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PubMed1974

Halophilic nuclease from a moderately halophilic Micrococcus varians.

The moderately halophilic bacterium Micrococcus varians, isolated from soy sauce mash, produced extracellular nuclease when cultivated aerobically in media containing 1 to 4 M NaCl or KCl. The enzyme, purified to an electrophoretically homogeneous state, had both ribonuclease and deoxyribonuclease activities. The nuclease had maximal activity in the presence of 2.9 M NaCl or 2.1 M KCl at 40 C. The enzymatic activity was lost by dialysis against low-salt buffer, whereas when the inactivated enzyme was dialyzed against 3.4 M NaCl buffer as much as 77% of the initial activity could be restored.

Cell-Free System↗
PubMed1977

Killer toxin for sake yeast: properties and effects of adenosine 5'-diphosphate and calcium ion on killing action.

The killer character of strain isolated from the main mash of sake brewing which produces a killer substance for sake yeast was transmitted to hybrids of the strain and a standard strain of Saccharomyces cerevisiae through a cytoplasmic determinant. The character was eliminated at 41 degrees C by incubation followed by growth at 30 degrees C. The killer strain produced the killer toxin in a growth-associated manner. A preparation of crude killer toxin extract showed first-order inactivation and a linear Arrhenius plot between 25 and 40 degrees C, with an activation of energy of 55.0 kcal/mol. Addition of 1% of synthetic polymer protected the toxin from inactivation by agitation but not by heat. Enhancement of the killer action toward sensitive yeast cells by only the nucleotide adenosine 5'-diphosphate (ADP) was observed after plating on agar medium as well as after incubation in liquid medium. The addition of CaCl2 reversed the enhancing effect of ADP on killing activity. This action of CaCl2 was inhibited by cycloheximide, suggesting that protein synthesis is required for recovery of toxin-induced cells in the presence of CaCl2. Further, CaCl2 overcame the decrease in the intracellular level of adenosine 5'-triphosphate (ATP) enhanced by ADP in killer-treated cells and also inhibited leakage of ATP from the cells with immediate response. The mode of killing action is discussed in terms of a transient state of the cells and the action of ADP and CaCl2.

Adenosine Diphosphate↗
PubMed1989

Correlation between depression of catabolite control of xylose metabolism and a defect in the phosphoenolpyruvate:mannose phosphotransferase system in Pediococcus halophilus.

Pediococcus halophilus X-160 which lacks catabolite control by glucose was isolated from nature (soy moromi mash). Wild-type strains, in xylose-glucose medium, utilized glucose preferentially over xylose and showed diauxic growth. With wild-type strain I-13, xylose isomerase activity was not induced until glucose was consumed from the medium. Strain X-160, however, utilized xylose concurrently with glucose and did not show diauxic growth. In this strain, xylose isomerase was induced even in the presence of glucose. Glucose transport activity in intact cells of strain X-160 was less than 10% of that assayed in strain I-13. Determinations of glycolytic enzymes did not show any difference responsible for the unique behavior of strain X-160, but the rate of glucose-6-phosphate formation with phosphoenolpyruvate (PEP) as a phosphoryl donor in permeabilized cells was less than 10% of that observed in the wild type. Starved P. halophilus I-13 cells contained the glycolytic intermediates 3-phosphoglycerate, 2-phosphoglycerate, and PEP (PEP pool). These were consumed concomitantly with glucose or 2-deoxyglucose uptake but were not consumed with xylose uptake. The glucose transport system in P. halophilus was identified as a PEP:mannose phosphotransferase system on the basis of the substrate specificity of PEP pool-starved cells. It is concluded that, in P. halophilus, this system is functional as a main glucose transport system and that defects in this system may be responsible for the depression of glucose-mediated catabolite control.

Aldose-Ketose Isomerases↗
PubMed2006

Differentiation of trophoblast giant cells and their metabolic functions are dependent on peroxisome proliferator-activated receptor beta/delta.

