bluuebunny/crossref_metadata_2025_split huggingface dataset:
The effect of hyperglycaemia on cerebral potentials evoked by rapid rectal distension in healthy humans
Authors: Russo A. , Smout A. J. P. M. , Kositchaiwat C. , Rayner C. , Sattawatthamrong Y. , Semmler J. , Horowitz M. , Sun W. M. 
Published: March 2003

BackgroundAcute hyperglycaemia affects the perception of sensations arising from the gastrointestinal tract. The mechanisms responsible for this effect are unknown. Recordings of cerebral evoked potentials (EPs) can be used to assess the integrity of visceral afferent pathways. Our aim was to determine whether hyperglycaemia affects EPs elicited by rectal distension in healthy humans.Materials and methodsTwelve healthy men, aged 19–31 years, were studied. A manometric catheter, incorporating a rectal balloon, was positioned 7–10 cm from the anal verge. Balloon distensions at both ‘low’ (∼ 20 mL) and ‘high’ (∼ 28 mL) volumes were performed, in a single‐blind, randomized order, during both euglycaemia (4 mmol L−1) and hyperglycaemia (12 mmol L−1). EPs were recorded from a midline scalp electrode (Cz, International 10–20 system) and averaged for each series of 50 distensions. EP latencies and interpeak amplitudes were calculated.ResultsPolyphasic EPs were recorded in all but one subject. Although the blood glucose concentration had no significant effect on the latencies of the EP peaks elicited by either ‘low’‐ or ‘high’‐volume balloon distension, the interpeak amplitude (P1–N1) was greater during hyperglycaemia than during euglycaemia at the ‘low’ balloon volume (6.3 ± 1.2 μV vs. 4.8 ± 1.0 μV, P < 0.05). The blood glucose concentration had no significant effect on the perception of rectal balloon distension.ConclusionsWe conclude that in normal subjects acute hyperglycaemia increases the amplitude of the cerebral EP elicited by rectal balloon distension at low balloon volumes, suggesting that the effects of hyperglycaemia on gastrointestinal sensation may be mediated by central mechanisms.
Immunohistochemical localization of somatostatin receptor sst2A in sarcoid granulomas
Authors: Ten Bokum  , Hofland  , De Jong  , Bouma  , Melief  , Kwekkeboom  , Schonbrunn  , Mooy  , Laman  , J. Lamberts  , Van Hagen  
Published: March 2003

BackgroundIn a previous study, we demonstrated the presence of receptors for somatostatin, a neuropeptide with immunoregulatory properties, in the inflammatory lesions of patients suffering from sarcoidosis and other granulomatous diseases by in vivo somatostatin receptor scintigraphy and in vitro autoradiography. However, it was not possible to identify exactly which cell types expressed the somatostatin receptors and which subtype was expressed. In this study we used a polyclonal antiserum directed against the sst2A receptor to identify more accurately the sst2A‐expressing cells in sarcoidosis and other granulomatous diseases.DesignTissue biopsies from 12 patients with sarcoidosis, one patient with giant cell arteritis and one patient with Wegener's granulomatosis were studied by immunohistochemistry with the sst2A‐specific antiserum. Two of the sarcoidosis patients were treated with the somatostatin analogue octreotide (100 μg t.i.d.).ResultsEpithelioid cells, multinucleated giant cells and a subset of CD68+ macrophages stained positive for sst2A in 9 out of 12 of the sarcoid biopsies and in both non‐sarcoid granuloma biopsies. Treatment with octreotide resulted in clinical improvement in one out of two treated patients.ConclusionThe identification of somatostatin receptors on granuloma macrophages, epithelioid cells and giant cells, and the successful treatment of one patient with sarcoidosis with a somatostatin analogue, may offer new possibilities for treatment of granulomatous diseases.
Induction of myocardial nitric oxide synthase by Coxsackie B3 virus in mice
Authors: Robinson  , Zhang  , Bevan  , De Belder  , Moncada  , Martin  , Archard  
Published: March 2003

