bluuebunny/crossref_metadata_2025_split huggingface dataset:
Protein adducts in type I and type II fibre predominant muscles of the ethanol‐fed rat: preferential localisation in the sarcolemmal and subsarcolemmal region
Authors: Worrall S. , Niemela O. , Parkkila S. , Peters T. J. , Preedy V. R. 
Published: March 2003

Background Chronic alcoholic myopathy is characterised by reduced muscle strength and structural changes including a decrease in the diameter of Type II (glycolytic, fast‐twitch, anaerobic) fibres. In contrast, the Type I fibres (oxidative, slow‐twitch, aerobic) are relatively protected. It is possible that adduct formation with reactive metabolites of ethanol may be a contributory process.Materials and Methods We analysed skeletal muscles from rats fed nutritional‐complete liquid diets containing ethanol as 35% of total dietary energy; control rats were fed the same diet in which ethanol was replaced by isocaloric glucose. Reduced‐acetaldehyde, unreduced‐acetaldehyde, malondialdehyde, malondialdehyde‐acetaldehyde and α‐hydroxyethyl protein‐adducts in both soleus and plantaris were analysed by ELISA or immunohistochemistry with comparative studies in liver.Results After 6 weeks, the weights of the plantaris, but not the soleus, were decreased. ELISA analyses for protein adducts showed increased amounts of unreduced‐acetaldehyde adducts in soleus (P < 0·025) and plantaris (P < 0·025). Reduced‐acetaldehyde, malondialdehyde, malondialdehyde‐acetaldehyde and α‐hydroxyethyl protein‐adducts in both soleus and plantaris muscles from ethanol‐fed rats were not significantly different from their pair‐fed controls (P > 0·05). In contrast, liver from ethanol‐fed rats showed significantly higher levels of unreduced‐acetaldehyde (P < 0·025), reduced‐acetaldehyde (P < 0·01), malondialdehyde (P < 0·01), malondialdehyde‐acetaldehyde (P < 0·025) and α‐hydroxyethyl radical (P < 0·01) protein adducts compared to pair‐fed controls. Immuno‐histochemical analysis using an antiserum reacting with both reduced‐ and unreduced‐acetaldehyde adducts showed adducts were increased in soleus (P < 0·05) and plantaris (P < 0·025), confirming ELISA analysis. Adducts were located within the sarcolemmal (i.e. muscle membrane) and subsarcolemmal regions.Conclusion This is the first report of adduct formation in myopathic skeletal muscle due to chronic alcohol ingestion and suggests a role for acetaldehyde in the aetiology of alcoholic myopathy.
Butyrate and the cytokine‐induced α1‐proteinase inhibitor release in intestinal epithelial cells
Authors: Faust D. , Hormann S. , Friedrich‐Sander M. , Milovic V. , Stein J. 
Published: March 2003

Background α1‐proteinase inhibitor (α1‐PI), an anti‐inflammatory protein thought to play a role in the intestinal inflammation, is synthesised by and released from the intestinal epithelial cells. IL‐1β is a key proinflammatory cytokine in the abnormal immune response that occurs in inflammatory bowel disease. Butyrate is a normal luminal constituent in the colon, known to be of benefit in preventing inflammatory bowel disease. Direct modes of action of butyrate in intestinal inflammation have been poorly studied so far. The aim of this study was to investigate the effects of butyrate on cytokine‐mediated α1‐PI release in intestinal epithelial cells.Methods Differentiated Caco‐2 cells were incubated with IL‐1β in the presence or absence of 2 mM butyrate. α1‐PI expression in the cells was evaluated by Western blot analysis and α1‐PI release by ELISA.Results Treatment with butyrate alone had no effect on α1‐PI expression in differentiated Caco‐2 cells. However, treatment of the cells with 2 mM butyrate significantly reduced the α1‐PI level in IL‐1β‐treated cells. In the cell culture medium, the presence of butyrate impaired the IL‐1β‐induced α1‐PI release to 17–35%. The treatment induced no change in the number of detached cells or the percentage of viable cells.Conclusion Our data show that butyrate inhibits α1‐PI release from Caco‐2 colonocytes treated with IL‐1β. It is therefore likely that anti‐inflammatory actions of butyrate occur via a mechanism that does not involve direct regulation of cytokine‐induced anti‐inflammatory protein expression in intestinal epithelial cells.
Dietary epoxy fatty acids are absorbed in healthy women
Authors: Wilson R. , Fernie C. E. , Scrimgeour C. M. , Lyall K. , Smyth L. , Riemersma R. A. 
Published: March 2003

