Relations among multiple peer influences, body dissatisfaction, eating disturbance, and self-esteem: a comparison of average weight, at risk of overweight, and overweight adolescent girls

OBJECTIVE: The goal of this study was to evaluate peer-related influences on appearance, body dissatisfaction, eating disturbance, and self-esteem in average weight, at risk of overweight, and overweight adolescent girls. METHODS: Three hundred twenty-five adolescent girls from high schools in Florida were assessed. Ninety met criteria for being at risk of overweight or overweight. Logistic and multiple regression analyses were used to evaluate group differences on all variables and to assess the amount of variance accounted for by peer-influence variables in the prediction of body dissatisfaction, eating disturbance, and self-esteem. RESULTS: Overweight and at risk of overweight girls scored higher than average weight girls on body dissatisfaction, dieting, and a peer measure that assessed negative comments and attributions about appearance. They also scored lower than average weight girls on self-report measures that assessed conversations about appearance and anti-dieting advice. How influential friends were in determining one's body image was a unique predictor of body dissatisfaction but only for the overweight and at risk of overweight group. CONCLUSIONS: Possible implications for clinical intervention programs are discussed along with directions for future research.     

HDL in Children with CKD Promotes Endothelial Dysfunction and an Abnormal Vascular Phenotype

Endothelial dysfunction begins in early CKD and contributes to cardiovascular mortality. HDL is considered antiatherogenic, but may have adverse vascular effects in cardiovascular disease, diabetes, and inflammatory conditions. The effect of renal failure on HDL properties is unknown. We studied the endothelial effects of HDL isolated from 82 children with CKD stages 2–5 (HDL^CKD), who were free of underlying inflammatory diseases, diabetes, or active infections. Compared with HDL from healthy children, HDL^CKD strongly inhibited nitric oxide production, promoted superoxide production, and increased vascular cell adhesion molecule-1 expression in human aortic endothelial cells, and reduced cholesterol efflux from macrophages. The effects on endothelial cells correlated with CKD grade, with the most profound changes induced by HDL from patients on dialysis, and partial recovery observed with HDL isolated after kidney transplantation. Furthermore, the in vitro effects on endothelial cells associated with increased aortic pulse wave velocity, carotid intima-media thickness, and circulating markers of endothelial dysfunction in patients. Symmetric dimethylarginine levels were increased in serum and fractions of HDL from children with CKD. In a longitudinal follow-up of eight children undergoing kidney transplantation, HDL-induced production of endothelial nitric oxide, superoxide, and vascular cell adhesion molecule-1 in vitro improved significantly at 3 months after transplantation, but did not reach normal levels. These results suggest that in children with CKD without concomitant disease affecting HDL function, HDL dysfunction begins in early CKD, progressing as renal function declines, and is partially reversed after kidney transplantation.Patients with CKD no longer die from renal failure but from cardiovascular disease. There is an independent, graded association between a reduced eGFR and the risk of death and cardiovascular events.¹ Typically, patients with CKD develop calcification in the tunica media of their arteries,² but a concomitant process of endothelial damage leading to atherosclerosis is also³ present beginning in predialysis CKD.^4,5LDL is crucially involved in the pathogenesis of atherosclerotic cardiovascular disease in the general population,⁶ whereas HDL is thought to be antiatherogenic by promoting reverse cholesterol transport and exerting direct protective endothelial effects.⁷ HDL from healthy participants increases the bioavailability of nitric oxide (NO) by activating endothelial NO synthase inducing vasodilation and decreasing arterial BP. Moreover, HDL diminishes the production of reactive oxygen species such as superoxide (SO) radicals, which have been demonstrated to reduce NO bioavailability leading to endothelial dysfunction and promoting atherogenesis. However, recent evidence suggests that HDL may lose its vasoprotective properties in patients with manifest cardiovascular disease (e.g., coronary artery disease), diabetes, or inflammatory disease states (e.g., antiphospholipid syndrome).^8–10 Similarly, in adults on dialysis, HDL has reduced cholesterol efflux capacity and proinflammatory effects on mononuclear cells.^11–13 Observational studies have shown a strong association between high HDL levels and reduced risk of cardiovascular disease in the general population¹⁴ but not in dialysis patients.¹⁵Cardiac and vascular damage has also been documented in children on dialysis,^2,16,17 and cardiovascular disease accounts for the majority of deaths in pediatric dialysis patients.¹⁷ In contrast with adult patients with CKD, in whom cardiovascular risk factors such as diabetes dyslipidemia, hypertension, and smoking are highly prevalent,¹⁸ CKD in children is mainly caused by inherited disorders such as malformations of the kidney or urinary tract.¹⁸ Accordingly, examining HDL function in children who are free of “traditional” cardiovascular risk factors and underlying inflammatory diseases and who are nonsmokers gives us an unique opportunity to study the effects of renal failure on the vascular functions of HDL.We studied the endothelial properties of HDL in a cohort of children at different stages of CKD on dialysis and after transplantation and compared them with healthy children. Furthermore, to determine the clinical relevance of in vitro effects of HDL, we examined its relationship with clinical measures of the vascular phenotype as well as circulating markers of endothelial dysfunction. Finally, to show a causal link between renal function and HDL properties, we examined children on dialysis and 3 months after kidney transplantation. This study allowed us to examine when HDL dysfunction develops during the natural history of renal decline, its effects on vascular function, and the potential for recovery after kidney transplantation.     