BackgroundInducible nitric oxide synthase (iNOS) expression is regulated by cytokines. This study investigated whether Coxsackie group B virus (CVB) myocarditis resulted in an environment suitable for induction of NOS in the murine heart.Materials and methodsMyocardium was removed from mice infected with CVB3 and from controls. Histology, reverse transcriptase polymerase reaction (RT‐PCR) for murine iNOS, NOS enzyme activity and immunohistochemistry were assessed.ResultsHistology revealed severe myocarditis 7 days after infection with CVB3 but not in controls. RT‐PCR using primers for murine iNOS detected iNOS mRNA in infected mice but not in controls. Calcium‐independent NOS activity increased by day 5 after infection with a peak at day 7. Calcium‐dependent NOS activity was present throughout, with a trend to lower levels during peak calcium‐independent activity. Immunohistochemistry revealed iNOS to be localized to inflammatory cells rather than to myocytes.ConclusionThis study demonstrates the development of calcium‐independent NOS activity and de novo gene transcription for iNOS in the murine myocardium in response to CVB3 infection. The nitric oxide produced at such high output may act at times as part of the immune defence as an antiviral agent and may be toxic to host tissue.
Gallbladder motility and cholesterol crystallization in bile from patients with pigment and cholesterol gallstones
Authors: Portincasa  , Di Ciaula  , Vendemiale  , Palmieri  , Moschetta  , VanBerge‐Henegouwen  , Palasciano  
Published: March 2003

BackgroundLittle is known about gallbladder motility in patients with black pigment stones when compared to cholesterol gallstone patients, or about their relationship to biliary composition, crystallization and stone characteristics.DesignFasting and postprandial gallbladder volumes were studied by ultrasonography in 49 gallstone patients with pigment (n = 14) or cholesterol (n = 35) stones and 30 healthy controls. After cholecystectomy stone composition, gallbladder wall inflammation, cholesterol saturation index and appearance of platelike cholesterol crystals in bile were evaluated in gallstone patients.ResultsFasting gallbladder volume was significantly (P < 0.05) increased in cholesterol stone patients (31.7 ± 1.9 mL) but not in pigment stone patients (21.9 ± 3.1 mL), compared to controls (21.0 ± 1.5 mL). Postprandial emptying was delayed in patients (half‐emptying time: 31 ± 2 min, 35 ± 3 min, 24 ± 2 min in cholesterol stone patients, pigment stone patients and controls, respectively, P < 0.05) and incomplete (residual volume: 43.2 ± 2.7%, 40.0 ± 4.3%, 15.8 ± 1.6% min in cholesterol stone patients, pigment stone patients and controls, respectively, P < 0.05). The inflammation of the gallbladder wall was mild or absent in all cases. Biliary cholesterol saturation index was 152.3 ± 8.5% and 92.9 ± 4.8% in patients with cholesterol and pigment stones, respectively (P < 0.01). Whereas cholesterol crystals never appeared during 21 days in biles from patients with pigment stones, crystal observation time in patients with cholesterol gallstone was 5 days (median) and was significantly shorter in patients with multiple (4 days) than in patients with solitary (12 days) cholesterol stones (P = 0.0019).ConclusionsPatients with black pigment stones who do not have excess cholesterol and do not grow cholesterol crystals in bile have decreased gallbladder emptying, although to a lesser extent than patients with cholesterol stones. Thus, gallbladder stasis is likely to put a subset of subjects at risk for the formation of pigment gallstones, and pathogenic mechanisms need to be further investigated.
Gastrotonometry represents dramatic increase in Pc	o2 after acetazolamide administration
Authors: Taki  , Oogushi  , Tozuka  
Published: March 2003

