bluuebunny/crossref_metadata_2025_split huggingface dataset:
Antibiotic Susceptibility Testing (Agar Disk Diffusion and Agar Dilution) of Clinical Isolates of <i>Enterococcus faecalis</i> and <i>E. faecium:</i> Comparison of Mueller-Hinton, Iso-Sensitest, and Wilkins-Chalgren Agar Media
Authors: Traub Walter H. , Geipel Udo , Leonhard Birgit 
Published: April 2003

Forty-two isolates of <i>Enterococcus faecalis</i> and 56 isolates of <i>Enterococcus faecium,</i> including 8 vancomycin-resistant strains, were examined for comparative susceptibility to 27 antimicrobial drugs with the agar dilution method, employing Mueller-Hinton (MHA), Iso-Sensitest (ISTA), and Wilkins-Chalgren (WCA) agar. The Bauer-Kirby agar disk diffusion method was used to comparatively test 24 of the agents in parallel. The enterococci yielded better growth on ISTA and WCA. However, WCA completely antagonized co-trimoxazole and, though less, fosfomycin. Importantly, WCA slightly reduced the activities of teicoplanin (minimal inhibitory concentrations, MICs, raised up to twofold) and vancomycin (MICs raised two- to fourfold) against enterococci and staphylococcal quality control strains. Therefore, WCA was judged unsuitable for susceptibility testing of enterococci. For <i>E. faecalis</i> no discrepancies between agar dilution MICs and inhibition zone diameters were encountered with augmentin, ampicillin, ampicillin-sulbactam, chloramphenicol, mupirocin, oxacillin, teicoplanin, and co-trimoxazole. Overall, MHA yielded fewer very major (category I) and major (category II) discrepancies than ISTA. However, numerous minor (category III), slight (category IV), minimal (category V), and/or negligible (category VI) discrepanices were encountered with ciprofloxacin, doxycycline, erythromycin, fosfomycin, fusidic acid, meropenem, ofloxacin and rifampin. With respect to <i>E. faecium,</i> only cefotaxime, mupirocin, oxacillin, and teicoplanin yielded nondiscrepant results. Several very major (I) and major (II) discrepancies were observed with augmentin, ampicillin, ampicillin-sulbactam, doxycycline, fusidic acid, imipenem, and penicillin G. Minor discrepancies (categories III–VI) were particularly numerous with augmentin, chloramphenicol, ciprofloxacin, doxycycline, and piperacillin. The largest numbers of negligible (VI) discrepancies were noted with fosfomycin, fusidic acid, and ofloxacin. It is recommended to test one cephalosporin (cefuroxime or the like) in parallel for educational purposes and to exclude fosfomycin, fusidic acid, and rifampin from test batteries because of the wide scatter of test results. The large number of minimal (V) discrepancies of ciprofloxacin against <i>E. faecalis,</i> the numerous minor (III) and slight (IV) discrepancies of chloramphenicol against <i>E. faecium,</i> and the not insignificant number of very major (I) and minor (III) discrepancies observed with meropenem against isolates of <i>E. faecalis</i> necessitated proposals for new disk intermediate susceptibility criteria.
Inhibitory Action of Natural Carrageenans on Herpes simplex Virus Infection of Mouse Astrocytes
Authors: Carlucci M.J. , Scolaro L.A. , Damonte E.B. 
Published: April 2003

The effects of the carrageenans 1T1 (λ-type), 1C1 (κ/ι-type) and 1C3 (ιι/ν-type), isolated from the red seaweed <i>Gigartina skottsbergii,</i> on herpes simplex virus type 1 (HSV-1) and type 2 (HSV-2) infection of murine astrocytes were investigated. The three compounds were effective inhibitors of virus replication, as determined by a virus yield inhibition assay, in astrocytes as well as in Vero cells. The 50% inhibitory concentration was in the range of 0.9–3.6 and 0.4–3.2 μg/ml for astrocytes and Vero cells, respectively, whereas the 90% inhibitory concentration ranged from 6.5 to 17.0 μg/ml in astrocytes and from 3.5 to 22.2 μg/ml in Vero cells. No cytotoxicity was detected at concentrations of up to 1,000 μg/ml, indicating high selectivity indices for these compounds. Inhibition of viral cytopathology and antigen expression was also detected in the presence of the carrageenans. The increase in the expression of glial fibrillary acidic protein (GFAP), an activated astrocyte marker, produced during the course of HSV-1 infection in astrocytes, was reversed in the presence of 1C1 and 1C3. By contrast, the λ-carrageenan 1T1 increased the expression of GFAP, independently of HSV-1 infection.
<i>Helicobacter pylori</i> Infection Decreases Gastric Alcohol Dehydrogenase Activity and First-Pass Metabolism of Ethanol in Man
Authors: Simanowski Ulrich A. , Egerer Gerlinde , Oneta Carl , Keil Thomas , Parés Xavier , Conradt Christian , Arce Luis , Waldherr Rüdiger , Stickel Felix , Russell Robert M. , Aderjan Rolf , Klee Fritz , Seitz Helmut K. 
Published: April 2003