Mutation of the nuclear receptor peroxisome proliferator-activated receptor beta/delta (PPARbeta/delta) severely affects placenta development, leading to embryonic death at embryonic day 9.5 (E9.5) to E10.5 of most, but not all, PPARbeta/delta-null mutant embryos. While very little is known at present about the pathway governed by PPARbeta/delta in the developing placenta, this paper demonstrates that the main alteration of the placenta of PPARbeta/delta-null embryos is found in the giant cell layer. PPARbeta/delta activity is in fact essential for the differentiation of the Rcho-1 cells in giant cells, as shown by the severe inhibition of differentiation once PPARbeta/delta is silenced. Conversely, exposure of Rcho-1 cells to a PPARbeta/delta agonist triggers a massive differentiation via increased expression of 3-phosphoinositide-dependent kinase 1 and integrin-linked kinase and subsequent phosphorylation of Akt. The links between PPARbeta/delta activity in giant cells and its role on Akt activity are further strengthened by the remarkable pattern of phospho-Akt expression in vivo at E9.5, specifically in the nucleus of the giant cells. In addition to this phosphatidylinositol 3-kinase/Akt main pathway, PPARbeta/delta also induced giant cell differentiation via increased expression of I-mfa, an inhibitor of Mash-2 activity. Finally, giant cell differentiation at E9.5 is accompanied by a PPARbeta/delta-dependent accumulation of lipid droplets and an increased expression of the adipose differentiation-related protein (also called adipophilin), which may participate to lipid metabolism and/or steroidogenesis. Altogether, this important role of PPARbeta/delta in placenta development and giant cell differentiation should be considered when contemplating the potency of PPARbeta/delta agonist as therapeutic agents of broad application.

Animals↗
PubMed1997

Patients' rights in England and the United States of America: The Patient's Charter and the New Jersey Patient Bill of Rights: a comparison.

The Patient's Charter has been in effect for nearly five years. This article considers the purpose and value of the document through a comparison with the New Jersey Patient Bill of Rights. Patient rights statements have been posted in American hospitals for more than twenty years. However, the New Jersey document and the patient rights programme it established seven years ago, have proven to be economically effective, successful in their representation of patients and enforceable, due to the adoption of state legislation and regulation to oversee the process. Several examples of how the programme works are included in the comparison, with a similar review of The Patient's Charter. In the comparison the author argues that for the programme to succeed as it has done in New Jersey, the government will need to develop legislative backing to ensure enforcement, and an efficient system for monitoring compliance. The programme will need to become credible in the eyes of the health service user. The author suggests this may be best achieved by developing an efficient, accessible and user-friendly means of redress, should the patient consider his or her rights have been violated. A "mish-mash" of quality assurance standards and levels of care which patients can "expect" from the health service providers only serves to distract the health service user from the government's failure to commit the resources that would empower the patients rights portion of The Patient's Charter.

Delivery of Health Care↗
PubMed1995

A survey of the incidence of Salmonella species and Enterobacteriaceae in poultry feeds and feed components.

Between July 1990 and April 1991 the rate of contamination with Salmonella species of poultry feeds and feed components used by the Dutch feed industry was surveyed. Ten per cent of 360, 10 g samples of poultry feeds were found to be contaminated. Mash feeds, mostly used for layer-breeders, were far more frequently (21 per cent) contaminated than pelleted feeds (1.4 per cent). The rate of contamination of 130 samples of fish meal was 31 per cent, of 83 samples of meat and bone meal 4 per cent, 58 samples of tapioca 2 per cent and of 15 samples of maize grits 27 per cent. Twenty-eight serotypes of salmonellae were isolated, but no Salmonella enteritidis was found, despite the occurrence of an epidemic in poultry caused by this serotype since 1987. The serotypes isolated most frequently were not the same as those encountered in poultry flocks. The Enterobacteriaceae isolated from the feedstuffs were predominantly thermotrophic. They were shown to be useful markers of the rate of contamination with salmonellae and of the efficiency of decontamination of the feedstuffs by pelletisation.

Animal Feed↗
PubMed1998

Dynamic MR defecography with a superconducting, open-configuration MR system.