BackgroundWe sought to evaluate the parameters of CO2 transport during the administration of acetazolamide in order to assess the role of carbonic anhydrase in CO2 transport.Materials and methodsThe partial pressure of carbon dioxide in tissue (Pt
co2), arterial blood (Pa
co2) and end‐tidal gas (PET
co2) were monitored to study the correlation between Pa
co2, Pt
co2 and PET
co2 in spontaneously breathing healthy volunteers after the intravenous administration of acetazolamide 6 mg kg−1.ResultsAt 60 min after the administration of acetazolamide, the Pt
co2 peaked at more than 60 mmHg, and although it decreased by 90 min, it then remained stable above the baseline value. The Pa
co2 did not change and the PET
co2 decreased significantly. The changes in Pt
co2 were greater than those of either Pa
co2 or PET
co2. The minute ventilation increased progressively throughout the study.ConclusionsWe concluded that gastrotonometry represents a new method for monitoring the dramatic increase in Pt
co2 induced by drugs such as acetazolamide clinically, and that it could be a warning against acetazolamide administration in severe patients without keeping a ventilation and circulation reserve.
Metabolic and inflammatory responses to pulmonary exacerbation in adults with cystic fibrosis
Authors: Bell  , Bowerman  , Nixon  , Macdonald  , Elborn  , Shale  
Published: March 2003

BackgroundWe hypothesized that increased resting energy expenditure in adults with cystic fibrosis was related to chronic inflammation secondary to pulmonary infection and could be modified by treatment of the underlying infection.MethodTo determine the relationship between resting energy expenditure and the inflammatory and metabolic responses, we studied 22 adults with cystic fibrosis and chronic Pseudomonas aeruginosa infection before and after treatment of a respiratory exacerbation. Resting energy expenditure was measured by indirect calorimetry. Spirometry and circulating concentrations of C‐reactive protein, neutrophil elastase α1–antiproteinase complex, catecholamines, non‐esterified fatty acids and glycerol were determined.ResultsThe mean (95% confidence interval)% predicted FEV1 was 28.5% (20.6, 36.4) and mean body weight 50.7 kg (47.4, 54.1). Following treatment, 1‐s forced expiratory volume (FEV1) and weight increased, while C‐reactive protein (P < 0.0001) and neutrophil elastase α1‐antiproteinase complex concentrations (P < 0.0001) were reduced. Resting energy expenditure decreased from 6.8 (6.3, 7.2) to 6.25 (5.9, 6.6) MJ day−1 by day 15 (P < 0.001). Changes in resting energy expenditure and C‐reactive protein were related (r = 0.66, P < 0.0001). Weight gain was inversely related to resting energy expenditure (r = 0.43, P = 0.02) and unrelated to energy intake (r = 0.02, P = 0.47). Post‐treatment reduction in norepinephrine was related to changes in heart rate (r = 0.57, P < 0.01), resting energy expenditure (r = 0.51, P = 0.001) and non‐esterified fatty acids (r = 0.42, P < 0.05).ConclusionsA parallel reduction in the host inflammatory and catabolic responses followed treatment of a respiratory exacerbation and may have contributed to weight gain.
The effect of apolipoprotein B xbaI polymorphism on plasma lipid response to dietary fat
Authors: López‐Miranda  , Marín  , Castro  , Gómez  , González‐Amieva  , Paz  , Bravo  , Ordovas  , Jimenez‐Pereperez  , Pérez‐Jiménez  
Published: March 2003

