bluuebunny/crossref_metadata_2025_split huggingface dataset:
Effects of Intravenous Calcitriol on Lipid Profiles and Glucose Tolerance in Uraemic Patients with Secondary Hyperparathyroidism
Authors: Lin Shih-Hua , Lin Yuh-Feng , Lu Kuo-Cheng , Diang Liang-Kuang , Chyr Shoou-Hwa , Liao Wen-Kuei , Shieh Shang-Der 
Published: August 2015

1. Secondary hyperparathyroidism in chronic renal failure may contribute to abnormalities of lipid metabolism and glucose tolerance. Amelioration of secondary hyperparathyroidism has been reported to mitigate the hyperlipidaemia and improve glucose tolerance experimentally.
2. The effect of the partial suppression of hyperparathyroidism by intravenous calcitriol on lipid levels and glucose tolerance was studied in 15 haemodialysis patients with secondary hyperparathyroidism. All received intravenous calcitriol 1 μg at the end of haemodialysis thrice weekly for eight weeks. Oral glucose tolerance test and plasma lipid profiles including triglyceride, total cholesterol, high density lipoprotein cholesterol (HDL-C), low density lipoprotein cholesterol (LDL-C), apoprotein A-I and apoprotein B were determined simultaneously before and after eight weeks of therapy.
3. Before calcitriol treatment, uraemic patients with secondary hyperparathyroidism displayed a significant higher triglyceride and a significant lower HDL-C and apoprotein A-I as well as marked glucose intolerance with an increment of the area below the glucose curve when compared with healthy control subjects.
4. After eight weeks of calcitriol treatment, there was a significant decrement in serum intact parathyroid hormone (476.45 ± 48.33 versus 191 37 ± 30.17 ng/l, P &lt; 0.001) and plasma triglyceride (2.24 ± 0.34 versus 1.80 ± 0.29 mmol/l, P &lt; 0.05) as well as a significant increment of plasma apoprotein A-I (38.13 ± 2.14 versus 44.19 ± 2.18 μmol/l, P &lt; 0.05), whereas there was no significant change in serum total cholesterol, LDL-C, HDL-C, and apoprotein B. These patients also became more glucose tolerant with a significant decrease of the area below the glucose curve and a significant rise in the area under the insulin curve after glucose load. Furthermore, the insulinogenic index increased significantly.
5. It was concluded that in addition to 1,25-dihydroxyvitamin D3 deficiency, secondary hyperparathyroidism may participate in the abnormal lipid metabolism, glucose tolerance and insulin secretion seen in dialysis patients and these abnormalities could be, at least in part, improved by intravenous calcitriol treatment.
Regional Fat Distribution by Dual-Energy X-Ray Absorptiometry: Comparison with Anthropometry and Application in a Clinical Trial of Growth Hormone and Exercise
Authors: Taaffe Dennis R. , Lewis Barbara , Marcus Robert 
Published: August 2015

1. The purpose of this study was to determine the suitability of ratios derived from dual-energy X-ray absorptiometry (DXA) whole body scans to assess regional fat distribution in older men and women by comparing them with the waist-to-hip ratio (WHR) and to evaluate their clinical utility by applying them in a clinical trial involving resistance exercise and recombinant human growth hormone.
2. Sixty-four healthy older adults (39 women and 25 men), aged 65–82 years, served as subjects. The ratios of trunk fat-to-total fat, trunk fat-to-body weight, trunk fat-to-limb fat and trunk fat % were determined by DXA. WHR was assessed on the same day, as was the ratio of subscapular/triceps skinfolds in men. Cardiovascular disease risk factors, functional capacity and serum lipids were also assessed.
3. A moderate relationship (r = 0.36-0.54) between the WHR- and DXA-derived ratios were observed for both men and women. Both DXA and WHR showed similar associations with cardiovascular disease risk factors. However, in men, all DXA ratios were able to detect subtle changes in regional fat distribution resulting from daily administration of recombinant human growth hormone in conjunction with resistance exercise for 10 weeks, whereas the WHR or subscapular/triceps ratios did not.
4. This suggests that DXA-derived ratios may be more sensitive than conventional anthropometric methods in the assessment and categorization of body fat distribution.
Sulphonamides as Anti-Inflammatory Agents: Old Drugs for New Therapeutic Strategies in Neutrophilic Inflammation?
Authors: Ottonello Luciano , Dapino Patrizia , Scirocco Maria C. , Balbi Alessandro , Bevilacqua Maurizio , Dallegri Franco 
Published: August 2015