PURPOSE: To evaluate dynamic magnetic resonance (MR) defecography performed with a superconducting, open-configuration system in diagnosis of defecation disorders. MATERIALS AND METHODS: Five healthy volunteers and 15 patients with defecation disorders were studied with MR defecography performed with a superconducting, open-configuration system; the patients also underwent fluoroscopic defecography. Before MR imaging, the rectum was filled with 300 mL of mashed potatoes mixed with 1.5 mL of gadopentetate dimeglumine. T1-weighted gradient-echo images were acquired every 2 seconds in the midsagittal plane with the patient at rest, at maximal contraction of the anal sphincter, during straining, and during defecation. RESULTS: MR defecography permitted analysis of the anorectal angle, anal canal, puborectal muscle, and descent of the pelvic floor. Owing to the high signal intensity of the intraluminal contrast material, the rectal walls were well demonstrated on the MR images, permitting visualization of intussusception and rectocele. Concomitant demonstration of structures surrounding the anorectal canal was helpful in assessment of spastic pelvic floor syndrome and descending perineum syndrome. MR defecography was superior to fluoroscopic defecography and allowed detection of all clinically relevant pathologic conditions except for one. CONCLUSION: Dynamic MR defecography is an attractive alternative for evaluation of defecation disorders.

Aged↗
PubMed2003

Processing of vegetable-borne carotenoids in the human stomach and duodenum.

Carotenoids are thought to diminish the incidence of certain degenerative diseases, but the mechanisms involved in their intestinal absorption are poorly understood. Our aim was to obtain basic data on the fate of carotenoids in the human stomach and duodenum. Ten healthy men were intragastrically fed three liquid test meals differing only in the vegetable added 3 wk apart and in a random order. They contained 40 g sunflower oil and mashed vegetables as the sole source of carotenoids. Tomato purée provided 10 mg lycopene as the main carotenoid, chopped spinach (10 mg lutein), and carrot purée (10 mg beta-carotene). Samples of stomach and duodenal contents and blood samples were collected at regular time intervals after meal intake. all-trans and cis carotenoids were assayed in stomach and duodenal contents, in the fat and aqueous phases of those contents, and in chylomicrons. The cis-trans beta-carotene and lycopene ratios did not significantly vary in the stomach during digestion. Carotenoids were recovered in the fat phase present in the stomach during digestion. The proportion of all-trans carotenoids found in the micellar phase of the duodenum was as follows (means +/- SE): lutein (5.6 +/- 0.4%), beta-carotene (4.7 +/- 0.3%), lycopene (2.0 +/- 0.2%). The proportion of 13-cis beta-carotene in the micellar phase was significantly higher (14.8 +/- 1.6%) than that of the all-trans isomer (4.7 +/- 0.3%). There was no significant variation in chylomicron lycopene after the tomato meal, whereas there was significant increase in chylomicron beta-carotene and lutein after the carrot and the spinach meals, respectively. There is no significant cis-trans isomerization of beta-carotene and lycopene in the human stomach. The stomach initiates the transfer of carotenoids from the vegetable matrix to the fat phase of the meal. Lycopene is less efficiently transferred to micelles than beta-carotene and lutein. The very small transfer of carotenoids from their vegetable matrices to micelles explains the poor bioavailability of these phytomicroconstituents.

Adult↗
PubMed1993

Effect of aging and bolus variables on pharyngeal and upper esophageal sphincter motor function.

Effect of aging, bolus volume, temperature, and consistency on the pharyngeal peristalsis, as well as the effect of aging on the upper esophageal sphincter (UES) resting pressure and its response to esophageal distension by air and balloon, were studied in 14 young and 12 healthy elderly volunteers. In both age groups there was no significant volume or temperature effect on amplitude, duration, or velocity of the pharyngeal peristalsis. Compared with water swallows, mashed potato swallows resulted in a significant increase in the amplitude and duration of the hypopharyngeal peristaltic pressure wave (P < 0.05). For water swallows, the amplitude and duration of the peristaltic pressure wave in the hypopharynx were significantly increased in the elderly compared with the young group (P < 0.01). UES resting pressure in the elderly measured 43 +/- 5 (SE) mmHg and was significantly less than that of the young (71 +/- 8 mmHg; P < 0.01). Magnitude of the UES pressure decrease because of esophageal distension by air, as well as magnitude of its pressure increase because of esophageal balloon distension, was similar among young and elderly. 1) Contrary to common expectations, the parameters of the pharyngeal peristaltic pressure wave do not deteriorate in the elderly in their seventh and eighth decade. 2) Compared with the young, hypopharyngeal pressure wave amplitude and duration are significantly increased in the elderly. This increase could be caused by an adaptation response to a pharyngeal outflow compromise. 3) Pharyngeal peristaltic pressure wave amplitude and duration, but not its velocity, are modulated by the bolus consistency. This modulatory mechanism is preserved in the elderly. 4) Although UES resting pressure is significantly decreased in the elderly, its pressure response to esophageal distension by air and balloon is preserved.

