bluuebunny/crossref_metadata_2025_split huggingface dataset:
Oral Clearance and Acid Production of Dairy Products during Interaction with Sweet Foods
Authors: Linke Harald A.B. , Riba Hicham K. 
Published: April 2003

Oral clearance and acid production were observed in 30 volunteers following the ingestion of sharp cheddar cheese (CC) and in 9 volunteers following the ingestion of milk chocolate (MC) and low-fat yogurt, and then when MC was eaten immediately after CC (CC/MC) and when CC was eaten following MC (MC/CC). After each test food or food combination had been ingested the volunteers were monitored at five different tooth sites. At each site, using an absorbent paper point, 4 oral fluid samples were collected at 30 min intervals. The five paper points from each sampling occasion were pooled, extracted with 1 ml of water and analyzed qualitatively and quantitatively for both carbohydrates and organic acids using HPLC. Data obtained for each food was averaged and subjected to statistical evaluation. With the CC, glucose clearance was prolonged, due to intermediate lactose degradation into galactose and glucose. The quantity of lactic acid produced during the four intervals was monitored for each of the test foods and their combinations. <i>Results:</i> CC, MC, CC/MC, MC/CC 30 min after ingestion: 1.64, 3.47, 4.68, 2.97; after 60 min: 1.30, 1.24, 1.28, 1.43; after 90 min: 1.58, 1.02, 0.76, 0.43; after 120 min: 1.27, 0.90, 0.70, 0.42 mmol lactic acid/l oral fluid, respectively. The average total amount of lactic acid obtained during the two hour test period was (highest) CC/MC > MC > CC > MC/CC (lowest). The lowest amount of intra-oral lactic acid was observed (Student’s t test, p < 0.05) when cheddar cheese (CC) was eaten immediately after the milk chocolate (MC). <i>Clinical Significance:</i> Consumption of cheese (cheddar), immediately after a sweet meal, significantly reduces (approx. 30%) the amount of lactic acid produced in the oral cavity, when compared to the amount of acid obtained from the sweet food alone.
Long-Term On-Line Hemodiafiltration Reduces Predialysis Beta-2-Microglobulin Levels in Chronic Hemodialysis Patients
Authors: Lin Chun-Liang , Yang Chih-Wei , Chiang Chin-Chen , Chang Ching-Tung , Huang Chiu-Ching 
Published: April 2003

<i>Background:</i> Hemodiafiltration (HDF) is effective in delaying the surgical need for carpal tunnel syndrome in chronic hemodialysis patients, however, predialysis β<sub>2</sub>-microglobulin levels were not reduced in most short-term studies. The aim of this study was to assess the effect of long-term and differing frequencies of on-line HDF on serum β<sub>2</sub>-microglobulin levels in comparison to high-flux hemodialysis (HD). <i>Methods:</i> One hundred and twelve patients in the Chang Gung Memorial Hospital Dialysis Unit were divided into three groups to receive different frequencies of on-line HDF alternating with high-flux HD. Group 1 was treated once with HDF and twice with high-flux HD per week (n = 21). Group 2 was treated twice with HDF and once with high-flux HD per week (n = 33). Group 3 was treated with HDF three times per week (n = 58). Analysis was performed to compare the serum β<sub>2</sub>-microglobulin levels in these groups and to high-flux HD. <i>Results:</i> After receiving HDF for a mean of 7.9 months, group 3 patients had a reduced predialysis β<sub>2</sub>-microglobulin level (22.2 ±5.3 vs. 34.8 ±6.3 mg/l, p < 0.001), postdialysis β<sub>2</sub>-microglobulin level (6.3 ± 2.0 vs. 13.8 ± 6.8 mg/l, p < 0.001) and an increased β<sub>2</sub>-microglobulin reduction rate (76.1 ± 5.6 vs. 61.1 ± 13.3%, p = 0.03) when compared to high-flux HD. A significant improvement in URR (p = 0.0004), Kt/V (p = 0.0002) and TAC urea levels (p = 0.006) but not nPCR (p = 0.122) was found after patients had been treated with on-line HDF. The β<sub>2</sub>-microglobulin reduction rate was positively correlated with the overall volume of the replacement solution per session (p < 0.0001). Patients in group 3 had lower predialysis β<sub>2</sub>-microglobulin levels than those in group 1 and group 2 (22.2 ± 5.3 vs. 25.2 ± 7.2 vs. 26.0 ± 4.2 mg/l, p = 0.02). Furthermore, an inverse correlation was found between the predialysis β<sub>2</sub>-microglobulin level and the duration of HDF, if patients were treated for more than 12 months (p = 0.031). <i>Conclusion:</i> On-line HDF has an increased dialysis efficiency compared to high-flux dialysis. Long-term HDF further reduced predialysis β<sub>2</sub>-microglobulin levels, thus, it may provide an improved modality for renal replacement therapy.
Prevention of Heart Failure
Authors: Cohn J.N. 
Published: April 2003