AbstractBackground Epoxy fats in the diet may adversely affect human health. There are no data on the absorption of these fats in humans.Methods Triglycerides were synthesized containing two U‐13C‐labelled monoepoxy or diepoxy stearic acid molecules. Apparently healthy women consumed a standardized fatty meal (30 g fat) containing either 20 mg monoepoxy or 25 mg diepoxy fat (n = 6 and n = 7, respectively). Plasma lipid [U‐13C]monoepoxy and diepoxy stearate concentrations were determined (0–24 h) by gas chromatography‐mass spectrometry.Results Plasma triglycerides increased from 1·05 ± 0·12 to 1·83 ± 0·13 mmol L−1 (n = 6) and from 1·10 ± 0·19 to 1·41 ± 0·27 mmol L−1 (n = 7) (both P < 0·001). Plasma [U‐13C]monoepoxy and diepoxy stearate levels increased to 0·18 ± 0·07 µmol L−1 (n = 6) and to 0·08 ± 0·03 µmol L−1 (n = 7), respectively. Monoepoxy triglyceride was better absorbed than diepoxy triglyceride: 17 ± 4 vs. 8 ± 1% of dose (determined from area under curve (plasma 13C) normalized to that of absorbed triglycerides (plasma 12C); P < 0·02 after log transformation). The absorption of monoepoxy‐ and diepoxy‐labelled triglycerides was related to that of normal triglycerides (r = 0·80, P < 0·05 and r = 0·91, P < 0·001, respectively).Conclusions Monoepoxy fats are better absorbed than diepoxy fats in women (17 ± 4 vs. 8 ± 1% of dose, P = 0·02). This difference in absorption is important when considering the relative toxicity of epoxidized material in the food chain.
Addition of glucose to a fatty meal delays chylomicrons and suppresses VLDL in healthy subjects
Authors: Westphal S. , Leodolter A. , Kahl S. , Dierkes J. , Malfertheiner P. , Luley C. 
Published: March 2003

AbstractBackground Postprandial lipemia has been shown in a number of studies to be associated with atherosclerosis. However, the test meals used in these studies were heterogeneous particularly in their carbohydrate content, which may be important for the resulting lipemia and which makes comparison between different studies difficult. We studied the effect of 75 g glucose added to a fatty meal on various lipoproteins and on gastric emptying.Materials and methods Fourteen healthy young volunteers were studied in the fasting state and until 7 h postprandially. In a crossover design, each subject received an oral fat load (1 g fat kg−1 body weight) with or without 75 g glucose. Triacylglycerol (TG) and free fatty acids (FFA) were then measured in whole blood and lipoproteins were separated off by ultracentrifuging. Gastric emptying was determined by the 13C breath test.Results The addition of 75 g glucose to a fatty meal had two different effects. Gastric emptying was delayed by about 2 h and the chylomicron response was consequently postponed. In addition, the postprandial increase in VLDL triacylglycerol was reduced by 40%, which may be due to the pronounced FFA depression during the glucose‐induced rise in insulin.Conclusions 75 g glucose added to an oral fat load causes a delay of the chylomicron response and a marked suppression of the postprandial increase in VLDL.
Impaired estrogen‐induced negative feedback on gonadotropin secretion in patients with gonadotropin‐secreting and nonfunctioning pituitary adenomas
Authors: Lania A. , Gangi E. , Romoli R. , Losa M. , Travaglini P. , Meringolo D. , Ambrosi B. , Faglia G. , Beck‐Peccoz P. , Spada A. 
Published: March 2003