Adult↗
PubMed1997

Effect of pharyngeal water stimulation on esophageal peristalsis and bolus transport.

Sensory stimuli originating from the pharynx inhibit esophageal peristalsis induced by a dry swallow. Our aims were to determine the effect of these stimuli on esophageal bolus transport and esophageal peristalsis induced by swallowing different volumes of liquid and semisolid boluses. We studied nine healthy volunteers age 35 +/- 4 yr in the supine position by intraluminal esophageal manometry as well as concurrent videofluoroscopy and manometry. In all subjects progression of peristalsis induced by swallowing of different volumes of water and mashed potato boluses was inhibited at all sites by pharyngeal water injection. Threshold volume for inhibition of the peristalsis induced by swallows of 5 and 10 ml of water was similar but significantly higher compared with dry swallows (P < 0.05). Pharyngeal water injection invariably halted transit of the barium boluses through the esophagus. Sensory impulses originating from the pharynx 1) inhibit esophageal bolus transit and 2) are capable of overcoming the facilitating effect of a liquid bolus on the swallowing apparatus. This phenomenon may explain the mechanism of some of the failed esophageal peristalsis observed in clinical practice.

Adult↗
PubMed1982

Developmental study of adipose cellularity in lateral hypothalamic-lesioned Zucker obese rats.

Ten-week-old lean and obese Zucker rats were sham lesioned or received bilateral, electrolytic lesions of the lateral hypothalamus (LH). They were maintained on a wet mash diet until killing at 15 or 32 wk of age; control lean and obese rats were also killed at 6 and 10 wk. Body composition analyses were performed and adipocyte cellularity of epididymal, retroperitoneal, and subcutaneous depots were calculated. Changes in body composition of LH-lesioned rats, though similar in the two genotypes on an absolute basis, differed on a percentage basis due to the extreme adiposity of the obese rats. Retarded development of protein depots in both lesioned lean and obese rats was apparent at 15 but not 32 wk. Relative to genotypic controls, lesioned lean and obese rats had smaller adipose depots by 32 wk due to decreased adipocyte size in lean rats and reduced adipocyte number in the obese. This genotype-specific response was probably due to the chronic hyperplasia of adipocytes unique to the obese rats. This distinctive developmental pattern of the epididymal depot is discussed.

Adipose Tissue↗
PubMed1984

Regeneration may mediate the sparing of VMH obesity observed with prior vagotomy.

The extent to which the vagus nerve is involved in mediating the development of obesity in animals with lesions of the ventromedial hypothalamus (VMH) was determined. Female rats were given either VMH lesions or sham lesions 100 days after they had received vagotomy with pyloroplasty, sham vagotomy with pyloroplasty, or sham vagotomy with sham pyloroplasty. For the first 7 postlesion wk, the animals were fed a wet mash diet, then they were maintained on a high-fat diet for 10 wk, and finally they were fed a highly palatable supermarket diet for 4 wk. VMH-lesioned animals with prior vagotomy and pyloroplasty displayed 65% of the obesity observed in lesioned animals with prior sham vagotomy. This expression was increased to 72% of the full VMH obesity during the supermarket diet phase. Assessment of vagotomy suggested that vagal regeneration and, in some cases, recovery of vagally stimulated insulin secretion had occurred. This reorganization may have contributed to the residual obesity expressed in VMH-lesioned animals with prior vagotomy.

Animals↗
PubMed1993

Abdominal vagotomy dissociates the anorectic mechanisms for peripheral serotonin and cholecystokinin.