Heart failure (HF) is a progressive process and the objective of treatment should be to prevent progression. Treatment should begin at the stage of asymptomatic left ventricular dysfunction (LVD), not only to reduce mortality but also to preserve exercise capacity and quality of life. To prevent clinical progression in patients with asymptomatic LVD or HF, left ventricular remodelling and dilatation must be prevented. The SOLVD prevention trial – the only clinical trial on the prevention of HF – showed that ACE inhibition significantly reduced the development of HF, but did not significantly reduce mortality. Plasma norepinephrine is elevated in patients with asymptomatic LVD, is further elevated in patients with overt HF, and is correlated with increased mortality. Inhibition of the sympathetic nervous system by administration of β-blocking agents is therefore a logical treatment for patients with HF or asymptomatic LVD. Clinical trials have shown that β-blocking agents increase left ventricular ejection fraction and reduce left ventricular dimensions in patients with HF, indicating regression of left ventricular remodelling. Almost all the patients in these studies were receiving an ACE inhibitor as part of their background medication, therefore the relative efficacy of β-blocking agents and ACE inhibitors in the regression of remodelling is not known. CARMEN, a double-blind, randomised, parallel group study of carvedilol versus enalapril versus carvedilol + enalapril in 450 patients with mild HF, will provide this information.
Effects of Chronic Nitrate Therapy on Left-Ventricular Volume in Patients with Heart Failure Secondary to Coronary Disease Already Treated with Captopril: A Withdrawal Study
Authors: Wieshammer Siegfried , Hetzel Martin , Hetzel Jürgen , Henze Eberhard , Hombach Vinzenz 
Published: April 2003

<i>Objective:</i> This randomized, double-blind, placebo-controlled study with treatment lasting 16 weeks and withdrawal lasting 6 weeks tried to determine whether stopping nitrates has an effect on left-ventricular end-systolic volume in patients with heart failure who were chronically treated with captopril and diuretics. <i>Patients and Methods:</i> The study group comprised 29 patients with previous myocardial infarction, symptoms of mild-to-moderate heart failure, ejection fraction below 40%, no exercise-induced angina and no electrocardiographic signs of ischemia. After all patients had been treated with captopril (target dose: 25 mg twice daily), diuretics and the study drug (target dose: 40 mg isosorbide dinitrate twice daily or placebo) for 16 weeks, the study drug was withdrawn. The patients were then maintained on captopril and diuretics at constant doses for a 6-week withdrawal period. Radionuclide ventriculography with right-heart catheterization was performed at rest and during supine bicycle exercise after 16 weeks of double-blind treatment and at the end of the 6-week withdrawal period. <i>Results:</i> The changes in resting parameters following the withdrawal of the study drug were not different between the groups. At comparable maximum workload (placebo group 68 ± 15 W, nitrate group 68 ± 20 W), nitrate withdrawal caused a decrease in ejection fraction (placebo withdrawal: +0.8 ± 4.0%; nitrate withdrawal: –2.7 ± 4.3%, p < 0.02) and increases in left-ventricular end-diastolic volume (–9 ± 35 vs. 23 ± 48 ml, p < 0.02) and end-systolic volume (–9 ± 33 vs. +24 ± 47 ml; p < 0.01). <i>Conclusion: </i>The addition of nitrates to a baseline therapy with captopril and diuretics might reduce exercise-induced left-ventricular dilatation in patients with heart failure from coronary disease.
A New Guidewire Technique for Difficult Cardiac Catheterization
Authors: Liau Chiau-Suong , Ho Shinn-Ge , Chen Sung-Nan , Yang Li-Fen 
Published: April 2003

