Jinnah Medical & Dental College

Introduction Sleep deprivation is an escalating public health concern among young adults, as it impairs cognitive function and increases the risk of cardiovascular disease (CVD). Existing studies have linked chronic sleep deficiencies to mental confusion, reduced cognitive performance, and early signs of cognitive decline. Research also indicates that inadequate sleep contributes to metabolic dysregulation and autonomic system instability, both of which elevate cardiovascular risk. However, the overall effects of sleep deprivation on cognitive function and cardiovascular markers in young adults require further exploration. This study aims to examine the relationship between sleep deprivation, brain fog, early cognitive decline, and cardiovascular risk factors in this population. Methods This cross-sectional study involved 300 participants aged 18-30 from Pakistan and various other countries. Participants were selected using non-probability purposive sampling. Data were collected using four validated instruments: the Pittsburgh Sleep Quality Index, the Cognitive Failures Questionnaire, the Mini-Mental State Examination, and the Perceived Stress Scale. Data analysis was conducted using IBM SPSS Statistics for Windows, Version 26.0 (Released 2019; IBM Corp., Armonk, NY, USA), applying chi-square tests, independent sample t-tests, ANOVA, Pearson correlation, and logistic regression to assess associations between sleep deprivation, cognitive performance, and cardiovascular outcomes. Results Participants with shorter sleep durations had significantly higher scores in cognitive failures (p < 0.01) and perceived stress (p < 0.01). Poor sleep quality was associated with reduced cognitive performance (r = -0.114, p < 0.05), and it also increased the likelihood of developing cardiovascular risk factors. Participants with a family history of CVD exhibited significantly higher cognitive failure scores (t = 5.540, p < 0.001). Furthermore, a decline in sleep quality was associated with increased cardiovascular risk (B = 0.035, p = 0.019), although sleep disorders were not significantly influenced by sleep quality deterioration (B = 0.012, p = 0.400). Employment status and smoking habits were also found to impact both sleep quality and cognitive function (p < 0.01). Conclusions This study highlights the adverse impact of insufficient sleep on cognitive function and cardiovascular health in young adults aged 18-30. Poor sleep quality is associated with increased cognitive errors, heightened stress levels, and a greater risk of cardiovascular issues. These findings emphasize the importance of targeted health interventions aimed at improving sleep hygiene and lifestyle behaviors to reduce the risk of early cognitive decline and cardiovascular conditions. Future research should employ longitudinal designs and objective sleep tracking to strengthen causal inferences.

This parallel two-arm randomized trial assessed skeletal changes following en masse and two-step anterior retraction using mini-implants. Of 110 patients screened, 14 were excluded due to ineligibility or refusal, leaving 96 participants randomized equally into two groups (48 each). All received the assigned intervention. During follow-up, 16 participants were lost because of bracket debonding, mini-implant failure, or discontinuation, resulting in 80 subjects (40 per group) included in the final analysis. All patients were treated with pre-adjusted edgewise appliances. After alignment and leveling, bilateral mini-implants were inserted between the maxillary second premolars and first molars, followed by extraction of the maxillary first premolars. Retraction was carried out according to group allocation either en masse or two-step. Lateral cephalograms taken before treatment and after incisor retraction were used to evaluate skeletal changes. Data were expressed as mean and standard deviation, with Wilcoxon signed-rank and Mann-Whitney U-tests applied for intra- and intergroup comparisons. Both methods produced significant sagittal and vertical changes. Although the two-step approach showed slightly greater maxillary retraction and ANB reduction, these differences likely related to baseline variation and biomechanics rather than true superiority. Vertical parameters increased in both groups, indicating posterior mandibular rotation, suggesting both techniques are equally effective.

Rhinophyma recurrence after surgical excision poses a significant therapeutic challenge, often stemming from the incomplete removal of deep hyperplastic pilosebaceous units. We present the case of a 66-year-old male with a third occurrence of rhinophyma after two prior failed cold-steel excisions. The definitive intervention consisted of a modified deep tangential excision, removing all rhinophymatous tissue to a deep dermal plane that approached, but did not violate, the nasal perichondrium, thereby eradicating the pathologic glandular nidus while preserving the deepest adnexal remnants essential for re-epithelialization. The wound was primarily managed by secondary intention healing, guided by selective, tension-free suture re-approximation of key wound edges to optimize contour. Cold-steel excision was specifically chosen to ensure a specimen free of thermal artifact for definitive histopathology, a critical step in a recurrent case, which ultimately confirmed marked sebaceous gland hypertrophy and excluded malignancy. The postoperative course was uneventful, and at an 18-month follow-up, the patient demonstrated a stable, successfully restored nasal contour with no signs of recurrence. This case demonstrates that for severe, recurrent rhinophyma, a surgical strategy that balances thorough debulking of pathologic tissue with meticulous preservation of deep adnexal structures is critical for achieving a durable, long-term outcome.

OBJECTIVES:Diabetes mellitus (DM) has a strong bidirectional relationship with mental disorders, collectively increasing the risk of mortality. We aim to analyze the mortality trends related to DM and associated mental disorders while exploring demographic and regional disparities in the United States from 1999 to 2023. METHODS:Death records were obtained from the Centers for Disease Control and Prevention-Wide-ranging ONline Data for Epidemiologic Research (CDC WONDER) database from 1999 to 2023. Crude and age-adjusted mortality rates (AAMRs), measured per 100,000 people, were calculated and standardized to the 2000 US standard population. Annual percent changes (APCs) in AAMRs and crude mortality rates (CMRs) were computed through the Joinpoint regression program and data stratification was done based on sex, race, age, and geographical regions. RESULTS:A total of 1,332,198 death records indicated the presence of both DM and mental disorders. AAMR increased fourfold from 1999 (9.5) to 2023 (40.4) per 100,000 population. Notable increase shifts were noted in AAMR across different periods between 1999 and 2021 (APC: 1999-2005: 14.98; 2005-2018: 2.92; 2018-2021: 8.98), after which it declined sharply until 2023 (APC: -6.42). Males (36.8) had elevated AAMRs in comparison to females (22.4). Non-Hispanic (NH) American Indians contributed to most of the AAMR (39.8). CMR was 11-fold higher in older adults as compared to those aged between 35 and 64 years. Regionally, AAMRs in nonmetropolitan areas (35.9) and Midwest regions (34.7) were the highest. CONCLUSIONS:Further research and targeted interventions are needed for in-depth evaluation of these rising mortality trends to find the root cause and lower the burden of DM and associated mental disorders.