AbstractBackground Several in vitro studies suggest that gonadotropin‐secreting pituitary adenomas (Gn‐omas) and non functioning pituitary adenomas (NFPA) originate from gonadotroph cells. Patients with Gn‐oma and NFPA frequently show abnormal gonadotropin response to TRH. The aim of the study was to investigate whether the estrogen‐induced negative feedback is operating in either patients with Gn‐oma or NFPA.Materials and methods Serum gonadotropin levels were evaluated at 24 h after ethinylestradiol administration (1 mg per os; EE2 test) in seven patients with a diagnosis of Gn‐oma, based on the presence of high follicle‐stimulating hormone (FSH) and/or lutenising hormone (LH) levels with normal or high levels of sex steroids, in 22 patients with NFPA with normal or low levels of gonadotropin and sex steroids, and 30 sex‐ and age‐matched healthy subjects. A normal response to EE2 test was arbitrarily defined as a serum LH and FSH decrease of at least 40 and 30% below basal levels.Results Among patients with Gn‐oma, only one had a normal FSH inhibition and another, a normal LH inhibition. Among the 22 patients with NFPA, the EE2 test caused a normal FSH or LH reduction in 10 and 15, respectively, while a normal reduction of both FSH and LH was observed in nine.Conclusions The study demonstrates that estrogen‐induced negative feedback of gonadotropin secretion is disrupted in almost all patients with Gn‐oma and in half of those with NFPA. This defective feedback is reminiscent of the resistance to thyroid hormones and glucocorticoids observed in patients with thyroid‐stimulating hormone‐ (TSH‐) and adrenocorticotropic hormone‐ (ACTH‐)secreting adenomas, respectively.
Factorial study of the effects of atorvastatin and fish oil on dyslipidaemia in visceral obesity
Authors: Chan D. C. , Watts G. F. , Mori T. A. , Barrett P. H. R. , Beilin L. J. , Redgrave T. G. 
Published: March 2003

AbstractBackground  Dyslipidaemia may account for increased risk of cardiovascular disease in central obesity. Pharmacotherapy is often indicated in these patients, but the optimal approach remains unclear. We investigated the effects of atorvastatin and fish oil on plasma lipid and lipoprotein levels, including remnant‐like particle‐cholesterol and apolipoprotein C‐III, in dyslipidaemic men with visceral obesity.Methods  We carried out a 6‐week randomized, placebo‐controlled, 2 × 2 factorial intervention study of atorvastatin (40 mg day−1) and fish oil (4 g day−1) on plasma lipids and lipoproteins in 52 obese men (age 53 1 years, BMI 33·7 0·55 kg m−2) with dyslipidaemia and insulin resistance. Treatment effects were analysed by general linear modelling.Results  Atorvastatin had significant main effects in decreasing triglycerides (−0·38 0·02 mmol L−1, P = 0·002), total cholesterol (−1·89 0·17 mmol L−1, P = 0·001), LDL‐cholesterol (−1·78 0·14 mmol L−1, P = 0·001), remnant‐like particle‐cholesterol (−0·08 0·04 mmol L−1, P = 0·035), apolipoprotein B (−49 4 mg dL−1, P = 0·001), apolipoprotein C‐III (−12·6 6·1 mg L−1, P = 0·044) and in increasing HDL‐cholesterol (+0·10 0·04 mmol L−1, P = 0·007). Fish oil had significant main effects in decreasing triglycerides (−0·38 0·11 mmol L−1, P = 0·002) and in increasing HDL‐cholesterol (+0·07 0·04 mmol L−1, P = 0·041). There were no significant changes in weight or insulin resistance during the study.Conclusions  Atorvastatin and fish oil have independent and additive effects in correcting dyslipidaemia in viscerally obese men. Improvement in abnormalities in remnant lipoproteins may occur only with use of atorvastatin. Combination treatment with statin and fish oil may, however, offer an optimal therapeutic approach for globally correcting dyslipidaemia in obesity.
Heritability of left atrial size in the Tecumseh population
Authors: Palatini P. , Amerena J. , Nesbitt S. , Valentini M. , Majahalme S. , Krause L. , Tikhonoff V. , Julius S. 
Published: March 2003

