The 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.

Introduction: We 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. Methods: MSCs 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. Results: Link 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. Conclusions: Link 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.

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.

Background: Limb amputation is a life-altering event with substantial physical, psychological, and social consequences. Despite advances in healthcare, amputation remains a major global health concern, particularly in regions with high burdens of diabetes and vascular disease. This study aims to analyze demographic characteristics, etiologies, and trends in amputations over a ten-year period at a tertiary-care center. Methods: We retrospectively reviewed medical records of patients who underwent amputation at our tertiary-care hospital. Collected variables included patients’ demographics, etiology, level of amputation, type of admission, and surgical specialty involved. Descriptive statistics were used to summarize the data. Associations between categorical variables were analyzed using chi-square tests, with post hoc pairwise comparisons adjusted using the Bonferroni method where applicable. Continuous variables were compared using the Mann–Whitney U test. A p-value of <0.05 was considered statistically significant. All analyses were conducted using IBM SPSS version 26.0. Results: A total of 647 patients underwent amputation, with a mean age of 56 years and a male predominance (65%). Diabetic complications were the leading cause (67.7%), followed by trauma (11.7%) and vascular diseases (11.6%). Lower limb amputations were more prevalent, with toe amputations being the most frequent (39%). Emergency procedures accounted for 72% of cases, and vascular surgery was the most involved specialty, followed by orthopedic surgery. Conclusions: Our study highlights a substantial burden of amputations, predominantly involving the lower limb, as well as a significant association with diabetic complications. These findings emphasize the urgent need for integrated diabetic care, early interventions, and public health strategies to reduce the burden of amputations in Saudi Arabia.

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.

Lumbar spinal stenosis (LSS) is a prevalent degenerative condition, with ligamentum flavum hypertrophy (LFH) contributing significantly to neural compression. Despite its clinical importance, few studies have evaluated longitudinal trends in LFH. This study investigates the temporal progression and demographic associations of LFH over the past decade. This retrospective cohort study included adult patients undergoing surgery for LSS at a tertiary academic center during two periods: 2013-2017 and 2018-2023. Exclusion criteria included prior spinal surgery, trauma, malignancy, or inadequate imaging. Two radiologists reviewed axial MRI images to measure ligamentum flavum thickness (≥4 mm indicated hypertrophy). Demographic data and coexisting spinal conditions were also recorded. A total of 202 patients were analyzed-98 from the initial and 104 from the later period. LFH prevalence rose from 24.5 % to 44.7 % over time. Patients aged ≥60 demonstrated significantly higher LFH rates in both periods (p = 0.004). Although female predominance persisted, it declined from 71.4 % to 55 %. LFH was most commonly associated with disc bulging, particularly at the same spinal level. Multilevel LFH increased from 25 % to 44.1 %, though L4-L5 remained the most affected segment. The incidence of LFH has increased substantially over the past decade, particularly among older adults. Given its role in LSS pathogenesis, greater attention to LFH in imaging and surgical planning is warranted. Further research is needed to clarify its etiology and guide effective management strategies.