Background: Congenital heart defects (CHDs) represent a significant cause of morbidity among pediatric patients, often associated with compromised endothelial function. Omega-3 fatty acids possess recognized anti-inflammatory and endothelial protective properties, yet their therapeutic potential in pediatric CHD populations remains inadequately explored. This study aimed to evaluate the efficacy of Omega-3 fatty acid supplementation on endothelial function in children diagnosed with congenital heart defects. Materials and Methods: A randomized controlled trial was conducted involving 60 pediatric CHD patients aged between 5-15 years. Participants were randomly allocated into two groups: the intervention group (n=30) received Omega-3 fatty acids (dosage 500 mg/day EPA and DHA combined) for 12 weeks, and the control group (n=30) received placebo capsules identical in appearance. Endothelial function was assessed at baseline and post-supplementation by measuring Flow-mediated dilation (FMD), circulating endothelial microparticles (EMPs), and inflammatory markers such as high-sensitivity C-reactive protein (hs-CRP). Results: Significant improvements in endothelial function parameters were observed in the Omega-3 supplementation group compared to the placebo. Post-intervention, FMD increased from baseline (6.2±1.5% to 10.8±1.7%; p<0.001), while EMP levels significantly decreased (from 1250±230 particles/µL to 810±150 particles/µL; p<0.001). hs-CRP levels also significantly reduced in the intervention group (from 3.5±0.8 mg/L to 1.8±0.5 mg/L; p<0.001). No significant changes were observed within the placebo group across any parameters. Conclusion: Omega-3 fatty acid supplementation significantly enhanced endothelial function in pediatric patients with congenital heart defects, as demonstrated by improved FMD, reduced EMPs, and decreased inflammatory markers. These findings suggest that Omega-3 supplementation could be a valuable adjunctive therapeutic approach in managing endothelial dysfunction among pediatric CHD patients.

Background & Methods: The aim is to study Efficacy of super-bioavailable itraconazole 130 mg and conventional-itraconazole 100 mg twice daily in glabrous tinea infection. Patients with KOH positive were given itraconazole in two different formulations. Patient with KOH negative were declared clinically cure. Results: We found KOH-negative Patient (After treatment) in Group A as super-bioavailable itraconazole 130 mg with 54% whereas Group B as conventional-itraconazole 100mg with 46%. (p=0.271669) Conclusion: Super-Bioavailable itraconazole 130 mg has better pharmacokinetic profile than conventional itraconazole 100 mg. This may not reflect in the form of better efficacy and safety than in the treatment of dermatophytosis. Multiple other factors might have a role to play in the lack of adequate clinical response of dermatophytosis to itraconazole. We could not find any better efficacy or safety of SB itraconazole as compared to conventional itraconazole.

Background: Dilated cardiomyopathy (DCM) is the most common non-ischemic cardiomyopathy subtype, characterized by progressive left ventricular dilation and systolic dysfunction. This study aimed to evaluate demographic, clinical, and echocardiographic profiles of DCM patients to identify etiology-specific patterns and severity markers. Methods: This cross-sectional observational study was conducted over 18 months at Dhiraj Hospital, Vadodara, involving 150 consecutively enrolled DCM patients. Inclusion criteria comprised adults (≥18 years) with heart failure symptoms and echocardiographic findings consistent with DCM (LVEF ≤40%, global hypokinesia, LVEDD >58.4 mm in men, >52.2 mm in women). Comprehensive clinical evaluation, 12-lead ECG, chest radiography, and transthoracic echocardiography were performed. Statistical analysis included correlation studies, multivariable logistic regression, and machine learning models for etiology prediction. Results: The cohort was predominantly male (74%) with mean age 52.6±12.4 years. Ischemic cardiomyopathy was most prevalent (38.7%), followed by peripartum (25.3%), alcoholic (20%), and diabetic (16%) subtypes. Mean LVEF was severely reduced at 30.7±6.4%, with ischemic patients showing the lowest values (25.4%). Universal heart failure symptoms were present across all etiologies, while chest pain discriminated ischemic cases (84.5%). Hypotension was the strongest predictor of severe systolic dysfunction (OR=3.67), followed by large LVEDD (OR=2.91) and ischemic etiology (OR=2.31). Machine learning models achieved 82.2% accuracy in etiology prediction. Conclusion: DCM demonstrates significant heterogeneity across etiologic subtypes, with ischemic cardiomyopathy representing the most severe phenotype. Comprehensive profiling incorporating clinical, electrocardiographic, and echocardiographic features enables improved risk stratification and supports personalized therapeutic approaches in this complex condition.

