Objectives To determine the usefulness of the Mini Nutritional Assessment (MNA) and plasma amino acid analysis in predicting the formation of pressure ulcers (PUs) in inpatients. Design Prospective, observational cohort study with a mean observation period of 62.2 ± 86.4 days. Setting Intermediate and acute care wards of a hospital in rural Japan. Participants Inpatients with an average age of 85.0 ± 7.6 (N = 422). Measurements Mini Nutritional Assessment, Subjective Global Assessment (SGA), Braden Scale (PU prognostic score), PU formation, and biochemical analysis including plasma amino acid concentrations. Results PUs developed in 7.1% of participants. A MNA score of less than 8 was more sensitive than a rating of moderate or severe malnourishment on the SGA combined with a Braden Scale score of less than 15 in predicting future PUs. The area under the receiver operating characteristic curve (AUC) of the MNA was superior to that of the Braden Scale. The Braden Scale nutrition subscore had the lowest AUC of the six Braden Scale subscores. Individuals who developed PUs had significantly lower plasma arginine concentrations than those who did not. Conclusion Mini Nutritional Assessment was able to predict the development of PUs. A MNA score of less than 8 performed better than the SGA, Braden Scale, and plasma arginine levels in predicting PU development. Although lower plasma arginine concentration at time of admission was associated with PU development, the AUC for arginine was not significantly different from 0.50. The findings from this prospective study support the use of nutritional assessment in inpatients to predict PU risk and target appropriate interventions.

BackgroundUrinary Ca2+ excretion increases with dietary NaCl. NaCl-induced calciuria may be associated with hypertension, urinary stone formation and osteoporosis, but its mechanism and long-term effects are not fully understood. This study examined alterations in the expressions of renal Ca2+ transporters, channels and claudins upon salt loading to better understand the mechanism of salt-induced urinary Ca2+ loss.MethodsEight-week old Wistar-Kyoto rats were fed either 0.3% or 8% NaCl diet for 8 weeks. Renal cortical expressions of Na+/Ca2+ exchanger 1 (NCX1), Ca2+ pump (PCMA1b), Ca2+ channel (TRPV5), calbindin-D28k, and claudins (CLDN-2, -7, -8, -16 and −19) were analyzed by quantitative PCR, western blot and/or immunohistochemistry.ResultsFractional excretion of Ca2+ increased 6.0 fold with high-salt diet. Renal cortical claudin-2 protein decreased by approximately 20% with decreased immunological staining on tissue sections. Claudin-16 and −19 expressions were not altered. Renal cortical TRPV5, calbindin-D28k and NCX1 expressions increased 1.6, 1.5 and 1.2 fold, respectively.ConclusionsChronic high-salt diet decreased claudin-2 protein and increased renal TRPV5, calbindin-D28k, and NCX1. Salt loading is known to reduce the proximal tubular reabsorption of both Na+ and Ca2+. The reduction in claudin-2 protein expression may be partly responsible for the reduced Ca2+ reabsorption in this segment. The concerted upregulation of more distal Ca2+-transporting molecules may be a physiological response to curtail the loss of Ca2+, although the magnitude of compensation does not seem adequate to bring the urinary Ca2+ excretion down to that of the normal-diet group.

Gamma-aminobutyric acid (GABA) is an important neurotransmitter, but recent reports have revealed the expression of GABAergic components in peripheral, non-neural tissues. GABA administration induces natriuresis and lowers blood pressure, suggesting renal GABA targets. However, systematic evaluation of renal GABAergic components has not been reported. In this study, kidney cortices of Wistar-Kyoto rats (WKY) were used to assay for messenger RNAs of GABA-related molecules using RT-PCR. In WKY kidney cortex, GABAA receptor subunits, α1, β3, δ, ε and π, in addition to both types of GABAB receptors, R1 and R2, and GABAC receptor ρ1 and ρ2 subunit mRNAs were detected. Kidney cortex also expressed mRNAs of glutamate decarboxylase (GAD) 65, GAD67, 4-aminobutyrate aminotransferase and GABA transporter, GAT2. Western blot and/or immunohistochemistry were performed for those molecules detected by RT-PCR. By immunofluorescent observation, co-staining of α1, β3, and π subunits was observed mainly on the apical side of cortical tubules, and immunoblot of kidney protein precipitated with π subunit antibody revealed α1 and β3 subunit co-assembly. This is the first report of GABAA receptor π subunit in the kidney. In summary, unique set of GABA receptor subunits and subtypes were found in rat kidney cortex. As GABA producing enzymes, transporters and degrading enzyme were also detected, a possible existence of local renal GABAergic system with an autocrine/paracrine mechanism is suggested.

The Na/K ratio is considered to be a useful index, the monitoring of which allows an effective Na reduction and K increase, because practical methods (self-monitoring devices and reliable individual estimates from spot urine) are available for assessing these levels in individuals. An intervention trial for lowering the Na/K ratio has demonstrated that a reduction of the Na/K ratio mainly involved Na reduction, with only a small change in K. The present study aimed to clarify the relationship between dietary Na intake and the urinary Na/K molar ratio, using standardized low- and high-salt diets, with an equal dietary K intake, to determine the corresponding Na/K ratio. Fourteen healthy young adult volunteers ingested low-salt (3 g salt per day) and high-salt (20 g salt per day) meals for seven days each. Using a portable urinary Na/K meter, participants measured their spot urine at each voiding, and 24-h urine was collected on the last day of each diet period. On the last day of the unrestricted, low-salt, and high-salt diet periods, the group averages of the 24-h urine Na/K ratio were 4.2, 1.0, and 6.9, while the group averages of the daily mean spot urine Na/K ratio were 4.2, 1.1, and 6.6, respectively. The urinary Na/K ratio tracked changes in dietary salt intake, and reached a plateau approximately three days after each change in diet. Frequent monitoring of the spot urine Na/K ratio may help individuals adhere to an appropriate dietary Na intake.

at many loci across the genome, 3 and that smoking-related changes in gene expression are epigenetically regulated. 4 Among EWAS-identified loci, the aryl-hydrocarbon receptor repressor (AHRR) gene has been noted as a promising candidate gene, with smoking-associated hypomethylation of AHRR CpG sites (e.g., cg05575921) detectable in DNA from peripheral lymphocytes and pulmonary macrophages. 5,6 AHRR encodes a transcription factor that can repress the aryl-hydrocarbon receptor pathway, which regulates the cytochrome P450 (CYP)-mediated catabolism of xenobiotics such as dioxin and polyaromatic hydrocarbons contained in tobacco smoke. 5 Although the exact relation-T obacco smoking is a leading preventable cause of morbidity and mortality in the world. Active smoking in adults increases the risk for a wide spectrum of chronic illness, such as cardiovascular and respiratory disease, and various forms of cancer. As self-reported smoking information is prone to inaccuracies due to recall bias and under-reporting, 1 an objective biomarker of longterm smoking behavior has been sought. Among current smokers, cotinine, a primary metabolite of nicotine, is a reliable measure of nicotine exposure, 2 but is not suited for the estimation of long-term smoking behavior due to its short half-life of 15-24 h.With the advent of epigenome-wide association studies (EWAS) in the last decade, it has become known that tobacco smoking has a broad effect on DNA methylation Editorial p ????