Parents\u27 perceptions and concerns about their children\u27s weight

Background: For parents to address overweight or obesity in their children, they first need to perceive their child to be overweight and to show some level of concern. We aimed to: (1) measure the level of misclassification between children&rsquo;s actual and parent-perceived weight status, and (2) determine the level of parent concern about their child&rsquo;s (actual) weight and whether concern varied according to the accuracy of parents&rsquo; perceptions.Methods: Participants were 1711 primary school children aged 5&ndash;12 years from the Barwon-South West region of Victoria, Australia. Height and weight were measured and weight status determined using international standards. Parents completed a Computer Assisted Telephone Interview (CATI) that included questions relating to their child&rsquo;s weight.Results: 448 children (26.2% of sample) were overweight or obese. Of these, weight status for almost half (48%) was underestimated by parents. This &lsquo;bias&rsquo; did not vary according to the child&rsquo;s gender, parent&rsquo;s education, or household socio-economic status but did for child&rsquo;s age and parent-respondent gender. More than half (57%) of the parents of overweight-obese children expressed no concern about their child&rsquo;s weight. Parents who underestimated the weight status of their overweight child were significantly less concerned (P &lt; 0.001) about their child&rsquo;s weight than those who correctly perceived their child as overweight.Conclusions: Parents were relatively poor judges of overweight or obesity in their own child and consequently there was a lack of appropriately directed concern. Education to help parents correctly classify their child&rsquo;s weight status should be part of efforts to prevent unhealthy weight gain.<br /

The anaplerotic node is essential for the intracellular survival of Mycobacterium tuberculosis

Enzymes at the phosphoenolpyruvate (PEP)–pyruvate–oxaloacetate or anaplerotic (ANA) node control the metabolic flux to glycolysis, gluconeogenesis, and anaplerosis. Here we used genetic, biochemical, and 13C isotopomer analysis to characterize the role of the enzymes at the ANA node in intracellular survival of the world's most successful bacterial pathogen, Mycobacterium tuberculosis (Mtb). We show that each of the four ANA enzymes, pyruvate carboxylase (PCA), PEP carboxykinase (PCK), malic enzyme (MEZ), and pyruvate phosphate dikinase (PPDK), performs a unique and essential metabolic function during the intracellular survival of Mtb. We show that in addition to PCK, intracellular Mtb requires PPDK as an alternative gateway into gluconeogenesis. Propionate and cholesterol detoxification was also identified as an essential function of PPDK revealing an unexpected role for the ANA node in the metabolism of these physiologically important intracellular substrates and highlighting this enzyme as a tuberculosis (TB)-specific drug target. We show that anaplerotic fixation of CO2 through the ANA node is essential for intracellular survival of Mtb and that Mtb possesses three enzymes (PCA, PCK, and MEZ) capable of fulfilling this function. In addition to providing a back-up role in anaplerosis we show that MEZ also has a role in lipid biosynthesis. MEZ knockout strains have an altered cell wall and were deficient in the initial entry into macrophages. This work reveals that the ANA node is a focal point for controlling the intracellular replication of Mtb, which goes beyond canonical gluconeogenesis and represents a promising target for designing novel anti-TB drugs

Losartan Improved Antioxidant Defense, Renal Function and Structure of Postischemic Hypertensive Kidney

Ischemic acute renal failure (ARF) is a highly complex disorder involving renal vasoconstriction, filtration failure, tubular obstruction, tubular backleak and generation of reactive oxygen species. Due to this complexity, the aim of our study was to explore effects of Angiotensin II type 1 receptor (AT1R) blockade on kidney structure and function, as well as oxidative stress in spontaneously hypertensive rats (SHR) after renal ischemia reperfusion injury. Experiments were performed on anaesthetized adult male SHR in the model of ARF with 40 minutes clamping the left renal artery. The right kidney was removed and 40 minutes renal ischemia was performed. Experimental groups received AT1R antagonist (Losartan) or vehicle (saline) in the femoral vein 5 minutes before, during and 175 minutes after the period of ischemia. Biochemical parameters were measured and kidney specimens were collected 24h after reperfusion. ARF significantly decreased creatinine and urea clearance, increased LDL and lipid peroxidation in plasma. Treatment with losartan induced a significant increase of creatinine and urea clearance, as well as HDL. Lipid peroxidation in plasma was decreased and catalase enzyme activity in erythrocytes was increased after losartan treatment. Losartan reduced cortico-medullary necrosis and tubular dilatation in the kidney. High expression of pro-apoptotic Bax protein in the injured kidney was downregulated after losartan treatment. Our results reveal that angiotensin II (via AT1R) mediates the most postischemic injuries in hypertensive kidney through oxidative stress enhancement. Therefore, blockade of AT1R may have beneficial effects in hypertensive patients who have developed ARF

Genome-wide association and functional follow-up reveals new loci for kidney function

Chronic kidney disease (CKD) is an important public health problem with a genetic component. We performed genome-wide association studies in up to 130,600 European ancestry participants overall, and stratified for key CKD risk factors. We uncovered 6 new loci in association with estimated glomerular filtration rate (eGFR), the primary clinical measure of CKD, in or near MPPED2, DDX1, SLC47A1, CDK12, CASP9, and INO80. Morpholino knockdown of mpped2 and casp9 in zebrafish embryos revealed podocyte and tubular abnormalities with altered dextran clearance, suggesting a role for these genes in renal function. By providing new insights into genes that regulate renal function, these results could further our understanding of the pathogenesis of CKD