<b>Background/Aims:</b> Ethanol is metabolized by alcohol dehydrogenase in the human stomach. This metabolism contributes to the so-called first-pass metabolism of ethanol which is affected by gender, medication, and morphological alterations of the gastric mucosa. Recently, it has been shown that <i>Helicobacter pylori</i> is capable to oxidize ethanol to acetaldehyde in vitro. Since <i>H. pylori</i> also injures gastric mucosa, the present study examines the effect of this bacterium on gastric alcohol dehydrogenase activity and systemic availability of ethanol in vivo. <b>Methods:</b> Thirteen volunteers (7 men and 6 women, aged 18–52 years) with gastric <i>H. pylori</i> infection diagnosed by a positive CLO test and positive gastric histology received ethanol (0.225 g/kg) either orally or intravenously before and after <i>H. pylori</i> elimination to determine systemic availability of ethanol. In addition, gastric biopsy specimens were taken from all subjects before and after <i>H. pylori</i> elimination for histological assessment of mucosal alterations and determinations of gastric alcohol dehydrogenase activity and phenotype of the enzyme. <b>Results:</b> In the presence of <i>H. pylori</i> the first-pass metabolism of ethanol was found to be significantly reduced (625 ± 234 vs. 1,155 ± 114 mg/dl/min, p = 0.046). This reduction of first-pass metabolism of ethanol was associated with a significant decrease in alcohol dehydrogenase activity (4.8 ± 1.5 vs. 12.1 ± 2.3 nmol/mg protein × min, p < 0.05) and an increase in the severity of mucosal damage as determined by a histological score (p < 0.05). <b>Conclusions:</b> <i>H. pylori</i> infection leads to gastric mucosal injury which is associated with a decrease in gastric alcohol dehydrogenase activity and first-pass metabolism of ethanol. Ethanol metabolism by <i>H. pylori</i> does not play an important role in vivo. However, gastric morphology is one important factor determining systemic availability of ethanol in man.
Comparison of Omeprazole, Metronidazole and Clarithromycin with Omeprazole/Amoxicillin Dual-Therapy for the Cure of <i>Helicobacter pylori</i> Infection
Authors: Miehlke Stephan , Meining Alexander , Lehn Norbert , Höchter Wilhelm , Weingart Josef , Simon Thomas , Krämer Walter , Klann Hermann , Bolle Karl-Heinz , Sommer Albrecht , Stolte Manfred , Bayerdörffer Ekkehard 
Published: April 2003

In this randomized, multicenter trial, we evaluated the effectiveness and side effect profile of a modified omeprazole-based triple therapy to cure <i>Helicobacter pylori</i> infection. The control group consisted of patients treated with standard dual therapy comprising omeprazole and amoxicillin. One hundred and fifty-seven <i>H. pylori</i> infected patients with duodenal ulcers were randomly assigned to receive either a combination of omeprazole 10 mg, clarithromycin 250 mg and metronidazole 400 mg (OCM) given three times daily for 10 days (n = 81), or a combination of omeprazole 20 mg and amoxicillin 1 g (OA) given twice daily for 14 days (n = 76). Prior to treatment and after 2 and 6 weeks, gastric biopsies from the antrum and corpus were obtained for histology and <i>H. pylori</i> culture. <i>H. pylori</i> infection was cured in 97.4% after OCM and in 65.8% after OA in the per-protocol analysis (p < 0.001) (intention-to-treat analysis: 93.4% and 63.2%, respectively). <i>H. pylori</i> was successfully cultured in 122 patients (77%). The overall rate of metronidazole resistance was 19.7% (24/122), no primary resistance to clarithromycin or amoxicillin was found. In the OCM group, all patients infected with metronidazole-sensitive <i>H. pylori</i> strains (n = 51) and those infected with strains of unknown susceptibility to metronidazole (n = 14) were cured (100%), while 77% (10/13) of those harboring metronidazole-resistant strains were cured of the infection (p = 0.36). Side effects leading to premature termination of treatment occurred in 2.5% of the patients in the OCM group and in 1.4% of the OA group. We conclude that combined treatment with omeprazole, clarithromycin and a higher dose of metronidazole is highly effective in curing <i>H. pylori</i> infection, and that this regimen remains very effective in the presence of metronidazole-resistant strains.
A Continuous Automated Method for the Determination of Intestinal Disaccharidase Activities
Authors: Sall I. , Férard G. 
Published: April 2003