AbstractBackground  Little is known about the determinants of atrial size, and no study has analyzed whether genetic factors are involved in the pathogenesis of LA enlargement.Materials and methods We studied the heritability of echocardiographic left atrial size in 290 parents from the Tecumseh Blood Pressure Study and 251 children from the Tecumseh Offspring Study. All data from the parents and children were obtained at the same field office in Tecumseh, USA. Left atrial dimension was determined echocardiographically in accordance with American Society of Echocardiography guidelines with the use of leading‐edge‐to‐leading‐edge measurements of the maximal distance between the posterior aortic root wall and the posterior left atrial wall at end systole.Results For correlation between the left atrial dimensions of the parents and their offspring, several models were generated to adjust the atrial dimensions in both groups for an increasing number of clinical variables. After removing the effect of age, gender, height, weight, skinfold thickness, and systolic blood pressure, parent–child correlation for left atrial size was 0·19 (P = 0·007). Further adjustment for left ventricular mass and for measuring left ventricular diastolic function increased the correlation to 0·25 (P = 0·001).Conclusions  The present data indicate that heredity can explain a small but definite proportion of the variance in left atrial dimension.
Lipid peroxidation and antioxidant status in professional American football players during competition
Authors: Schippinger G. , Wonisch W. , Abuja P. M. , Fankhauser F. , Winklhofer‐Roob B. M. , Halwachs G. 
Published: March 2003

AbstractBackground Oxidative stress occurs during strenuous physical exercise, perhaps as a result of increased consumption of oxygen.Materials and methods In this study, different markers of oxidative stress were determined in eight national league American football players. Before (March) and at three time‐points during the competition season (May, June, July) serum total peroxide concentrations, autoantibody titres against oxidized low‐density lipoprotein (oLab), and lag time of reactive oxygen species‐induced degradation of the fluorophore 1‐palmitoyl‐2‐((2‐(4‐(6‐phenyl‐trans‐1,3,5‐hexatrienyl)phenyl)ethyl)‐carbonyl)‐sn‐glycero‐3‐phosphocholine (DPHPC) were measured along with serum ascorbate, α‐ and γ‐tocopherol, and β‐carotene concentrations.Results Before the competition season, serum antioxidant concentrations were within the lower normal range; ascorbate concentrations increased significantly during the competition period (P < 0·05). Serum peroxide concentrations were within the normal range and increased significantly during the competition period (P < 0·05); in four of the eight subjects the increase was several times the baseline values, while four athletes did not show any increase. The oLab titres increased significantly at the mid‐competition period time‐point (P < 0·01), but levelled off thereafter.Discussion Given that it could not be predicted from the baseline oxidative stress and antioxidant status which subject would respond to strenuous exercise with an increase in oxidative stress status, it is concluded that oxidative stress should be monitored in all athletes.
Procoagulant and inflammatory response of virus‐infected monocytes
Authors: Bouwman J. J. M. , Visseren F. L. J. , Bosch M. C. , Bouter K. P. , Diepersloot R. J. A. 
Published: March 2003

