bluuebunny/crossref_metadata_2025_split huggingface dataset:
Bone turnover markers and sex hormones in men with idiopathic osteoporosis
Authors: Pietschmann P. , Kudlacek S. , Grisar J. , Spitzauer S. , Woloszczuk W. , Willvonseder R. , Peterlik M. 
Published: March 2003

Background In contrast to osteoporosis in postmenopausal women, osteoporosis in men has received much less attention.Patients and We determined various biochemical parameters of bone metabolism and sex hormones in 31 men with idiopathic osteoporosis and 35 age matched control subjects.Results In the men with osteoporosis, a significantly increased urinary excretion of deoxypyridinoline (5·3 ± 0·2 vs. 4·6 ± 0·2 nmol mmol−1 creatinine; P = 0·033) in addition to increased serum levels of the c‐terminal telopeptide of type I collagen (2677 ± 230 vs. 2058 ± 153 pmol; P = 0·037) were found. While parameters of bone formation were not significantly different in the patients and controls, serum bone sialoprotein levels were significantly decreased in the patients (3·7 ± 0·8 vs. 12·4 ± 4·0 ng mL−1; P = 0·021). Moreover, in men with idiopathic osteoporosis, lower levels of estradiol (91·3 ± 5·8 vs. 114·6 ± 7·8 pmol L−1; P = 0·044), higher levels of sex hormone binding globulin (31·5 ± 3·1 vs. 24·2 ± 1·4 nmol L−1; P = 0·034) and a decreased free androgen index (42·6 ± 5·2 vs. 56·4 ± 5·9; P = 0·016) were seen. Serum estradiol levels correlated negatively with several parameters of bone resorption.Conclusions In men with idiopathic osteoporosis, bone resorption is increased and exceeds bone formation. The excessive bone resorption seen in idiopathic male osteoporosis may be due to decreased estradiol levels and low levels of bioavailable testosterone.
Impaired nutritional status in common variable immunodeficiency patients correlates with reduced levels of serum IgA and of circulating CD4+ T lymphocytes
Authors: Muscaritoli M. , Fanfarillo F. , Luzi G. , Sirianni M. C. , Iebba F. , Laviano A. , Russo M. , Aiuti F. , Fanelli F. Rossi 
Published: March 2003

Background Common variable immunodeficiency (CVI) is a primary defect of the immune system. Infections, persistent diarrhoea and malabsorption may result in malnutrition, which may in turn contribute to increased morbidity. In this paper, the prevalence of malnutrition in CVI was evaluated.Patients and methods Forty CVI patients (20 male, 20 female, aged 17–75 years) underwent anthropometric measurements from which body mass index, arm fat and muscle area were calculated. Body mass index values < 18·5 and arm fat and muscle area values < 10th percentile were considered indicative of malnutrition. Patients were divided into four groups according to circulating CD4+ T cells (lower or greater than 300 µL−1) and serum immunoglobulin A (IgA) levels (detectable and undetectable).Results Body mass index < 18·5, arm fat and muscle area < 10th percentile were observed in 23%, 58% and 44%, respectively, of patients. Lower values of body mass index, arm fat and muscle area were more frequent in patients with low CD4+ cells and undetectable IgA. Low arm fat values were more frequent in patients with diarrhoea (P = 0·03). Infectious episodes were more frequent in undetectable IgA than in detectable IgA patients (P = 0·04).Conclusions Anthropometric measurements revealed an increased rate of malnutrition in CVI patients, particularly in those with low CD4+ and undetectable IgA, suggesting that selected CVI subjects could be considered for standard or specialized nutritional support.
Variation at the cholesteryl ester transfer protein gene in relation to plasma high density lipoproteins cholesterol levels and carotid intima‐media thickness
Authors: Kakko S. , Tamminen M. , Päivänsalo M. , Kauma H. , Rantala A. O. , Lilja M. , Reunanen A. , Kesäniemi Y. A. , Savolainen M. J. 
Published: March 2003