Identification and quantification of apoptosis in the kidney using morphology, biochemical and molecular markers

Renal cell apoptosis is important in both physiological conditions such as normal renal development and pathological processes affecting the glomerular, vascular or tubulointerstitial compartments. Apoptosis may result in the detrimental loss of cells following many renal diseases or damaging changes, with significant loss of function. In contrast, apoptosis may control and limit inflammatory processes in both the acute and chronic phases of renal disease. Investigators interested in the presence of apoptotic cells in different forms of renal disease and development need methods to accurately determine the level of apoptosis within the kidney. Apoptosis is a gene-driven mode of cell death that may be identified by distinct morphological features, endonuclease-initiated DNA degradation, and by the involvement of specific apoptosis-regulating proteins. Many research papers that analyse the presence of apoptosis use the in situ terminal deoxyribonucleotidyl transferase-mediated deoxyuridine triphosphate nick end labelling (TUNEL) assay that detects DNA strand breaks in situ in tissue sections. Localization of activated caspase-3 is now seen as an alternative to TUNEL. This review will discuss some methods of identifying apoptosis in the kidney, using both morphological and biochemical or molecular characteristics, and also discuss some of the pitfalls of entire reliance on biochemical means of apoptotic cell identification without some morphological checks and balances. Although there are some caveats to the methods for identifying apoptotic cells in renal disease, those investigators who take the time to undertake such analysis often gain insightful data that provide explanations for the disease or condition being studied

Apoptosis and Expression of Bcl-2, Bcl-XL, and Bax in Renal Cell Carcinomas

There are at present disparate published results with regard to the relevance of the Bcl-2 gene family, levels of apoptosis, and cell proliferation in the development and progression of renal cell carcinoma (RCC). The present study v analyses the interrelationship between the expression of representatives of the anti-apoptotic (Bcl-2, Bcl-X-L) or pro-apoptotic (Bax) Bcl-2 proteins, incidence of apoptosis, and mitosis in a selected small group of 22 graded RCCs that had paired normal renal tissue, or non-neoplastic tissue in the renal biopsy specimen. The cases were chosen to determine the feasibility of measuring these parameters as potential surrogate markers of progression or treatment failure of the cancers. The results showed that in approximately 50% of the RCCs, where Bcl-2 and/or Bcl-X-L expression was high, apoptosis it-as not detected, and when expression of these proteins was low or not found, increased levels of apoptosis were seen. In most of the remaining 50% of samples, high levels of Bcl-X-L but not Bcl-2 were negatively correlated with low levels of apoptosis (Bcl-X-L: r = -0.437, P = 0.07 and Bcl-2: r = + 0.560, P = 0.02). For the same group of samples, high Bax expression was found in association with apoptosis (r = + 0.578, P = 0,02). A novel finding was an association between low expression of Bcl-2 an/or Bcl-X-L in normal tissue and the level of expression of these proteins in the RCCs, an intrinsic variation that may be an individual patient factor. The results indicate that, in RCCs with increased expression of Bcl-2 and/or Bcl-X-L, levels of apoptosis are minimal and these combined factors may assist in progression of the cancers and resistance to treatments

Expression and localization of the retinoblastoma gene during radiation-induced apoptosis in neonatal rat kidney

An in vivo neonatal rat kidney model was used to study an association between expression and localization of the retinoblastoma tumor-suppressor gene (Rb), or its protein product (pRb), and localization of radiation-induced apoptosis. The rat kidney has two distinct zones of differentiation at birth-an outer nephrogenic zone, in which cells are undifferentiated and new nephrons are forming, and a differentiated zone internal to this zone that has essentially the adult kidney form. At 6 h after radiation (5 Gy), high levels of relatively synchronous apoptosis are induced in the nephrogenic zone, with little effect on the differentiated zone, and proliferation in the nephrogenic zone is almost totally inhibited by radiation treatment, again with little effect in the differentiated area. We have used our knowledge of this model to analyze control (sham-treated) surd irradiated renal tissue for Rb mRNA transcript levels and localization (Northern blot and in situ hybridization (ISH)), pRb expression (Western blot and immunolocalization), apoptosis and mitosis (light and electron microscopy, and DNA gel electrophoresis for apoptosis), and cells in S-phase ([H-3]thymidine uptake and autoradiography). Northern blots showed no detectable alteration in RX, transcript levels between control and irradiated tissues, whereas Western blots indicated increased expression of pRb in protein extracted fr om irradiated kidney compared with controls. ISH confirmed that Rb transcripts were not substantially altered in the nephrogenic and differentiated zones in control versus irradiated renal tissue. Immunolocalization of pRb demonstrated little effect in the differentiated zone, but in the nephrogenic zone pRb expression was increased, especially the S-shaped prenephrons, and was also found in many, but not all, apoptotic cells in this zone. The results link radiation-induced apoptosis and increased pRb expression in a zone of the neonatal kidney having a low level of cell differentiation. (C) 1997 Academic Press