bluuebunny/crossref_metadata_2025_split huggingface dataset:
Pentoxifylline Contributes to the Hepatic Cytoprotective Process in Rats Undergoing Hepatic Ischemia and Reperfusion Injury
Authors: Aslan A. , Karagüzel G. , Çelik M. , Uysal N. , Yücel G. , Melikoglu M. 
Published: April 2003

<i>Aim:</i> Considerable efforts have been made to find and/or eliminate the underyling causes of hepatic ischemia-reperfusion injury, but many points are still unclear. Pentoxifylline-related cytoprotection is one of these unclear points. Our study tests the effects of pentoxifylline on the hepatic cytoprotective process in an experimental model. <i>Materials and Methods:</i> The animals were divided into two groups: (1) placebo-pretreated rats and (2) pentoxifylline-pretreated rats. After pretreatment, all rats underwent the hepatic ischemia-reperfusion procedure which was performed by clamping the hepatoduodenal ligament. To evaluate the liver injury, serum levels of alanine transaminase (ALT) and aspartate transaminase (AST), and liver tissue levels of prostaglandin E<sub>2</sub> (PGE<sub>2</sub>) were measured before ischemia, immediately after ischemia and immediately after reperfusion. <i>Results: </i>Before ischemia and immediately after ischemia, there were no significant differences between ALT and AST levels of groups 1 and 2 (p >0.05). However, at the end of reperfusion, ALT and AST levels of group 2 were significantly decreased when compared with group 1 (p < 0.05 and p < 0.01, respectively). Additionally, tissue levels of PGE<sub>2</sub> that were obtained before ischemia, immediately after ischemia and immediately after reperfusion in group 2 were significantly higher than those of group 1 (p < 0.001). <i>Conclusion:</i> Pentoxifylline reduces reperfusion injury of the liver through significantly decreased transaminase levels, and contributes to hepatic cytoprotection by increasing tissue levels of PGE<sub>2</sub> significantly. These effects reflect the role of tissue PGE<sub>2</sub> in pentoxifylline-related hepatoprotection against ischemia-reperfusion injury of the liver.
Dye-Staining Stereomicroscopic Examinations for Fine Mucosal Structures of the Gallbladder
Authors: Aoki Tatsuya , Inoue Keiichiro , Tsuchida Akihiko , Kasuya Kazuhiko , Koyanagi Yasuhisa 
Published: April 2003

<i>Background:</i> In order to diagnose an unsuspected gallbladder carcinoma and to examine whether a differential diagnosis could be made between cancer and noncancerous lesions during surgery, we evaluated the findings of fine structures of various types of gallbladder mucosa. <i>Methods:</i> We used stereomicroscopy with a dye-contrast technique under water and measured the maximum blood vessel diameters of the gallbladder mucosa: normal gallbladder, chronic cholecystitis, and carcinoma. <i>Results:</i> All normal gallbladders showed fine-reticular-type findings. In chronic cholecystitis, 5.8% of the specimens (n = 69) had fine reticular type, 87.0% had rough reticular type, and 7.2% had atrophic type. All the cases of adenomyomatosis (n = 16) showed rough reticular type. In eight specimens of pancreaticobiliary maljunction, 75% of them showed high reticular type, and the other 25% showed papillary type. The two adenoma specimens showed fine granular type. In five gallbladder carcinomas, the lattice-like pattern completely disappeared and showed rough granular type. The average of maximum vessel diameters in the gallbladder mucosa were 41.0 µm in normal gallbladders, 99.1 µm in patients with chronic cholecystitis, and 614.8 µm in patients with a carcinoma. There were significant differences among them (p < 0.05). <i>Conclusion:</i> This study showed that differential diagnosis between cancer and noncancerous lesion is possible by dye-staining mucosal pattern and measurement of maximum vessel diameters by stereoscopic examination.
The Corrugated Esophagus, a Sign of Severe Reflux Disease: Radiographic and Endoscopic Appearance
Authors: Low Vincent H.S. , O’Connor J. Barry 
Published: April 2003

