Prevalence of polycystic ovarian syndrome and its association with circulatory gonadotropins (luteinizing hormone and follicle-stimulating hormone) and prolactin in different reproductive age groups: A brief survey

Polycystic ovarian syndrome can affect fertility due to anovulatory cycles, luteal phase defects, hyperprolactinemia, and sex hormone imbalance, it remains untreated. The present study aims prevalence of polycystic ovarian disease (PCOD) of clinical/subclinical infertile women, different age groups and to analyze the association between circulatory level of gonadotropins, luteinizing hormone and follicle-stimulating hormone (LH and FSH) and prolactin (PRL) in polycystic ovary syndrome (PCOS) women of different reproductive age and its impact on fertility of women. The hormonal reports for LH, FSH, and PRL of 100 female patients were analyzed. Women suffering from oligomenorrhea and amenorrhea are given priority in this study. These samples were categorized into five different age groups of 15–20 years, 21–25 years, 26–30 years, 31–35 years, and 36–40 years. Obtained hormonal data of LH, FSH, and PRL were pooled and the average was taken to compare with the normal range of hormone. A significant age-dependent variation observed in circulatory serum levels of gonadotropins (LH and FSH) and PRL. The study reveals that the highest PCOD patients were observed in the age group of 21–25 years. Whereas, 30% to 15–20 years, 60% to 21–25 years, 40% to 26–30 years, 30 % to 31–35 years, and 20 % to 36–40 years of reproductive age group. Most affected population of PCOS women ranges in between 21 and 25 age groups, whereas the 36–40 age group was least affected. Age-related alteration in the circulatory level of PRL (hyperprolactinemia) and pulsatility of LH and FSH can be considered as the important factor regulating neuronal mechanisms of hypophyseal gonadal and peripheral endocrine feedback.

Endothelial Nitric Oxide Synthase (eNOS) Gene Expression determine the abundance of circulatory Endothelial Progenitor Cells (EPC) in Premature Coronary Artery Disease (PCAD) Patients

Objectives: Several studies has reported a reduced circulatory level and impaired functionality of EPCs in coronary artery disease (CAD) patients and the role of endothelial nitric oxide Synthase (eNOS) in relation with reduced circulatory level of EPC and their impaired functionality has been revealed by in vitro and animal studies. However EPC’s eNOS gene expression profile in in vivo condition in PCAD patients is yet to be revealed as the prevalence of CAD at young age is markedly increased in developing countries. Our previous study has already reported a significantly reduced circulatory level of EPC in PCAD patients compared to control subjects and in continuation of that finding, present study aimed to investigate the eNOS gene expression of EPC in same study subjects as well as to establish the association between EPC’s eNOS gene expression and reduced circulatory level of EPC in PCAD patients. Results: Reduced eNOS gene expression in EPC from PCAD patients compared to healthy controls were found (0.998±0.096/1.063±0.107) with a p-value of 0.002 and this difference was persistent even after adjusting for confounding factors (p=0.002). A positive correlation was found between eNOS gene expression and level of EPC in circulation (r = 0.234 and p = 0.0664); data from previous study.

Endothelial Nitric Oxide Synthase (eNOS) Gene Expression determine the abundance of circulatory Endothelial Progenitor Cells (EPC) in Premature Coronary Artery Disease (PCAD) Patients

Objectives Several studies has reported a reduced circulatory level and impaired functionality of EPCs in CAD patients and the role of eNOS in relation with reduced circulatory level of EPC and their impaired functionality has been revealed by in vitro and animal studies. However EPC’s eNOS gene expression profile in in vivo condition in PCAD patients is yet to be revealed as the prevalence of CAD at young age is markedly increased in developing countries. Our previous study has already reported a significantly reduced circulatory level of EPC in PCAD patients compared to control subjects and in continuation of that finding, present study aimed to investigate the eNOS gene expression of EPC in same study subjects as well as to establish the association between EPC’s eNOS gene expression and reduced circulatory level of EPC in PCAD patients. Results Reduced eNOS gene expression in EPC from PCAD patients compared to healthy controls were found (0.998±0.096/1.063±0.107) with a p-value of 0.002 and this difference was persistent even after adjusting for confounding factors (p=0.002). A positive correlation was found between eNOS gene expression and level of CD34+/KDR+ cells in circulation (r = 0.234 and p = 0.0664); data from previous study.

Pentraxin 3 increases in adult overweight and obese men after weight loss by dietary modification with exercise training

The circulatory level of pentraxin 3 (PTX3), an anti-inflammatory cardioprotective protein, has been shown to be lower in obese individuals than in those with normal weight. However, reports on the effects of different weight-loss methods on PTX3 are limited. The present study aimed to investigate the effect of weight loss on circulating PTX3 levels in overweight and obese men and to examine the combined effect of dietary modification and exercise training on PTX3 levels. Forty-eight overweight and obese men were assigned to 2 groups: dietary modification (group D) or exercise training and dietary modification (group DE). Groups D and DE were composed of 27 and 21 participants, respectively. We observed a significant independent relationship between changes in PTX3 and body mass index (BMI) in all participants (β = −0.617, p < 0.01). Subsequently, we compared the effects of the 2 weight-loss methods on plasma PTX3 in groups D and DE. The magnitude of the increase in plasma PTX3 levels was similar in the 2 groups. Interestingly, we observed that PTX3 levels in group DE increased significantly more than those in group D in subjects who achieved normal weight, based on BMI, after interventions. Our study suggested that weight reduction after lifestyle modification significantly increased PTX3 levels in overweight and obese men, and the addition of habitual exercise to dietary modification enhanced the magnitude of the increase in PTX3 levels in obese individuals achieving normal weight after weight loss.