Terryflanagan1715
Patients are commonly reported to experience postoperative cognitive decline (POCD) and new ischemic lesions following surgery, which many researchers have hypothesised to result from emboli entering the cerebral circulation during surgery. Modern magnetic resonance imaging techniques have enabled clear and accurate identification of ischemic lesions. However, difficulties in assessing subtle changes in cognitive impairment clinically remain. The purpose of this systematic review is to discuss the literature that has investigated cognitive outcome in relation to new ischaemic brain lesions after cardiac surgery.
Risk of cardiovascular and metabolic disease is higher in adults who were relatively thin at birth and had subsequent accelerated weight gain. This specific pattern of weight gain may relate to unfavorable cardiometabolic markers already in childhood. We prospectively assessed whether children with different patterns of overweight development from age 3 months to 11 years had distinct levels of cardiometabolic markers at age 12 years.
We used data of 1500 children participating in the PIAMA birth cohort that started in 1996/1997. Parents reported height and weight during 10 waves of follow-up from age 3 months to 11 years. Four distinct overweight development patterns were derived using longitudinal latent class analysis; 'never'; 'early transient'; 'gradually developing' and 'persistent' overweight. Cardiometabolic markers (total-to-high-density lipoprotein cholesterol (TC/HDLC) ratio, blood pressure (BP), glycated hemoglobin (HbA1c)) were assessed at age 12 years in 1500 children.
Children who developlt cardiometabolic disease.
Children with gradually developing overweight, and those with persistent overweight had unfavorable cholesterol and blood pressure levels already at age 12 years, whereas children with early transient overweight avoided these unfavorable outcomes. Our results support the hypothesis that specific overweight patterns predispose to an adverse cardiometabolic profile, which is already apparent in early adolescence before progressing to adult cardiometabolic disease.
Various pathogens are implicated in the induction of obesity. Previous studies have confirmed that human adenovirus 36 (Ad36) is associated with increased adiposity, improved glycemic control and induction of inflammation. The Ad36-induced inflammation is reflected in the infiltration of macrophages into adipose tissue. However, the characteristics and role of adipose tissue macrophages (ATMs) and macrophage-secreted factors in virus-induced obesity (VIO) are unclear. Although insulin-like growth factor-1 (IGF-1) is involved in obesity metabolism, the contribution of IGF secreted by macrophages in VIO has not been studied.
Four-week-old male mice were studied 1 week and 12 weeks after Ad36 infection for determining the characteristics of ATMs in VIO and diet-induced obesity (DIO). In addition, macrophage-specific IGF-1-deficient (MIKO) mice were used to study the involvement of IGF-1 in VIO.
In the early stage of VIO (1 week after Ad36 infection), the M1 ATM sub-population increased, which increased the M1/M2 ratio, whereas DIO did not cause this change. In the late stage of VIO (12 weeks after Ad36 infection), the M1/M2 ratio did not change because the M1 and M2 ATM sub-populations increased to a similar extent, despite an increase in adiposity. By contrast, DIO increased the M1/M2 ratio. In addition, VIO in wild-type mice upregulated angiogenesis in adipose tissue and improved glycemic control. However, MIKO mice showed no increase in adiposity, angiogenesis, infiltration of macrophages into adipose tissue, or improvement in glycemic control after Ad36 infection.
These data suggest that IGF-1 secreted by macrophages may contribute to hyperplasia and hypertrophy in adipose tissue by increasing angiogenesis, which helps to maintain the 'adipose tissue robustness'.
These data suggest that IGF-1 secreted by macrophages may contribute to hyperplasia and hypertrophy in adipose tissue by increasing angiogenesis, which helps to maintain the 'adipose tissue robustness'.
Several studies have reported on associations of size at birth and early growth with general and central obesity; however, few have examined the potential effects of birth weight and postnatal growth on separate abdominal fat compartments. We investigated the effects of size at birth, linear growth and relative weight gain from birth to adulthood on visceral (VFT) and subcutaneous abdominal (SAFT) fat thicknesses at age 30 years.
A total of 2663 participants from the 1982 Pelotas (Brazil) birth cohort study had complete information on ultrasound measures of abdominal fat at age 30 years, and anthropometric measurements for at least five visits (0/2/4/23/30 years). We estimated weight and height Z-score changes, conditional relative weight gain and conditional height at several ages.
In both men and women, VFT and SAFT showed positive associations with conditional relative weight gain during all age periods beyond 2 years and birth, respectively (all P⩽0.01). Women born with intrauterine growth restriction (IUGR) had greater VFT than other women (difference=0.15 s.d., 95% CI 0.01-0.29), and they showed a stronger positive influence of infant weight gain 0-2 years on VFT (IUGR β=0.17 s.d., 95% CI 0.05-0.29; non-IUGR β=0.01 s.d., 95% CI -0.04 to 0.06; Pinteraction=0.02). Stunting at 2 years was associated with lower SAFT but not VFT, and it modified the influence of weight gain 2-4 years on SAFT in both sexes (both Pinteraction<0.05).
Our findings reinforce the advantages of being born with an appropriate birth weight, and the hazards of rapid postnatal gains in weight relative to linear growth, particularly after the critical window of the first 1000 days.
Our findings reinforce the advantages of being born with an appropriate birth weight, and the hazards of rapid postnatal gains in weight relative to linear growth, particularly after the critical window of the first 1000 days.