<i>Purpose:</i> To present the appearance of esophageal scarring resulting in a corrugated configuration seen on barium radiographs and through the endoscope. <i>Materials and Methods:</i> Barium radiographs and endoscopic images obtained in 8 patients with a fixed deformity of the esophagus which resulted in a corrugated pattern were retrospectively reviewed. All patients (6 males, 2 females) presented long histories of gastroesophageal reflux disease; they were aged 29–84 (mean 46.0) years. Six patients complained of obstructive symptoms (dysphagia or recurrent food impactions). <i>Results:</i> All of the lesions occurred in the mid or distal esophagus, with an average length of 11.1 (range 4–22) cm, and an average diameter of 15.4 (range 9–22) mm. Additional findings included hiatal hernia (n = 6), distal esophageal scarring (n = 3), esophageal fold thickening (n = 1) and intramural pseudodiverticula (n = 1). <i>Conclusion:</i> The finding of a corrugated pattern of the esophagus is suggestive of chronic severe gastroesophageal reflux disease. The reduction in esophageal caliber as a consequence often leads to symptomatic dysphagia.
NFκB Signaling in Posthypoxic Endothelial Cells: Relevance to E-Selectin Expression and Neutrophil Adhesion
Authors: Kokura Satoshi , Rhoads Carol Ann , Wolf Robert E. , Yoshikawa Toshikazu , Granger D. Neil , Aw Tak Yee 
Published: April 2003

Our previous studies have implicated the nuclear transcription factor ĸB (NFĸB) in the regulation of adhesion molecule expression in endothelial cells exposed to anoxia-reoxygenation (A/R) or a redox imbalance. The objectives of this study were (1) to define the kinetics of NFĸB activation by examining IĸBα degradation and the nuclear translocation of p65 in response to A/R or redox imbalance (induced by treatment of cells with diamide and buthionine sulfoximine) and (2) to determine whether the signal for IĸBα degradation, nuclear translocation of p65, and E-selectin-mediated neutrophil adhesion is related to the activity of protein tyrosine kinase (PTK), protein tyrosine phosphatase (PTPase) and/or protein kinase C (PKC). The results demonstrate that both A/R and redox imbalance led to IĸBα degradation within 30 min and the concomitant appearance of p65 in the nucleus, consistent with rapid cytosolic activation of NFĸB and subsequent nuclear translocation of the activated p65 subunit. Inhibition of PKC blocked IĸBα degradation and p65 translocation in A/R-challenged, but not redox-altered, endothelial cells. However, both A/R- and redox-induced NFĸB activation was blocked by inhibition of PTK. Similarly, A/R-induced E-selectin expression and neutrophil-endothelial cell adhesion were blocked by inhibition of PKC or PTK, while only PTK inhibited the redox-induced adhesion response. Pretreatment of cells with N-acetyl cysteine effectively blocked A/R- or redox-induced IĸB degradation and significantly attenuated the respective neutrophil adhesion responses. Collectively, these findings indicate that A/R-induced E-selectin expression and neutrophil-endothelial cell adhesion are mediated by both PKC and PTK, which signal rapid activation of NFĸB. This A/R-induced NFĸB signaling response appears to be mediated, at least in part, by intracellular redox imbalance.
Reduced PO<sub>2</sub> and Adenosine Formation Preserve Arteriolar Nitric Oxide Synthesis during Sympathetic Constriction in the Rat Intestine
Authors: Sauls Bryan A. , Boegehold Matthew A. 
Published: April 2003