Background: Alzheimer's disease (AD) and Parkinson's disease (PD) are distinct neurodegenerative disorders characterized by the accumulation of misfolded proteins—amyloid-beta (Aβ) and α-synuclein, respectively. Emerging evidence suggests that endoplasmic reticulum (ER) stress and the subsequent Unfolded Protein Response (UPR) may represent a common pathogenic pathway. However, a direct comparative analysis of the temporal progression and pathological contribution of ER stress in both diseases is lacking. Methodology: We used the 5xFAD transgenic mouse model for AD and the neurotoxin-based MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) model for PD. Brain tissues from the hippocampus (AD) and substantia nigra (PD) were collected at progressive disease stages (3, 6, and 9 months for 5xFAD; 1, 3, and 7 days post-MPTP injection) alongside age-matched wild-type controls. Key UPR markers (GRP78, p-PERK, XBP1s, CHOP) and neuronal degeneration markers (NeuN, Tyrosine Hydroxylase [TH]) were quantified using Western blotting and immunohistochemistry. Apoptosis was assessed via TUNEL staining. Results: In both 5xFAD and MPTP models, the ER chaperone GRP78 and the UPR initiator p-PERK were significantly elevated at the earliest time points, preceding significant neuronal loss. As the diseases progressed, downstream pro-apoptotic UPR marker CHOP became robustly upregulated. Critically, a strong positive correlation was found between CHOP expression levels and the degree of neuronal loss (loss of NeuN-positive cells in hippocampus, r = 0.89, p < 0.001; loss of TH-positive cells in substantia nigra, r = 0.92, p < 0.001). Immunohistochemical analysis confirmed the co-localization of CHOP in degenerating neurons. Conclusions: Our findings demonstrate that ER stress is not only an early and sustained pathological feature in both AD and PD models but also that its pro-apoptotic signaling directly correlates with the severity of neuronal degeneration. This positions the UPR, particularly the PERK-CHOP axis, as a critical, convergent mechanism of neurotoxicity, suggesting that therapeutic strategies targeting ER stress may have broad applicability across multiple proteinopathies.

Background: Cigarette smoking is a leading cause of preventable cardiovascular disease (CVD). The autonomic nervous system (ANS) plays a crucial role in cardiovascular regulation, and its dysfunction is implicated in the pathogenesis of CVD. Heart rate variability (HRV), the physiological variation in time between consecutive heartbeats, is a reliable non-invasive marker of cardiac autonomic function. Reduced HRV reflects impaired sympathovagal balance and is an independent predictor of adverse cardiovascular events. While smoking is known to affect the ANS, a detailed characterization of HRV alterations in chronic smokers remains pertinent. Methods: This cross-sectional study included 100 participants, divided into two groups: 50 chronic smokers (smoking ≥10 cigarettes/day for ≥5 years) and 50 healthy non-smokers. Participants were aged between 25 and 50 years and were free from any known cardiovascular, metabolic, or neurological diseases. After a 15-minute acclimatization period, a 5-minute continuous Lead-II electrocardiogram (ECG) was recorded in the supine position under standardized laboratory conditions. Time-domain (SDNN, RMSSD) and frequency-domain (LF power, HF power, LF/HF ratio) HRV parameters were analyzed. Group comparisons were performed using independent t-tests. Key Findings: Smokers and non-smokers were well-matched for age (38.2 ± 6.5 vs. 37.9 ± 6.8 years, p=0.81) and sex distribution. Smokers exhibited significantly lower values in time-domain parameters indicative of overall variability and vagal tone compared to non-smokers: SDNN (42.1 ± 10.5 ms vs. 55.2 ± 12.1 ms, p<0.001) and RMSSD (25.3 ± 8.1 ms vs. 38.5 ± 9.8 ms, p<0.001). In frequency-domain analysis, smokers showed significantly reduced high-frequency (HF) power, a marker of parasympathetic activity (320 ± 110 ms² vs. 550 ± 150 ms², p<0.001). Concurrently, the low-frequency/high-frequency (LF/HF) ratio, representing sympathovagal balance, was significantly elevated in the smoking group (2.8 ± 0.9 vs. 1.5 ± 0.5, p<0.001). Conclusion: Chronic cigarette smoking is strongly associated with significant alterations in HRV, characterized by reduced overall variability, parasympathetic withdrawal, and a shift towards sympathetic dominance. These findings demonstrate subclinical cardiac autonomic dysfunction in smokers, which may be a key mechanism underlying their increased risk for cardiovascular morbidity and mortality.

