Forecasting Atrial Fibrillation: The Predictive Power of N-terminal Prohormone of Brain Natriuretic Peptide in a Five-Year Study.

Introduction Atrial fibrillation (AF) is a major global health concern, and early prediction is essential for managing high-risk individuals. N-terminal prohormone of brain natriuretic peptide (NT-proBNP) has emerged as a crucial biomarker for predicting AF. While most studies have concentrated on cohorts already diagnosed with AF or other cardiac diseases, this research investigates the predictive value of NT-proBNP for AF development in a population without prior AF diagnosis. Methods and materials A five-year prospective observational study was conducted on 4090 individuals aged 45 to 75 with no previous diagnosis of AF. Baseline demographic characteristics, comorbid conditions, cardiac-specific measures, and NT-proBNP levels were systematically recorded. The primary endpoint was the onset of AF, confirmed through annual 12-lead ECG or 24-hour Holter monitoring. Univariate and multivariate analyses identified factors associated with AF onset. Results Out of the total population, 16.6% (679 individuals) developed AF. Notably, increased NT-proBNP levels (P=0.001), older age (P=0.001), and hypertension (P=0.001) were significantly associated with the onset of AF. The mean NT-proBNP levels in the AF group were significantly higher than in the non-AF group (P<0.001). The AF group also showed a higher mean age and a greater prevalence of hypertension (P<0.001 for both). Conclusion This study confirms the predictive value of NT-proBNP for AF onset in a non-AF population, highlighting older age and hypertension as significant risk factors for AF development. The findings underscore the potential of NT-proBNP not only as a predictive biomarker but also as a therapeutic target. These insights emphasize the potential role of NT-proBNP in early intervention and management strategies for AF, suggesting that future research should include additional variables, such as lifestyle factors and genetic predisposition, in assessing AF risk.

Effect of Ajwa date pits powder (Phoenix dactylifera L.) on body composition, lipid profile and blood pressure in patients with hyperlipidemia: A randomized clinical trial.

Objective: To evaluate the effect of Ajwa dates pit powder (ADP) on lipid profile, body composition and blood pressure in patients with hyperlipidemia. Materials and Methods: This randomized controlled clinical study was carried out on 40 patients with total cholesterol >200 mg/dl, triglycerides >150 mg/dl and BMI >25, of either sex, aged 30-50 years, who were recruited through written consent. The patients were divided into two groups (n=20 each): the ADP and the control group (CG). All patients received the doctor's prescribed class A statin (Rosuvastatin/ Atorvastatin) 10 mg/day, while 2.7 g ADP was given on daily basis before breakfast with lukewarm water for 40 days and the control group received the same amount of wheat flour. Body composition, blood pressure and lipid profile were determined at baseline, and after 20 and 40 days. Data were analyzed by using SPSS and GraphPad Prism. Results: ADP significantly reduced body weight (p<0.001), BMI (p<0.001), fat mass, body fat percentage, visceral fat area and waist circumference compared to the control group. Similarly, ADP significantly (p=0.000) decreased the serum level of total cholesterol and low-density lipoprotein. Conclusion: ADP may have the potential to improve dyslipidemia and obesity.

Improvement in cardio-metabolic health and immune signatures in old individuals using daily chores (Salat) as an intervention: A randomized crossover study in a little-studied population.

Background: Decline in cardio-metabolic health, immunity, and physical activity is associated with old age. Old people also find it difficult to engage in structured exercise programs. Therefore, there is a need to investigate common daily chores as an alternative for exercise that may also help in maintaining cardio-metabolic and immune health. Objective: We aimed to investigate whether Salat, an obligatory Islamic prayer involving various physical movements and closely resembling yoga, enhances the benefits conferred by the current guidelines for physical activity. Methods: A total of 30 overweight adults (mean (SD) age of 53.5 (8.7) years) participated in this study. For a 4-week duration, we compared the effects of Salat before/after meals (Pre-MS/Post-MS) on selected immunological and metabolic parameters in serum samples. We also compared the effects of both Pre-MS/Post-MS regimens in young and old subjects to observe any age-related effects. Results: Most of the baseline metabolic parameters and the count of immune cells were normal. Post-MS resulted in a significant reduction in body weight and percent body fat (%BF). Overall, Post-MS resulted in a clear leukocytosis with a significant increase in granulocytes, monocytes, and lymphocytes. When analyzing the lymphocyte compartment, a clear numerical increase was noted for T, B, and NK cells. The number of CD8+ T cells showed a statistically significant increase. Similarly, Post-MS induced leukocytosis in both young and old individuals, while the increase in granulocytes, monocytes, and lymphocytes was statistically significant in old subjects only. Conclusion: This study demonstrated that the Islamic obligatory and congressional Salat practice is capable of mimicking desirable pro-immune and pro-metabolic health effects. Clinical trial registration: (UMIN000048901).

