Alzheimer’s disease (AD) is the most common cause of dementia in elderly patients, affecting individuals older than 60 years. It is a complex degenerative brain disease characterized by progressive cognitive impairment. AD constitutes a major global health concern. A central role for inflammation has been implicated in the pathogenesis of AD. Despite the understanding of multiple molecular pathways in the pathophysiology of AD, novel treatment agents with a possible role in modifying the disease activity are still lacking. Our article provides a comprehensive review of various observational studies and randomized trials encompassing the use of anti-inflammatory agents in the management of AD patients and utilizes the conclusions derived therefrom to give recommendations in this regard.

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Stress has long been known to affect eating behaviors in humans. Stress-induced hyperphagia is considered a potential cause for the development of obesity. Given the high prevalence of obesity and its association with other cardiovascular and metabolic disorders, the subject of stress-induced eating has become even more important. We reviewed data from past studies to further elucidate the relationship between stress, appetite regulation and eating patterns in humans. Even though it is difficult to say with certainty that a person exposed to stress will undereat or overeat, but certain assumptions can be made. Generally, acute stress results in decreased eating whereas chronic stress results in increased eating. Glucocorticoids, the effector molecules of the stress response, increase the tendency to consume high-calorie, palatable foods. Further studies that can link the biological markers of stress-response with the hormones and neurotransmitters of appetite regulation can broaden our understanding of the subject. These studies can provide a groundwork for the development of effective anti-obesity strategies.

Background Data regarding the phenotypic correlates and prognostic value of albumin in heart failure with preserved ejection fraction (HFpEF) are scarce. The goal of the current study is to determine phenotypic correlates (myocardial hypertrophy, myocardial fibrosis, detailed pulsatile hemodynamics, and skeletal muscle mass) and prognostic implications of serum albumin in HFpEF. Methods and Results We studied 118 adults with HFpEF. All‐cause death or heart‐failure–related hospitalization was ascertained over a median follow‐up of 57.6 months. We measured left ventricular mass, myocardial extracellular volume, and axial muscle areas using magnetic resonance imaging. Pulsatile arterial hemodynamics were assessed with a combination of arterial tonometry and phase‐contrast magnetic resonance imaging. Subjects with lower serum albumin exhibited a higher body mass index, and a greater proportion of black ethnicity and diabetes mellitus. A low serum albumin was associated with higher myocardial extracellular volume (52.3 versus 57.4 versus 39.3 mL in lowest to highest albumin tertile, respectively; P =0.0023) and greater N‐terminal pro B‐type natriuretic peptide levels, but not with a higher myocardial cellular volume (123 versus 114 versus 102 mL; P =0.13). Lower serum albumin was also associated with an increased forward wave amplitude and markedly increased pulsatile power in the aorta. Serum albumin was a strong predictor of death or heart failure hospitalization even after adjustment for N‐terminal pro B‐type natriuretic peptide levels and the Meta‐Analysis Global Group in Chronic Heart Failure (MAGGIC) risk score (adjusted standardized hazard ratio=0.56; 95% CI=0.37–0.83; P <0.0001). Conclusions Serum albumin is associated with myocardial fibrosis, adverse pulsatile aortic hemodynamics, and prognosis in HFpEF. This readily available clinical biomarker can enhance risk stratification in HFpEF and identifies a subgroup with specific pathophysiological abnormalities.

Objectives Gallbladder disease is one of the most common diseases of the gastrointestinal tract. Various studies have shown an association between gallstones and an alteration in the serum lipids. The objective of this study was to compare serum lipid profile of gallstone patients with the controls. Methods This prospective cross-sectional study was conducted in the Surgical Department of the Services Institute of Medical Sciences from August 2017 to August 2018. A total of 50 patients were included in the study after screening through the inclusion criteria. A control group of 50 inpatients with no personal or family history of gallstones were also recruited for comparison. Results were expressed as mean with standard deviation. Students t-test was used to compare the data between the patients and the control groups (p < 0.05 was considered statistically significant). SPSS software, version 20 was used for statistical analysis. Results The mean age of the patients was 40.90 years and that of controls was 34.74 years. 46 patients were females and 44 controls were females. The serum cholesterol levels were high in the patients as compared to the controls but the comparison was not statistically significant. Serum triglycerides levels were high in the patients as compared to the controls and the analysis was statistically significant. Furthermore, the serum HDL levels were low in the patients as compared to the controls with a statistically significant p-value. However, the serum LDL levels were low in the patients as compared to the control group. Conclusion It was concluded that serum triglyceride levels and serum HDL levels were statistically significant in gallstone patients and there was a positive correlation between these parameters and gallstone disease.