bluuebunny/crossref_metadata_2025_split huggingface dataset:
Stability within the Chaos: The Koori Kids Mental Health Network
Authors: Mushin David , Potter Carol , Booth Anne , Geoghegan Kaye , Krupinska Ola , Paul Campbell , Wyatt Nareida 
Published: October 2003

Introduction: The Koori (Aboriginal term for Indigenous people from South Eastern Australia) Kids Mental Health Network is a child, adolescent and family psychiatric service based at the Victorian Aboriginal Health Service, a community health service which is controlled by the Victorian Koori community and based in Melbourne. The Koori Kids Mental Health Network is a collaborating group of Indigenous mental health workers from the Victorian Aboriginal Health Service and other health services together with a network of non-Indigenous workers from mainstream child and adolescent mental health services. Method: This article is a distillation of a 3-hour workshop involving seven members of the Koori Kids Mental Health Network. It comprised an introduction regarding the development of the Network, a section on the process by which Indigenous and mainstream workers have developed their working relationships and fostered each other's development according to the needs of Indigenous families, and a section on the nature of the service provided to these patients. Results: A child and adolescent psychiatric service, relevant to the needs of the Victorian Aboriginal community, has developed through the collaborative functioning of mainstream and aboriginal mental health workers. It has been critical for the development of such a service that it be coordinated by an Aboriginal mental health worker and located within a health service administered by the Aboriginal community. The workshop enabled presentation and discussion of material leading to an understanding of the Service and its development.
Comparative study of the effects of nitric oxide synthase and cyclo‐oxygenase inhibition on duodenal functions in rats anaesthetized with inactin, urethane or a‐chloralose
Authors: SABABI M. , NYLANDER O. 
Published: October 2003

This study was undertaken to investigate the effects of a cyclo‐oxygenase and a nitric oxide synthase (NOS) inhibitor on duodenal mucosal alkaline secretion (DMAS), motility and mucosal permeability in inactin‐, urethane‐ and α‐chloralose anaesthetized rats. Proximal duodenum was perfused with a 150 mm NaCl solution and DMAS was determined by back titration. Mucosal permeability was assessed by measuring blood to lumen clearance of 51Cr‐EDTA and duodenal motility by measuring intraluminal pressure. Mean arterial blood pressure and mucosal permeability were significantly lower in urethane‐ than in inactin‐ or α‐chloralose anaesthetized rats (urethane: 90±2 mm Hg and 0.15±0.02 mL min‐1 100 g‐1; inactin: 112±5 mm Hg and 0.62±0.15 mL min‐1 100 g‐1; α‐chloralose: 111±4 mm Hg and 0.61±0.06 mL min‐1 100 g‐1, respectively). Basal (pre‐drug) DMAS was significantly lower in urethane rats (6.2±1.0 μmol cm‐1 h‐1) than in α‐chloralose (9.3±1.2 μmol cm‐1 h‐1), but not different from that in inactin‐anaesthetized rats (7.5±0.8 μmol cm‐1 h‐1). No or very few spontaneous duodenal contractions occurred under the control (pre‐drug) conditions in any group. All animals responded to the cyclo‐oxygenase inhibitor indomethacin or the NOS inhibitor N‐nitro‐l‐arginine‐methyl‐ester (l‐NAME) with induction of duodenal motility and an increase in DMAS. The effect of indomethacin or l‐NAME on mucosal permeability was similar in all anaesthetic groups except that l‐NAME induced a transient increase in the inactin and α‐chloralose groups but a sustained increase in urethane‐anaesthetized animals. It is concluded that inactin‐ and α‐chloralose anaesthetized rats do not differ regarding the studied basal values. Urethane‐anaesthetized animals differed from rats given the other two anaesthetics in that basal mucosal permeability and mean arterial blood pressure were lower. Endogenous prostaglandins and NO contribute to the postoperative ileus and the low rate of DMAS also in urethane‐ and α‐chloralose anaesthetized rats.
Effect of cimetidine on basal and postprandial plasma concentrations of cholecystokinin and gastrin in humans
Authors: STØA‐BIRKETVEDT G. , WALDUM H.L. , VONEN B. , FLORHOLMEN J. 
Published: October 2003