Background and aimsLipid response to dietary fat and cholesterol is, to a large extent, genetically controlled. Apolipoprotein B (apo B) plays a dominant role in cholesterol homeostasis. Several polymorphic sites within or adjacent to the gene locus for apo B have been detected. The X+ allele of the XbaI restriction fragment polymorphism of the apo B gene has been found to be associated with higher serum cholesterol and/or triglyceride levels. In order to study the influence of this mutation on the plasma lipid response in diets of varying fat content, 72 healthy male subjects were studied, 21 X− X− (X−) and 51 X+ (X+ X− or X+ X+).Methods and resultsThese subjects followed three consecutive 28‐day diet periods: one rich in saturated fats (SAT diet; 38% fat, 20% saturated); a National Cholesterol Education Program type I diet (NCEP‐I diet) (28% fats, < 10% saturated); and a third monounsaturated (MUFA diet)(38% fats, 22% monounsaturated). The different genotypes can be observed to have significant effects on total and LDL cholesterol concentrations (P < 0.017). X+ individuals had higher levels of total and LDL cholesterol after the consumption of a SAT diet (P < 0.012; P < 0.006, respectively), NCEP diet (P < 0.060; P < 0.054, respectively) and MUFA diet (P < 0.022; P < 0.042, respectively) in comparison with X− individuals. A significant interaction between genotypes and dietary effects was observed for diet‐induced changes in plasma triglycerides (P < 0.032). Significant decreases in the absolute values of triglyceride concentrations (−0.18 mmol L−1, P < 0.024) were noted in the X− subjects after the high intake of a MUFA diet, while no significant differences were observed in the X+ individuals (0.006 mmol L−1, P < 0.858).ConclusionsOur results suggest that the total triglyceride response to diet is influenced by the apo B XbaI polymorphism.
Energy expenditure in chronic alcohol abuse
Authors: Levine  , Harris  , Morgan  
Published: March 2003

BackgroundIn healthy subjects, alcohol decreases lipid oxidation favouring fat deposition. However, individuals who chronically abuse alcohol are not obese. To investigate this paradox, we measured energy expenditure (EE) and fuel utilization in chronic alcohol abusers in relation to their drinking behaviour.MethodsResting and postprandial EE and nonprotein respiratory quotient (NPRQ) were measured using indirect calorimetry, in 36 alcohol abusers [mean (± SE) age 42 ± 2 years; weight 67 ± 2 kg; 21 with steatosis, eight with hepatitis; seven with cirrhosis] and in 36 gender‐, age‐ and weight‐matched healthy controls. Alcoholic patients were re‐evaluated either after 14 days (n = 14) or on days 2, 4, 6, 8, 14 and 42 (n = 6) after abstinence.ResultsWhen alcoholics were compared to healthy controls, mean energy intake was greater, 15 ± 1 MJ day−1 (38 ± 2% from alcohol) cf. 9 ± 1 MJ day−1 (P < 0.001), resting EE increased, 82 ± 2 cf. 65 ± 2 W (P < 0.001) and NPRQ decreased, 0.75 ± 0.02 cf. 0.82 ± 0.01 (P < 0.001). The postprandial increases in EE and NPRQ were of similar magnitude in both groups. Abstinence from alcohol for 14 days was accompanied by reduced energy intake, 16 ± 1 cf. 11 ± 1 MJ day−1 (P < 0.005) and decreased resting EE, 84 ± 5 cf. 73 ± 4 W (P < 0.05). The decrease in resting EE consistently occurred 4 days after abstinence from alcohol.ConclusionsChronic alcohol abuse is associated with energy wasting and inhibition of adipose tissue accumulation. This may explain why alcoholics are not obese despite high total energy intakes.
Predictors of diabetic renal lesions in type 2 diabetes associated with microalbuminuria
Authors: Kanauchi M. , Dohi K. 
Published: March 2003

Not all type 2 diabetic patients with microalbuminuria show the same pattern of renal tissue injury, and heterogeneity in renal lesions has been reported. We determine clinical and laboratory findings that predict the presence of typical diabetic glomerulosclerosis in type 2 diabetic patients with microalbuminuria.Twenty‐three type 2 diabetic patients with microalbuminuria who underwent renal biopsy were investigated. Two patterns of renal biopsy findings were defined as type D (typical diabetic glomerulosclerosis) and type A (atherosclerotic nephropathy without evidence of diabetic glomerulopathy).Thirteen patients (57%) were classified as type D, and 10 (43%) as type A. In stepwise multiple regression analysis, severity of diabetic retinopathy (P = 0·0006), relatively high urinary N‐acetyl‐beta‐D‐glucosaminidase activity (P = 0·0013), and relatively low serum creatinine concentration (P = 0·0303) significantly predicted type D findings as opposed to type A (R2 = 0·734, P < 0·001).Certain patient characteristics can predict the presence of typical diabetic glomerulosclerosis in type 2 diabetic patients with microalbuminuria.
Acute inhibitory effect of alcohol on fibrinolysis
Authors: Van De Wiel A. , Van Golde P. M. , Kraaijenhagen R. J. , Von Dem Borne P. A. K. , Bouma B. N. , Hart H. C. 
Published: March 2003