Background Cholesteryl ester transfer protein (CETP) plays a major role in lipoprotein metabolism. We have screened the CETP gene for mutations and polymorphisms regulating high density lipoproteins cholesterol (HDL‐C) levels and the development of atherosclerosis, and found some polymorphisms (I405V and R451Q) to have minor effects.Design The purpose of this study was to investigate the combined effect of the several polymorphisms of the CETP gene so far found on HDL‐C levels and carotid intima‐media thickness (IMT), and, in addition, to study whether the recently found functional polymorphism in the promoter region of the CETP gene (C to A, − 629 relative to the first transcribed nucleotide) explains the previous associations due to linkage disequilibrium. The genotypes were determined in a population sample of 481 men and women.Results There were no significant differences in plasma CETP activity or carotid IMT between the genotypes of the promoter polymorphism. The women with the CC genotype of the promoter polymorphism had the lowest HDL‐C levels (P < 0·001), but no such difference was seen in men. Detected polymorphisms of the CETP gene explained about 8% of the variation in HDL‐C in women and about 7 and 10% of the variation in carotid IMT in women and men, respectively. The associations of the promoter, I405V and R451Q‐A373P polymorphisms with HDL‐C and carotid IMT seemed to be independent of each other. The associations with IMT were independent of total HDL‐C levels, suggesting that HDL subfractions may have more effect on IMT.Conclusion The CETP gene locus was found to be polymorphic and its polymorphisms explained a reasonable proportion of the variation in the degree of carotid atherosclerosis.
Prevalence and risk of gingival enlargement in patients treated with anticonvulsant drugs
Authors: Brunet L. , Miranda J. , Roset P. , Berini L. , Farré M. , Mendieta C. 
Published: March 2003

BackgroundPredictors of gingival enlargement in patients treated with anti‐epileptics have not been previously assessed. This study was conducted to determine, with the aid of two indices that score vertical and horizontal overgrowth, the prevalence and risk factors for gingival enlargement in patients treated with phenytoin and other anticonvulsant drugs.Materials and MethodsA cross‐sectional study was conducted and data from 59 patients taking antiepileptics were compared with 98 controls. Gingival enlargement was evaluated with two indices to score vertical overgrowth [Gingival overgrowth index (GO] and horizontal overgrowth [Miranda‐Brunet index (MB)] . Gingival index, plaque index, and probing depth were also evaluated.ResultsThe prevalence of gingival enlargement was significantly higher (P < 0·0001) for both indices in the anticonvulsants treated groups than in the control group. Gingival overgrowth was significantly higher for both indices in the phenytoin group than in the non phenytoin group. Among the possible risk factors, only the gingival index showed a significant association with gingival enlargement. For the MB index the risk of gingival enlargement (odds ratio) associated to phenytoin therapy and other anticonvulsants therapy were 52·6 (13·5–205) and 6·6 (1·5–28·2). Gingival index‐adjusted odds ratios for the same drugs were 5·7 (1·3–24·7) and 18·1 (2–158), respectively. The concordance between GO and MB indices in the control group and in the phenytoin‐group and non phenytoin‐group showed a Kappa value of 0·773 and 0·697, respectively.ConclusionThis study reports significant differences in the prevalence and severity of gingival overgrowth in two groups of patients, one treated with phenytoin, and another treated with other anticonvulsants. Gingival inflammation is a significant risk factor for gingival enlargement in these patients.
Dysregulation of monocyte oxidative burst in streptococcal endocarditis
Authors: Presterl E. , Rokita E. , Graninger W. , Hirschl A. M. 
Published: March 2003

Background Streptococcal subacute endocarditis is characterized by low‐grade systemic inflammation. Although structural cardiac defects are pivotal, phagocytic cells, i.e. monocytes and neutrophils, are involved in the induction and the course of bacterial endocarditis. Decreased production of reactive oxygen metabolites was described in long‐lasting infections. We hypothesized that the oxidative burst of phagocytes induced by the infecting organism is defective in patients with streptococcal endocarditis.Patients and methods The monocytes and neutrophils of 11 patients with streptococcal native valve endocarditis were challenged with the respective pathogens and two control streptococcal strains, and the oxidative burst was determined by fluorescence‐activated cell sorter analysis. These experiments were done before any antibiotic therapy was administered, and repeated at least 12 months after recovery. Eight volunteers served as healthy controls.Results The monocyte response to the respective pathogens was decreased in the patient groups compared to the response to the control streptococci. After cure the monocyte response to the pathogens was not different to the response to the control strains. The monocyte response of the healthy volunteers did not show any differences between the patients' pathogens and the control strains. The neutrophil oxidative burst to the pathogens was similar to that to the control streptococci in both patient and the volunteer group.Conclusion The decreased response of patient monocytes to the pathogens may contribute to the low‐grade inflammatory response and to the course of streptococcal endocarditis.
Matrix‐bound fibroblasts regulate angiogenesis by modulation of VE‐cadherin
Authors: Martin T. A. , Harding K. , Jiang W. G. 
Published: March 2003