STØA‐BIRKETVEDT, G., WALDUM, H. L.,VONEN, B. & FLORHOLMEN, J. 1997. Effect of cimetidine on basal and postprandial plasma concentrations of cholecystokinin and gastrin in humans. Acta Physiol Scand159, 321–325. Received 12 June 1996, accepted 8 November 1996. ISSN 000–6772. Laboratory of Gastroenterology, Institute of Clinical Medicine, University of Tromsø, Tromsø, Physiological Laboratory, University School of Medicine, 6000 Trondheim and Department of Surgery, University Hospital of Tromsø, 9037 Tromsø, Norway.Cimetidine reduces the appetite and weight in healthy overweight subjects. Gastrointestinal regulatory peptides such as cholecystokinin (CCK) have been proposed to mediate the satiety signal from gut to brain. Therefore, the effect of cimetidine on basal and postprandial plasma concentrations of cholecystokinin and gastrin was studied. After an overnight fast, 12 healthy volunteers were given cimetidine (400 mg) on day 1, breakfast on day 2, and cimetidine 20 min before breakfast on day 3. Plasma concentrations of cholecystokinin and gastrin were measured by radioimmunoassay. Plasma cholecystokinin concentration increased with one major peak observed 30 min and one smaller peak observed 120 min after intake of cimetidine. The meal induced an increase in the plasma concentration of cholecystokinin, while cimetidine prior to the meal elicited a sustained postprandial cholecystokinin response. Cimetine had no effect on the basal plasma concentration of gastrin. The meal induced an increase in the plasma concentration of gastrin, while cimetidine prior to the meal elicited a sustained postprandial gastrin response. In conclusion, cimetidine increases the basal concentration of plasma cholecystokinin and elicits a sustained postprandial response of both cholecystokinin and gastrin. At least the cholecystokinin response may be one mechanism by which cimetidine reduces the appetite.
Oxygen, pHi and arrest of biosynthesis in brine shrimp embryos
Authors: HAND S.C. 
Published: October 2003

Embryos of the brine shrimp Artemia franciscana are able to withstand bouts of environmental anoxia for several years by entering a quiescent state, during which time metabolism is greatly depressed. Within minutes of oxygen removal, intracellular pH (pHi) drops at least 1.0 unit. This acidification has been strongly implicated in the arrest of both catabolic and anabolic processes in the cytoplasm. A global arrest of cytoplasmic translation accompanies the transition into anoxia or into aerobic acidosis (artificial quiescence imposed by intracellular acidification with CO2 in the presence of oxygen). Similarly, protein synthesis in isolated mitochondria from these embryos is also reduced markedly in response to acidic pH (80% reduction) or anoxia (79% reduction). The constancy of mRNA levels during quiescence indicates that protein synthesis is likely to be controlled at the translational level.Mitochondrial matrix pH is 8.2 during protein synthesis assays performed at the extramitochondrial pH optimum of 7.5. When this proton gradient is abolished with the K+/H+ ionophore nigericin, the extramitochondrial pH optimum for protein synthesis displays an alkaline shift of ≈0.7 pH unit. These data suggest the presence of proton‐sensitive translational components within the mitochondrion. The oxygen dependency of mitochondrial protein synthesis is not explained simply by blockage of the electron transport chain or by the increased redox state. Whereas oxygen deprivation substantially depresses protein synthesis by 77% after 1 h, normoxic incubations with saturating concentrations of cyanide or antimycin A have only a modest effect (36% reduction, cyanide; 20%, antimycin A). This cyanide‐ and antimycin‐insensitive, but hypoxia‐sensitive, inhibitory signature for the arrest of protein synthesis suggests the presence of a molecular oxygen sensor within the mitochondrion.
Cardiovascular and renal effects of endothelin receptor blockade with PD 145065 and interaction with urodilatin
Authors: DOBROWOLSKI L. , ENDLICH K. , SADOWSKI J. , STEINHAUSEN M. 
Published: October 2003