Previous reports by this laboratory have indicated that a flow-dependent fall in arteriolar wall PO<sub>2 </sub>may be a stimulus for the sustained release of endothelial nitric oxide (NO) during sympathetic vasoconstriction in the superfused rat intestine. In this study, we tested the hypothesis that locally formed adenosine serves as the link between the fall in local PO<sub>2</sub> and NO synthesis under these conditions. Adenosine applied via pressurized micropipettes directly onto the wall or at a distance of 25 µm from the wall of first-order arterioles (resting diameter = 54 ± 1 µm) elicited dose-dependent dilations of 15–46% that were significantly reduced by the NO synthase inhibitor N<sup>G</sup>-monomethyl-<i>L</i>-arginine (L-NMMA, 10<sup>–4</sup><i>M</i>). Arteriolar responses to sympathetic nerve stimulation were enhanced by 57–66% in the presence of L-NMMA or when tissue PO<sub>2</sub> was prevented from falling under a high O<sub>2</sub> superfusate. Adenosine deaminase (2.0 U/ml) or the selective A<sub>1</sub> receptor antagonist 8-cyclopentyl-1,3-dipropylxanthine (4 × 10<sup>–4</sup><i>M</i>) completely blocked the enhancing effect of L-NMMA on sympathetic constriction. These results are consistent with the hypothesis that the fall in arteriolar wall and/or tissue PO<sub>2</sub> that accompanies sympathetic arteriolar constriction in the rat intestine can lead to local adenosine production, which in turn preserves endothelial NO release.
Life and Death Cell Labeling in the Microcirculation of the Spontaneously Hypertensive Rat
Authors: Lim H.H. , DeLano F.A. , Schmid-Schönbein G.W. 
Published: April 2003

Spontaneously hypertensive rats (SHRs) have elevated numbers of apoptotic cells. However, the extent and pattern of cell death at the microvascular level is unexplored. We developed a technique to determine early forms of cell death in vivo in the mesentery by use of the life/death indicator ethidium bromide (EB). The mesenteric microvasculature was superfused with 5 µ<i>M</i> EB for a period of 3 min, rinsed and immediately viewed by digital fluorescence microscopy. EB-positive cell structures were observed both in the wall of microvessels as well as in the tissue parenchyma. The microvessels had about 2–4 EB-positive cell structures per 100 µm of vessel length. Larger arterioles (>25 µm) in the SHR had an increased EB-positive structure density. After normalization of the blood pressure in the SHR with adrenalectomy, no significant differences remained between Wistar-Kyoto (WKY) rats and SHRs. After dexamethasone treatment, the adrenalectomized SHRs had a higher EB-positive cell density in the smaller class of microvessels than the WKY rats. In addition, EB-positive cell fragments (0.5–2 µm) were observed in the mesentery microvessel wall, and with TUNEL labeling, they were demonstrated to represent DNA fragments. The percentage of microvessels with EB-positive fragments was higher in the SHR arterioles and capillaries. Capillaries and larger venules (>30 µm) in the SHR had higher levels of cell fragments per vessel length. After adrenalectomy, no significant differences remained between WKY rats and SHRs in any of the mcirovessel categories. When adrenalectomized rats were treated with dexamethasone, a higher number of EB-positive fragments was detected in the wall of SHR capillaries. These results indicate that the mesentery microcirculation in both strains is subject to an early and nonuniform pattern of cell death, as detected by EB, but is enhanced in selected individual microvascular segments of the SHR by a glucocorticoid-driven mechanism.
Assessment of the Peripheral Microcirculation Using Computer-Assisted Venous Congestion Plethysmography in Post-Traumatic Complex Regional Pain Syndrome Type I
Authors: Schürmann Matthias , Zaspel Johannes , Gradl Georg , Wipfel Alexander , Christ Frank 
Published: April 2003

