The Effect of Social Support and Workplace Breastfeeding Conditions of Mothers Working in an Education Research Hospital on Breastfeeding Period

Objective: Breast milk is considered to be natural, reference nutrition for infants. The American Academy of Pediatrics and World Health Organization recommend that infants should be exclusively breastfed for about 6 months and breasteeding should be continued at least for 12 months as long as both the mother and the infant desire. It is known that mothers who started to work during breastfeeding period have difficulty in continuing breastfeeding due to inconvenient workplace conditions and breastfeeding breaks. Social support, known to have a role in coping with stress, has also been shown to be effective in maintaining breastfeeding. The aim of our study is to evaluate the problems faced by the mothers working in a training and research hospital related to the workplace environment and conditions and their social support. Method: The study group consisted of mothers who had children under three years of age and working in a training and research hospital. Eighteen questions prepared by the researchers, and questions in the Multidimensional Scale of Perceived Social Support were addressed to the mothers participating in the study about their breastfeeding period, return time to their work, breast-feeding permission, and milking, etc. Results: Fifty-one working mothers were reached during the study period. It was seen that 29 (56.9%) working mothers used formula during breastfeeding period. When mothers exclusively breastfed their infants, and those used formula during breastfeeding period were compared, it was seen that the mothers who used formula returned earlier to work (p = 0.036). Conclusion: Study results supported that the period of maternity leave should be longer to avoid using formulas more frequently, and to support exclusive breastfeeding for the first 6 months. It was concluded that employers should provide more suitable conditions for breastfeeding mothers to support breastfeeding

Epicardial adipose tissue and pericoronary fat thickness measured with 64-multidetector computed tomography: potential predictors of the severity of coronary artery disease

OBJECTIVE: The aim of the present study was to investigate the relationship between pericoronary fat and the severity and extent of atherosclerosis, quantified using 64-multidetector computed tomography, in patients with suspected coronary artery disease. METHODS: The study population consisted of 131 patients who were clinically referred for noninvasive multislice computed tomography coronary angiography for the evaluation of coronary artery disease. Patients were classified as follows: no atherosclerosis, Group 1; nonobstructive atherosclerosis (luminal narrowin

‘Browning’ the cardiac and peri-vascular adipose tissues to modulate cardiovascular risk

Excess visceral adiposity, in particular that located adjacent to the heart and coronary arteries is associated with increased cardiovascular risk. In the pathophysiological state, dysfunctional adipose tissue secretes an array of factors modulating vascular function and driving atherogenesis. Conversely, brown and beige adipose tissues utilise glucose and lipids to generate heat and are associated with improved cardiometabolic health. The cardiac and thoracic perivascular adipose tissues are now understood to be composed of brown adipose tissue in the healthy state and undergo a brown-to-white transition i.e. during obesity which may be a driving factor of cardiovascular disease. In this review we discuss the risks of excess cardiac and vascular adiposity and potential mechanisms by which restoring the brown phenotype i.e. “re-browning” could potentially be achieved in clinically relevant populations

A fatal complication after repair of post-infarction ventricular septal rupture: heparin-induced thrombocytopenia with thrombosis: case report

interior, theater, 196

Galectin-3: A biochemical marker to detect paroxysmal atrial fibrillation?

Purpose: Atrial fibrillation (AF) is the most common form of arrhythmia. AF leads to electrical remodelling and fibrosis of the atria; however, the mechanism(s) remain poorly understood. Galectin-3 is a potential mediator of cardiac fibrosis. The present study aimed to examine the relationship between serum galectin-3 levels and paroxysmal AF. Methods: Forty-six patients with paroxysmal AF and preserved left ventricular systolic function, and 38 age- and gender-matched control subjects, were involved in the study. Serum galectin-3 levels were analyzed with an enzyme-linked immunosorbent assay (ELISA). Results: Serum galectin-3 levels (median 1.38 ng/mL; 1.21 ng/mL-1.87 ng/mL; p < 0.001) were significantly elevated in patients with paroxysmal AF compared with the control. Left atrial diameter was significantly higher in patients with paroxysmal AF (41.2±3.0 mm vs. 39.6±3.3 mm). Left atrial diameter was found to be significantly correlated with serum galectin-3 levels in patients with paroxysmal AF (r= 0.378, p= 0.001). Conclusion: Serum galectin-3 levels are significantly elevated and significantly correlated with left atrial diameter in patients with paroxysmal AF. © 2016 CIM