Background Vascular endothelial cadherin (VE‐cadherin/cadherin‐5) has previously been described as playing a specific role in angiogenesis due to its localisation at areas of intercellular contact, where it functions in maintenance of tubular architecture. Matrix‐bound fibroblasts have been show to produce a number of factors that are important in inducing angiogenesis and to promote tubule‐formation by human endothelial cells, an indicator of angiogenic potential.Results Tubule formation stimulated by fibroblast‐derived growth factors can be prevented by the addition of monoclonal antibody to VE‐cadherin. In addition, fibroblasts‐derived growth factors are able to modulate the expression and hence the regulation of this endothelial cell specific cadherin.Conclusions The change in VE‐cadherin expression of human endothelial cells by fibroblast‐derived growth factors may contribute to the regulation of angiogenesis.
Impact of genetic defects on atherosclerosis in patients suspected of familial hypercholesterolaemia
Authors: Descamps O. S. , Gilbeau J‐P. , Leysen X. , Van Leuven F. , Heller F. R. 
Published: March 2003

Among patients with severe hypercholesterolaemia and a family history of early cardiovascular disease, we assessed whether patients with mutations of low‐density lipoprotein (LDL) receptor and apolipoprotein B genes related to familial hypercholesterolaemia (FH) have a different degree of atherosclerosis than those without such mutations.In our lipid clinics, 273 patients were selected on the basis of a severe hypercholesterolaemia (cholesterol above 95th percentile) and a family history of early cardiovascular disease. By molecular genetic test, 122 patients were classified as FH. Atherosclerosis was evaluated by the ultrasonographic measurement of intima‐media thickness (IMT) in the carotid and femoral arteries.Despite the fact that non‐FH individuals had a higher prevalence of obesity, hypertension, diabetes and hypertriglyceridaemia, FH individuals had significantly greater carotid and femoral IMT than non‐FH patients: difference between carotid and femoral IMT, respectively, 0·19 mm (95% CI, 0·08–0·29; P < 0·001) and 0·20 mm (95% CI, 0·09–0·35; P = 0·001), respectively. These differences remained statistically significant after adjustment for the various risk factors as well as in sub‐analysis restricted to the patients with LDL‐cholesterol between 240 and 300 mg dL−1 (range with similar distribution in the two groups). When classified according to the severity of their mutations, FH individuals with null LDL receptor allele tended to have thicker carotid IMT than FH individuals carrying the LDL receptor‐defective allele.Among patients with severe hypercholesterolaemia and a family history of early cardiovascular disease, the presence of a genetically ascertained FH is associated with a higher degree of atherosclerosis. This suggests that molecular genetic identification of FH may be helpful to evaluate better the coronary heart disease risk in these patients.
Histidine induces lipolysis through sympathetic nerve in white adipose tissue
Authors: Yoshimatsu H. , Tsuda K. , Niijima A. , Tatsukawa M. , Chiba S. , Sakata T. 
Published: March 2003

AbstractBackground Hypothalamic neuronal histamine has been shown to increase lipolysis in white adipose tissue. The present study aimed to clarify whether peripheral loading with L‐histidine, a precursor of neuronal histamine, may affect lipid metabolism in adipose tissue.Materials and methods The in vivo microdialysis study was used to assess lipolysis in rat epididymal adipose tissue by measuring the release of glycerol in response to administration of L‐histidine. In addition, electrophysiological measurements were performed to record changes in activity of sympathetic nerve innervating adipose tissue following histidine treatment.Results Sequential administration of isoproterenol, a β‐adrenoceptor agonist, through the microdialysis cannula at concentrations of 10−8 to 10−6 M increased the glycerol concentration in the dialysate dose‐dependently (P < 0·05). Intraperitoneal administration of L‐histidine at a dosage of 0·35 mmol kg−1 also increased the glycerol concentration compared to that of phosphate buffered saline (P < 0·05). Concomitantly, the administration of histidine increased the serum concentration of free fatty acid compared to control treatment (P < 0·05). The accelerating effects of histidine on lipolysis were mimicked by the infusion of 102 nmol rat−1 L‐histamine into the third cerebroventricle (P < 0·05). Electrophysiological measurement demonstrated that administration of histidine at a dosage of 0·35 mmol kg−1 increased the activity of efferent sympathetic nerve, innervating adipose tissue more than the infusion of phosphate buffered saline (P < 0·05).Conclusion The present results indicate that histidine accelerates lipolysis in white adipose tissue through activation of the sympathetic nerve. The regulation of lipolysis may therefore involve histamine neurons in the brain, probably through the conversion of L‐histidine to histamine in the hypothalamus.
Homocysteine and the stage of atherosclerotic disease: a study in patients suffering from clinically silent and clinically manifest atherosclerotic disease
Authors: Pasterkamp G. , Algra A. , Grobbee D. E. , De Jaegere P. P. T. , Banga J. D. , Van Der Graaf Y. 
Published: March 2003