A reliable method for the measurement of various disaccharidase activities such as maltase, isomaltase and sucrase is introduced. It is based on the continuous measurement of liberated glucose by a commercially available glucose dehydrogenase reagent. The procedures were first optimized for enzymes from rat intestinal mucosa. The pH optima were similar (6.3–6.7) for the three enzymes tested, and the apparent K<sub>m</sub>s were estimated to be 18, 12 and 19 mmol/l for maltase, isomaltase and sucrase, respectively. The procedures were adapted on a Cobas Mira automated analyzer. The assays correlated strongly with the conventional method of Dahlqvist. They were reliable, rapid, easy to perform and validate because the progress curve of each reaction rate can be continuously monitored. The method described has also been applied to human intestinal mucosa (Caco-2 cells).
Augmentation of Water-Immersion Stress- Induced Gastric Mucosal Lesions in BALB/c Mice Infected with <i>Helicobacter felis</i>
Authors: Matsushima Yumi , Kinoshita Yoshikazu , Watanabe Makoto , Hassan Sazzad , Fukui Hirokazu , Maekawa Toru , Okada Akihiko , Kawanami Chiharu , Kishi Kiyohiko , Watanabe Norihiko , Nakao Masafumi , Chiba Tsutomu 
Published: April 2003

<i>Background and Aims:</i> Inoculation of Helicobacter felis into the murine stomach has been reported to induce chronic gastric inflammation and may be a model of Helicobacter pylori-induced chronic gastritis. In this study, to characterize H. felis-induced gastritis, the gastric production of interleukin-1β (IL-1β) and hepatocyte growth factor (HGF) was measured in mice. <i>Methods:</i> Gastric mucosal lesions were induced in H. felis-infected BALB/c mice by water-immersion stress. The severity score of gastric erosions per stomach was measured as the sum of the length of erosions. Gene expression of IL-1β and HGF were analyzed by Northern blot analysis and production of HGF was examined using the enzyme immunoassay method. <i>Results:</i> Water-immersion stress induced gastric mucosal lesions accompanied by increased expression of IL-1β mRNA. H. felis infection evoked enhanced expression of IL-1β and HGF genes. When H. felis-infected mice were stressed by water immersion, the mucosal lesions were more severe than those in non-infected mice. Moreover, IL-1β gene expression as well as HGF production was further increased. <i>Conclusions:</i> Although H. felis inoculation did not cause gastric mucosal erosions by itself, it augmented the stress-induced erosions.
<i>Helicobacter pylori</i> and the Risk of Colonic Adenomas
Authors: Breuer-Katschinski B. , Nemes K. , Marr A. , Rump B. , Leiendecker B. , Breuer N. , Goebell H. 
Published: April 2003

<i>Aims:</i> Previous studies have found a positive association between <i>Helicobacter pylori</i> infection and colorectal adenomas. The aim of the present study was to examine this association while taking possible confounding factors into account. <i>Methods:</i> 98 serum samples were available from 182 patients with colorectal adenomas who entered a case-control study of colorectal adenomas and diet. The <i>H. pylori</i> status in patients was compared with a hospital control group and a population control group. <i>Results:</i> <i>H. pylori</i> IgG antibodies were more common in colorectal polyp patients compared with either control group, the prevalence being 79% in cases compared with 62% in both control groups. The corresponding RR was 1.4 (0.76–2.6) compared with hospital controls and 2.1 (1.1–3.9) compared with population controls. After adjusting for possible confounding variables the association between <i>H. pylori</i> status and adenoma risk was even more marked. There was an RR of 1.6 (0.80–3.4) compared with hospital controls and an RR of 2.6 (1.3–5.4) compared with population controls, the latter association being statistically significant. <i>Conclusion:</i> These findings suggest a statistically significant association between <i>H. pylori</i> infection and colorectal polyps. A possible mechanism might be increased gastrin levels in <i>H. pylori</i>-infected subjects which exhibit a trophic effect on colonic mucosa.
Fragmentation Pattern of Mucins in Normal and Diseased Gastric Mucosae: A Glycoprotein Fractionates with Gastric Mucins Purified from Mucosal Scrapings of Cancer and Peptic Ulcer Patients
Authors: Mall Anwar S. , McLeod Heather A. , Hickman Rosemary , Kahn Delawir , Dent David M. 
Published: April 2003