Time-restricted feeding regulates molecular mechanisms with involvement of circadian rhythm to prevent metabolic diseases.

Lifestyle and genetic perturbation of circadian rhythm can trigger the incidence and severity of metabolic diseases. Time-restricted feeding (TRF) regulates the circadian rhythm of food intake that protects against metabolic disorders induced by adverse nutrient intake. TRF also executes host metabolism from nutrient availability to optimize nutrient utilization. Circadian clock and nutrient-sensing pathways coordinate to regulate metabolic health through the feeding/fasting cycle. Concurrently, TRF imposes diurnal rhythm in nutrient utilization, thereby preserving cellular homeostasis. However, modulation of daily feeding and fasting periods calibrates the circadian clock, which protects against the lethal effects of nutrient imbalance on metabolism. Therefore, TRF also improves and restores metabolic rhythms that ultimately lead to better fitness by reversing the alteration in genotype-specific gene expression. The aim of this review was to summarize that TRF is an emerging dietary approach that maintains robust circadian rhythms in support of a steady daily feeding and fasting cycle. TRF also encourages the coordination between circadian clock components and nutrient-sensing pathways via molecular effectors that exert a protective role in the prevention of metabolic diseases.

Predominant Role of Immunoglobulin G in the Pathogenesis of Splenomegaly in Murine Lupus.

Systemic lupus erythematosus (SLE) is characterized by high levels of autoantibodies and multiorgan tissue damage. The pathogenesis of splenomegaly in SLE remains unknown. In this study, the role of immunoglobulin G (IgG) generation and deposition in the inflammation of the spleen and associated dysfunction in SLE was investigated. In the lupus mice, we observed the development of spontaneous splenomegaly, and we found that lupus serum IgG is an important pathological factor involved in the initiation of inflammation and further germinal center (GC) and plasma cell formation. We discovered that macrophages of the splenic marginal zone are dispensable for the GC response induced by lupus IgG, but red pulp macrophages are important for GC responses. Furthermore, we found that pathogenic lupus IgG promotes inflammation and GC formation through the macrophage-mediated secretion of TNF-α. Syk inhibitor treatment suppressed the changes in the histopathology of the spleen induced by lupus IgG. This study will contribute to the understanding of the pathogenesis of splenomegaly in lupus and promote the development of an effective therapeutic strategy for SLE.

Role of Hepatic Deposited Immunoglobulin G in the Pathogenesis of Liver Damage in Systemic Lupus Erythematosus.

The onset of hepatic disorders in patients with systemic lupus erythematosus (SLE) is frequent; however, the etiology and liver pathogenesis of SLE remain unknown. In the present study, the role of hepatic deposited immunoglobulin G (IgG) in SLE-derived liver damage was investigated. From a retrospective analysis of the medical records of 404 patients with lupus and from experimental studies on mice models, we found that liver dysfunction is common in SLE and liver damage with IgG deposition spontaneously develops in lupus-prone mice. Liver injury was recreated in mice by injecting IgG from lupus serum intrahepatically. The inflammation intensity in the liver decreased with IgG depletion and the lupus IgG-induced liver inflammation in FcγRIII-deficient mice was comparatively low; while, inflammation was increased in FcγRIIb-deficient mice. Macrophages, Kupffer cells, natural killer cells, and their products, but not lymphocytes, are required for the initiation of SLE-associated liver inflammation. Blocking IgG signaling using a spleen tyrosine kinase (Syk) inhibitor suppressed the liver damage. Our findings provided evidence of spontaneously established liver damage in SLE. They also suggested that hepatic-deposited lupus IgG is an important pathological factor in the development of liver injury and that hepatic inflammation is regulated by the Syk signaling pathway. Thus, Syk inhibition might promote the development of a therapeutic strategy to control liver damage in patients with SLE.

The role of neutrophils in skin damage induced by tissue-deposited lupus IgG.

Skin injury is the second most common clinical manifestation in patients with systemic lupus erythematosus (SLE). Neutrophils are crucial effector cells in the immune system but the significance of neutrophils in the pathogenesis of SLE is not clear. This study is to explore the role of neutrophils in the skin damage of SLE. We used lupus-prone mice and a C57BL/6 mouse model of lupus serum IgG-induced skin inflammation to investigate the role of neutrophils in skin damage of SLE. We found that a few neutrophils infiltrated the inflammatory sites of skin in lupus-prone mice and the lupus-IgG-induced skin damage mouse model. Depletion of neutrophils did not affect the development of skin inflammation caused by lupus IgG, and lupus IgG can induce apoptosis of neutrophils. The apoptosis of neutrophils induced by lupus IgG is related to FcγRIII and Fas/Fas ligand pathways. Our study indicates that neutrophils are not major contributors in the skin damage caused by tissue-deposited lupus IgG but death of neutrophils caused by lupus IgG may provide a resource of a large amount of autoantigens in SLE.