<i>Purpose:</i> To propose a simple guidewire technique to resolve the problem of difficulty in advancing catheters or guidewires during vascular and cardiac catheterization. <i>Methods:</i> A 0.035-inch J-tip guidewire was reshaped manually at the distal 7- to 8-cm portion, including the flexible part and 2–3 cm of the stiff part, into zigzag shape. With this modification, the guidewire became much more trackable and could be advanced to the right position. <i>Results:</i> In the past 2 years, this ‘zigzag wire technique’ was applied in cardiac catheterization with high success rates for cases with difficulty in advancing either catheters or guidewires. This wire technique was applied in peripheral arterial tortuosity or stenosis (18 cases, with success in 17), aortic aneurysm (successful in all 7 cases), aortic stenosis (11 cases, successful in 8), and dilated right heart chambers (successful in all 6 cases). No complications resulted from the use of this guidewire technique. <i>Conclusion:</i> This simple method of guidewire modification would be very helpful in difficult vascular and cardiac catheterization when difficulty in advancing catheters or wires was encountered.
Pathophysiology of Acute Ischemic Stroke: New Concepts in Cerebral Embolism
Authors: Futrell Nancy 
Published: April 2003

Cerebral embolism was once thought to be the etiology of only a small percentage of ischemic strokes. In earlier classification schemes stroke was generally referred to as (1) ‘embolic’ (definite only if a source of embolism was proven, suspected if cerebral infarcts were bilateral), (2) ‘hemodynamic’ (if there was a tight carotid stenosis thought to produce stroke by decreased flow past the stenosis or if there was decreased cardiac output or decreased blood pressure), (3) ‘lacunar’ (implying ‘hypertensive small-vessel disease’ if the stroke was small and deep, even though the patient may not have a history of hypertension) and (4) ‘thrombotic’ (if none of the other 3 ‘mechanisms’ could be demonstrated), which was thought to be the major mechanism for stroke.
Controlling Acute Elevation of Plasma Fibrinogen with Ancrod
Authors: Cole C.Wm. 
Published: April 2003

Elevated plasma fibrinogen is an independent risk factor for generalized atherosclerosis. Markers of elevated fibrinogen include cigarette smoking, diabetes, hypertension and a sedentary life-style; all are associated with vascular occlusive disease. A variety of molecular mechanisms have been proposed by which fibrinogen could directly influence the vessel wall [1]. In addition, fibrinogen degradation products stimulate macrophages to produce a variety of factors including interleukin 6, an important mediator of inflammation. For this reason, atherosclerosis could be described as a low-grade, generalized inflammatory condition of the arterial wall. As illustrated in figure 1, the exact role of fibrinogen in these processes is complex and multifocal. This discussion will focus on the management of acute elevations of fibrinogen using ancrod, a thrombin-like enzyme, that triggers a cascade of normal reactions. When these are carefully controlled, fibrinogen can be safely depleted to achieve clinical benefit.
Glycine Antagonist (GV150526) in Acute Stroke: A Multicentre, Double-Blind Placebo-Controlled Phase II Trial
Authors: Lees K.R. , Lavelle J.F. , Cunha L. , Diener H.C. , Sanders E.A.C.M. , Tack P. , Wester P. 
Published: April 2003