The relationship between lipoprotein(a) and coronary artery disease, as well as its variable nature following myocardial infarction

Purpose: The present study aimed to investigate the relationship between the severity of coronary artery disease (CAD) and level of Lipoprotein (LP)(a). Methods: The study included 52 CAD patients and a control group consisting of 38 individuals. The patients were classified into three groups based on the clinical form of CAD (stable angina pectoris, SAP, unstable angina pectoris,UAP, and myocardial infarction,MI), and were further divided into three groups based on CAD severity (1-, 2- and 3-vessel). Serum Lp(a) levels were monitored 4, 8, and 24 h, 10 and 30 days following acute MI in 18 patients. Results: Based on regression analysis, Lp(a) was not correlated with other lipoproteins or with risk factors of CAD, such as body mass index, smoking, family history, diabetes, age, gender, and hypertension (r = 0.08-0.22). 72% of the patients in the CAD group and 24% of the control group had an Lp(a) level > 30 mg dL–1 (P = 0.004), and Lp(a) levels were higher in 3-vessel patients than in 2-vessel and 1-vessel CAD patients (86% vs. 68%, P = 0.02 and 86% vs. 62%, P=0.01, respectively). Serum Lp(a) levels were higher in the UAP and MI groups than in the SAP group (48 ± 44.7 mg dL–1, 49 ± 36.1 mg dL–1 and 31.2 ± 22.3 mg dL–1 , respectively,P=0.02). Lp(a) levels increased after acute MI, and reached peak levels 10 days post-MI (41% increase, P=0.001) and remained considerably elevated (18%) 30 days post-MI (P=0.01). Conclusion: Serum Lp(a) was higher in the UAP and MI patients in comparison with the SAP patients, and was higher in 3-vessel CAD in comparison with 1- and 2-vessel CAD patients

Adropin: A New Marker for Predicting Late Saphenous Vein Graft Disease after Coronary Artery Bypass Grafting

Purpose: Saphenous vein graft disease (SVGD), defined as an occlusion of 50% or more of the SVG excluding distal anastomotic occlusion, is an important predictor of morbidity after coronary artery bypass grafting (CABG). Late graft occlusion is a serious complication that often limits the use of the saphenous vein as a coronary bypass graft. Late graft occlusion is particularly common in old, degenerated venous grafts with advanced atherosclerotic plaques. Adropin has been implicated in the homeostatic control of metabolism. The purpose of this study was to investigate whether serum adropin levels are associated with late SVGD following CABG. Methods: Thirty-eight patients with SVGD involving at least one graft (occluded group; 14 females, 24 males) and 42 patients with a patent saphenous vein graft (patent group; 15 females, 27 males) were enrolled in this study. Venous blood samples were taken from all of the participants to measure plasma adropin levels using an enzyme-linked immunsorbent assay kit. Results: The mean adropin level was significantly lower in the occluded group than in the patent group (3.2 ± 0.71 vs. 4.9 ± 1.51 ng/mL, p < 0.001). Multivariate regression analysis showed that the adropin level was the independent predictor of late saphenous vein graft occlusion. Conclusions: Adropin levels are lower in patients with late saphenous vein graft occlusion and these reduced adropin levels, together with other factors, may lead to saphenous vein graft occlusion. Larger and prospective studies are needed to determine if adropin plays a role in the pathogenesis of SVGD