These studies compared the effects of total abdominal vagotomy (VGX) on ingestive actions produced by peripheral serotonergic and cholecystokinergic (CCKergic) stimulation in rats. Subcutaneous injection of 0.01-0.16 mumol/kg of the serotonin (5-HT) analogue 5-carboxamidotryptamine (5-CT) dose-dependently reduced mash intake equally in VGX rats and their laparotomized (LAP) controls but concurrently stimulated drinking only in the controls. The sulfated octapeptide of cholecystokinin (CCK-8, 4.0 nmol/kg ip) also reduced food intake only in the controls. In a second set of rats, vagotomy did not alter anorexia after intraperitoneal administration of either 2.0 or 8.0 mumol/kg of 5-HT or of 0.03 mumol/kg of 5-CT but abolished anorexia after a large dose of CCK-8 (8.0 nmol/kg). The completeness of vagotomy was verified histologically by immunohistochemical staining of the vagal bundles for the high molecular weight form of neurofilament-H protein. We report for the first time that 5-CT produces anorexia by a vagally independent mechanism. In contrast, 5-CT stimulates drinking by a pathway that does involve vagal function. Finally, we confirm the prediction that vagotomy dissociates the neural mechanisms for the anorectic action of peripheral 5-HTergic and CCKergic stimulation.

Abdomen↗
PubMed1995

Lesions of area postrema attenuate but do not prevent anorectic action of peripheral serotonin in rats.

These studies assessed the effect of selectively ablating the area postrema (AP) on the action of peripheral serotonin [5-hydroxytryptamine (5-HT)] to reduce food intake in rats. Intraperitoneal 5-HT (0, 2.0, 4.0, and 8.0 mumol/kg) reduced the intakes of sweetened mash during a 30-min test in controls (APC) and in AP-lesioned rats (APX). The anorexia was dose dependent in controls but the dose-response function was flat after AP lesions. In another study, 2.0 mumol/kg 5-HT reduced intakes of both groups by approximately 25%, but AP lesions blunted the effect at 8.0 mumol/kg 5-HT (APX, -30% vs. APC, -85%). Behavioral analysis revealed that, compared with controls, AP lesions eliminated the decrease in frequency of feeding and reduced the incidence of resting and of an aberrant posture observed after 8.0 mumol/kg. Thus peripheral 5-HT decreases food intake in rats with AP lesions. Multiple mechanisms appear to be involved in the ability of peripheral 5-HT to reduce feeding. A high dose of 5-HT promotes responses associated with satiation but also produces behavioral toxicity; these effects involve the AP. Lower doses appear to engage processes that do not rely on the function of this circumventricular organ.

Animals↗
PubMed1999

A functional role for central glucagon-like peptide-1 receptors in lithium chloride-induced anorexia.

The present study sought to determine whether central glucagon-like peptide-1 (GLP-1)-receptor signalling contributes to the anorexigenic effects of systemically administered lithium chloride (LiCl). Male Sprague-Dawley rats with chronic intracerebroventricular (ICV) cannulas were acclimated to a feeding schedule that included daily 30-min access to palatable mash. In the first experiment, ICV infusion of a GLP-1-receptor antagonist [exendin-4-(3-39)] significantly attenuated (10 microgram dose) or completely blocked (20 microgram dose) the inhibition of food intake produced by subsequent ICV infusion of GLP-1-(7-36) amide (5 microgram). In the second experiment, rats were infused with 0, 10, or 20 microgram of the GLP-1-receptor antagonist ICV, followed by injection of 0.15 M LiCl (50 mg/kg ip) or the same volume of 0.15 M NaCl. The ability of LiCl treatment to suppress food intake was significantly attenuated in rats that were pretreated with the GLP-1-receptor antagonist. These results support the view that central mechanisms underlying LiCl-induced anorexia include a prominent role for endogenous GLP-1 neural pathways.

Animals↗
PubMed2002

Validation of the DLW method in Japanese quail at different water fluxes using laser and IRMS.