GV150526 is a novel glycine antagonist at the NMDA receptor complex. It is a potent neuroprotective agent in animal models of acute stroke including permanent middle cerebral artery occlusion in the rat. GV150526 was very well tolerated in early human studies. The purpose of this randomised, double-blind, multicentre, placebo-controlled trial was to assess the safety and population pharmacokinetics of GV150526 in patients with a clinical diagnosis of acute stroke. Exploratory assessment of efficacy, quality of life and resource utilisation was also undertaken. Upon clinical diagnosis of acute stroke within 12 h of onset of symptoms, patients were treated with a loading dose of 800 mg GV150526 (or placebo), followed by 5 maintenance doses of 400 mg GV150526 (or placebo) given every 12 h over 3 days. Following observation of asymptomatic hyperbilirubinaemia, the maintenance dose was reduced mid-study to 200 mg. CT/MRI scanning was not mandatory prior to treatment. The study treated 128 patients (38 with GV 800 mg/400 mg, 48 with GV 800 mg/200 mg and 42 with placebo). Fewer patients with mild stroke (NIH scores ≤5) were enrolled in the GV150526-treated groups than in the placebo group (placebo 38%, GV 800 mg/400 mg 18%, GV 800 mg/200 mg 15%). There was also an imbalance in the proportion of patients with haemorrhagic strokes (placebo 5%, GV 800 mg/400 mg 3%, GV 800 mg/200 mg 15%). Mortality at 1 month was unbalanced between treatment groups, being 10, 18 and 17% in the placebo, GV 800 mg/400 mg and GV 800 mg/200 mg groups, respectively (no significant difference). Similarly, adverse events, though consistent with an acute stroke population, appeared more often in the GV 800 mg/200 mg group. Functional outcomes at 1 month also showed imbalances, the percentage of patients with a Barthel Index score of ≧95 at 1 month being 52, 39 and 27% in the placebo, GV 800 mg/400 mg and GV 800 mg/200 mg groups, respectively. These results probably reflect a prognostically significant baseline difference between the groups rather than the effect of GV150526. GV150526 was generally well tolerated in patients with a clinical diagnosis of acute stroke and formal efficacy studies were considered justified.
Antiepileptic Treatment in Patients with Early Postischemic Stroke Seizures: A Retrospective Study
Authors: Gilad Ronit , Lampl Yair , Eschel Yehiel , Sadeh Menachem 
Published: April 2003

Early seizures caused by stroke are a common cause of epilepsy in adults. The protocol for treatment in such a case is not clear. Patients were studied retrospectively after early poststroke seizures. Two groups of patients were compared: one treated group included 35 patients who continued therapy for 2 years; the second group of 23 patients were untreated following a first attack, receiving anticonvulsive therapy only after a second seizure. The data of 61 patients (35 treated and 26 untreated) were analyzed. In the treated group, 24 patients were on treatment with carbamazepine, 9 with valproic acid and 2 with phenytoin. Seizure-free rate after 2 years was 85% in group I and 61% in group II (p = 0.042). Comparing the seizure rate and the event-free period (number/follow-up at risk) during the 2 years of no anticonvulsive therapy, both groups experienced about the same seizure rate (4.8 vs. 6.2%, p = 0.605) and similar seizure-free curve survival analysis (p = 0.85). We conclude that treatment of seizures immediately after the first attack after cerebral infarctions decreases the risk of recurrent seizure during the first 2 years of antiepileptic treatment. This subgroup of patients receiving antiepileptic medication immediately after the first poststroke seizure continues to be at the same rate of risk after treatment was stopped as the untreated group during the first 2 years. Antiepileptic therapy is an option in the medical management of poststroke seizure patients, but has no influence on the development of recurrent seizures after discontinuing medication.
Effect of Patient Weight on the Anticoagulant Response to Adjusted Therapeutic Dosage of Low-Molecular- Weight Heparin for the Treatment ofVenous Thromboembolism
Authors: Wilson S. Jo-Anne , Wilbur Kerry , Burton Erica , Anderson David R. 
Published: April 2003

