Prevalence of Work-Related Musculoskeletal Disorders in Iranian Physical Therapists: A Cross-sectional Study

Objective

The purpose of this study was to determine the prevalence of musculoskeletal disorders among Iranian physical therapists.

The relative locations of the supraorbital,infraorbital, and mental foramina: A cadaveric study

The purpose of this study is to investigate the applicability of the current surgical guideline stating that the main facial foramina that transmit cutaneous nerves to the face (supraorbital notch/foramen, infraorbital foramen, and mental foramen) are equidistant from the midline in European and Hispanic populations. Previous studies suggest this surgical guideline is not applicable for all ethnicities; however, to our knowledge, no data have been published regarding the accuracy of this guideline pertaining to the Hispanic population. An experimental study was performed on 67 cadavers donated to the Human Anatomy Program at UT Health San Antonio. The supraorbital, infraorbital, and mental foramina were dissected and midline structures including the crista galli, internasal suture, anterior nasal spine, and mandibular symphysis were identified. The distance from each foramen to midline was recorded using a digital caliper. For all cadavers/ethnicities studied, the supraorbital, infraorbital, and mental foramina were 25.32 mm, 29.57 mm, and 25.55 mm to the midline, respectively. Thus, the infraorbital foramen is located significantly more lateral compared to the supraorbital (p < 0.0001) and mental foramina (p < 0.0001). After dividing the sample based on ethnicity, this relationship was also true for the European sample and tended to be true for the Hispanic sample. Significant anatomical variations exist in the current surgical guideline stating that the supraorbital foramen, infraorbital foramen, and mental foramen are equidistant from the midline. Clinicians may need to adjust their methodology during surgical procedures of the face in order to optimize patient care.     

Elevated IL-38 Serum Levels in Newly Diagnosed Multiple Sclerosis and Systemic Sclerosis Patients

ObjectiveInterleukin (IL)-38 is a newly discovered member of the IL-1 cytokine family with a proposed anti-inflammatory profile. We studied the probable role of this cytokine in the pathogenesis of two autoimmune diseases: multiple sclerosis (MS) and systemic sclerosis (SSc).Subjects and MethodsA total of 87 MS patients and 86 SSc patients (40 new and recently untreated cases and 46 treated cases) were selected for this study. Eighty-seven and 80 age- and sex-matched healthy subjects were included as controls for MS and SSc, respectively. Clinical and paraclinical features of the patients were recorded at the time of sampling. Serum IL-38 was measured by ELISA.ResultsLevels of serum IL-38 did not significantly differ between the total MS or SSc patients compared to controls. However, levels of IL-38 were significantly higher in newly diagnosed patients of MS (206.43 ± 38.97 pg/mL, p < 0.0001) than in those previously treated (158.04 ± 39.45 pg/mL). Similarly, new/recently untreated cases of SSc patients showed increased IL-38 levels (185.19 ± 36.27 pg/mL, p = 0.001) compared to treated patients (166.82 ± 33.08 pg/mL). IL-38 levels in newly diagnosed MS patients (p = 0.007) and new/recently untreated SSc patients (p = 0.032) were significantly higher than those in healthy controls.ConclusionThe higher serum levels of IL-38 in new or recently untreated cases of MS and SSc patients than in treated patients and healthy controls suggest the possible role of this cytokine in the development of these diseases or as part of a feedback loop to attenuate the inflammatory conditions in early stages of these diseases.     

Genetic activation of pyruvate dehydrogenase alters oxidative substrate selection to induce skeletal muscle insulin resistance

