Iqbal Alam

Background: Chronic Obstructive Pulmonary Disease (COPD) is associated with diaphragm dysfunction and reduced functional capacity. Altered deep core muscle function, particularly of deep abdominal muscles may further compromise postural stability and functional performance. However, objective clinical assessment of deep core muscle activation across COPD severity remains underexplored. Purpose: To explore potential associations between deep core muscle function using a pressure biofeedback unit (PBU) and Pulmonary Function parameters (PFT) across Global Initiative for Chronic Obstructive Lung Disease (GOLD) stages in individuals with COPD. Methods: In this cross‐sectional exploratory study, 84 individuals with COPD were assessed. Pulmonary function (FEV ₁ , FVC and FEV ₁ /FVC) was measured using spirometry. Deep core muscle function was evaluated using a Pressure Biofeedback Unit (PBU) during the Abdominal Drawing‐In Maneuver (ADIM) in prone position. Associations between PBU measures and pulmonary function parameters were examined using Spearman's correlation including exploratory analysis across GOLD stages. Results: Deep core muscle function demonstrated statistically significant negative correlations with pulmonary function parameters, including FEV ₁ /FVC ( ρ = −0.55; p < 0.001), FEV ₁ ( ρ = −0.72; p < 0.001) and FVC ( ρ = −0.59; p < 0.001). Mean PBU pressure values progressively increased across GOLD stages (Kruskal–Wallis H (3) = 50.053; p < 0.001; Ɛ ² = 0.59). Stage‐wise exploratory analyses demonstrated variable correlations across GOLD stages, however findings should be interpreted cautiously due to small subgroup sample sizes. Discussion: Deep core muscle function assessed via pressure biofeedback demonstrated exploratory association with pulmonary function and varied across COPD severity categories. Participants with greater airflow limitation generally exhibited poorer deep abdominal muscle activation. These findings indicate a possible association between COPD severity and altered deep core muscle activation patterns. However, due to the exploratory cross‐sectional design and methodological limitations, the findings should be considered hypothesis‐generating rather than confirmatory. Longitudinal and interventional studies are required to further investigate these associations. Trial Registration: The data for the present study were collected as part of a PhD thesis and the study was registered with the Clinical Trials Registry of India (CTRI/2022/12/048039)

Background: Preeclampsia (PE) is a leading cause of maternal and fetal morbidity and mortality. It involves systemic inflammation, oxidative stress, and endothelial dysfunction. High Mobility Group Box 1 (HMGB1), a danger-associated molecular pattern (DAMP), may contribute to these processes. Objective: To evaluate the role of extracellular HMGB1 in endothelial dysfunction in a rat model of PE induced by NG-nitro-L-arginine methyl ester (L-NAME), and to assess the therapeutic effect of glycyrrhizic acid (GA), an HMGB1 inhibitor. Methods: Pregnant Wistar rats were divided into four groups: control, pregnant control, PE (L-NAME-treated), and PE+GA. On gestational day 21, systolic, diastolic, and mean arterial pressure, proteinuria, and heart rate were measured. Plasma and placental nitric oxide (NO), oxidative stress markers (MDA, SOD, GSH), and inflammatory markers (HMGB1, IL-6, TNF-α, ICAM-1, NE, vWF) were analyzed via ELISA. Immunofluorescence was used to evaluate HMGB1, IL-6, NE, and vWF expression in placentae. Results: L-NAME treatment resulted in increased blood pressure, proteinuria, and elevated HMGB1 and inflammatory markers, with decreased NO and antioxidant levels. GA treatment improved NO bioavailability, reduced inflammation, and normalized endothelial markers. Conclusion: HMGB1 contributes to endothelial dysfunction and oxidative stress in PE. GA attenuates these effects, indicating its potential as a therapeutic agent targeting HMGB1 in preeclampsia.

Background: Type 2 diabetes mellitus (T2DM) is characterized by insulin resistance, which impairs the metabolism of carbohydrates, lipids, and proteins. Recent findings indicate that skeletal muscle atrophy, decreased muscle strength, and reduced muscle performance have become prevalent complications of diabetes. Additionally, dysfunction of cardiac autonomic nerves also leads to skeletal muscle impairment. These issues further exacerbate diabetes, thereby leading to a vicious cycle. This study investigates the association between muscle performance and cardiac autonomic neuropathy in middle-aged T2DM patients. Material and Methods: In this case–control study, we included 51 diagnosed T2DM patients aged 30-55 years, with a duration of T2DM less than 5 years and HbA1C level below 8%. We also included 51 age-, sex-, and BMI-matched healthy control subjects. Muscle performance was assessed by evaluating the core endurance through the trunk flexor endurance test (TFET), trunk lateral endurance test (TLET), trunk extensor endurance test (TEET), along with hamstring muscle flexibility through the active knee extension (AKE) test. Cardiac autonomic function was evaluated using the heart rate variability test. Statistical analyses were performed using GraphPad Prism version 9. The Mann–Whitney test was used to compare the two groups, and data were represented as median (interquartile range). Values were considered statistically significant at P value ≤ 0.05. Results: We observed a significant decrease in core endurance (TFET, TLET, TEET) with P values < 0.001, as well as reduced hamstring muscle flexibility shown by a decrease in the degree of AKE test with P value < 0.001 in the T2DM patients when compared with the controls. Furthermore, heart rate variability in both time domain parameters (SDRR, CVRR, SDSD, RMSSD, pRR50%) and frequency domain parameters (Total power, VLF, LF, HF, LF/HF) also showed significant decreases, with P values < 0.001 in the T2DM group compared to the control group. Conclusion: The observed decrease in muscle performance and heart rate variability parameters in middle-aged newly diagnosed T2DM patients suggests early skeletal muscle atrophy and cardiac autonomic dysfunction.