Data evaluating the safety of using weight-based dosing of low-molecular-weight heparin (LMWH) in obese patients are limited. Some manufacturers have recommended a maximum daily dose of LMWH not to be exceeded. The purpose of this study was to determine if body weight influenced the anticoagulant response to a weight-based dose of LMWH for the treatment of venous thromboembolism. Patients with serum creatinine levels <150 µmol/l receiving the LMWH , dalteparin 200 anti-Xa IU/kg based on actual body weight subcutaneously once daily for the treatment of deep vein thrombosis or pulmonary embolism, were eligible for the study. Patients received a minimum of 5 days LMWH treatment. Patients had peak anti-Xa levels (IL Test Chromogenic assay) measured 3–4 h following their day 3 injection and trough anti-Xa levels measured immediately prior to injections on day 3 and 5. No dose adjustments were made on the basis of the anti-Xa levels. Patients were a priori stratified into three weight classes: (A) within 20% of ideal body weight (IBW) (n = 13); (B) 20–40% of IBW (n = 14), and (C) greater than 40% of IBW (n = 10). The largest patient weighed 190 kg and had a body mass index of 58. Mean daily LMWH doses were 14,030, 17,646 and 23, 565 IU for groups A, B and C, respectively. Mean (SD) trough anti-Xa levels on day 3 were 0.12 (0.05) anti-Xa IU/ml for group A, 0.11 (0.03) anti-Xa IU/ml for group B and 0.11 (0.03) anti-Xa IU/ml for group C (p > 0.2). Similar trough anti-Xa levels were observed on day 5. Mean (SD) peak anti-Xa levels on day 3 were 1.01 (0.20) anti-Xa IU/ml, 0.97 (0.21) anti-Xa IU/ml and 1.12 (0.22) anti-Xa IU/ml for groups A, B and C, respectively (p > 0.2). No thromboembolic or bleeding complications occurred during LMWH therapy in any patients. These findings suggest that body mass does not appear to have an important effect on the response to LMWH up to a weight of 190 kg in patients with normal or near normal renal function.
Estradiol Stimulates Gene Expression of Norepinephrine Biosynthetic Enzymes in Rat Locus coeruleus
Authors: Serova Lidia , Rivkin Mark , Nakashima Akira , Sabban Esther L. 
Published: April 2003

Gender-specific differences in susceptibility to a number of disorders related to catecholaminergic systems, including depression and hypertension, have been postulated to be mediated, at least in part, by estrogens. In this study, we examined if estrogens may regulate gene expression of norepinephrine biosynthetic enzymes. Administration of five injections of 15 or 40 µg/kg estradiol benzoate to ovariectomized (OVX) female rats elicited a dose-dependent elevation in mRNA levels of tyrosine hydroxylase (TH) in locus coeruleus, to as great as 3-fold over control. Dopamine β-hydroxylase (DBH) mRNA levels were also similarly increased. To examine the mechanism, PC12 cells were cotransfected with luciferase reporter constructs under control of DBH or TH promoters [pDBH/Luc(–2,236/+21) or pTH/Luc(–272/+27 or –773/+27)] with an expression vector for estradiol receptor α. The cells were treated with 17β-estradiol (E<sub>2</sub>) for 12–36 h. E<sub>2</sub> triggered a several fold increase in luciferase activity under control of the DBH promoter in a dose-dependent fashion. Omission of estrogen receptor α or addition of the estrogen receptor antagonist ICI 182,780 prevented the DBH promoter-driven increase in luciferase. When E<sub>2</sub> was given with 0.2 m<i>M</i> CPT-cAMP, reporter activity with pDBH/Luc(–2,236/+21) was increased greater than with either treatment alone. In contrast, addition of E<sub>2</sub> to cells transfected with pTH/Luc(–272/+27) elicited no change in basal luciferase activity nor in the response to 0.2 m<i>M</i> CPT-cAMP. These findings are the first to reveal that estrogen can stimulate DBH gene expression. Differing mechanisms may underlie the regulation of TH and DBH gene expression by estrogens.
Mucin-Like Glycoprotein Associated with Photoreceptor Cells in the Postnatal Developing Rat Retina
Authors: Uehara Fumiyuki , Ohba Norio , Ozawa Masayuki 
Published: April 2003