The pyruvate dehydrogenase complex (PDH) has been hypothesized to link lipid exposure to skeletal muscle insulin resistance through a glucose-fatty acid cycle in which increased fatty acid oxidation increases acetyl-CoA concentrations, thereby inactivating PDH and decreasing glucose oxidation. However, whether fatty acids induce insulin resistance by decreasing PDH flux remains unknown. To genetically examine this hypothesis we assessed relative rates of pyruvate dehydrogenase flux/mitochondrial oxidative flux and insulin-stimulated rates of muscle glucose metabolism in awake mice lacking pyruvate dehydrogenase kinase 2 and 4 [double knockout (DKO)], which results in constitutively activated PDH. Surprisingly, increased glucose oxidation in DKO muscle was accompanied by reduced insulin-stimulated muscle glucose uptake. Preferential myocellular glucose utilization in DKO mice decreased fatty acid oxidation, resulting in increased reesterification of acyl-CoAs into diacylglycerol and triacylglycerol, with subsequent activation of PKC-θ and inhibition of insulin signaling in muscle. In contrast, other putative mediators of muscle insulin resistance, including muscle acylcarnitines, ceramides, reactive oxygen species production, and oxidative stress markers, were not increased. These findings demonstrate that modulation of oxidative substrate selection to increase muscle glucose utilization surprisingly results in muscle insulin resistance, offering genetic evidence against the glucose-fatty acid cycle hypothesis of muscle insulin resistance.Lipid-induced muscle insulin resistance plays a major role in the pathogenesis of type 2 diabetes (T2D), but the cellular mechanisms remain unknown (1, 2). More than 50 y ago Randle et al. (3) postulated the glucose-fatty acid cycle to explain the impairment of insulin-stimulated glucose disposal by fatty acids in muscle. In this model, fat oxidation increases mitochondrial acetyl-CoA/CoA and NADH/NAD⁺ ratios. Acetyl-CoA and NADH allosterically inhibit pyruvate dehydrogenase complex (PDH), the mitochondrial enzyme that links glycolysis to the TCA cycle by converting pyruvate to acetyl-CoA. Additionally, fatty acid-derived acetyl-CoA produces citrate, which inhibits phosphofructokinase. This in turn increases glucose-6-phosphate (G6P), a potent allosteric inhibitor of hexokinase. By these mechanisms, increased fatty acid oxidation was hypothesized to reduce glycolytic flux and prevent further muscle glucose uptake. However, in vivo studies of human skeletal muscle metabolism have challenged the Randle hypothesis. Five hours of a lipid infusion, combined with heparin to activate lipoprotein lipase, raised plasma fatty acids and induced muscle insulin resistance in healthy individuals, yet intramyocellular G6P and glucose concentrations were reduced compared with control glycerol infusion studies, implicating defects in insulin-stimulated glucose transport activity (4, 5). An alternative hypothesis to explain the muscle insulin resistance associated with lipid exposure posits that accumulation of bioactive lipid intermediates initiates signaling cascades that impair insulin action. Lipid species implicated include diacylglycerols (DAGs) (6–10), ceramides (11, 12), and long-chain acyl-CoAs (13). DAG activation of PKC-θ in skeletal muscle has been shown to impair canonical insulin signaling at the level of insulin receptor substrate-1 (IRS-1) tyrosine phosphorylation through increased IRS-1 serine phosphorylation at the 1101 position (2, 6, 7, 14).More recently, incomplete fat oxidation and subsequent accumulation of mitochondrially derived acylcarnitines has been proposed to contribute to lipid-induced muscle insulin resistance (15–17). According to this model, insulin resistance stems from increased fat oxidation, leading to increased conversion of acyl-CoA to medium- and long-chain acylcarnitines, which may mediate insulin resistance via unknown mechanisms. In contrast, short-chain acylcarnitines have been suggested to promote metabolic flexibility. The shortest acylcarnitine, acetylcarnitine, is synthesized from acetyl-CoA and carnitine by carnitine acetyltransferase (CrAT), a mitochondrial matrix enzyme, and is responsible for buffering the mitochondrial acetyl-CoA pool and mitigating acetyl-CoA inhibition of PDH (18). Consistent with the notion that CrAT regulates substrate selection by modulating PDH flux, mice with muscle-specific deletion of CrAT exhibited reduced PDH activity during the fed-to-fasted transition, resulting in glucose intolerance and metabolic inflexibility, a term coined by Kelley and Mandarino (19) to explain the impairment in the ability to adjust fuel oxidation to fuel availability.Although these studies emphasize the importance of PDH in the promotion of metabolic inflexibility, the role of PDH and mitochondrial oxidative substrate selection in the regulation of basal and insulin-stimulated muscle glucose metabolism has not been directly assessed in vivo. To examine this question, we sought to determine whether modulation of oxidative substrate selection in a genetic mouse model with constitutively active PDH activity would affect insulin sensitivity in skeletal muscle.     

Association of endothelial nitric oxide synthase gene variant (G894T) with coronary artery disease in Western Iran

There are conflicting reports about the association of endothelial nitric oxide synthase (eNOS) gene polymorphism and the risk of coronary artery disease (CAD). To determine the frequency of eNOS G894T variant and to find the possible association between this polymorphism with CAD we studied 207 unrelated patients with total CAD (with and without diabetes) and 92 controls. The eNOS variants were detected by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP). The presence of GT + TT genotype was associated with 2.1-fold (P = .006), 2.29-fold (P = .006), and 1.93-fold (P = .032) increased risk of CAD in total CAD, CAD with diabetes, and in CAD without diabetes patients, respectively. The presence of T allele of eNOS increased the risk of CAD 2.15-fold (P = .001). The levels of low-density lipoprotein cholesterol (LDL-C) and triglycerides (TG) tended to be higher in patients carrier for T allele compared to those with G allele. The results of present study revealed that eNOS G894T polymorphism is associated with increased risk of CAD in our population.     

Osseous reaction to implantation of two endodontic cements: Mineral trioxide aggregate (MTA) and calcium enriched mixture (CEM)

Aim: The aim of the present in vivo study was to determine bone tissue reaction to calcium enriched mixture (CEM) and mineral trioxide aggregate (MTA) using a rat femur model. Study Design: Sixty-three rats were selected and randomly divided into three groups of 21 each [experimental groups (n=15), control (n=6)]. Implantation cavities were prepared in each femoral bone and randomly filled with the biomaterials only in the experimental groups. The animals in three groups were sacrificed 1, 4, and 8 weeks postoperatively. Histologic evaluations comprising inflammation severity and new bone formation were blindly made on H&E-stained decalcified 6-μm sections. Results: At 1, 4, and 8 weeks after implantation number of inflammatory cells had decreased in the CEM, MTA and control groups, respectively, with no statistically significant differences. Conversely, new bone formation had increased in all the experimental and control groups, without statistically significant differences. Conclusion: The results suggest that biocompatibility of MTA, as gold standard, and CEM cement as a new endodontic biomaterial are comparable.