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Query: UMLS:C0033036 (APC)
 10,214 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The following hematological and biochemical reference values were determined in 150 hares: hematocrit, blood count and leucocytic formula, Na, K, Cl, P, Ca, Mg, Cu, Zn, glucose, urea, creatinine, uric acid, cholesterol, bilirubin, triglycerides, proteins and fractions, PAL, PAC, TGO, TGP, amylase, GGT, LDH. Once the effects of sex and age have been established, the references defined here will be used as a base for interpreting disturbances linked either to pathology or nutrition.
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PMID:[Contribution to the definition of reference values in the hare: hematology -- blood biochemistry (author's transl)]. 57 73

The aim of the present study is to explore whether the renal and cardiovascular response to clonidine in type II diabetic patients is different from that in control subjects, and to clarify the role of central alpha 2-receptor in the regulation of cardiovascular response and sodium handling in type II diabetes mellitus (DM). Thirty-five diabetic inpatients aged 30-71 years (54.1 +/- 9.7) and ten control subjects (N) were enrolled in this study after their fasting plasma glucose had been improved. To evaluate the peripheral sympathetic nerve activity, 24-hour urinary catecholamine was measured, and pulse rate (PR) responses to a 30-second standing test was determined. On another day, blood pressure (BP), PR, plasma norepinephrine (PNE), cyclic AMP (p-cAMP), renin activity (PRA), aldosterone (PAC) and growth hormone (p-GH) were measured at 0, 30, 60, 90, 120, 150, 180 minutes following the oral administration of clonidine (150 micrograms). Type II DM were classified as DM with hyper-response (DM-HR, n = 12) when their PR decreased after clonidine more than that of N, and if not, they were classified as DM with normal response (DM-NR, n = 23). Urinary catecholamine excretions in type II DM were within the normal range. BP, PNE and p-cAMP were markedly decreased with clonidine in similar fashion in DM-NR, DM-HR and N. The percent changes of PNE were correlated positively with the changes of p-cAMP in both N and DM-NR (r = 0.660 and 0.449, respectively), but not in DM-HR. No significant difference in the changes of p-GH (delta p-GH) and integral of GH (the area under the curve) following clonidine administration was observed in the three groups. The decrease in PR was correlated with neither delta p-GH (N: r = 0.082, DM-NR: r = -0.400, DM-HR: r = 0.242) or integral of GH (N: r = 0.191, DM-NR: r = 0.382, DM-HR: r = 0.162). The fractional excretion of sodium (FENa) decreased in N (p < 0.01), increased in DM-NR (p < 0.05) and did not change in DM-HR. The changes of FENa were not correlated with those of PRA and PAC.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Altered responses of heart rate, renal sodium handling and plasma growth hormone to clonidine in type II diabetic patients]. 133 89

Brain alpha-adrenoceptor (alpha-AR) binding was examined as a possible explanation for the persistence of diet-induced obesity (DIO) or resistance (DR) in rats after they were returned to chow from a high-energy, fat and sucrose diet (CM diet). Adult Sprague-Dawley rats (n = 28) were fed the CM diet for 12 weeks. Those that gained more weight than chow-fed controls were classified as DIO and those that gained the same weight as controls were called DR. The 10 heaviest DIO and 8 lightest DR rats were then placed on chow for an additional 14 weeks. After the entire 26-week period, the body weights of DIO rats were still 21 per cent greater and those of the DR rats were 9 per cent less than 7 chow-fed controls. DIO retroperitoneal fat pads were also 62 per cent heavier while DR pads were equal to controls. Plasma insulin and glucose levels were comparable in all 3 groups. Receptor autoradiographic studies of brain alpha 1-AR (3H prazosin; PRZ) and alpha 2-AR (3H-paraminoclonidine; PAC) adrenoceptor binding were carried out using these animals at the end of 26 weeks. Binding to alpha 1-AR was comparable in all groups but alpha 2-AR binding was 47-103 per cent higher in DIO compared to DR and chow-fed controls in 14 of 17 brain areas assessed. These included the dorsomedial, ventromedial and paraventricular hypothalamic n. and all amygdalar areas. Such widespread differences in alpha 2-AR binding in rats fed the same diet but of differing body weights suggest that alpha 2-AR binding is a marker for differences in body weight regulation and may be important in the control of the differences in weight gain.
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PMID:Increased brain 3H-paraminoclonidine (alpha 2-adrenoceptor) binding associated with perpetuation of diet-induced obesity in rats. 197 22