In complex regional pain syndrome type I (CRPS-I), edema of the affected limb is a common finding. Therefore, the changes in macro- and microcirculatory parameters were investigated to elucidate the underlying pathophysiology. Twenty-four patients with post-traumatic CRPS-I and 25 gender- and age-matched healthy subjects were examined by means of an advanced computer-assisted venous congestion strain-gauge plethysmograph. The recording of the volume response of the forearm to a stepwise inflation of an occlusion cuff placed at the upper arm enabled the calculation of the arterial blood flow into the arm (Q<sub>a</sub>), the vascular compliance (C), the peripheral venous pressure (P<sub>v</sub>), the isovolumetric venous pressure (P<sub>vi</sub>; = hydrostatic pressure needed to achieve net fluid filtration) and the capillary filtration capacity (CFC) – an index of microvascular permeability. The study revealed no difference in any of the parameters between the right and left hand of healthy subjects. In CRPS-I patients, however Q<sub>a</sub>, P<sub>v</sub>, P<sub>vi</sub> and CFC were significantly (p < 0.01/0.001) elevated in the affected arm (Q<sub>a</sub> 11.2 ± 7.0 ml min<sup>–1</sup> 100 ml<sup>–1</sup>, P<sub>v</sub> 20.2 ± 8.1 mm Hg, P<sub>vi</sub> 24.7 ± 4.2 mm Hg, CFC 0.0058 ± 0.0015 ml min<sup>–1</sup> 100 ml<sup>–1</sup> mm Hg<sup>–1</sup>) compared to the unaffected arm (Q<sub>a</sub> 4.2 ± 2.4 ml min<sup>–1</sup> 100 ml<sup>–1</sup>, P<sub>v</sub> 10.0 ± 5.1 mm Hg, P<sub>vi</sub> 13.2 ± 3.7 mm Hg, CFC 0.0038 ± 0.0005 ml min<sup>–1</sup> 100 ml<sup>–1</sup> mm Hg<sup>–1</sup>) and the values obtained in healthy controls (Q<sub>a</sub> 5.1 ± 1.3 ml min<sup>–1</sup> 100 ml<sup>–1</sup>, P<sub>v</sub> 10.4 ± 4.3 mm Hg, P<sub>vi</sub> 15.7 ± 3.3 mm Hg, CFC 0.0048 ± 0.0012 ml min<sup>–1</sup> 100 ml<sup>–1</sup> mm Hg<sup>–1</sup>). Whereas the values in the unaffected arm of CRPS-I patients revealed no difference in Q<sub>a</sub>, P<sub>v</sub> and P<sub>vi</sub> but a lower CFC (p < 0.01) compared to those from healthy controls. These results suggest profound changes in both macro- and microvascular perfusion in the affected arm of CRPS-I patients. The high CFC contributes to the edema formation, and combined with the elevated P<sub>vi</sub>, they are in agreement with the hypothesis of an inflammatory origin of CRPS.
Endothelin-1, a Regulator of Angiogenesis in the Chick Chorioallantoic Membrane
Authors: Cruz Amauri , Parnot Charles , Ribatti Domenico , Corvol Pierre , Gasc Jean-Marie 
Published: April 2003

We investigated the angiogenic properties of endothelin-1 (ET-1) using a novel experimental approach involving the constant production and release of ET-1, which was achieved by grafting stably transfected Chinese hamster ovary (CHO) (CHO-ET-1) cell aggregates onto the chorioallantoic membrane (CAM) ectoderm. Macroscopic observation showed that CHO-ET-1 cell aggregates formed highly vascularized nodules surrounded by radially rearranged vessels, with a strong angiogenic response. 5-Bromo-2′-deoxy-uridine (BrdU) studies showed an increase in endothelial cell proliferation in the CAM vasculature around CHO-ET-1 nodules. An angiogenic response was also observed with gelatin sponges containing conditioned medium from CHO-ET-1 cells. The specific involvement of ET-1 in the angiogenic effect mediated by CHO-ET-1 was demonstrated by the reduction or abolition of neovascularized CHO-ET-1 nodules by (1) bosentan, a mixed antagonist of ET<sub>A</sub>/ET<sub>B</sub> receptors, (2) an ET<sub>A</sub> receptor antagonist (Ru69986) and (3) phosporamidon, an inhibitor of endothelin-converting enzyme-1 (ECE-1). We also demonstrated that VEGF was involved in CHO-ET-1-mediated angiogenesis, by using a specific inhibitor of VEGF tyrosine kinase receptor activity (PTK787/ZK 222584), which abolished CHO-ET-1 nodule formation and CAM neovascularization. Thus, our results show that exogenous ET-1 mediates angiogenesis in vivo.
Study on Pancreatic Insufficiency (Chronic Pancreatitis) and Steatorrhea in Japanese Patients with Low Fat Intake
Authors: Nakamura Teruo , Tando Yusuke , Yamada Naoko , Watanabe Taku , Ogawa Yoshiji , Kaji Asako , Imamura Ken-ichi , Kikuchi Hiroaki , Suda Toshihiro 
Published: April 2003