1. It is well known that neutrophils act as mediators of tissue injury in a variety of inflammatory diseases. Their histotoxic activity is presently thought to involve proteinases and oxidants, primarily hypochlorous acid (HOCl). This oxidant is also capable of inactivating the specific inhibitor of neutrophil elastase (α1-antitrypsin), thereby favouring digestion of the connective matrix.
2. In the present work, we found that sulphanilamide and some sulphanilamide-related anti-inflammatory drugs such as dapsone, nimesulide and sulphapyridine reduce the availability of HOCl in the extracellular microenvironment of activated neutrophils and prevent the inactivation of α1-antitrypsin by these cells in a dose-dependent manner. The ability of each drug to prevent α1-antitrypsin from inactivation by neutrophils correlates significantly with its capacity to reduce the recovery of HOCl from neutrophils. Five other non-steroidal anti-inflammatory drugs were completely ineffective.
3. Therefore, sulphanilamide-related drugs, i.e. dapsone, nimesulide and sulphapyridine, have the potential to reduce the bioavailability of neutrophil-derived HOCl and, in turn, to favour the α1-antitrypsin-dependent control of neutrophil elastolytic activity. These drugs appear as a well-defined group of agents which are particularly prone to attenuate neutrophil histotoxicity. They can also be viewed as a previously unrecognized starting point for the development of new compounds in order to plan rational therapeutic strategies for controlling tissue injury during neutrophilic inflammation.
Cigarette Smoking Influences Cytokine Production and Antioxidant Defences
Authors: Tappia Paramjit S. , Troughton Kerry L. , Langley-Evans Simon C. , Grimble Robert F. 
Published: August 2015

1. Smoking exerts an inflammatory stimulus on lung macrophages, and smokers generally have low intakes of antioxidant micronutrients. This study was performed to investigate the relationship between whole-blood tumour necrosis factor production, plasma interleukin-6 and acute-phase protein concentration and antioxidant vitamins in smokers and non-smokers.
2. Measurement of tumour necrosis factor was conducted in whole blood stimulated with endotoxin (lipopolysaccharide), and interleukin-6 concentrations were measured in the plasma of smokers and non-smokers. Enzyme and dietary antioxidant concentrations and acute-phase proteins were determined in the two groups.
3. Tumour necrosis factor production and plasma interleukin-6 concentrations were 38% (P = 0.01) and 16% (P = 0.07) greater, respectively, in smokers than in non-smokers. Plasma vitamin A and E concentrations were unaffected by smoking; however, a 21% lower plasma vitamin C (P = 0.04) concentration was observed in smokers, than in non-smokers despite a similar intake of this vitamin by the two groups.
4. Concentrations of the acute-phase proteins α1-acid glycoprotein, caeruloplasmin and α2-macroglobulin were increased in the plasma of smokers compared with non-smokers by 39%, 28% and 12% respectively (P &lt; 0.01). Our studies indicate that smokers have a compromised antioxidant status and elevated concentrations of tumour necrosis factor and interleukin-6 as a consequence of smoking.
5. These observations may provide some insight into the biological mechanisms underlying the pathology associated with smoking.
Plasma Metadrenalines: Do they Provide Useful Information about Sympatho-Adrenal Function and Catecholamine Metabolism?
Authors: Eisenhofer Graeme , Friberg Peter , Pacak Karel , Goldstein David S. , Murphy Dennis L. , Tsigos Constantine , Quyyumi Arshed A. , Brunner Han G. , Lenders Jacques W. M. 
Published: August 2015

1. The clinical utility of plasma metadrenalines for examination of sympatho-adrenal function and catecholamine metabolism was assessed from plasma measurements of these metabolites in a number of clinical conditions (hypertension, cardiac failure, bilateral adrenalectomy and X-chromosomal deletions of the gene for monoamine oxidase), and before and during activation of sympathetic outflow or infusions of noradrenaline and adrenaline.
2. Plasma concentrations of normetadrenaline were less than 25% of those of noradrenaline, concentrations of metadrenaline and adrenaline were similar and those of sulphate-conjugated metadrenalines were 20- to 30-fold higher than free metadrenalines. Hypertensive patients had elevated plasma concentrations of adrenaline, noradrenaline and conjugated but not free metadrenalines. Cardiac failure patients had 2- to 4-fold increases in plasma noradrenaline and free and conjugated normetadrenaline. Adrenalectomy resulted in undetectable plasma concentrations of adrenaline, 91–97% decreases in free and conjugated metadrenaline and a 40% decrease in normetadrenaline relative to noradrenaline. Patients with X-chromosomal deletions of the gene for monoamine oxidase had 6- and 16-fold increases in plasma free and conjugated normetadrenaline and 2- and 4-fold increases in free and conjugated metadrenaline.
3. Infusion of catecholamines increased plasma concentrations of free metadrenalines by less than 6% of increases in precursor amines, indicating that most plasma normetadrenaline (84%) and metadrenaline (90%) is derived from metabolism of catecholamines before their entry into the circulation. Considerable O-methylation of catecholamines within the adrenals explains why sympatho-adrenal activation resulted in smaller proportional increases in plasma metadrenalines than catecholamines.
4. Plasma metadrenalines provide supplementary information about sympatho-adrenal activity to that provided by catecholamines, but are more useful for examination of the extraneuronal inactivation of catecholamines, particularly detection of neurochemical phenotypes in genetic disorders of catecholamine metabolism. Significant formation of metadrenalines within chromaffin tissue explains why measurements of plasma metadrenalines provide an extraordinarily sensitive method for diagnosis of phaeochromocytoma.
Glucocorticoid-Suppressible Hyperaldosteronism: Effects of Crossover Site and Parental Origin of Chimaeric Gene on Phenotypic Expression
Authors: Jamieson Andrew , Slutsker Liliya , Inglis Gordon C. , Fraser Robert , White Perrin C. , Connell John M. C. 
Published: August 2015