Two-photon excitation improves multifocal structured illumination microscopy in thick scattering tissue

Multifocal structured illumination microscopy (MSIM) provides a twofold resolution enhancement beyond the diffraction limit at sample depths up to 50 µm, but scattered and out-of-focus light in thick samples degrades MSIM performance. Here we implement MSIM with a microlens array to enable efficient two-photon excitation. Two-photon MSIM gives resolution-doubled images with better sectioning and contrast in thick scattering samples such as Caenorhabditis elegans embryos, Drosophila melanogaster larval salivary glands, and mouse liver tissue.Fluorescence microscopy is an invaluable tool for biologists. Protein distributions in cells have an interesting structure down to the nanometer scale, but features smaller than 200–300 nm are blurred by diffraction in widefield and confocal fluorescence microscopes. Superresolution techniques like photoactivated localization microscopy (1), stochastic optical reconstruction microscopy (2), or stimulated emission depletion (STED) (3) microscopy allow the imaging of details beyond the limit imposed by diffraction, but usually trade acquisition speed or straightforward sample preparation. And although STED can provide resolution down to 40 nm, STED-specific fluorophores are recommended and it often requires light intensities that are orders of magnitude above widefield and confocal microscopy. On the other hand, structured illumination microscopy (SIM) (4) gives twice the resolution of a conventional fluorescence microscope with light intensities on the order of widefield microscopes and can be used with most common fluorophores. SIM uses contributions from both the excitation and emission point spread functions (PSFs) to substantially improve the transverse resolution and is generally performed by illuminating the sample with a set of sharp light patterns and collecting fluorescence on a multipixel detector, followed by image processing to recover superresolution detail from the interaction of the light pattern with the sample. A related technique, image scanning microscopy (ISM), uses a scanned diffraction-limited spot as the light pattern (5, 6). Multifocal SIM (MSIM) parallelizes ISM by using many excitation spots (7), and has been shown to produce optically sectioned images with ∼145-nm lateral and ∼400-nm axial resolution at depths up to ∼50 µm and at ∼1 Hz imaging frequency. In MSIM, images are excited with a multifocal excitation pattern, and the resulting fluorescence in the multiple foci are pinholed, locally scaled, and summed to generate an image [multifocal-excited, pinholed, scaled, and summed (MPSS)] with root 2-improved resolution relative to widefield microscopy, and improved sectioning compared with SIM due to confocal-like pinholing. Deconvolution is applied to recover the final MSIM image which has a full factor of 2 resolution improvement over the diffraction limit.MSIM works well in highly transparent samples (such as zebrafish embryos), but performance degrades in light scattering samples (such as the Caenorhabditis elegans embryo). Imaging in scattering samples can be improved by two-photon microscopy (8) and although the longer excitation wavelength reduces the resolution in nondescanned detection configurations, this can be partially offset by descanned detection and the addition of a confocal pinhole into the emission path. Whereas the nondescanned mode collects the most signal, the addition of a pinhole in the emission path of a point-scanning system can improve resolution when the pinhole is closed (9). In practice this is seldom done for biological specimens because signal-to-noise decays as the pinhole diameter decreases (9–11).SIM is an obvious choice in improving resolution without a dramatic loss in signal-to-noise, but the high photon density needed for efficient two-photon excitation is likely difficult to achieve in the typical widefield SIM configuration. This has led to other methods, such as line scanning (12) to achieve better depth penetration than confocal microscopy and up to twofold improvements in axial resolution (but with only ∼20% gain in lateral resolution). Multiphoton Bessel plane illumination (13) achieved an anisotropic lateral resolution of 180 nm (only in one direction) but requires an instrument design with two objectives in an orthogonal configuration. Cells and embryos can be readily imaged, but the multiaxis design may hinder the intravital imaging of larger specimens. Here, a combination of multiphoton excitation with MSIM is shown to improve both lateral and axial resolutions twofold compared with conventional multiphoton imaging while improving the sectioning and contrast of MSIM in thick, scattering samples.     

