Determinants of Slow Walking Speed in Ambulatory Patients Undergoing Maintenance Hemodialysis

Walking ability is significantly lower in hemodialysis patients compared to healthy people. Decreased walking ability characterized by slow walking speed is associated with adverse clinical events, but determinants of decreased walking speed in hemodialysis patients are unknown. The purpose of this study was to identify factors associated with slow walking speed in ambulatory hemodialysis patients. Subjects were 122 outpatients (64 men, 58 women; mean age, 68 years) undergoing hemodialysis. Clinical characteristics including comorbidities, motor function (strength, flexibility, and balance), and maximum walking speed (MWS) were measured and compared across sex-specific tertiles of MWS. Univariate and multivariate logistic regression analyses were performed to examine whether clinical characteristics and motor function could discriminate between the lowest, middle, and highest tertiles of MWS. Significant and common factors that discriminated the lowest and highest tertiles of MWS from other categories were presence of cardiac disease (lowest: odds ratio [OR] = 3.33, 95% confidence interval [CI] = 1.26–8.83, P<0.05; highest: OR = 2.84, 95% CI = 1.18–6.84, P<0.05), leg strength (OR = 0.62, 95% CI = 0.40–0.95, P<0.05; OR = 0.57, 95% CI = 0.39–0.82, P<0.01), and standing balance (OR = 0.76, 95% CI = 0.63–0.92, P<0.01; OR = 0.81, 95% CI = 0.68–0.97, P<0.05). History of fracture (OR = 3.35, 95% CI = 1.08–10.38; P<0.05) was a significant factor only in the lowest tertile. Cardiac disease, history of fracture, decreased leg strength, and poor standing balance were independently associated with slow walking speed in ambulatory hemodialysis patients. These findings provide useful data for planning effective therapeutic regimens to prevent decreases in walking ability in ambulatory hemodialysis patients.     

Ionic control of renal gluconeogenesis IV. Effect of extracellular phosphate concentration

Isolated rat renal tubules from glucose from pyruvate, malate, glycerol and α-ketoglutarate. The rate of glucose formation from all but glycerol is enhanced by an increase in Ca²⁺ concentration. Because changes in inorganic phosphate concentrations influence the uptake and retention of calcium by isolated cells, the effect of changes in phosphate concentration upon renal gluconeogenesis was examined. It was found that changing phosphate concentration altered the metabolism of isolated rat renal tubules in three ways which dependend upon the Ca²⁺ concentration. In the absence of Ca²⁺, increasing phosphate concentration from 0.07 to 1.2 mM led to a stimulation of the decarboxylation of [U-¹⁴C]malate, [1-14C]pyruvate, [2-¹⁴C]-pyruvate, α-keto[5-¹⁴C]glutarate and [1,3-¹⁴C₂]glycerol, and to an increase in ATP concentration but had no effect upon the rate of glucose formation from malate, pyruvate, α-ketoglutarate but a slight stimulation of glucose production from glycerol. A further increase in phosphate above 1.2 mM had no effect on any of these parameters. In the presence of either low (0.2 mM) or high (2.0 mM) Ca²⁺, changing phosphate concentration had no effect upon the decarboxylation of any of these substrates except glycerol whose decarboxylation was stimulated by increasing medium phosphate concentration. In the presence of calcium, increasing phosphate concentration led to an inhibition of glucose formation from malate, pyruvate and α-ketoglutarate but not from glycerol. Also in the presence of calcium both parathyroid hormone and cyclic AMP stimulated glucose formation, and under these conditions increasing phosphate concentration led to an inhibition of glucose formation. In tubules treated with parathyroid hormone an increase in phosphate concentration from 0.07 to 6.0 mM led to a significant increase in cyclic AMP concentration even though the rate of glucose formation decreased.Analysis of metabolite concentrations and rates of substrates decarboxylations, under a variety of conditions, revealed that P_i altered renal gluconeogenesis at a site different from those controlled by changes in Ca²⁺ concentration. The P_i-control site was tentatively identified as the glyceraldehyde phosphate dehydrogenase-glycerate kinase reaction sequence. However, the effect of changing P_i concentration upon parathyroid hormone-induced alterations in cyclic AMP concentration could not be explained by this action of P_i, and was probably due to an effect of P_i upon cellular calcium distribution. Thus, changes in P_i concentration appear to have two cellular effects, only one of which is related to a change in cellular calcium metabolism.     