The incidence of steatorrhea is said to be lower and its grade milder in Japanese because their fat intake is lower than that of Europeans and Americans. Failure to take this into account creates difficulties when attempting to compare data on pancreatic exocrine insufficiency in different countries. The authors examined the incidence and grade of steatorrhea in Japanese chronic pancreatitis (CP) patients whose daily fat intake was <40 g (25 patients) or &#8805;40 g (35 patients). In addition, 23 CP patients with steatorrhea and daily fecal fat excretion &#8805;5 g were given a pancreatic enzyme preparation at a dose 3–8 times higher than the usual dose to investigate its effect on fecal fat excretion. Among CP patients whose fat intake was <40 g, the incidence of fecal fat excretion <5 g was 56% and that of fecal fat excretion &#8805;10 g (severe steatorrhea) was 8%. In CP patients whose fat intake was &#8805;40 g, the incidences were 27.9 and 34.9%, respecetively; a significant increase in the number of affected patients was noted when fat intake was &#8805;40 g. The fat absorption rate was 76.2% among patients whose fat intake was <40 g and 77.8% among patients whose fat intake was &#8805;40 g, revealing no significant difference between the two groups. The proportion of CP patients whose fat absorption rate ≦80% was 32% at a fat intake <40 g and 39% at a fat intake &#8805;40 g, revealing no significant difference between the two groups.
Autoimmunity to Keratinocyte Acetylcholine Receptors in Pemphigus
Authors: Grando Sergei A. 
Published: April 2003

Pemphigus autoimmunity is not limited to antides- moglein antibodies. Nondesmoglein antibodies induce pemphigus-like lesions in neonatal mice. Acantholytic activity of pemphigus IgG harbors pharmacologic effects on keratinocyte shape and adhesion. Acantholytic antireceptor autoantibodies target: (1) a novel human α9 acetylcholine receptor regulating keratinocyte adhesion, and (2) pemphaxin, a novel keratinocyte annexin-like molecule binding acetylcholine. A ‘multiple-hit’ hypothesis reconciles recent findings of anti-acetylcholine-receptor autoimmunity in pemphigus and the fact that pemphigus patients also develop autoantibodies to adhesion molecules. The antiacantholytic activity of cholinergic agonists suggests a novel avenue for the development of a nonhormonal treatment of pemphigus.
<i>Scytalidium dimidiatum</i> Melanonychia and Scaly Plantar Skin in Four Patients from the Maghreb: Imported Disease or Outbreak in a Belgian Mosque?
Authors: Arrese J.E. , Piérard-Franchimont C. , Piérard G.E. 
Published: April 2003

<i>Scytalidium dimidiatum</i> is a geophilic dematiaceous, non-dermatophyte mould that can become a pathogen for plants and humans particularly in tropical and subtropical regions. We report 4 cases of <i>S. dimidiatum</i> onychomycosis presenting clinically as thickened and dark toenails. The skin of the soles was scaly. The time and location of the contaminations were uncertain. Indeed, the patients were ancient immigrants from the Maghreb to Belgium. They were also regularly travelling to their countries of origin. They were also often barefoot in the same Belgian mosque. The disease was unresponsive to current oral antifungal treatments.
Asthma, Rhinitis and Dermatitis Triggered by Fungal Infection: Therapeutic Effects of Terbinafine
Authors: Hürlimann A. , Fäh J. 
Published: April 2003