<i>Background/Aims:</i> Gastric cancer, a fatal malignancy, is prevalent in the Western Cape region of South Africa. The aim of this study was a biochemical characterisation of gastric mucins in this disease, compared with gastric ulceration and controls from transplant donors. <i>Methods:</i> Mucins were extracted in a denaturing medium (to prevent endogenous proteolysis) and purified by caesium chloride density gradient ultracentrifugation. Analysis of mucin was by gel filtration, SDS-PAGE and Western blotting methods. <i>Results:</i> All samples of mucin when analysed by gel filtration were found to contain polymeric glycoprotein together with varying amounts of lower-molecular-weight glycoprotein. SDS-PAGE and Western blot analysis showed that diseased stomachs had glycopeptides of a wider range in size and antigenicity with a greater number of smaller fragments immunoreactive to monoclonal antibodies 2–12M1 and 9–13M1. We identified by SDS-PAGE a glycoprotein which co-fractionates in a caesium chloride density gradient with mucins isolated from gastrectomy specimens resected for carcinoma and peptic ulceration and which was absent from mucins of the transplant donor control group. This neuraminidase-sensitive glycoprotein resisted dissociation from mucin during purification in a 3.5 <i>M</i> CsCl density gradient but was partially separable by Sepharose 2B gel chromatography and heat treatment (100°C, 2.0 min) in SDS. Chemical analysis of the glycoprotein by HPLC favours it being an N-linked glycoprotein. Its non-ideal electrophoretic properties make its exact size estimation difficult and we ascribe to it a broad size range of M<sub>r</sub> ∼55–65 kD. <i>Conclusion:</i> We conclude that mucins from diseased stomachs were more degraded than those from donors and that the diseased mucosa reproducibly secretes a M<sub>r</sub> ∼55–65 kD glycoprotein, the role of which needs to be established.
Epidermal Growth Factor Protects against Pancreatic Damage in Cerulein-Induced Pancreatitis
Authors: Warzecha Zygmunt , Dembinski Artur , Konturek Peter Ch. , Ceranowicz Piotr , Konturek Stanislaw J. 
Published: April 2003

Epidermal growth factor (EGF) exhibits gastroprotective and ulcer-healing action. These observations prompted us to determine the influence of EGF on cerulein-induced pancreatitis (CIP) in the rat. Acute pancreatitis was induced by subcutaneous infusion of cerulein (10 μg/kg/h) for 5 h. Initially EGF was administrated twice at doses of 1, 5, 10 or 100 μg/kg s.c. (first injection 30 min prior to cerulein infusion, and the second injection 2.5 h after the start of cerulein infusion) and from this part of study 10 μg/kg was chosen for the next experiments. CIP led to a significant decrease in DNA synthesis and a reduction in pancreatic blood flow (PBF) by 42 and 30%, respectively, as well as a significant increase in pancreatic weight, plasma amylase concentration, plasma interleukin-1β (IL-1β) level and the development of the histological signs of pancreatic damage with marked edema, leukocyte infiltration and vacuolization of acinar cells. Treatment with EGF attenuated the pancreatic tissue damage in CIP as manifested by partial reversal of the drop in DNA synthesis and improvement of pancreatic histology. Moreover, EGF administration attenuated the fall in PBF and significantly reduced the cerulein-evoked increase in pancreatic weight. Also plasma amylase and IL-1β were decreased in rats treated with EGF. We conclude that: (1) EGF exerts a protective effect against CIP, and (2) the beneficial activity of EGF in CIP seems to depend on the increase in pancreatic cell proliferation, the reduction in cytokine generation and the attenuation of the fall in PBF.
Ultra-High-Dose Lanreotide Treatment in Patients with Metastatic Neuroendocrine Gastroenteropancreatic Tumors
Authors: Faiss S. , Räth U. , Mansmann U. , Caird D. , Clemens N. , Riecken E.-O. , Wiedenmann B. 
Published: April 2003