<i>Purpose:</i> To examine the developmental expression of mucin-like glycoprotein associated with photoreceptor cells (MLGAPC), and to confirm that MLGAPC with a relative mass of 120 and 135 kD correspond to the cone and rod types, respectively. <i>Methods:</i> We isolated the cDNA of the core protein of rat MLGAPC, prepared an anti-rat MLGAPC core protein antibody and then examined the expression of the MLGAPC core protein in postnatal developing rat retinas by means of Western blotting and immunohistochemistry. <i>Results:</i> On postnatal early days when cone photoreceptor cells were thought to be developing, MLGAPC was detected as a single band of 120 kD and was found to be positive in the apical portion of the neuroblastic layer. After postnatal day 7, when rod photoreceptor cells were developing, MLGAPC was detected as a minor band of 120 kD and an additional major band of 135 kD and was present throughout the differentiated photoreceptor and outer plexiform layers. <i>Conclusions:</i> The present findings revealed the developmental expression of MLGAPC and confirmed that MLGAPC of 120 and of 135 kD correspond to the cone and rod types, respectively. This demonstration is advantageous for studying the physiological roles of MLGAPC in the photoreceptor and outer plexiform layers, since the cone- and rod-associated glycoproteins should be investigated separately.
Acute Effects of Serotonin on Rat Bladder Contractility
Authors: Kim Hyung Jee , Lee Gilho , Kim Dong Hee , Lee Suk Jae , Yoon Duck Ki , Cho Jae Heung 
Published: April 2003

<i>Introduction:</i> The purpose of this study is to investigate in vitro the effects of serotonin on the rat detrusor. In particular, it examines which drugs inhibit the serotonin-induced detrusor contractions. <i>Materials and Methods:</i> Isometric tension changes of isolated rat bladder muscle strips were recorded in an organ bath using a force transducer. Acute effects of serotonin (0.0001–0.01 m<i>M</i>) on resting tension were assessed. Electrical field stimulation (EFS); bethanechol (0.0001–0.01 m<i>M</i>); ATP (1–3 m<i>M</i>)- or KCl (63.5–254 m<i>M</i>)-induced contractions using an application in an organ bath were compared with serotonin-induced contractions. In order to examine the action mechanism of serotonin-induced stimulation, EFS-, bethanechol-, ATP- or KCl-induced contraction on serotonin treatment (0.001 m<i>M</i>) was assessed and serotonin (0.001–0.1 m<i>M</i>) was cumulatively added to the organ bath following preincubation with propranolol, ketanserin, tropisetron, propiverine, sodium nitroprusside or doxazosin. <i>Results:</i> The serotonin-induced response has two phases: an initial transient contraction and a prolonged tonic phase. Serotonin produced a reversible and dose-dependent contraction of the detrusor strips. Responses to bethanechol significantly increased with a concentration of 0.001 m<i>M</i> serotonin (p < 0.05). There was no effect on the responses to ATP, KCl, or EFS on 0.001 m<i>M</i> serotonin. The 5-HT<sub>2</sub> receptor is mainly responsible for serotonin-induced contractions of the detrusor (p < 0.05), while the 5-HT<sub>1</sub> receptor is partially responsible. Doxazosin and propiverine each significantly suppressed the response to serotonin, while sodium nitroprusside and tropisetron each had no effect (p < 0.05). <i>Conclusions:</i> Because the 5-HT<sub>2</sub> antagonist blocked the effect of serotonin-induced bladder contractions and the stimulation of the adrenoreceptors, the 5-HT<sub>2</sub> antagonist seems to improve lower urinary tract symptoms.