In Japanese quail (Coturnix c. japonica; n = 9), the doubly labeled water (DLW) method ((2)H, (18)O) for estimation of CO(2) production (l/day) was validated. To evaluate its sensitivity to water efflux levels (r(H(2))O(e); g/day) and to assumptions of fractional evaporative water loss (x; dimensionless), animals were repeatedly fed a dry pellet diet (average r(H(2))O(e) of 34.8 g/day) or a wet mash diet (95.8 g/day). We simultaneously compared the novel infrared laser spectrometry (LS) with isotope ratio mass spectrometry. At low r(H(2))O(e), calculated CO(2) production rate exhibited little sensitivity to assumptions concerning x, with the best fit being found at 0.51, and only little error was made employing an x value of 0.25. In contrast, at high r(H(2))O(e), sensitivities were much higher with the best fit at x = 0.32. Conclusions derived from isotope ratio mass spectrometry and LS were similar, proving the usefulness of LS. Within a threefold range of r(H(2))O(e), little error in the DLW method is made when assuming one single x value of 0.25 (recommended by Speakman JR, Doubly Labelled Water. Theory and Practice. London: Chapman & Hall, 1997), indicating its robustness in comparative studies.

Animal Feed↗
PubMed1996

Energy expenditure and substrate oxidation rates of obese rats during a 12-day treatment with dexfenfluramine.

Serotoninergic neuronal networks are included in regulation and modification of eating behavior and energy metabolism. Dexfenfluramine (dF), a serotonin releaser and reuptake inhibitor, was used to investigate changes in food intake, body weight development, energy expenditure, respiratory quotient, and substrate oxidation rates for 12 days. Rats which had been made obese by postnatal overfeeding received an energy-controlled mash diet and water ad libitum and were intraperitoneally injected with either saline or 5 or 10 mg dF/kg. As compared with controls, food intake and energy expenditure were significantly decreased in a dose-dependent manner, especially during the first 6 days. Lipid oxidation was increased, while the oxidation of carbohydrates was decreased. The body weight was only slightly reduced after 2 days of dF treatment. After 4 days, dF-treated rats resumed body weight, but as compared with controls both dF groups exhibited lower body weights at the end of the experiment. After 12 days the plasma glucose concentration was unchanged, whereas plasma free fatty acids were significantly decreased. Plasma insulin levels were unchanged after dF, but 10 mg dF/kg led to increased muscle and, especially liver glycogen contents, indicating an improved nonoxidative glucose disposal. Muscle pyruvate kinase was slightly but not significantly increased after dF treatment but that of the liver was significantly decreased, indicating a reduced glycolytic activity of the liver. Whereas the renal N excretion was rather decreased, the plasma concentrations of urea, citrulline, arginine, and ornithine were increased, and the liver contents of glutamine and arginine were decreased. Possibly, there is a shift of ammonia removal from glutamine synthesis to production of urea. The sum of all large neutral amino acids in muscle was significantly decreased after dF treatment, indicating a diminished proteolysis. Pair-feeding experiments over 2 days revealed that this was not solely a result of diminished food intake, but also an additional metabolic effect of dF, different from its anorectic effect. It is concluded that both increased oxidation of endogenous fat and reduced food intake could mediate the body weight reducing effect of dF.

Amino Acids↗
PubMed2003

Alimentary tract innervation deficits and dysfunction in mice lacking GDNF family receptor alpha2.

Subsets of parasympathetic and enteric neurons require neurturin signaling via glial cell line-derived neurotrophic factor family receptor alpha2 (GFRalpha2) for development and target innervation. Why GFRalpha2-deficient (Gfra2-/-) mice grow poorly has remained unclear. Here, we analyzed several factors that could contribute to the growth retardation. Neurturin mRNA was localized in the gut circular muscle. GFRalpha2 protein was expressed in most substance P-containing myenteric neurons, in most intrapancreatic neurons, and in surrounding glial cells. In the Gfra2-/- mice, density of substance P-containing myenteric ganglion cells and nerve bundles in the myenteric ganglion cell layer was significantly reduced, and transit of test material through small intestine was 25% slower compared to wild-type mice. Importantly, the knockout mice had approximately 80% fewer intrapancreatic neurons, severely impaired cholinergic innervation of the exocrine but not the endocrine pancreas, and increased fecal fat content. Vagally mediated stimulation of pancreatic secretion by 2-deoxy-glucose in vivo was virtually abolished. Retarded growth of the Gfra2-/- mice was accompanied by reduced fat mass and elevated basal metabolic rate. Moreover, the knockout mice drank more water than wild-type controls, and wet-mash feeding resulted in partial growth rescue. Taken together, the results suggest that the growth retardation in mice lacking GFRalpha2 is largely due to impaired salivary and pancreatic secretion and intestinal dysmotility.

Animals↗