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Background:As part of the Healthy, Hunger-Free Kids Act, snacks, and desserts sold in K-12 schools as of the 2014-2015 school year are required to meet the "Smart Snacks" nutritional guidelines. Although studies exist in tracking progress in local and national efforts, the proportion of snack food procured by school districts compliant with the Smart Snacks standard prior to its full implementation is unknown. Methods: We repurposed a previously untapped database, Interflex, of public bid records to examine the nutritional quality of snacks and desserts procured by school districts. We selected 8 school districts with at least 90% complete data each year during 2011-2012, 2012-2013, and 2013-2014 school years and at locations across different regions of the United States. We quantified the amount of calories and sugar of each product contained in the won bids based on available online sources and determined whether the produce complied with Smart Snack guidelines. Results: In all 8 districts (snack expenditure analyzed ranging from $152,000 to $4.4 million), at least 50% of snack bids were compliant with the US Department of Agriculture Smart Snacks standard during the 2013-2014 school year. Across sampled districts, we observed a general trend in lower caloric density (kcal per product) and sugar density (grams of sugar per product) over a 3-year period. Conclusions: Many districts across the country have made headway in complying with the Smart Snack guidelines, though gaps remain.

APOL1 G1 and G2 variants are established risk factors for nondiabetic kidney disease. The presence of two APOL1 risk variants in donor kidneys negatively impacts kidney allograft survival. Because of evolutionary pressure, the APOL1 risk variants have become common in people from Africa and in those with recent African ancestry. APOL1 risk variant proteins are expressed in kidney cells and can cause toxicity to these cells. In this issue of the JCI, Zhang, Sun, and colleagues show that recipient APOL1 risk variants negatively affect kidney allograft survival and T cell-mediated rejection rates, independent of donor APOL1 genotype or recipient ancestry. The authors provide evidence that APOL1 risk variants play an immunomodulatory role in T cells and NK cells in the setting of kidney transplantation. These findings have important clinical implications that require further investigation., APOL1 and kidney risk Two genome sequence variants in the APOL1 gene on chromosome 22q strongly associate with an increased risk of non-diabetic kidney diseases such as focal segmental glomerulosclerosis, [...]

Detecting acute rejection in kidney transplantation has been traditionally done using histological analysis of invasive allograft biopsies, but this method carries a risk and is not perfect. Transplant professionals have been working to develop more accurate or less invasive biomarkers that can predict acute rejection or subsequent worse allograft survival. These biomarkers can use tissue, blood or urine as a source. They can comprise individual molecules or panels, singly or in combination, across different components or pathways of the immune system. This review highlights the most recent evidence for biomarker efficacy, especially from multicenter trials., Author(s): Vikas R. Dharnidharka [sup.1] , Andrew Malone [sup.2] Author Affiliations: (Aff1) 0000 0001 2355 7002, grid.4367.6, Division of Pediatric Nephrology, Hypertension and Pheresis, Washington University in St Louis & [...]

Background Many COL4A5 splice region variants have been described in patients with X-linked Alport syndrome, but few have been confirmed by functional analysis to actually cause defective splicing. We sought to demonstrate that a novel COL4A5 splice region variant in a family with Alport syndrome is pathogenic using functional studies. We also describe an alternative method of diagnosis. Methods Targeted next-generation sequencing results of an individual with Alport syndrome were analyzed and the results confirmed by Sanger sequencing in family members. A splicing reporter minigene assay was used to examine the variant's effect on splicing in transfected cells. Plucked hair follicles from patients and controls were examined for collagen IV proteins using immunofluorescence microscopy. Results A novel splice region mutation in COL4A5, c.1780-6T>G, was identified and segregated with disease in this family. This variant caused frequent skipping of exon 25, resulting in a frameshift and truncation of collagen [alpha]5(IV) protein. We also developed and validated a new approach to characterize the expression of collagen [alpha]5(IV) protein in the basement membranes of plucked hair follicles. Using this approach we demonstrated reduced collagen [alpha]5(IV) protein in affected male and female individuals in this family, supporting frequent failure of normal splicing. Conclusions Differing normal to abnormal transcript ratios in affected individuals carrying splice region variants may contribute to variable disease severity observed in Alport families. Examination of plucked hair follicles in suspected X-linked Alport syndrome patients may offer a less invasive alternative method of diagnosis and serve as a pathogenicity test for COL4A5 variants of uncertain significance., Author(s): Andrew F. Malone [sup.1] , Steven D. Funk [sup.1] , Tarek Alhamad [sup.1] , Jeffrey H. Miner [sup.1] Author Affiliations: (1) 0000 0001 2355 7002grid.4367.6Division of Nephrology, Department of [...]

Mechanical circulatory support (MCS) devices, such as left ventricular assist devices (LVADs) are very useful in improving outcomes in patients with advanced‐stage heart failure. Despite recent advances in LVAD development, pump thrombosis is one of the most severe adverse events caused by LVADs. The contact of blood with artificial materials of LVAD pumps and cannulas triggers the coagulation cascade. Heat spots, for example, produced by mechanical bearings are often subjected to thrombus build‐up when low‐flow situations impair washout and thus the necessary cooling does not happen. The formation of thrombus in an LVAD may compromise its function, causing a drop in flow and pumping power leading to failure of the LVAD, if left unattended. If a clot becomes dislodged and circulates in the bloodstream, it may disturb the flow or occlude the blood vessels in vital organs and cause internal damage that could be fatal, for example, ischemic stroke. That is why patients with LVADs are on anti‐coagulant medication. However, the anti‐coagulants can cause a set of issues for the patient—an example of gastrointestinal (GI) bleeding is given in illustration. On account of this, these devices are only used as a last resort in clinical practice. It is, therefore, necessary to develop devices with better mechanics of blood flow, performance and hemocompatibility. This paper discusses the development of LVADs through landmark clinical trials in detail and describes the evolution of device design to reduce the risk of pump thrombosis and achieve better hemocompatibility. Whilst driveline infection, right heart failure and arrhythmias have been recognised as LVAD‐related complications, this paper focuses on complications related to pump thrombosis, especially blood coagulopathy in detail and potential strategies to mitigate this complication. Furthermore, it also discusses the LVAD implantation techniques and their anatomical challenges. [ABSTRACT FROM AUTHOR]