Gujarat Adani Institute of Medical Sciences

Abstract Introduction Minimally invasive surgical techniques including Robotic-Assisted thoracoscopic surgery (RATS) have advanced the treatment of lung cancer and enhanced patient outcomes from early recovery to improved quality of life. The “July effect” hypothesizes that morbidity and mortality outcomes worsen during the beginning of academic year when new residents and fellows begin training. We investigated the impact of the same on outcomes of RATS among lung cancer patients. Methods Using the National Inpatient Sample (2016-2019), we identified adults(ages≥18 years) with lung cancer who underwent RATS(lobectomy/sublobar resection) at urban teaching centers(UTC). Patients were stratified by surgical timing: July-September versus other months. Multivariable logistic regression compared perioperative outcomes between groups, adjusting for confounders. Results We analyzed 25,480 RATS procedures, with 25.59% performed during July-September. Baseline characteristics were comparable between groups regarding sex, race (White, Hispanic), insurance type, comorbidity burden, and age; however, fewer Black patients underwent surgery during July-September (Table 1a). Multivariable logistic regression revealed no significant differences in perioperative outcomes between the July-September and other months of the year. Evaluated outcomes included thoracic complications like pneumonia (aOR 0.89, 95% CI 0.62-1.28, p = 0.526), pneumothorax (aOR 1.07, 95% CI 0.85-1.34, p = 0.583), air leak (aOR 0.98, 95% CI 0.79- 1.22, p = 0.873), respiratory failure (aOR 0.9, 95% CI 0.50-1.63, p = 0.729) , atelectasis (aOR 1.12, 95% CI 0.88-1.42, p = 0.372), thromboembolic events like pulmonary embolism (aOR 0.63, 95% CI 0.13-2.97, p = 0.557), deep venous thrombosis (aOR 1.01, 95% CI 0.65-1.57, p = 0.952), bleeding complications like transfusion (aOR 0.95, 95% CI 0.55-1.64, p = 0.866), hemothorax/hemoperitoneum/hematoma (aOR 0.58, 95% CI 0.22-1.52, p = 0.264), renal complications (aOR 1.00, 95% CI 0.32-3.17, p = 0.994), conversion to open surgery (aOR 0.53, 95% CI 0.11-2.47, p = 0.417), extended length of stay (>7 days) (aOR 0.96, 95% CI 0.78-1.17, p = 0.667), and in-hospital mortality (aOR 0.57, 95% CI 0.21-1.50, p = 0.250)(Table 1b). Conclusions Our study suggested no “July effect” in the perioperative outcomes of RATS. This demonstrates the robust hospital support systems ensuring the safe transition of resident classes without affecting the patient care negatively. This abstract is funded by: None

Background:Adherence to medication is a critical factor that affects the glycemic control in patients with type 2 diabetes mellitus (T2DM) and influences both short-term and long-term complications. The objective of the study was to assess the impact of medication adherence and glycemic control in patients with T2DM on oral hypoglycemic agents (OHAs) and insulin. Materials and Methods:This 12-month prospective study involved 220 T2DM patients at a tertiary care hospital. The study cohort was divided into those on OHAs (n = 120) and insulin therapy (n = 100). Adherence was measured by the Morisky Medication Adherence Scale, and glycemic control was measured by levels of glycated hemoglobin (HbA1c). Results:The average age of the participants was 55.2 ± 11.8 years, and males were overrepresented (60%). Adherence was high among 68% of patients receiving OHAs and 52% of those receiving insulin (P = 0.02). The average HbA1c was lower in the OHA group (7.4% ±1.1%) than in the insulin group (8.2% ± 1.4%, P < 0.001). Glycemic control was also better in patients with high adherence (HbA1c 7.1% ± 0.9%) than low adherence (8.6% ± 1.3%, P < 0.001). Complexity of treatment, dose frequency, and injection fear were some factors that affected adherence in the insulin group. Conclusion:This study demonstrates that adherence is higher in patients treated with OHA and that it is associated with better glycemic control. Interventions to improve adherence in the insulin group are crucial for better management of diabetes.