High-fat diets (HFDs) induce systemic inflammation, gut microbial derangements and disturb metabolic homeostasis, resulting in weight gain, insulin resistance and nonalcoholic fatty liver (NAFL). Numerous antioxidants and prebiotic/probiotics per se may prevent HFD-associated comorbidities, but there are no reports related to their combination.
In the present study, we aim to evaluate a cobiotic combination of lycopene (antioxidant) and isomalto-oligosaccharides (IMOs, a prebiotic) for prevention of HFD-induced alterations.
Male Swiss albino mice were fed either normal pellet diet (NPD) or HFD and lycopene (5 and 10 mg kg(-1)), IMOs (0.5 and 1 g kg(-1)) or their combination for 12 weeks. Systemic adiposity, glucose tolerance, insulin sensitivity, feeding regulators in hypothalamus, hepatosteatosis and liver inflammation, cecal short chain fatty acids (SCFAs), serum inflammatory cytokines, gut morphology and alterations in selected gut microbes were studied.
Lycopene, IMOs and their combination preventnctional foods for their application against HFD-associated pathological complications.
In the popular news media, public health officials routinely emphasize the health risks of obesity and portray weight as under personal control. These messages may increase support for policies designed to reduce rates of obesity, but can also increase antifat stigma. Less often, the media cover 'Health at Every Size' or 'Fat Rights' perspectives that may have the opposite effects. We investigated how exposure to different 'fat frames' shifts attitudes about weight and support for obesity policies.
Across four experiments (n=2187), people read constructed news articles framing fatness as negative (unhealthy, controllable, acceptable to stigmatize) or positive (healthy, uncontrollable, unacceptable to stigmatize).
Compared with people who read fat-positive frames, people who read fat-negative frames expressed more belief in the health risks of being fat (d=0.95-1.22), belief weight is controllable (d=0.38-0.55), support for charging obese people more for health insurance (d=0.26-0.77), antifat prejudice ealth risks and weight-based stigma. selleck chemicals Shifting policy attitudes, however, is more challenging.
Recent reports indicate that inter/intramuscular adipose tissue (IMAT), composed by adipocytes underneath the deep fascia of the muscles, is positively correlated with aging, obesity and insulin resistance in humans. However, no molecular/cellular evidence is available to support these interactions. The current study aimed to better characterize human skeletal muscle-derived adipogenic progenitors obtained from obese volunteers and investigate the impact of derived adipocytes on insulin action in primary skeletal muscle cells.
Primary cultured stroma-vascular fraction (SVF) obtained from vastus lateralis muscle biopsies of middle-aged obese subjects was immunoseparated (magnetic beads or flow cytometry). The characteristics and/or metabolic phenotype of CD56(+), CD56(-) and CD56(-)CD15(+) cellular fractions were investigated by complementary approaches (flow cytometry, cytology, quantitative PCR and metabolic assays). The effects of conditioned media from CD56(-)CD15(+) cells differentiated into adipocytemuscle adipocytes are able to impair insulin action and signaling of muscle fibers. This paracrine effect could explain, at least in part, the negative association between high levels of IMAT and insulin sensitivity in obesity and aging.Genetic studies have identified a glutamate-ammonia ligase gene (GLUL) polymorphism associated with cardiovascular disease morbidity and mortality among people with type 2 diabetes (T2D). We sought to determine whether GLUL rs10911021 is associated prospectively with adjudicated cardiovascular composite end points among overweight/obese individuals with T2D and whether a lifestyle intervention resulting in weight loss could diminish this association. Look AHEAD is a randomized, controlled trial to determine the effects of intensive lifestyle intervention (ILI), including weight loss and physical activity, relative to diabetes support and education, on cardiovascular outcomes. Look AHEAD participants included in this report were 3,845 overweight/obese individuals with T2D who provided consent for genetic analyses. Over a median of 9.6 years of follow-up, the risk (C) allele for GLUL rs10911021 was significantly associated with the primary composite end point of death from cardiovascular causes, nonfatal myocardial infarction, nonfatal stroke, or hospitalization for angina among individuals with no history of cardiovascular disease (CVD) at baseline using additive genetic models (hazard ratio 1.17 [95% CI 1.01-1.36]; P = 0.032). Results appeared more consistent in recessive models and among individuals with no known history of CVD at baseline; ILI did not alter these associations. These results extend the association of GLUL rs10911021 to incident CVD morbidity and mortality in the setting of T2D.Circulating microRNAs (miRNAs) have emerged as novel biomarkers of diabetes. The current study focuses on the role of circulating miRNAs in patients with type 1 diabetes and their association with diabetic retinopathy. A total of 29 miRNAs were quantified in serum samples (n = 300) using a nested case-control study design in two prospective cohorts of the DIabetic REtinopathy Candesartan Trial (DIRECT) PROTECT-1 and PREVENT-1. The PREVENT-1 trial included patients without retinopathy at baseline; the PROTECT-1 trial included patients with nonproliferative retinopathy at baseline. Two miRNAs previously implicated in angiogenesis, miR-27b and miR-320a, were associated with incidence and with progression of retinopathy the odds ratio per SD higher miR-27b was 0.57 (95% CI 0.40, 0.82; P = 0.002) in PREVENT-1, 0.78 (0.57, 1.07; P = 0.124) in PROTECT-1, and 0.67 (0.50, 0.92; P = 0.012) combined. The respective odds ratios for higher miR-320a were 1.57 (1.07, 2.31; P = 0.020), 1.43 (1.05, 1.94; P = 0.021), and 1.48 (1.