AbstractBackground Elevated serum levels of homocysteine are considered a risk factor for cardiovascular disease. It has been suggested that homocysteine is a late stage predictor of adverse cardiovascular events, which might explain reported controversies in literature. The objective of the present study was to study the relationship between homocysteine levels and the stage of atherosclerotic disease.Methods In a cross‐sectional study we compared the prevalence of hyperhomocysteinemia in high risk patients without silent or clinically overt atherosclerosis (group I, n= 196) with two patient groups: patients with clinically manifest atherosclerosis in the past or asymptomatic atherosclerosis (group II, n= 364) and patients who currently suffer from a clinically relevant manifestation of ischemic cardiovascular disease (group III, n= 967). In addition, we related homocysteine levels with a cumulative index of atherosclerotic disease (SMART‐score).Results Homocysteine levels (µmol L−1) for the different groups were 13·5 ± 8·9 (group I), 13·7 ± 8·2 (group II) and 14·7 ± 7·7 (group III). After adjustment for age, body mass index, creatinine levels and current use of vitamins, no significant differences in the prevalence of hyperhomocysteinemia were observed, compared with the reference category. Linear regression analysis revealed a significant relationship between Smart score and homocysteine levels that remained after adjustment for potential confounders (Beta = 0·36 (0·14–0·59), P = 0·001).Conclusion If homocysteine levels are associated with the presence and indicators of atherosclerotic plaque burden, then this relationship is apparently not affected by the stage of atherosclerotic disease.
LDL‐receptors expression in HIV‐infected patients: relations to antiretroviral therapy, hormonal status, and presence of lipodystrophy
Authors: Petit J. M. , Duong M. , Duvillard L. , Florentin E. , Portier H. , Lizard G. , Brun J. M. , Gambert P. , Verges B. 
Published: March 2003

AbstractBackground Abnormalities in lipid levels and lipodystrophy (LD) have been commonly reported after commencement of highly active antiretroviral therapy (HAART). A major mechanism by which plasma low‐density lipoprotein (LDL) cholesterol levels may be influenced is via the regulation of hepatic LDL receptor expression. The activity of LDL receptors is under hormonal control. Moreover, HIV infection and HAART are associated with important modifications of hormonal status. As the cause of these adverse reactions is unknown, the effects of HAART and lipodystrophy on LDL receptors were evaluated.Materials and methods Thirty‐nine HIV treated patients (21 with a protease inhibitor (PI) containing regimen, 18 without PI use) and 22 control subjects were tested for insulin resistance (HOMA model assessment), lipid profile, serum concentration of dehydroepiandrosterone (DHEA) and LDL‐R expression. LDL‐R on mononuclear cells were quantified by flow cytrometry.Results Among the 39 HIV infected patients, 14 patients had a lipodystrophy (LD). Patients with LD had significantly higher levels of triglyceride (TG) and insulin resistance compared to patients without LD. There was no significant difference in LDL‐R count between patients with or without PI use. In contrast, LDL‐R count was significantly lower in patients with LD compared with those without (8504 ± 3901 vs. 13 200 ± 4532, P = 0·001). There was no difference in LDL‐R count between patients without LD and control subjects. Patients with LD had lower levels of DHEA compared to patients without LD. In HIV‐infected patients, we found a significant correlation between LDL‐R expression and TG (r = −0·32; P = 0·04) and LDL cholesterol (r = −0·33; P = 0·04). In contrast, we did not observe a correlation between DHEA level and LDL‐R count or LDL cholesterol level.Conclusions HIV‐lipodystrophy is associated with a lower expression of LDL‐R. This decreased expression of LDL‐R seems independent of DHEA or insulin secretion.
Effect of trefoil factors on the viscoelastic properties of mucus gels
Authors: Thim L. , Madsen F. , Poulsen S. S. 
Published: March 2003