AbstractBackground Monocytes play a prominent role in inflammation, coagulation and atherosclerosis by their ability to produce tissue factor (TF) and cytokines. The aim of the present study was to establish whether virus‐infected monocytes initiate coagulation. In addition, the production of cytokines by monocytes may accelerate the chronic process of atherosclerosis and may contribute to coronary syndromes by eliciting plaque instability.Materials and methods Monocytes were isolated by Vacutainer®, BD Biosciences, Alphen aan den Rijn, Netherlands and subsequent magnetic cell sorting (MACS®, Milteny Biotec, Bergish Gladbach, Germany). Coagulation times in normal pooled plasma and Factor VII‐deficient plasma were measured after infection with cytomegalovirus (CMV), Chlamydia pneumoniae (Cp) and influenza A\H1N1. Anti‐TF antibodies were added to neutralize TF expressed on monocytes. Interleukins (IL) 6, 8 and 10 were measured in the supernatants.Results Chlamydia pneumoniae‐ and CMV‐infected monocytes decreased the clotting time by 60%, and influenza‐infected monocytes by 19%, as compared to uninfected monocytes. Procoagulant activity was absent when Factor VII‐deficient plasma or anti‐TF antibodies were used. Monocytes produced both IL‐6 and IL‐8 after infection with CMV (317 pg mL−1 and 250 pg mL−1) or Cp (733 pg mL−1 and 268 pg mL−1). Similar results were obtained for influenza virus‐infected monocytes, but the levels of both cytokines were 3–5‐fold higher (1797 pg mL−1 and 725 pg mL−1). Interleukin‐10 was not produced by infected monocytes.Conclusion The procoagulant activity of virus‐infected monocytes is TF‐dependent. Although influenza infection did not generate a significant reduction in clotting time, the pronounced expression of IL‐6 and IL‐8 may induce local and/or systemic inflammatory reactions, which may be associated with plaque rupture and atherosclerosis. The lack of production of the anti‐inflammatory cytokine IL‐10 may even accelerate these processes.
Selectin‐P and interleukin‐8 plasma levels in coronary heart disease patients
Authors: Romuk E. , Skrzep‐Poloczek B. , Wojciechowska C. , Tomasik A. , Birkner E. , Wodniecki J. , Gabrylewicz B. , Ochala A. , Tendera M. 
Published: March 2003

AbstractBackground  Alterations of the immune system are now believed to play crucial role in the pathogenesis of atherosclerosis. The aim of this study was analysis of soluble forms of selectin‐P and interleukin‐8 levels in patients with different form of coronary heart disease. Materials and methods: In the study took part 18 patients with stable coronary heart disease, 20 patients with unstable coronary heart disease and 15 healthy persons from control group. Soluble selectin‐P and interleukin‐8 levels were measured in EDTA plasma with the use of enzyme immunoassay ELISA.Results The level of soluble selectin‐P was significantly higher in unstable coronary heart disease patients in comparison to the stable coronary heart disease patients (P ≤ 0·01) and nonsignificantly higher in comparison to the control group. The level of interleukin‐8 were significantly higher in unstable coronary heart disease patients in comparison to the stable coronary heart disease patients (P ≤ 0·01) and in comparison to the control group (P ≤ 0·02). Conclusion: Our findings suggest that soluble form of selectin‐P and interleukin‐8 may be useful clinical predictors of unstable coronary heart disease. The assessment of the risk for the development of coronary heart disease requires further serial investigation.
Effect of Sildenafil on hypertensive lower oesophageal sphincter
Authors: Bortolotti M. , Pandolfo N. , Giovannini M. , Mari C. , Miglioli M. 
Published: March 2003

AbstractBackground Sildenafil relaxes the muscle cells of the penis arterioles by inhibiting phosphodiesterase‐type 5 (PD‐5), inactivating the nitric oxide‐stimulated cyclic guanosine monophosphate. We investigated whether this effect of Sildenafil is also displayed on the muscles of the hypertensive lower oesophageal sphincter (LES).Methods In 14 patients with symptomatic hypertensive LES, oesophageal motility was recorded by means of a low‐compliance manometric system with five manometric ports for the oesophageal body and a sleeve for the sphincter. After a basal period of 60 min a tablet of Sildenafil 50 mg (group A; seven patients) or one of placebo (group B; seven patients) ground and dissolved in 20 cc of water was infused in the stomach, randomly and in double‐blind manner. Recording continued for a further 60 min. Sphincter tone and pressure wave amplitude were measured each minute and the values averaged for each 5‐min period for the post‐infusion period of 60 min. The values of the whole post infusion period, the lowest values among the 5‐min periods (nadir values) and the values of the last 5‐min periods were compared with the basal values in each group, and those of group A were compared with the corresponding values of group B.Results Sphincter tone and wave amplitude showed after Sildenafil a significant decrease comparable that of the basal period and the placebo. The inhibitory effect reached its maximum 10 min after the infusion and lasted approximately 1 h.Conclusions Sildenafil inhibits the lower oesophageal sphincter tone and pressure wave amplitude of patients with symptomatic hypertensive LES. These findings suggest a clinical application of PD‐5 inhibitors in the treatment of spastic oesophageal motor disorders.
Influence of atherosclerosis on age‐related changes in renal size and function
Authors: Bax L. , Van Der Graaf Y. , Rabelink A. J. , Algra A. , Beutler J. J. , Mali for the Smart Study Group W. P. Th. M. 
Published: March 2003

