BackgroundThe relationship between the sleep/wake habits and the academic performance of medical students is insufficiently addressed in the literature. This study aimed to assess the relationship between sleep habits and sleep duration with academic performance in medical students.MethodsThis study was conducted between December 2009 and January 2010 at the College of Medicine, King Saud University, and included a systematic random sample of healthy medical students in the first (L1), second (L2) and third (L3) academic levels. A self-administered questionnaire was distributed to assess demographics, sleep/wake schedule, sleep habits, and sleep duration. Daytime sleepiness was evaluated using the Epworth Sleepiness Scale (ESS). School performance was stratified as “excellent” (GPA ≥3.75/5) or “average” (GPA <3.75/5).ResultsThe final analysis included 410 students (males: 67%). One hundred fifteen students (28%) had “excellent” performance, and 295 students (72%) had “average” performance. The “average” group had a higher ESS score and a higher percentage of students who felt sleepy during class. In contrast, the “excellent” group had an earlier bedtime and increased TST during weekdays. Subjective feeling of obtaining sufficient sleep and non-smoking were the only independent predictors of “excellent” performance.ConclusionDecreased nocturnal sleep time, late bedtimes during weekdays and weekends and increased daytime sleepiness are negatively associated with academic performance in medical students.

IntroductionWe previously showed that Link N can stimulate extracellular matrix biosynthesis by intervertebral disc (IVD) cells, both in vitro and in vivo, and is therefore a potential stimulator of IVD repair. The purpose of the present study was to determine how Link N may influence human mesenchymal stem cell (MSC) differentiation, as a prelude to using Link N and MSC supplementation in unison for optimal repair of the degenerated disc.MethodsMSCs isolated from the bone marrow of three osteoarthritis patients were cultured in chondrogenic or osteogenic differentiation medium without or with Link N for 21 days. Chondrogenic differentiation was monitored by proteoglycan staining and quantitation by using Alcian blue, and osteogenic differentiation was monitored by mineral staining and quantitation by using Alzarin red S. In addition, proteoglycan secretion was monitored with the sulfated glycosaminoglycan (GAG) content of the culture medium, and changes in gene expression were analyzed with real-time reverse transcription (RT) PCR.ResultsLink N alone did not promote MSC chondrogenesis. However, after MSCs were supplemented with Link N in chondrogenic differentiation medium, the quantity of GAG secreted into the culture medium, as well as aggrecan, COL2A1, and SOX9 gene expression, increased significantly. The gene expression of COL10A1 and osteocalcin (OC) were downregulated significantly. When MSCs were cultured in osteogenic differentiation medium, Link N supplementation led to a significant decrease in mineral deposition, and alkaline phosphatase (ALP), OC, and RUNX2 gene expression.ConclusionsLink N can enhance chondrogenic differentiation and downregulate hypertrophic and osteogenic differentiation of human MSCs. Therefore, in principle, Link N could be used to optimize MSC-mediated repair of the degenerated disc.

IntroductionWe previously showed that type X collagen, a marker of late stage chondrocyte hypertrophy (associated with endochondral ossification), is constitutively expressed by mesenchymal stem cells (MSCs) from osteoarthritis patients and this may be related to Naproxen (Npx), a nonsteroidal anti-inflammatory drug used for therapy. Hedgehog (HH) signaling plays an important role during the development of bone. We tested the hypothesis that Npx affected osteogenic differentiation of human MSCs through the expression of Indian hedgehog (IHH), Patched-1 (PTC1) and GLI family members GLI1, GLI2, GLI3 in vitro.MethodsMSCs were cultured in osteogenic differentiation medium without (control) or with 0.5 μM Npx. The expression of collagen type X, alpha 1 (COL10A1), alkaline phosphatase (ALP), osteopontin (OPN), osteocalcin (OC), collagen type I, alpha 1 (COL1A1) was analyzed with real-time reverse transcription (RT) PCR, and the ALP activity was measured. The osteogenesis of MSCs was monitored by mineral staining and quantification with alizarin red S. To examine whether Npx affects osteogenic differentiation through HH signaling, the effect of Npx on the expression of IHH, GLI1, GLI2, GLI3 and PTC1 was analyzed with real-time RT PCR. The effect of cyclopamine (Cpn), a HH signaling inhibitor, on the expression of COL10A1, ALP, OC and COL1A1 was also determined.ResultsWhen MSCs were cultured in osteogenic differentiation medium, Npx supplementation led to a significant decrease in ALP gene expression as well as its activity, and had a tendency to decrease mineral deposition. It also decreased the expression of COL1A1 significantly. In contrast, the gene expression of COL10A1 and OPN were upregulated significantly by Npx. No significant effect was found on OC expression. The expression of IHH, PTC1, GLI1, and GLI2 was increased by Npx, while no significant difference was observed on GLI3 expression. Cpn reversed the effect of Npx on the expression of COL10A1, ALP, OPN and COL1A1.ConclusionsThese results indicate that Npx can affect gene expression during osteogenic differentiation of MSCs, and downregulate mineral deposition in the extracellular matrix through IHH signaling. Therefore, Npx could affect MSC-mediated repair of subchondral bone in OA patients.