<i>Background: </i>Symptomatic control and occasionally even tumor regression of functional neuroendocrine tumors (NET) of the gastroenteropancreatic (GEP) system can be achieved by somatostatin analogues. Assuming a dose-dependent antiproliferative effect of somatostatin analogues, we performed a study with the somatostatin analogue lanreotide in ultra-high dosages in patients with progressive, metastatic GEP NET. <i>Patients and Methods: </i>30 patients with metastatic GEP NET, progressive during treatment with somatostatin analogues (≤1.5 mg/day) and/or interferon-α, underwent ultra-high-dose lanreotide therapy (5 mg lanreotide s.c. three times a day). Tumor growth was evaluated every 3 months. Serum chromogranin A, serum serotonin as well as urinary 5-hydroxyindoleacetic acetic acid levels were also determined at 3-month intervals. In patients with functional tumors, tumor-related symptoms were documented. <i>Results: </i>After a 1-year treatment period with ultra-high-dose lanreotide, 1 complete and 1 partial remission were observed in patients with functional midgut NET. Eleven patients had stable disease and 11 patients showed continuing tumor growth after 3–12 months of treatment. Symptoms decreased significantly during therapy. <i>Conclusions: </i>Our data show that ultra-high-dose lanreotide treatment in patients with metastatic GEP NET can lead to control of both symptoms and proliferation in at least some patients refractory to conventional therapies.
Effect of Ecabet Disodium, a Novel Locally-Acting Antiulcer Drug, on Epithelial Restitution following Injury by Hypertonic NaCl in Bullfrog Stomach in vitro
Authors: Furukawa Osamu , Kume Eisuke , Sugamoto Shinich , Kawauchi Shoji , Takeuchi Koji 
Published: April 2003

<i>Background:</i> The antiulcer drug ecabet 2Na (12-sulfodehydroabietic acid disodium salt) exhibits a gastroprotective activity, mainly through a local action, involving endogenous prostaglandins (PGs) and nitric oxide (NO). In the present study, we examined the effect of ecabet on the epithelial restitution of the bullfrog gastric mucosa in vitro following injury by hypertonic NaCl. <i>Methods:</i> Bullfrog fundic mucosa was mounted in an Ussing chamber. The tissue injury was induced by exposure of the mucosa to 1.25 <i>M</i> NaCl for 5 min, and transmucosal potential difference (PD) and electrical resistance (R) were measured during a 4-hour test period. Ecabet (3–30 mg/ml) was added to the luminal solution for 10 min before or after NaCl, while 16,16-dimethyl PGE<sub>2</sub> (dmPGE<sub>2</sub>: 1× 10<sup>–6</sup> <i>M</i>) or NOR-3 (a NO donor: 1 × 10<sup>–4</sup> <i>M</i>) was added to the nutrient solution 10 min before NaCl. <i>Results:</i> Mucosal application of 1.25 <i>M</i> NaCl caused an immediate reduction of PD and R, followed by a gradual normalization, reaching about 70% of the pre-exposure levels within 4 h. Ecabet, added before NaCl, significantly expedited the recovery of PD and R in a concentration-dependent manner; this effect was mimicked by posttreatment with ecabet and significantly mitigated by prior addition of indomethacin (1 × 10<sup>–5</sup> <i>M</i>) or N<sup>G</sup>-nitro-<i>L</i>-arginine methyl ester (L-NAME: 1 × 10<sup>–3</sup> <i>M</i>). The epithelial restitution was also significantly promoted by serosal application of either dmPGE<sub>2</sub> or NOR-3. The mucosal exposure to ecabet significantly increased the luminal release of PGE<sub>2</sub> and NO metabolites, the effects being attenuated by indomethacin and L-NAME, respectively. The mucous secretion was increased by ecabet as well as dmPGE<sub>2</sub> and NOR-3, and the effect of ecabet was significantly suppressed by both indomethacin and L-NAME. The inhibitory effects of L-NAME on the ecabet action were all significantly antagonized by concurrent addition of <i>L</i>-arginine. <i>Conclusion:</i> These results suggest that ecabet significantly expedited the restitution following gastric surface cell injury, and this action is mediated by endogenous NO as well as PGs and may be functionally associated with an increase of mucous secretion.
Combined Immunoglobulin and Azathioprine in Multiple Sclerosis
Authors: Kalanie Hossein , Tabatabai Seid Shahabbedin 
Published: April 2003

In an attempt to prevent exacerbations of multiple sclerosis, immunoglobulin therapy was combined with azathioprine (AZA). Intravenous immunoglobulin (IVIG) 2 g/kg was given in divided doses over 3 consecutive days followed by monthly booster doses (0.2 g/kg) for 3 years to 38 patients with relapsing-remitting multiple sclerosis (MS). In the 34 patients who completed the trial, the relapse rate decreased (from 1.7 relapses per year to 0 during the 3-year trial period). The Kurtzke Expanded Disability Status Scale decreased from 3.4 ± 0.72 to 3.0 ± 0.70. The results suggest that combined IVIG and AZA suppress the ongoing pathologic process in relapsing-remitting MS.