1. Genetic analysis of five kindreds with glucocorticoid-suppressible hyperaldosteronism, four of whom had not been subjected to any previous genetic analysis, revealed three different crossover breakpoints within the five kindreds clustered in the exon 3-intron 4 region of the chimaeric gene. The site of the crossover point had no effect on blood pressure within the kindreds studied.
2. The gene causing glucocorticoid-suppressible hyperaldosteronism was in strong linkage disequilibrium with an allele of a newly described restriction enzyme polymorphism of the aldosterone synthase gene promoter region, suggesting a possible role for this allele in the development of the chimaeric gene.
3. A novel observation on subjects inheriting glucocorticoid-suppressible hyperaldosteronism from their mothers showed that they had significantly higher plasma aldosterone concentrations and mean arterial blood pressures than those inheriting glucocorticoid-suppressible hyperaldosteronism from their fathers.
4. These results raise the possibility that chronic exposure in utero to elevated plasma aldosterone concentrations may result in the permanent programming of mineralocorticoid-dependent blood pressure regulatory mechanisms, which is amplified in later life by the elevated plasma aldosterone concentrations found in glucocorticoid-suppressible hyperaldosteronism.
Differential Nitric Oxide Synthase Activity in Human Platelets during Normal Pregnancy and Pre-Eclampsia
Authors: Delacrétaz Etienne , de Quay Nicolas , Waeber Bernard , Vial Yvan , Schulz Pierre-E. , Burnier Michel , Brunner Hans R. , Bossart Hans , Schaad Nicolas C. 
Published: August 2015

1. Nitric oxide released from endothelial cells is a potent vasodilator that might play an important role in cardiovascular regulation during pregnancy. Platelets, like endothelial cells, contain a constitutive form of nitric oxide synthase.
2. The present study aimed to measure the activity of this nitric oxide-forming enzyme in normotensive pregnant and non-pregnant women, as well as in women who had developed pre-eclampsia. Nitric oxide synthase activity was measured in the platelets of 21 normotensive pregnant women, 16 non-pregnant women and seven pregnant women who had developed pre-eclampsia.
3. The nitric oxide synthase activity was significantly higher in normotensive pregnant women [36.8 ± 2.7 pmol h−1 mg−1 of protein (mean ± SEM), P &lt; 0.001] than in non-pregnant control subjects (16.8 ± 1.4 pmol h−1 mg−1 of protein) and in women with pre-eclampsia (24.5 ± 2.1 pmol h−1 mg−1 of protein, P &lt; 0.01).
4. These data suggest that nitric oxide synthesis is increased during normal pregnancy, possibly contributing to the vasodilatation associated with this condition. Nitric oxide generation, however, may be inappropriately low in pregnant women developing pre-eclampsia, thus leading to an enhanced vasoconstriction.
Tricarboxylic Acid Cycle Intermediates during Incremental Exercise in Healthy Subjects and in Patients with McArdle's Disease
Authors: Sahlin K. , Jorfeldt L. , Henriksson K.-G. , Lewis S. F. , Haller R. G. 
Published: August 2015