In subjects with impaired insulin action, alterations of the serum sodium and potassium concentrations have been reported. The resulting cationic imbalance, along with the osmotic effect of the elevated sugar levels, could influence the course of diabetes mellitus management. Therefore, this study was conducted to compare the fasting blood glucose and HbA1c levels with those of the serum electrolytes. Blood samples were collected for assessment of HbA1c, fasting blood glucose (FBS), and electrolytes using different automated methods. A significant association between the serum sodium and FBS levels among types 1 and 2 insulin-treated patients, and type 2 oral agent patients was observed. A total of 138 diabetic subjects were randomly selected from any gender aged between 25 and 65 years at the University Diabetes Center, King Saud University, Riyadh KSA. The subjects were classified into types 1 or 2 DM using ADA criteria. Blood samples were collected for assessment of HbA1c, FBS, and electrolytes using different automated methods. It showed a significant association between serum sodium, FBS among type 1, type 2 insulin treated, and type 2 oral agent groups. However, the association of sodium and HbA1c was insignificant when analyzed individually. A statistically significant association (P < 0.001) was observed between the levels of serum sodium and the fasting blood glucose levels. This study demonstrated significant reduction in serum sodium level among types 1 or 2 diabetic patients especially among insulin-treated patients. No significant association was demonstrated by serum potassium with FBS and degree of diabetes control.

No abstract

No abstract

Several studies have shown that type X collagen (COL X), a marker of late-stage chondrocyte hypertrophy, is expressed in mesenchymal stem cells (MSCs) from osteoarthritis (OA) patients. We recently found that Naproxen, but not other nonsteroidal anti-inflammatory drugs (NSAIDs) (Ibuprofen, Celebrex, Diclofenac), can induce type X collagen gene (COL10A1) expression in bone-marrow-derived MSCs from healthy and OA donors. In this study we determined the effect of Naproxen on COL X protein expression and investigated the intracellular signaling pathways that mediate Naproxen-induced COL10A1 expression in normal and OA hMSCs. MSCs of OA patients were isolated from aspirates from the intramedullary canal of donors (50-80 years of age) undergoing hip replacement surgery for OA and were treated with or without Naproxen (100 μg/mL). Protein expression and phosphorylation were determined by immunoblotting using specific antibodies (COL X, p38 mitogen-activated protein kinase [p38], phosphorylated-p38, c-Jun N-terminal kinase [JNK], phosphorylated-JNK, extracellular signal-regulated kinase [ERK], and phosphorylated-ERK). Real-time reverse transcription polymerase chain reaction (RT-PCR) was performed to determine the expression of COL10A1 and Runt-related transcription factor 2 gene (Runx2). Our results show that Naproxen significantly stimulated COL X protein expression after 72 h of exposure both in normal and OA hMSCs. The basal phosphorylation of mitogen-activated protein kinases (MAPKs) (ERK, JNK, and p38) in OA hMSCs was significantly higher than in normal. Naproxen significantly increased the MAPK phosphorylation in normal and OA hMSCs. NSAID cellular effects include cyclooxygenase, 5-lipoxygenase, and p38 MAPK signaling pathways. To investigate the involvement of these pathways in the Naproxen-induced COL10A1 expression, we incubated normal and OA hMSCs with Naproxen with and without inhibitors of ERK (U0126), JNK (BI-78D3), p38 (SB203580), and 5-lipoxygenase (MK-886). Our results showed that increased basal COL10A1 expression in OA hMSCs was significantly suppressed in the presence of JNK and p38 inhibitors, whereas Naproxen-induced COL10A1 expression was suppressed by 5-lipoxygenase inhibitor. This study shows that Naproxen induces COL X both at transcriptional and translational levels in normal and OA hMSCs. Elevated basal COL10A1 expression in OA hMSCs is probably through the activation of MAPK pathway and Naproxen-induced COL10A1 expression is through the increased 5-lipoxygenase signaling.

Case: We report a 27-year-old man who presented with thigh swelling and inability to bear weight after blunt trauma 24 hours before. Based on the clinical assessment, the patient was diagnosed with anterior compartment syndrome of the thigh and underwent fasciotomy. Postoperatively, 1.5 L of blood were drained from his wound in the first 30 minutes after the operation. Angiography was performed demonstrating bleeding from the lateral femoral circumflex which was successfully embolized. Conclusions: Our case represents the underlying arterial injury that was initially undiagnosed as a cause for thigh compartment syndrome. Physicians should consider associated injuries (beyond muscle crush) when making a diagnosis of compartment syndrome.