AbstractBackground Renal size and function reflect the health of the kidney. These parameters are associated with age, gender and body weight. The kidneys are also influenced by micro‐ and macrovascular diseases. Atherosclerotic markers and risk factors may influence the age‐related changes of renal size and function.Methods Data of 1056 patients who entered the SMART‐study (Second Manifestations of ARTerial disease) were used to assess the effect of atherosclerosis on the relationship between age and renal size and function and to study the effect of atherosclerosis on renal size and function. Patients who were newly referred to the hospital with manifestations of vascular disease were screened for asymptomatic atherosclerosis with noninvasive tests. The carotid intima‐media thickness (IMT) and albuminuria were used as estimates for the atherosclerotic burden. Renal size was defined as the mean pole‐to‐pole length of both kidneys measured by ultrasonography. Renal function was represented by serum creatinine.Results Intima‐media thickness was a significant effect modifier of the age‐renal size relationship (P = 0·041). The increase of serum creatinine with age was more pronounced in the highest tertile of IMT (P = 0·048). Renal size decreased equally with age in patients with and without hypertension or diabetes mellitus (DM). The same held true for the age‐renal function relationship. Albuminuria and DM were independent predictors of renal size and function.Conclusion Atherosclerosis accelerates the decrease of renal size and the increase of serum creatinine with age. Renal size and function are determined by albuminuria and DM.
Lactose intolerance: analysis of underlying factors
Authors: Vonk R. J. , Priebe M. G. , Koetse H. A. , Stellaard F. , Lenoir‐Wijnkoop I. , Antoine J.‐M. , Zhong Y. , Huang C.‐Y. 
Published: March 2003

AbstractBackground We studied the degree of lactose digestion and orocecal transit time (OCTT) as possible causes for the variability of symptoms of lactose intolerance (LI) in a sample of a population with genetically determined low lactase activity.Methods Lactose digestion index (LDI) was measured by the recently developed 13C‐lactose/2H‐glucose test. The OCTT was determined using the breath hydrogen test. Based on a 6‐h symptom score (SSC) after a challenge dose of 25 g of lactose the subjects were divided into a tolerant group (T: n= 15; SSC = 0) and an intolerant group (IT: n= 28; SSC 1–40). The intolerant group was subdivided according to the severity of symptoms: group ITa (n = 17; mild symptoms without diarrhoea) and group ITb (n = 11; with diarrhoea).Results The LDI was lower in the intolerant group (0·34 ± 0·14) (mean ± SD) than in the tolerant group (0·47 ± 0·14) (P = 0·008). The OCTT of group IT (60, 30–90 min) (median, quartiles) was significantly shorter than that of group T (105, 60–120 min) (P = 0·003) and was positively correlated with the LDI (P = 0·050). In groups ITa and ITb the OCTT (60, 30–90 min; 60, 26–83 min) and LDI (0·30 ± 0·14; 0·39 ± 0·14) were similar.Conclusions Lactose digestion capacity, which is determined by small intestinal lactase activity as well as by OCTT, affects the occurrence of lactose intolerance. However, the major difference in intolerance symptoms is caused by differences in the colonic processing of maldigested lactose.