Adherence to transition guidelines in European paediatric nephrology units

Background

There is increasing focus on the problems involved in the transition and transfer of young adult patients from paediatric to adult renal units. This situation was addressed by the 2011 International Pediatric Nephrology Association/International Society of Nephrology (IPNA/ISN) Consensus Statement on transition.

Methods

We performed a survey of transition practices of 15 paediatric nephrology units across Europe 2 years after publication of the consensus statement.

Results

Two thirds of units were aware of the guidelines, and one third had integrated them into their transition practice. Forty-seven per cent of units transfer five or fewer patients with chronic kidney disease (CKD) stage 5 per year to a median of five adult centres, with higher numbers of CKD stages 2–4 patients. Seventy-three per cent of units were required by the hospital or government to transfer patients by a certain age. Eighty per cent of units commenced transition planning after the patient turned 15 years of age and usually within 1–2 years of the compulsory transfer age. Forty-seven per cent of units used a transition or transfer clinic. Prominent barriers to effective transition were patient and parent attachment to the paediatric unit and difficulty in allowing the young person to perform self-care.

Conclusions

Whereas awareness of the consensus statement is suboptimal, it has had some impact on practice. Adult nephrologists receive transferred patients infrequently, and the process of transition is introduced too late by paediatricians. Government- and hospital-driven age-based transfer policies distract focus from the achievement of competencies in self care. Variable use of transition clinics, written patient information and support groups is probably due to economic and human-resource limitations. The consensus statement provides a standard for evolving and evaluating transition policies jointly agreed upon by paediatric and adult units.     

Encapsulating peritoneal sclerosis in children

Encapsulating peritoneal sclerosis (EPS) is a rare but extremely serious complication of peritoneal dialysis (PD). While EPS has been well recognized in adults on long-term PD, and children can spend many years on PD before a transplant becomes available, only a small number of children with EPS have been described. Two European pediatric registries have recently reported on the prevalence, potential risk factors and outcomes of EPS in children. Although the prevalence of EPS is comparable to that published in adult registries, the outcome of pediatric EPS is significantly better and carries a lower mortality. All studies have shown a greater risk of EPS with a longer dialysis vintage, but it is not known why some individuals are susceptible to EPS development. In this review we discuss current views on the epidemiology, pathogenesis and management strategies for EPS. The hope of the authors is that this review will alert pediatric nephrologists to this rare but extremely serious complication of chronic PD. In the future, collaborative research and the establishment of a pediatric EPS registry may be of importance in helping pediatric nephrologists to recognize the early warning signs of EPS development and thereby to develop strategies for its prevention and optimal management.     

A common haplotype at the CD36 locus is associated with high free fatty acid levels and increased cardiovascular risk in Caucasians

CD36 is a class B scavenger receptor recognizing a variety of ligands including long-chain fatty acids and modified LDL. We investigated whether genetic variability at this locus is a determinant of free fatty acid (FFA) plasma levels and risk of coronary artery disease (CAD) in Caucasians. Typing of 21 polymorphic markers, evenly spanning the CD36 gene, revealed two linkage disequilibrium (LD) blocks that could be tagged by five polymorphisms (-33137A>G, -31118G>A, 25444G>A, 27645del>ins and 30294G>C). In 585 non-diabetic individuals of Caucasian origin, the 30294G>C polymorphism was significantly associated with FFA levels (P = 0.02)--an effect that was especially visible among men (P = 0.009). A similar association was observed in this gender at -33137 (P = 0.008) and -31118 (P = 0.028). When the five tag polymorphisms were considered together, men carrying the AGGIG haplotype had 31% higher FFA (P = 0.0002) and 20% higher triglycerides (P = 0.025) than non-carriers. The same haplotype was associated with increased risk of CAD in 197 type 2 diabetic individuals from the US (OR = 2.3, 95% CI 1.2-4.2). A similar tendency was observed in a group of 321 type 2 diabetic individuals from Italy (OR = 1.4, 0.9-2.3), resulting in an overall relative risk of 1.6 (1.1-2.3, P = 0.015) in the two populations considered together. By targeted resequencing, we identified a common variant in the CD36 promoter that is in strong LD with the AGGIG haplotype and could be partly responsible for these findings. In conclusion, this comprehensive study of CD36 variability indicates that the common polymorphisms at this locus modulate lipid metabolism and cardiovascular risk in Caucasians.