and their chaperon, CD147, on both sarcolemmal and mitochondrial membrane, separately, in healthy and type 2 diabetic rats. Diabetes was induced by injection of low dose of streptozotocin and feeding with high-fat diet. Insulin resistance was confirmed by homeostasis model assessment-estimated insulin resistance index and accuracy of two membranes separation was confirmed by negative control markers (glucose transporter 1 and cytochrome c oxidase. Real-time PCR and western blotting were used for mRNA and protein expression, respectively. Diabetes dramatically reduced MCT1 and MCT4 mRNA and their expression on sarcolemmal membrane whereas the reduction in MCT1 expression was less in mitochondrial membrane. Training increased the MCT1 mRNA and protein expression in both membranes and decreased insulin resistance as an adaptive consequence. In both tissues increase in CD147 mRNA was only parallel to MCT1 expression. The response of MCT1 on sarcolemmal and mitochondrial membranes was different between cardiac and skeletal muscles which indicate that intracellular lactate kinetic is tissue specific that allows a tissue to coordinate whole organism metabolism.

Traumatic brain injury (TBI) is a leading cause of mortality and long-lasting disability globally. Although novel treatment options have been investigated, no effective therapeutic opportunities for TBI exist. Accumulating studies demonstrated that the paracrine mechanisms of stem cells may allow them to orchestrate regenerative processes after TBI. So far, very little attention has been paid to the beneficial effects of human neural stem cells (hNSCs) in comparison to their exosomes as a paracrine mechanism. This study is aimed at comparing the effect of hNSCs with their exosomes in a TBI model. For in vitro assessments, we cultured hNSCs using the neurosphere method and isolated hNSC-derived exosomes from culture supernatants. For in vivo experiments, male rats were divided into three groups ( n = 8 /group): TBI group: rats were subjected to a unilateral mild cortical impact; hNSC group: rats received a single intralesional injection of 2 × 10 6 hNSCs after TBI; and exosome group: rats received a single intralesional injection of 63 μg protein of hNSC-derived exosomes after TBI. Neurological assessments, neuroinflammation, and neurogenesis were performed at the predetermined time points after TBI. Our results indicated that the administration of exosomes improved the neurobehavioral performance measured by the modified neurological severity score (mNSS) on day 28 after TBI. Furthermore, exosomes inhibited the expression of reactive astrocytes as a key regulator of neuroinflammation marked by GFAP at the protein level, while enhancing the expression of Doublecortin (DCX) as a neurogenesis marker at the mRNA level. On the other hand, we observed that the expression of stemness markers (SOX2 and Nestin) was elevated in the hNSC group compared to the exosome and TBI groups. To sum up, our results demonstrated that the superior effects of exosomes versus parent hNSCs could be mediated by improving mNSS score and increasing DCX in TBI. Considerably, more work will need to be done to determine the beneficial effects of exosomes versus parent cells in the context of TBI.

Scan to discover online Background & Objective: Concentration of low-density lipoprotein (LDL) is a known risk factor for cardiovascular disease which is routinely measured or calculated as LDL-C in clinical laboratories. In order to decrease the cost, instead of its measuring, it is recommended to calculate it using multiple formulas that have been introduced up to now. The aim of this study was to assess the results of various formulas and comparison of these results with those of measuring method and to clarify the best formula for the Iranian population. Methods: Concentrations of total cholesterol (TC), triglyceride (TG), cholesterol of high-density lipoprotein (HDL-C) and LDL-C in serums of 471 overnight fasting individuals were measured and also LDL-Cs of these samples were calculated by eleven different formulas according to their TC, TG, and HDL-C concentrations. Subsequently, results of measured and calculated LDL-C were analyzed statistically by paired t-test, correlation coefficient, and Passing-Bablok regression. In addition, for clinical evaluation, the differences between calculated and measured mean results were calculated and compared with an allowable total error. Results: Paired t-test unraveled a significant difference between the results of measured and calculated LDL-C by various formulas. But for some formulas, these differences were not clinically significant. The best clinical and statistical agreement (correlation coefficient) was obtained by the Friedewald equation. Conclusion: By using validated methods which have correct calibration and control system for measuring TC, TG, and HDL-C, we can use the Friedewald formula for calculating LDL-C in serum samples with TG up to 400 mg/dL.

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SummaryBackgroundGlycated hemoglobin (HbA1c) measuring has a critical role in the monitoring and diagnosis of diabetes. So, the analytical performance of its measuring method must be acceptable. Clinical laboratories should continuously monitor the performance of their commercial methods, both by using proper internal quality control (IQC) and by participating in external quality assessment schemes (EQAS).MethodsIn January and August 2016, two different freshly prepared commutable patient QC samples were sent to over 1000 laboratories, but 682 and 925 different laboratories which were used five common commercial methods for measuring HbA1c, included in this study during 23th and 24th runs of the external quality assessment program (EQAP), respectively. Target values for total group and also for peer groups were calculated. The performance of each method and laboratory were determined according to two different allowable total errors (TEa), including ±6% and ±20%, which are suggested by the National Glycohemoglobin Standardization Program (NGSP) and Reference Health Laboratory of Iran, respectively.ResultsConsidering TEa of ±20% in evaluating HbA1c commercial methods and laboratory performances, pass rates ranged from 97% to 98% during EQAP-23 and EQAP-24, respectively. But when this evaluation was performed according to TEa of ±6%, pass rates decreased significantly to 60% and 62%, respectively.ConclusionsUsing improper analytical goals has led to misinterpretation of EQA results. In order to maintain the clinical usefulness of HbA1c results, we need to reduce TEa of ±20% to ±6% and improve HbA1c measuring method performance. Although, with TEa of ±6% our pass rates are not so bad.