1. The importance of the level of tricarboxylic acid cycle intermediates (malate, citrate and fumarate) for energy transduction during exercise has been investigated in six healthy subjects and in two patients with muscle phosphorylase deficiency (McArdle's disease).
2. Healthy subjects cycled for 10 min at low (50 W), moderate [130 ± 6 W (mean ± SEM)] and high (226 ± 12 W) work rates, corresponding to 26, 50 and 80% of their maximal O2 uptake, respectively. Patients with McArdle's disease cycled for 11–13 min at submaximal (40 W) rates, and to fatigue at maximal work rates of 60–90 W.
3. In healthy subjects, phosphocreatine was unchanged during low work rates, but decreased to 79 and 32% of the initial level during moderate and high work rates. In patients with McArdle's disease, phosphocreatine decreased to 82 and 34% of the initial level during submaximal and peak exercise. Muscle lactate increased in healthy subjects during exercise at moderate and high work rates, but remained low in patients with McArdle's disease.
4. In healthy subjects, tricarboxylic acid cycle intermediates were similar at rest and at low work rates (0.48 ± 0.04 mmol/kg dry weight), but increased to 1.6 ± 0.2 mmol/kg dry weight and 4.0 ± 0.3 mmol/kg dry weight at moderate and high work rates. The tricarboxylic acid cycle intermediate level in patients with McArdle's disease was similar to that in healthy subjects at rest, but was markedly reduced during exercise when compared at the same relative intensity. The peak level of tricarboxylic acid cycle intermediates in patients with McArdle's disease was 22% of that in healthy subjects. However, when compared at the same absolute workload, tricarboxylic acid cycle intermediates were similar in patients with McArdle's disease and in healthy subjects.
5. The decrease in glutamate and increase in alanine suggest that the alanine aminotransaminase reaction was the major anaplerotic process in healthy subjects. However, in patients with McArdle's disease (n = 1), muscle alanine remained unchanged and the purine nucleotide cycle may instead be the route of a limited anaplerosis during maximal exercise. The muscle content of glutamate and glutamine (n = 1) was markedly reduced in patients with McArdle's disease.
6. It is concluded that the tricarboxylic acid cycle intermediate level is related to the work rate in healthy subjects, and that the attenuated peak level in patients with McArdle's disease may be a limitation for aerobic energy transduction.
Ventricular Expression and Circulating Levels of Insulin-Like Growth Factor 1 in Heart Transplant Recipients
Authors: Ationu ART , Burch Michael , Singer Donald , De Leval Marc , Whitehead Bruce , Carter Nicholas 
Published: August 2015

1. Insulin-like growth factor I is a major mediator of growth-promoting activities. We studied the ventricular insulin-like growth factor I gene expression at mRNA and peptide levels in 24 heart transplant recipients (14 children and 10 adults), using ‘slot blot' hybridization with insulin-like growth factor I cDNA probe and a specific radioimmunoassay.
2. Ventricular insulin-like growth factor I mRNA was detected in all the cardiac transplant children but was below the limit of detection in the cardiac transplant adults. Ventricular insulin-like growth factor I levels were significantly higher in the transplant children [174 ± 15 (SEM; range 39–950) pg/mg soluble protein] than in transplant adults [39 ± 2 (range 14–85) pg/mg soluble protein, P &lt; 0.01, n = 14]. Circulating levels of insulin-like growth factor I in the cardiac transplant children [164 ± 10 (range 105–192) ng/ml] and adults [176 ± 15 (range 126–244) ng/ml] were within normal ranges for children and adults.
3. These results suggest that the human heart is a site for insulin-like growth factor I production and provide support for an autocrine role for insulin-like growth factor I in the ventricle, despite cardiac denervation.
Contribution of Vascular Nitric Oxide to Basal Blood Pressure in Conscious Spontaneously Hypertensive Rats and Normotensive Wistar Kyoto Rats
Authors: Minami Naoyoshi , Imai Yutaka , Hashimoto Jun-Ichiro , Abe Keishi 
Published: August 2015