Background: Chronic inflammatory disorders (CIDs), such as Rheumatoid Arthritis (RA) and Inflammatory Bowel Disease (IBD), represent a significant global health burden. The nucleotide-binding oligomerization domain-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome, a key component of the innate immune system, has been implicated in the pathogenesis of individual CIDs, but its comparative role across different disorders and its association with disease severity remain poorly defined. Methodology: We conducted a cross-sectional case-control study involving 150 participants: 50 patients with RA, 50 patients with IBD (Crohn's disease or ulcerative colitis), and 50 age- and sex-matched healthy controls (HC). Peripheral blood mononuclear cells (PBMCs) and plasma were isolated from all participants. NLRP3 inflammasome activation was quantified by measuring the protein expression of its core components (NLRP3, ASC, and cleaved Caspase-1) in PBMCs using Western blot analysis, and the plasma levels of its downstream cytokines (IL-1β and IL-18) using enzyme-linked immunosorbent assay (ELISA). Disease activity was assessed using the Disease Activity Score 28-C-reactive protein (DAS28-CRP) for RA and the Harvey-Bradshaw Index (HBI) for IBD. Results: Patients with RA and IBD exhibited significantly higher expression of NLRP3, ASC, and cleaved Caspase-1 in their PBMCs compared to healthy controls (p<0.001 for all). Plasma concentrations of IL-1β and IL-18 were also markedly elevated in both patient cohorts (p<0.001). A strong, positive correlation was observed between plasma IL-1β levels and disease activity scores in both the RA (r = 0.72, p<0.001) and IBD (r = 0.68, p<0.001) groups. Conclusions: Our findings provide direct comparative evidence that NLRP3 inflammasome hyperactivation is a common pathological feature in both RA and IBD. The strong correlation between inflammasome-derived cytokines and disease severity suggests that this pathway is not only involved in pathogenesis but also contributes to disease progression. These results highlight the NLRP3 inflammasome as a potential biomarker for disease activity and a promising pan-therapeutic target for a range of CIDs.

Background: Neural tube defects (NTDs) are among the most common congenital malformations, and meningocele represents a less severe but clinically significant form. Early detection of small meningocele (even sub centimeter size) during the first trimester has become feasible with advances in high- resolution ultrasonography. Objective: To describe the sonographic characteristics, incidence, and outcomes of meningocele diagnosed at even 11–14 weeks of gestation. Methods: A prospective observational study was conducted on 100 pregnancies with suspected anomalies about neurology undergoing routine first-trimester ultrasound (11–14 weeks), in which 3 cases of meningocele was identified, including one case of a small (even sub centimeter size) meningocele. Data recorded included gestational age at diagnosis, lesion size and location, associated anomalies, pregnancy decision, and neonatal outcome. Conclusion: First-trimester ultrasound can reliably detect small (even sub centimeter size) meningocele, enabling earlier counseling and management even in rare isolated cases.

Background: Systemic autoimmune diseases (SADs), such as Systemic Lupus Erythematosus (SLE) and Systemic Sclerosis (SSc), are characterized by heterogeneous clinical presentations and unpredictable courses, making diagnosis and management challenging. There is a critical need for non-invasive biomarkers to improve disease assessment. Circulating microRNAs (miRNAs)—stable, small non-coding RNAs found in body fluids—have emerged as promising candidates due to their roles in regulating immune responses. Methodology: In this cross-sectional case-control study, we recruited 150 participants: 50 patients with SLE, 50 with SSc, and 50 age- and sex-matched healthy controls (HC). Serum levels of miR-146a, miR-155, and miR-21 were quantified using reverse transcription-quantitative polymerase chain reaction (RT-qPCR). Disease activity was assessed using the Systemic Lupus Erythematosus Disease Activity Index 2000 (SLEDAI-2K) for SLE and the modified Rodnan Skin Score (mRSS) for SSc. Receiver operating characteristic (ROC) curve analysis was used to evaluate diagnostic accuracy, and Spearman's correlation was used to assess the association with disease activity. Results: Serum levels of miR-146a and miR-155 were significantly upregulated in both SLE and SSc patients compared to HCs (p<0.001). Notably, miR-21 expression was significantly elevated only in the SSc cohort (p<0.001 vs. HCs and SLE). ROC analysis demonstrated that the miRNA panel had high diagnostic accuracy for distinguishing patients from controls (Area Under the Curve [AUC] = 0.92 for SLE; AUC = 0.94 for SSc). Furthermore, miR-155 levels showed a strong positive correlation with SLEDAI-2K scores in SLE patients (r = 0.75, p<0.001), while miR-21 levels strongly correlated with mRSS in SSc patients (r = 0.79, p<0.001). Conclusions: Our findings indicate that circulating miR-146a, miR-155, and miR-21 exhibit distinct expression profiles in SLE and SSc. This panel of miRNAs serves as a promising non-invasive biomarker for the diagnosis of these diseases, while specific miRNAs (miR-155 for SLE, miR-21 for SSc) show strong potential for monitoring disease-specific activity.