Half the rats fed a high-energy diet develop diet-induced obesity (DIO); the remainder are diet-resistant (DR). Since alpha-adrenoceptors modulate both food intake and body weight, this study was conducted to identify potential differences in brain alpha-receptor binding which might predispose some animals to become DIO (DIO-prone) and others DR (DR-prone) when fed a high energy diet. DIO-prone rats can be prospectively identified by high and DR-prone rats by a low plasma norepinephrine (NE) response to i.v. glucose. Here 28 chow-fed rats were tested for glucose-induced NE release and the 6 highest and 6 lowest plasma NE responders were identified as being most likely to be DIO- and DR-prone, respectively. Binding to brain alpha-adrenoceptors was studied in these 12 rats by receptor autoradiography using 1 nM [3H]prazosin (PRZ; alpha 1-) and 1 nM [3H]paraminoclonidine (PAC; alpha 2-). There were no differences in [3H]PRZ binding in any of 18 brain areas examined. However, DIO-prone [3H]PAC binding was only 14-39% of DR-prone levels in 9 areas including 4 amygdalar nuclei, the lateral area, dorso- and ventromedial nuclei of the hypothalamus, median eminence and medial dorsal thalamic n. Although it is unclear whether this widespread decrease in [3H]PAC binding implicates brain alpha 2-adrenoceptors in the pathophysiology of DIO, it does correlate with a phenotypic marker (increase glucose-induced NE release) which predicts the subsequent development of DIO on a high-energy diet.
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PMID:Obesity-prone and -resistant rats differ in their brain [3H]paraminoclonidine binding. 215 28

Evidence indicates that hypothalamic norepinephrine (NE), acting via alpha 2-noradrenergic receptors, and also circulating glucose both have an important role in the control of normal feeding behavior in rats. In this report, we studied the relationship between glucose and the alpha 2-noradrenergic system, by manipulating blood glucose levels and analyzing changes in the binding of [3H]p-aminoclonidine [( 3H]PAC) to alpha 2-noradrenergic receptors in discrete hypothalamic areas. Brief periods (1-3 hr) of food deprivation, at the onset of the dark cycle, produced a significant decline in serum glucose levels and a simultaneous decrease in alpha 2-receptor binding sites, specifically in the hypothalamic paraventricular nucleus (PVN) as opposed to other hypothalamic areas. Restoration of circulating glucose levels, by refeeding for 0.5 hr after 2.5 hr food deprivation or by administration of glucose to 1 hr food-deprived rats, prevented this decline in serum glucose, as well as the reduction in PVN alpha 2-noradrenergic receptor density. In each of these experiments, a strong positive correlation between circulating glucose levels and PVN alpha 2-noradrenergic receptor sites was obtained. These findings suggest that blood glucose has direct impact upon alpha 2-noradrenergic receptor activity in the PVN and may affect feeding behavior, in part, through this neurochemical system.
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PMID:Glucose-dependent changes in alpha 2-noradrenergic receptors in hypothalamic nuclei. 285 87

A variety of bacterial lipopolysaccharide (LPS) preparations with highly defined primary polysaccharide chemical structure and/or aggregate macromolecular composition have been employed to examine the molecular requirements for activation of the classical and alternative pathways of human serum complement. Evidence is presented for two independent modes of polysaccharide dependent activation of the APC by LPS. One mechanism is dependent upon specific O-antigen polysaccharides and the second is defined by a specific L-glycero-D-mannoheptose/glucose region of the core oligosaccharide. LPS O-antigen polysaccharide but not core oligosaccharide determinants can convert sheep erythrocytes to cells capable of initiating the APC. The data presented provide convincing evidence that the tertiary assembly of individual LPS subunits into an aggregate macromolecule is a critical determinant in the expression of APC activity by LPS. The results of these studies provide strong evidence that CPC activation by LPS is restricted to the Re-chemotype and isolated lipid A. LPS isolated from other R-chemotypes as well as native wild type LPS preparations do not activate the CPC, in spite of the fact that the former LPS preparations contain more lipid A than polysaccharide on a percentage by wt basis. The presence of core polysaccharide L-glycero-D-mannoheptose, which provides a critical recognition role for activation of the APC, appears to negatively regulate CPC activation in a similar inverse relationship. In addition, the presence of polysaccharide containing LPS subunits in synthetic mixed LPS micellar aggregates can also restrict CPC activation by Re LPS subunits, most probably by steric hindrance at the LPS macromolecular surface. Our data are consistent with the hypothesis that activation of either pathway of human serum complement by a given LPS preparation is a mutually exclusive event dictated by the presence or absence of L-glycero-D-mannoheptose.
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PMID:Activation of human serum complement by bacterial lipopolysaccharides: structural requirements for antibody independent activation of the classical and alternative pathways. 330 24