Intestinal fatty acid–binding protein (I-FABP) has gained attention as a biomarker of gut epithelial injury in heart failure (HF), a condition increasingly recognized as involving multisystem dysfunction. This review synthesizes current evidence on I-FABP’s role in HF pathophysiology, prognosis, and its potential therapeutic relevance. Elevated I-FABP levels have been consistently linked with worse clinical outcomes across diverse HF presentations, including acute decompensated HF, cardiogenic shock, chronic HF, and HF following myocardial infarction. In these contexts, I-FABP reflects intestinal injury caused by splanchnic hypoperfusion or venous congestion, providing prognostic insight beyond traditional cardiac markers. In chronic HF, I-FABP correlates with gut microbiota alterations and reduced microbial diversity, supporting its role in gut barrier dysfunction and systemic inflammation through the gut-heart axis. Compared with other fatty acid–binding proteins, such as H-FABP (myocardial injury), L-FABP (hepatic and renal stress), and A-FABP (metabolic inflammation), I-FABP captures a distinct and clinically relevant dimension of HF-related organ involvement. Thus, I-FABP shows a strong potential as a multimodal biomarker for risk stratification, disease monitoring, and possibly guiding novel gut-targeted therapies in HF. Further research is warranted to validate its clinical utility and explore its integration into routine HF management.

Background: Acute exacerbation of chronic obstructive pulmonary disease (AECOPD) is a leading cause of hospitalization and constitutes the principal driver of COPD-related healthcare expenditure, with prolonged hospital stay representing a major contributor to this burden. Methods: This retrospective observational study analyzed medical records of 205 patients admitted with AECOPD at ABC Hospital over a one-year period. COPD was diagnosed per GOLD criteria and exacerbation severity classified using The Rome Proposal; prolonged length of hospital stay (LHS) was defined as ≥7 days. Clinical, demographic, and investigational parameters were extracted, and their associations with LHS were evaluated using binary and multiple logistic regression analysis with statistical significance set at p <0.05. Results: The mean LHS was 10.7 ± 5.1 days, with 144 patients (70.2%) experiencing prolonged hospitalization. The cohort was predominantly male (89.8%), with a mean age of 64.2 ± 8.4 years, and 68.3% presented with type II respiratory failure. Binary logistic regression identified advancing age (p = 0.04), prior AECOPD hospitalizations (p = 0.03), arterial hypoxemia (p = 0.04), NIV requirement (p = 0.01), and severe AECOPD (p = 0.004) as significantly associated with prolonged LHS. On multiple logistic regression, severe AECOPD at admission was the only independent predictor of prolonged hospitalization (OR: 5.0; 95% CI: 1.4–18.2; p = 0.01). Conclusion: Severe AECOPD at admission is the strongest independent determinant of prolonged hospitalization, highlighting the importance of early severity stratification to guide timely intervention and optimize resource utilization in AECOPD management.

Fear, anxiety, and suicidality are often conceptualized along a severity continuum; however, this view fails to capture critical mechanistic differences in how threat is processed and regulated in the brain. Here, we propose a circuit-based framework in which these states represent distinct modes of neural organization defined by their temporal dynamics, network configurations, and regulatory control. Fear is mediated by phasic, stimulus-bound processing within amygdala-centered microcircuits that enable rapid and precise responses to immediate threat. Anxiety emerges through temporal expansion of threat processing, involving recruitment of bed nucleus of the stria terminalis (BNST) circuits, interoceptive amplification via insula-anterior cingulate cortex (ACC) networks, and reduced prefrontal regulation, resulting in sustained anticipatory activation. Suicidal states reflect a further reconfiguration in which threat becomes internalized within self-referential systems. Altered interactions between default mode network (DMN) regions and salience-related systems may contribute to persistent negative self-referential processing, while dysfunction in frontostriatal circuits and reduced serotonergic regulation may contribute to impaired behavioral inhibition and increased behavioral vulnerability. Across these states, three partially overlapping processes temporal persistence, internalization of threat, and impaired action regulation are proposed to represent dynamic reconfigurations within shared neural systems rather than fixed sequential stages.