AbstractBackground Trefoil peptides (TFFs) are expressed and secreted in a tissue‐specific manner in the gastrointestinal tract. Evidence of coexpression of trefoil peptides and mucins has been demonstrated in most mucus‐producing cells in the gastrointestinal tract. The expression of trefoil peptides is up‐regulated in gastric ulceration and colitis. It is believed that TFF peptides interact with mucin to increase viscosity but this has never been confirmed. The aims of the present study were to elucidate the direct effect of trefoil peptides on mucus gel formation.Materials and methods The viscosity of mucin solutions was measured by means of a rotational rheometer after adding three mammalian trefoil peptides: TFF1, TFF2, and TFF3.Results Adding TFF2 (0·3%) to the mucin solutions (8%) resulted in more than a factor 10 increase in viscosity and elasticity, and the mucin solution was transformed into a gel‐like structure with serpentine‐like complexes between the mucin and TFF2. The dimer form of TFF3 also increased viscosity but resulted in a spider's web‐like structure. The monomer forms of TFF1 and TFF3 had very little effect on the viscosity and elasticity of the mucin solutions.Conclusions The addition of TFF2 to mucin solutions results in significantly increased viscosity and elasticity, under which the mucin solutions are transformed into a gel‐like state. The ability of some trefoil peptides to catalyse the formation of stable mucin complexes may be one of the ways by which these peptides exert their protective and healing functions.
Serum homocysteine, creatinine, and glucose as predictors of the severity and extent of coronary artery disease in asymptomatic members of high‐risk families
Authors: Pajunen P. , Syvänne M. , Nieminen M. S. , Kareinen A. , Viitanen L. , Lehto S. , Laakso M. 
Published: March 2003

AbstractBackground There has been no previous study to determine the severity and extent of coronary artery disease (CAD) in subjects with no diagnosis or symptoms of CAD at the time of the angiography.Methods Fifty‐three subjects, who were siblings of patients with early onset CAD, underwent coronary angiography. Indices to describe per‐patient characteristics of CAD were calculated, based on computer‐aided quantitative coronary angiography. Clinical and laboratory characteristics were correlated to the angiographic parameters.Results Serum total homocysteine (ρ = 0·29, P < 0·05) and creatinine (ρ = 0·47, P = 0·001) levels were related to the global atheroma burden index. The median of the atheroma burden index was two times higher in the top homocysteine quartile compared to the lowest quartile. The overall atheroma burden index correlated significantly with the fasting blood glucose level in all subjects. Diabetes, especially when albuminuria was present, was a powerful risk factor. In a multivariate analysis, only age and sex were independent predictors of atheroma burden.Conclusions Serum homocysteine and creatinine concentrations, and diabetes with albuminuria were found to be markers of the severity and extent of CAD in subjects of high‐risk families without symptoms of CAD.
Long‐term sequelae of HFE deletion in C57BL/6 × 129/O1a mice, an animal model for hereditary haemochromatosis
Authors: Lebeau A. , Frank J. , Biesalski H. K. , Weiss G. , Srai S. K. S. , Simpson R. J. , McKie A. T. , Bahram S. , Gilfillan S. , Schümann K. 
Published: March 2003

AbstractBackground HFE knockout mice (C57BL/6 × 129/Ola strain) mimic the functional aberrations of human hereditary haemochromatosis (HH) in short‐term experiments. The present study investigates functional and morphological long‐term changes.MethodsHFEo/o, HFE+/oand HFE+/+mice were maintained on iron‐rich and control diets for 2 weeks, 3, 12 and 18 months. Light microscopic tissue iron distribution, pathomorphological alterations, tissue iron content and oxidative stress were analysed in liver, pancreas, spleen, gastrointestinal tract, kidneys and myocardium. Additionally, duodenal59Fe absorption and59Fe whole body loss were measured.ResultsIron distribution between organs and microscopic iron deposition in the tissues resembled the patterns described in HH. After 3 months of iron‐rich feeding duodenal59Fe absorption decreased to ∼15% of iron‐adequate controls but remained about twice as high in HFEo/oas in HFE+/+mice. Hepatic iron concentrations reached only half the values known to induce hepatic fibrosis in rats and humans, while whole body59Fe loss was about twice as high. Consequently no hepatic fibrosis developed, although massive hepatocellular iron deposition and indication for oxidative stress were observed.ConclusionC57BL/6 × 129/O1a HFEo/omice mimic HH iron distribution and the regulation of intestinal iron absorption after long‐term feeding. However, characteristic morphological late changes in untreated HH are not modelled.