In contrast to a reduced risk of coronary heart disease (CHD) with light to moderate alcohol consumption, heavy alcohol intake and binge drinking are associated with increased cardiovascular mortality. Alcohol has an acute and profound effect on fibrinolysis that may be relevant to the pathogenesis of CHD.The short‐term effects of a low (two glasses, 250 mL, 20 g ethanol) and a high (six glasses, 750 mL, 60 g ethanol) intake of red wine were studied in male volunteers and compared to the intake of mineral water. To find a threshold for inhibition of fibrinolysis and to study a binge effect, a second experiment was performed comparing the intake of four (500 mL, 40 g ethanol) and eight (1000 mL, 80 g ethanol) glasses of red wine with mineral water. Plasminogen activator inhibitor‐1 (PAI‐1), tissue‐type plasminogen activator (t‐PA), plasmin–antiplasmin (PAP) complexes and clot lysis time were measured.In contrast to the circadian rhythm with an enhanced fibrinolysis in the evening that was found in the mineral water group, an intake above four glasses of wine inhibited fibrinolysis significantly. After the intake of two glasses no significant disturbance of the circadian rhythm was observed. Five hours after the consumption of six glasses of wine, a dramatic increase occurred of PAI‐1 antigen (77 ± 42 μg L−1 vs. − 5 ± 10 μg L−1 in the mineral water controls; P < 0·001) and PAI‐1 activity (27 ± 15 U mL−1 vs. − 2 ± 3 U mL−1 in mineral water controls; P < 0·001). Despite a rise in t‐PA antigen, t‐PA activity dropped (− 0·5 ± 0·2 U mL−1 vs. − 0·1 ± 0·2 in controls; P < 0·001) as did PAP complexes (− 103 ± 55 μg L−1 vs. − 26 ± 57 μg L−1 in controls; P < 0·01). After the consumption of eight glasses of wine, the clot lysis assay indicated continued inhibition of fibrinolysis the following morning.Drinking a large amount of alcohol in the evening results in an acute inhibition of fibrinolysis, persisting the following morning. This may predispose to accelerated atherosclerosis and set the stage for thrombotic coronary events, explaining the higher cardiovascular mortality risk in binge drinkers.
Platelet‐associated and secreted PAF‐acetylhydrolase activity in patients with stable angina: sequential changes of the enzyme activity after angioplasty
Authors: Goudevenos J. , Tselepis A. D. , Vini M. P. , Michalis L. , Tsoukatos D. C. , Elisaf M. , Ninio E. , Sideris D. A. 
Published: March 2003