Changes in Brain Tissue and Behavior Patterns Induced by Single Short-Term Fasting in Mice

In humans, emaciation from long-term dietary deficiencies, such as anorexia, reportedly increases physical activity and brain atrophy. However, the effects of single short-term fasting on brain tissue or behavioral activity patterns remain unclear. To clarify the impact of malnutrition on brain function, we conducted a single short-term fasting study as an anorexia model using male adult mice and determined if changes occurred in migratory behavior as an expression of brain function and in brain tissue structure. Sixteen-week-old C57BL/6J male mice were divided into either the fasted group or the control group. Experiments were conducted in a fixed indoor environment. We examined the effects of fasting on the number of nerve cells, structural changes in the myelin and axon density, and brain atrophy. For behavior observation, the amount of food and water consumed, ingestion time, and the pattern of movement were measured using a time-recording system. The fasted mice showed a significant increase in physical activity and their rhythm of movement was disturbed. Since the brain was in an abnormal state after fasting, mice that were normally active during the night became active regardless of day or night and performed strenuous exercise at a high frequency. The brain weight did not change by a fast, and brain atrophy was not observed. Although no textural change was apparent by fasting, the neuronal neogenesis in the subventricular zone and hippocampus was inhibited, causing disorder of the brain function. A clear association between the suppression of encephalic neuropoiesis and overactivity was not established. However, it is interesting that the results of this study suggest that single short-term fasting has an effect on encephalic neuropoiesis.     

Chemistry of Benzeneglycols

Diacetyl-trans-aminodeoxybenzeneglycol (trans-1-acetamido-2-acetoxy-cyclohexadiene-3, 5) was synthesized by starting from α-B. T. C.-cis-diol²⁾ through its dehydrochlorination, NaN₃ treatment, reduction, and then dehalogenation with zinc. During NaN₃ treatment, the formation of some diazido compounds was also observed.     

Syntheses of Paromamine and Its Related Compounds

Paromamine and its related compounds were synthesized by a modified Königs-Knorr reaction of 3,4,6-tri-O-acetyl-2-(2′,4′-dinitroanilno)-α-d-glucopyranosyl bromide with isopropylidene derivatives of 2-deoxystreptamine, streptamine and dihydroconduramine F–4. The condensed products were isolated as their poly N-acetyl derivatives and proved to have α-configuration by PMR spectroscopy in D₂O.     

Leptin reduces Atlantic salmon growth through the central pro-opiomelanocortin pathway

Leptin (Lep) is a key factor for the energy homeostasis in mammals, but the available data of its role in teleosts are not conclusive. There are large sequence differences among mammalian and teleost Lep, both at the gene and protein level. Therefore, in order to characterize Lep function in fish, the use of species-specific Lep is crucial. In this study, the cDNA sequence of salmon leptin a1 (lepa1) was used to establish a production protocol for recombinant salmon LepA1 (rsLepA1) in Escherichia coli, that enabled a final yield of 1.7 mg pure protein L^?1 culture. The effects of 20-day administration of rsLepA1 on growth and brain neuroendocrine peptide gene expression [npy, cart, agrp (-1 and -2), pomc (-a1, -a2, -a2s, and -b)] were studied in juvenile, immature Atlantic salmon (96.5 ± 2.1 g) fed a commercial diet to satiation. Intraperitoneal osmotic pumps were used to deliver rsLepA1 at four different concentrations (calculated pumping rates were 0, 0.1, 1.0 and 10 ng g^?1 h^?1). In the highest dosage group (10 ng g^?1 h^?1), the growth rate was significantly reduced, and pomc-a1 gene expression was higher than in controls. The results support the lipostatic hypothesis and suggest that sLepA1 reduces growth in Atlantic salmon by affecting food intake through the central pro-opiomelanocortin pathway.