We report 2 atopic patients suffering from tinea unguium caused by <i>Trichophyton rubrum</i>. In addition, both patients had symptoms of allergies: one had perennial rhinoconjunctivitis and bronchial asthma, the other had chronic dermatitis of the face and neck. In both cases, their allergy symptoms improved dramatically during oral therapy with the antifungal agent terbinafine (250 mg/day) and relapsed after its discontinuation.
Relevance of Underlying Disease and Bacterial <i>vacA</i> and <i>cagA</i> Status on the Efficacy of <i>Helicobacter pylori</i> Eradication
Authors: Rudi Jochen , Reuther Susanne , Sieg Andreas , Hoerner Martin , Stremmel Wolfgang 
Published: April 2003

<i>Aim:</i> To study the effects of <i>Helicobacter pylori</i> associated diseases and the bacterial <i>vacA</i> and <i>cagA</i> statuses on the efficacy of <i>H. pylori</i> eradication. <i>Methods:</i> A prospective study in a consecutive series of outpatients of a gastroenterological institution and of a primary practice. A series of 146 <i>H. pylori</i> positive patients with peptic ulcer disease (PUD; n = 40) or nonulcer dyspepsia (NUD; n = 106) were evaluated. <i>H. pylori vacA</i> genotpyes and <i>cagA</i> status were determined directly in gastric biopsy specimens by polymerase chain reaction. The patients were treated with triple-therapy regimens consisting of a proton pump inhibitor and two antibiotics twice daily for 7 days. Reevaluation of <i>H. pylori</i> was determined 4–5 weeks later by endoscopy or <sup>13</sup>C urea breath test. <i>Results:</i> 123 patients completed the study. In 8 patients, colonization with two or more <i>H. pylori</i> strains was found. The overall cure rate was 84.6% (104/123). The eradication rates were significantly higher in patients with PUD (94.4%, 34/36) than in those with NUD (81.6%, 71/87; p < 0.05). In patients with <i>cagA-</i>positive<i> H. pylori</i> strains, the eradication rate was 89.0% (73/82) as compared with 78.8% (26/33) in those with <i>cagA-</i>negative strains (p = 0.15). The <i>vacA</i> genotype had no effect on the efficacy of <i>H. pylori</i> eradication. <i>Conclusion:</i> Using 1-week triple-therapy regimens, treatment of <i>H. pylori</i> infection is more effective in patients with PUD than in those with NUD.
Relationship between the Effects of Cisapride on Gastric Emptying and Plasma Glucose Concentrations in Diabetic Gastroparesis
Authors: Horowitz Michael , Jones Karen L. , Harding Philip E. , Wishart Judith M. 
Published: April 2003

<i>Background/Aims: </i>The effect of erythromycin on gastric emptying is attenuated during hyperglycaemia. The aim of this study was to determine in patients with diabetic gastroparesis whether the effect of cisapride on gastric emptying of solids and liquids is influenced by the plasma glucose concentration. <i>Methods:</i> Nineteen patients with type 1 diabetes mellitus, who had delayed gastric emptying of solids and/or liquids, were studied. On 2 separate days, each patient received cisapride (20 mg) or placebo orally 60 min before scintigraphic measurement of gastric emptying of a mixed solid (ground beef) and liquid (dextrose) meal. The plasma glucose concentrations were measured at –5, 30, 60, 90, and 120 min during each gastric emptying measurement. <i>Results:</i> Cisapride accelerated both solid (retention at 100 min 43 ± 4 vs. 69 ± 4%, p < 0.001) and liquid (T<sub>50</sub> 27 ± 2 vs. 39 ± 2 min, p < 0.001) gastric emptying. The mean plasma glucose level was not significantly different after placebo when compared with cisapride (19.5 ± 1.1 vs. 18.2 ± 1.0 mmol/l). The change in the 50% emptying time (T<sub>50</sub>) for liquid, but not solid, emptying was related (r = 0.55, p = 0.01) to the change in the plasma glucose AUC from 0 to 30 min between the placebo and cisapride tests, i.e., the acceleration was greater if the plasma glucose concentration was relatively less during the gastric emptying test performed on cisapride. <i>Conclusion:</i> The effect of cisapride on gastric emptying, at least that of liquids, in patients with diabetic gastroparesis appears to be dependent on the plasma glucose concentration.