The elimination of ethanol (ETOH) as a gas in human insensible perspiration (PAC) was investigated following the oral administration of 0.5 g/kg or 0.75 g/kg of alcohol. Simultaneous breath alcohol analysis (AAC) was also carried out for comparison purposes. To determine reproducibility, one subject experienced five trials at each dose over a period of six months, in addition to a single dose (0.5 g/kg) trial with five other subjects. All ETOH concentrations were determined by gas chromatography (GLC). A one-compartment open model with first order absorption and pseudo-zero-order elimination was used to compute the pharmacokinetic parameters. The average first order absorption rate constant (K alpha) and pseudo-zero-order elimination rate constant (beta) for ten trials in a single subject were: K alpha AAC = 1.60 h-1 and 1.39 h-1, beta AAC = 0.154 g/l/h and 0.192 g/l/h. K alpha PAC = 1.27 h-1 and 1.11 h-1, beta PAC = 0.109 g/l/h and 0.141 g/l/h for 0.5 g/kg and 0.75 g/kg ETOH, respectively. In all experiments, AAC was consistently higher than PAC during active absorption, with significantly higher (p less than 0.05) average peak concentration (Cmax) and shorter (p less than 0.05) average time to peak (tmax). However, during the later stages of elimination, AAC falls below PAC, with a significantly faster (p less than 0.05) elimination rate (beta). The data indicates that ETOH elimination via perspiration does not parallel the breath and that the pharmacokinetic parameters are significantly different.
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PMID:The pharmacokinetics of alcohol excretion in human perspiration. 407 88

There is evidence that central infusion of brain-derived neurotrophic factor (BDNF) induces weight loss in rats. We have begun to investigate the physiological basis for BDNF-induced weight loss by assessing its relationship to (a) appetite, (b) serum indices of metabolic and renal toxicity, and (c) brain monoamine activity in areas associated with feeding or motor function. BDNF (0-6 microgram/day) was infused into the lateral ventricle (LV) of male Long-Evans rats for 14 days. Body weight and food intake were monitored throughout infusion and recovery periods. BDNF induced severe, dose-dependent appetite suppression and weight loss. Although appetite began to recover after the 10th infusion day, body weight had not returned to control values at the end of the recovery period. The weight loss observed in BDNF-infused rats was related to appetite suppression, since uninfused rats that were pair-fed to high dose BDNF-treated rats showed comparable weight loss. Despite severe weight loss, serum BUN, creatinine, thyroxine, glucose, and total protein were not affected by BDNF infusion. Striatal DO-PAC/DA was similarly unaffected by BDNF. In contrast, BDNF-infused rats showed a dose-dependent increase in hypothalamic 5-HIAA/5-HT that was not observed in pair-fed rats, suggesting that the observed increase in hypothalamic 5-HIAA/5-HT was a direct effect of BDNF infusion rather than a secondary effect of food restriction. These data suggest that BDNF may induce appetite suppression and weight loss through a central mechanism.
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PMID:Characteristics of BDNF-induced weight loss. 753 21

The aim was to determine whether proton magnetic resonance spectroscopy (MRS) could grade human colorectal cells of differing malignant potential. A cell model of tumour development and progression comprising 2 non-tumorigenic adenoma lines and 4 carcinoma lines of increasing tumorigenicity was chosen. A gradual reduction in cellular differentiation and an accumulation of genetic alterations from adenoma to carcinoma characterized the selected cell lines. One-dimensional and 2-dimensional MRS showed that reduced differentiation in the cell model correlated with an increase in the levels of lipid, metabolites, the glycosylation intermediate uridine diphospho-N-acetylglucosamine and cell-surface fucosylation. Mutations involving the K-ras, APC and DCC genes are present both in adenoma- and in carcinoma-derived lines in this model, but the first evidence of an abnormality in the p53 gene was concomitant with the cells' ability to grow as a tumour in athymic nude mice. This genetic change coincided with the detection, by MRS, of UDP-hexose (ribose moiety, 2D MRS cross peak between H2 at 4.38 ppm and HI at 5.99 ppm) and the appearance of an additional fucosyl resonance (cross peak between-CH3 at 1.41 and H5 at 4.30 ppm) in the least tumorigenic of the carcinoma cell lines. An increase in complexity of the fucosylation spectral pattern was observed with further cellular de-differentiation and increased tumorigenicity. Collectively these data support the existence of an adenoma-carcinoma sequence.
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PMID:Correlation of cellular differentiation in human colorectal carcinoma and adenoma cell lines with metabolite profiles determined by 1H magnetic resonance spectroscopy. 792 26

The use of whole cell biotransformations for single and multistep enzyme conversions is gaining widespread application. In this study the naphthalene dioxygenase nah A gene was transferred into Pseudomonas aeruginosa PAC 1R, Escherichia coli JM107 and Pseudomonas putida PpG 277. The effect of ethanol on these genetically engineered Gram-negative bacteria was studied by measurement of enzyme activity, stability and cell integrity. Ethanol has been used in biotransformations as a co-substrate carbon source for co-factor recycling and as a co-solvent increasing dissolved substrate and product levels. Ethanol increased the dissolved substrate (naphthalene) concentration slightly and dissolved product ((+)-cis-(1R,2S)-dihydroxy-1,2-dihydronaphthalene) by approximately 30% at 4% (w/v) ethanol. Both P. aeruginosa PAC 1R and P. putida PpG 277 showed decreased activity with increasing ethanol concentration whilst E. coli enzyme activity increased with increasing ethanol concentration being comparable to that when glucose was used as a carbon source. This project highlighted the many factors involved in the selection of microbial hosts for whole cell biotransformation processes.
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PMID:Choice of microbial host for the naphthalene dioxygenase bioconversion. 875 40


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