Role of endogenous endothelins (ET) in the control of cardiovascular system and renal function, and ET interaction with urodilatin (URO) were studied in anaesthetized rats. Activity of ET was blocked using PD 145065 (5 mg kg‐1 body wt i.v.), a non‐selective antagonist of ETA and ETB receptors. PD 145065 decreased mean arterial blood pressure (MBP) from 114±4 to 109±4 mmHg and the renal blood flow (RBF) from 6.6±0.3 to 5.8±0.4 mL min‐1 (P<0.02) and increased renal vascular resistance (RVR) from 17.7±1.2 to 20.1±2.1 mmHg min mL‐1. Heart rate (HR) and renal function were not affected. URO was infused i.v. at 0.1 nmol min‐1 kg‐1 body wt without or with previous ET receptor blockade. After pre‐treatment with PD 145065, infusion of URO decreased MBP more than did URO alone: 15±3% vs. 7±2% (P<0.05). RVR and HR did not change after URO alone but decreased with URO given to PD 145065 treated rats (19±5% and 14±3%, respectively, P<0.01). It is concluded that in anaesthetized surgically prepared rats endogenous ET can cause renal vasodilation, in contrast to constriction of systemic vasculature. Enhancement by ET blockade of vascular systemic and renal effects of URO supports ET interaction with natriuretic peptides in the control of cardiovascular and renal function.
Brain natriuretic peptide (BNP) gene expression in the heart of vasopressin‐deficient Brattleboro rats
Authors: ARJAMAA O. , TASKINEN T. , VUOLTEENAHO O. , LEPPÄLUOTO J. 
Published: October 2003

Brain natriuretic peptide (BNP) messenger RNA was measured with a semiquantitative method from heart auricles and ventricles of vasopressin‐deficient Brattleboro rats (DI) and from desmopressin treated Brattleboro rats (DI+DDAVP). Desmopressin had been injected peripherally and Long‐Evans rats (LE) served as controls. The 3‐day substitution treatment had shifted the fluid balance of DI almost to that of LE. In the present study, the amount of BNP mRNA, normalized to the glyceraldehyde‐3‐phosphate‐dehydrogenase mRNA content, was constant in all three groups in the right auricle. No changes were seen when the right auricular and left auricular mRNA levels were compared within each group. In the left auricle, desmopressin treatment increased significantly (P<0.05) the amount of BNP mRNA compared with that of LE rats (from 1.09±0.21, n=7 to 1.72±0.17, n=8, arbitrary units). In all groups, the left ventricle had significantly (P<0.05) higher mRNA content than the right ventricle (LE: 2.24±0.23 vs. 0.67±0.13, n=6; DI: 2.30±0.60 vs. 0.33±0.05, n=8; DI+DDAVP: 2.36±0.29 vs. 0.37±0.07, n=10). In the right ventricle, both DI and DI+DDAVP rats had significantly (P<0.05) lower mRNA content than LE rats (0.33±0.5 vs. 0.67±0.13 and 0.37±0.07 vs. 0.67±0.13, respectively).To conclude, these findings suggest that brain natriuretic peptide gene expression dissociates from, or rapidly adapts to, the chronic effects of peripheral desmopressin treatment which have shifted the fluid balance to almost normal in Brattleboro rats. The left ventricular pressure appears to regulate the brain natriuretic peptide gene expression.
The future of Helicobacter pylori eradication: a personal perspective
Authors: MARSHALL B. J. 
Published: October 2003

Future changes in the use of Helicobacter pylori eradication therapy first will involve a decision‐making process to determine which individuals require testing. Clearly, only persons who require therapy need to be diagnosed and, at present, the indications for therapy are constantly expanding. The author takes the view that everyone with H. pylori would be better off without the bacterium, but accepts that in many countries resources are inadequate to achieve this goal.Where antibiotic therapy for H. pylori fails due to a resistant organism, second treatment must include a different class of antibiotic. When a third therapy is contemplated, antibiotic sensitivity studies are usually necessary.In developing counties where reinfection with H. pylori is common, lesser goals than permanent cure might be appropriate. Thus, selected patients could have H. pylori suppressive therapy to prevent full expression of H. pylori‐associated disease, or to prevent reinfection after an initial eradicative therapy.After considering all these alternatives, one must conclude that a vaccination strategy, if safe and cost effective, is the ideal future therapy.
Outcomes research in Helicobacter pylori infection
Authors: FENDRICK A. M. 
Published: October 2003