1. The aim of this study was to clarify the extent to which vascular nitric oxide contributes to basal blood pressure in conscious spontaneously hypertensive rats and normotensive Wistar Kyoto rats.
2. The contribution of vascular nitric oxide to maintenance of blood pressure was estimated by measuring the pressor response to an intravenous injection of nitric oxide synthase inhibitor, Nω-l-arginine methyl ester, given after serial injections of captopril, vasopressin V1-receptor antagonist (V1-antagonist) and ganglion blocker (pentolinium) in conscious spontaneously hypertensive and Wistar Kyoto rats aged 20–28 weeks. To estimate the ‘amplifier property’ of hypertrophied vasculature in spontaneously hypertensive rats, which is known to modulate pressor responses, the lower blood pressure plateau after serial injections of captopril, V1-antagonist and pentolinium and the maximum blood pressure elicited by subsequent injection of increasing doses of phenylephrine were also measured.
3. The serial injections of captopril, V1-antagonist and pentolinium decreased mean arterial pressure from 164 ± 9 mmHg to 67 ± 2 mmHg and from 117 ± 2 mmHg to 49 ± 1 mmHg in spontaneously hypertensive and Wistar Kyoto rats respectively. The subsequent injection of Nω-l-arginine methyl ester restored mean arterial pressure almost to its control levels in both spontaneously hypertensive and Wistar Kyoto rats. The absolute changes in mean arterial pressure elicited by Nω-l-arginine methyl ester were significantly greater in spontaneously hypertensive than in Wistar Kyoto rats (P &lt; 0.01), but there was no significant difference in the responses to Nω-l-arginine methyl ester when they were expressed as percentages of either the lower blood pressure plateau or maximum blood pressure.
4. These results indicate that basal blood pressure in both spontaneous hypertensive and Wistar Kyoto rats is maintained by a balance between vascular nitric oxide and major pressor systems. They also suggest that the vasodilatory effect of vascular nitric oxide does not differ between spontaneously hypertensive and Wistar Kyoto rats, and that the increased pressor effect of Nω-l-arginine methyl ester in spontaneously hypertensive rats is due to a vascular amplifier mechanism.
Effect of Dietary Restriction on Protein Synthesis and Wound Healing after Surgery in the Rat
Authors: Emery Peter W. , Sanderson Peter 
Published: August 2015

1. The healing of an abdominal muscle wound after surgery is associated with a considerable increase in the rate of protein synthesis. We have investigated whether this increase in protein synthesis is affected by chronic undernutrition, and whether this causes a delay in wound healing.
2. A group of rats was fed 58% of the voluntary food intake of a matched control group. After 7 days half the rats in each group underwent abdominal surgery. Forty-eight hours later all the rats were killed and muscle protein synthesis rate was measured by the flooding dose technique.
3. In a second experiment using the same dietary regimen rats were placed in metabolic cages after surgery and killed 7 days later. In addition to measurements of muscle protein synthesis, wound breaking strength was measured with a tensiometer and collagen content was also measured at the wound site.
4. Dietary restriction caused a loss of body weight, a decrease in nitrogen balance and a deficit in muscle protein mass. It also caused a decrease in protein synthesis rate in gastrocnemius muscle and in parts of the abdominal muscle distant from the site of the wound. However, it had no effect on the rate of muscle protein synthesis at the site of the wound either 2 or 7 days after surgery. The tensile strength and the collagen content of the wound were also unaffected by food restriction.
5. It is concluded that the wound healing process is uniquely protected from the effects of moderate undernutrition such as might be experienced by a chronically ill patient.
Expression and Regulation of Glycosyltransferases for N-Glycosyl Oligosaccharides in Fresh Human Surgical and Murine Tissues and Cultured Cell Lines
Authors: Li M. , Andersen V. , Lance P. 
Published: August 2015

1. Mammalian membrane and serum proteins are glycosylated by the addition of heterogeneous N-linked oligosaccharides. It has been widely speculated that oligosaccharide diversity is achieved by corresponding heterogeneity of expression of the glycosyltransferases that are responsible for oligosaccharide synthesis.
2. We surveyed mRNA levels of three sequentially acting glycosyltransferases, N-acetylglucosaminyltransferase I, β1,4-galactosyltransferase and α2,6-sialyltransferase, in 11 human tissues and confirmed the expected variations.
3. The size heterogeneity of α2,6-sialyltransferase transcripts reported in rat tissues was evident neither in the human tissue survey nor in a panel of murine RNAs. Tissue distributions of alternative terminal sialyltransferases, α2,6-sialyltransferase and α2,3-sialyltransferase, were distinct.
4. Relative glycosyltransferase mRNA levels in four transformed human cell lines cultured in vitro did not fully reflect levels in the corresponding human tissues.
5. Expression of α2,6-sialyltransferase mRNA was approximately 2.6-fold greater in adenocarcinomatous than in normal human colon, and β1,4-galactosyltransferase expression was approximately 1.8-fold greater in normal than in adenocarcinomatous colon.
6. n-Butyrate (0.003–0.005 mol/l), a short-chain fatty acid that is produced by colonic bacterial fermentation, caused approximately 80% inhibition of α2,6-sialyltransferase, approximately 2.5-fold induction of β1,4-galactosyltransferase and approximately 6-fold induction of N-acetylglucosaminyltransferase mRNAs in T84 (colonic) cells. The effects on α2,6-sialyltransferase and β1,4-galactosyltransferase were near maximal by 6 h, but induction of N-acetylglucosaminyltransferase was fully apparent only after exposure for 24 h.