BackgroundPlatelet‐activating factor (PAF), the lipid mediator of inflammation and potent platelet agonist, can be hydrolysed and inactivated by PAF‐acetylhydrolase (PAF‐AH). We investigated the PAF‐AH activity in relation to PAF formation in platelets from patients with stable angina undergoing elective percutaneous transluminal coronary angioplasty (PTCA).Twenty‐seven patients with stable angina, undergoing PTCA, and 30 age‐ and sex‐matched controls were studied. The platelet‐associated and secreted PAF‐AH activity was measured, before PTCA, as well as at 4 h, 48 h and 6 months afterwards. PAF formation by thrombin‐stimulated platelets and the platelet aggregation responses to PAF and ADP were also determined.ResultsThe PAF‐AH activity secreted by thrombin‐stimulated platelets before PTCA (in pmol/109 cells/h) was significantly higher compared to controls (892 ± 222 vs. 624 ± 144, P < 0·001). The enzyme activity was not altered at 4 h after PTCA, but was significantly increased at 48 h (1284 ± 312, P < 0·005) to return to the levels observed in the control group 6 months afterwards. Detectable levels of PAF in thrombin‐stimulated platelets were found only at 6 months after PTCA. Furthermore, the cell‐associated enzyme activity in resting platelets before PTCA was significantly lower compared with controls. Unlike in controls, the platelet‐associated enzyme activity in the patient group was not increased after stimulation with thrombin and it was associated by a platelet hyperaggregability to PAF. Both the intact cell‐associated activity and the platelet hyper‐reactivity to PAF were restored at 6 months after PTCA.ConclusionsAlterations in the platelet PAF‐AH activity, which affect the PAF formation in thrombin‐stimulated platelets and are associated by an increased aggregatory response to PAF, are observed in patients with stable angina and are completely restored after PTCA.
The 13C/2H‐glucose test for determination of small intestinal lactase activity
Authors: Vonk R. J. , Stellaard F. , Priebe M. G. , Koetse H. A. , Hagedoorn R. E. , De Bruijn S. , Elzinga H. , Lenoir‐Wijnkoop I. , Antoine J.‐M. 
Published: March 2003

To diagnose hypolactasia, determination of lactase enzyme activity in small intestinal biopsy material is considered to be the golden standard. Because of its strongly invasive character and the sampling problems, alternative methods have been looked for.We analysed the 13C‐glucose response in serum after consumption of 25 g of naturally enriched 13C‐lactose. As an internal standard, 0·5 g of 2H‐glucose was added and the 2H‐glucose response in serum was measured simultaneously. The studies were performed in healthy volunteers with a background of genetically determined lactase nonpersistence (n = 12; low lactase activity) and lactase persistence (n = 27; high lactase activity). The results were compared with those of the lactose hydrogen breath test, the lactose 13CO2 breath test and the previously described 13C‐lactose digestion test.After consumption of 13C‐lactose and 2H‐glucose, the mean ratio 13C‐glucose/2H‐glucose concentration in serum at 45–75 min was 0·26 ± 0·09 in the low lactase activity group and 0·93 ± 0·17 in the high lactase activity group (P < 0·01). Threshold of the ratio between digesters and maldigesters was calculated as 0·46. Accuracy of the new test was superior to all other tests.We conclude that the 13C/2H‐glucose test has the potential of determining the small intestinal lactase activity in vivo and of estimating the amount of lactose which is digested in the small intestine.
IgG subclasses of anti Saccharomyces cerevisiae antibody in inflammatory bowel disease
Authors: Oshitani N. , Hato F. , Jinno Y. , Sawa Y. , Nakamura S. , Matsumoto T. , Seki S. , Kitagawa S. , Arakawa T. 
Published: March 2003

Elevation of serum anti Saccharomyces cerevisiae antibody (ASCA) has been reported in patients with Crohn's disease. We analysed the subclasses of Immunoglobulin (Ig) G reaction in ASCA in sera from patients with inflammatory bowel disease, healthy controls, and patients with intestinal Behçet's disease.Serum samples were obtained from 29 patients with Crohn's disease, 30 patients with ulcerative colitis, 7 patients with intestinal Behçet's disease, and 12 healthy controls. Serum IgG subclasses IgG1, IgG2, IgG3, and IgG4 of ASCA were analysed using ELISA.IgG4 ASCA was significantly increased in patients with inflammatory bowel disease. In patients with intestinal Behçet's disease, IgG1, IgG3, and IgG4 ASCA were increased.Differential responses, in terms of subclasses in ASCA, were found in patients with inflammatory bowel disease and patients with intestinal Behçet's disease, which may represent different pathophysiologies of these intestinal inflammatory diseases.