A 25-year-old female presented to us in the outpatient department with complaints of progressive exertional dyspnea, palpitations, and occasional dizziness over the past year. Vital signs revealed a heart rate of 110 bpm, blood pressure of 110/70 mmHg, respiratory rate of 18 breaths per minute, and oxygen saturation of 92% on room air. On general examination there was 2+ pedal edema, but no cyanosis, clubbing, icterus, pallor or lymphadenopathy. An electrocardiogram (ECG) demonstrated sinus tachycardia, right atrial enlargement, and incomplete right bundle branch block. Chest X-ray showed significant cardiomegaly with a globular-shaped heart and decreased pulmonary vascular markings. Based on clinical findings and imaging studies, a diagnosis of Ebstein’s anomaly was confirmed. The patient’s condition was classified as Carpentier Type C (markedly atrialized right ventricle with severely restricted leaflet mobility). She underwent a cone reconstruction procedure; a surgical technique designed to restore tricuspid valve competence and optimize right ventricular function. The surgery was successful, with intraoperative findings confirming severe tricuspid valve deformity and extensive atrialization of the right ventricle.

Background: Less than 5% of gastrointestinal cancers are small intestine cancers, making them an uncommon type of cancer.  Black people have a greater prevalence rate than white people, with an estimated yearly incidence of 0.3 to 2.0 cases per 100,000 people. Case Presentation: A 55-year-old male patient presented to us with a complaint of swelling over the medial aspect of right thigh. The patient also had an associated complaint of pain over the swelling. On elaborating origin, duration and progression, the patient noticed the swelling two weeks ago and was of the same size. The lesions were located along the neurovascular bundle. Conclusions: The larger lesion measured approximately 8.8(cc)×3.5(w)×2.2(AP) cm. No perilesional edema was seen. On the basis of MRI findings, a provisional diagnosis of nerve sheath tumor was made. Metastatic Adenocarcinoma of Small Intestine was to be done. Diagnosis was made on the basis of CT results, supported by the results of FNAC of supraclavicular lymph node and biopsy of the tumor on the thigh. Patient was managed conservatively with chemotherapy. The patient was given Oxaliplatin 180mg and Capecitabine 500mg for 14 days in 21 cycles. The patient was also referred for radiotherapy. The patient was doing well as of his last follow-up.

Background and Methods: This observational study assessed the impact of omitting prophylactic preoperative and postoperative antibiotics in 251 clean plastic surgery cases. Patients aged below 40 years with proper hygiene and no comorbidities were included. Antibiotics were intentionally withheld in select cases based on clinical judgment and informed consent. Results: Among 136 patients receiving antibiotics, 5.20% developed surgical site infections (SSIs), while 6.97% of the 115 patients without antibiotics experienced SSIs. The difference was not statistically significant. Conclusion: The results suggest that routine antibiotic prophylaxis may be unnecessary in well-selected clean surgeries when stringent aseptic protocols are followed. The study supports individualized antibiotic use, promotes cost-effective care, and contributes to reducing antimicrobial resistance in surgical practice.

Introduction: Inferior wall myocardial infarction (IWMI) may often affect the right ventricle (RV), which is overlooked in clinical assessments. RV dysfunction has been associated with poor outcomes, including increased mortality and complications. Echocardiography, a non-invasive and widely used tool, can effectively evaluate RV function using parameters like TAPSE and MPI.  Aims: Aim of the present study is to assess the RV function in Acute Inferior Wall Myocardial Infarction patients and it’s correlation on treatment outcome. Materials & Methods: The study was Cross sectional Descriptive type of study. This study was completed within one and half year, One Year for data collection and management (2024-2025). Department of medicine, Agartala Government Medical College and GB Pant Hospital. And total sample size 110 acute inferior wall myocardial infarction patients. Result: In our study, hypertension was the most common comorbid condition, observed in 54 patients (49.1%), and followed by diabetes in 23 patients (20.9%). Dyslipidaemia was present in 8 patients (7.3%), and a family history of cardiovascular diseases (FHO CVDs) was noted in 2 patients (1.8%). Notably, 23 patients (20.9%) had no comorbid conditions. The value of z is 8.0482. The value of p is < .00001. The result is significant at p < .05. We found that Patients with RV dysfunction in inferior wall myocardial infarction experienced significantly higher rates of mortality, shock, heart failure, and longer hospitalization. These findings reinforce RV dysfunction as a poor prognostic marker, necessitating early identification and aggressive supportive management in affected individuals. Conclusion: We concluded that the research demonstrates the substantial influence of right heart dysfunction in inferior wall MI patient’s outcome. The most common co morbidity was found to be hypertension, which affected 54 patients and was statistically significant

Over 90% of people with diabetes have diabetic neuropathy, a common side effect of both type 1 and type 2 diabetes. Despite being one of the primary signs of diabetic neuropathy, the pathophysiological mechanisms behind pain are still unclear. Although the harmful consequences of hyperglycemia are generally acknowledged to be a significant factor in the development of this complication, a number of alternative theories have been proposed.  Derived from Clostridium botulinum, botulinum neurotoxin (BoNT) has been utilized globally to treat neurologic conditions like stiffness and dystonia in addition to cosmetic therapeutic uses. Because of its good safety profile and long-lasting therapeutic effects following a single course of injection, BoNT type A offers therapeutic utility in treating idiopathic trigeminal neuralgia or refractory neuropathic pain.  Patients with preserved heat sensitivity in the pain location and/or induced deep pain with pain paroxysms appear to have the best responder profiles to BoNT A. To sum up, a deeper comprehension of the processes behind botulinum toxin's effects on diabetic neuropathic pain may help both the search for novel treatments and the development of improved guidelines for maximizing pain management with already existing medications.

We retrospectively evaluated early postoperative outcomes following the Modified Bentall‑de Bono procedure using the coronary‑button technique in 60 patients from January 2018 to August 2024 at a single tertiary centre. Most patients were aged 30–49 years; hypertension was the most common comorbidity. Aortic dissection was present in 30 % of cases, and 23 % were operated emergently. Mean cardiopulmonary bypass and cross‑clamp times were 283 and 213 minutes, respectively. Re‑exploration for bleeding was required in 8.3 %, three patients needed permanent pacemakers. Overall early mortality was 11.6 %, notably higher in emergency vs. elective cases (28.5 % vs. 6.5 %). The Modified Bentall remains effective with acceptable early outcomes in elective settings, though emergency operations and preoperative instability are associated with increased risk. 

Background: The medical curriculum is globally recognized for its rigorous and demanding nature, making medical students highly susceptible to psychological stress. The period surrounding professional examinations represents a time of peak academic pressure, which can significantly impact students' mental well-being and academic performance. Understanding the extent of this stress and the coping strategies employed is crucial for developing effective support systems. Methods: A descriptive, cross-sectional study was conducted among 100 MBBS students at a tertiary care medical college one week prior to their professional examinations. Participants were selected via convenience sampling. Data were collected using an anonymous, self-administered questionnaire that included sociodemographic details, the 10-item Perceived Stress Scale (PSS-10) to measure stress, and the Brief COPE inventory to assess coping mechanisms. Data were analyzed using SPSS version 26.0. The Independent Samples t-test and Chi-square test were used for comparisons, with a p-value <0.05 considered significant. Results: The mean age of the participants was 21.1 ± 2.3 years. The overall mean PSS-10 score was high at 24.8 ± 5.6, with 79% of students falling into the high-stress category (score >20). Students in their clinical years reported significantly higher mean stress scores than their pre-clinical counterparts (26.3 ± 4.9 vs. 23.3 ± 5.8; p=0.018). The most frequently used adaptive coping strategies were planning (85%), active coping (83%), and acceptance (76%). However, the use of maladaptive strategies was also common, including self-blame (52%) and behavioral disengagement (35%). Female students were significantly more likely to use emotion-focused coping strategies such as seeking emotional support (70% vs. 45%; p=0.021) compared to male students. Conclusion: A substantial majority of medical students experience high levels of stress during examinations, with the burden being greater in the clinical years. While students actively use problem-focused coping, there is a concerning reliance on maladaptive strategies like self-blame. These findings underscore the urgent need for medical institutions to implement targeted mental health support and stress-management programs to foster resilience and healthier coping skills among future physicians.

Tissue engineering offers a promising approach in medicine, aiming to repair and replace damaged or abnormal tissues. Using stem cells, this field seeks to create functional tissue constructs that can restore normal physiological functions. In this paper, we explore the application of tissue engineering in the context of congenital heart disease (CHD). We review recent advancements from in vitro experiments, preclinical animal models, and early clinical studies, highlighting both the progress made and the limitations encountered. Key challenges such as immune rejection and integration with host tissue are discussed. Finally, we outline future directions and the potential of tissue engineering to transform the treatment landscape for CHD.