While the medical community has accepted the role of H. pylori in the pathogenesis of peptic ulcer disease, confusion persists among clinicians regarding when and on which patients to attempt H. pylori eradication. Thus, the objective for outcomes research in H. pylori is to help clinicians identify which patients benefit from H. pylori eradication and to determine the cost‐effective strategies for their diagnosis, treatment and follow‐up care.Economic evaluation of the impact of H. pylori infection has focused primarily on assessment of patient with documented peptic ulcer disease, with particular attention to costs of pharmaceuticals. However, drug costs are only one portion of the total costs of management for patients with acid‐related disorders and therefore must be put in the appropriate context. Additional aspects of patient benefit (e.g. patient satisfaction) and health‐care expenditures (e.g. over‐the‐counter medications, specialist visits, hospitalizations) must be included in an evaluation of the value of a particular diagnostic test, treatment, clinical guideline or disease management strategy.As a result of the high quality and quantity of data emerging, it can be safely said that H. pylori eradication is cost‐effective in selected patient populations: newly documented peptic ulcer disease; history of peptic ulcer disease and taking maintenance therapy; and suspected peptic ulcer disease using a serological test to guide initial treatment. The role of eradication in other areas, for example, patients with non‐ulcer dyspepsia and screening to prevent gastric cancer, remains to be seen. In addition to the performance of rigorous studies, researchers must respond to the ‘information overload’ on busy clinicians, by effectively disseminating their findings. If data generated from outcomes research are not integrated into everyday clinical practice, the enormous benefits associated with H. pylori eradication will not be achieved.
Randomized comparison of differing periods of twice‐a‐day triple therapy for the eradication of Helicobacter pylori
Authors: LAINE L. , ESTRADA R. , TRUJILLO M. , FUKANAGA K. , NEIL G. 
Published: October 2003

Background: We assessed the efficacy, compliance, and tolerability of the twice‐a‐day triple therapy, amoxycillin, omeprazole, and clarithromycin, for Helicobacter pylori and studied the effect of treatment duration (7, 10 or 14 days) on these factors. Methods: One‐hundred and fifty subjects with H. pylori infection documented by 13C‐urea breath test were randomly assigned to a 7, 10 or 14‐day course of amoxycillin 1 g b.d., omeprazole 20 mg b.d. and clarithromycin 500 mg b.d. Subjects returned at the end of therapy for pill count and assessment of side‐effects. Subjects returned for a repeat 13C‐urea breath test 4 weeks after the end of therapy. Results: Poor compliance (<80% of medications taken) was seen in 0 subjects at 7 days, 6% at 10 days, and 10% at 14 days (P=0.03 by χ2 test for trend; difference for 7 vs. 14 days=10%; 95% CI, −2% to 18%; P=0.056). Intention‐to‐treat eradication rates were 86% at 7 days, 90% at 10 days and 92% at 14 days. Per‐protocol eradication rates were 86% at 7 days, 91% at 10 days, and 95% at 14 days (P=0.11; difference for 7 vs. 14 days=9%; 95% CI, −2% to 21%; P=0.17). Conclusions: One week of twice‐a‐day amoxycillin, omeprazole and clarithromycin is well tolerated and provides a good rate of H. pylori eradication. Increasing the duration of therapy decreases compliance but has the potential to modestly improve efficacy if the patient takes the full complement of medication.
Long‐term treatment with lansoprazole of patients with duodenal ulcer and basal acid output of more than 15mmol/h
Authors: HIRSCHOWITZ B. I. , MOHNEN J. , SHAW S. 
Published: October 2003

Background: About 10% of patients with duodenal ulcers have marked gastric acid hypersecretion with basal acid output (BAO) of more than 15 mmol/h, which is in the range found in Zollinger–Ellison syndrome. Patients and study design: We report long‐term, up to 4 years, prospective treatment using lansoprazole in nine male patients with duodenal ulcers and a BAO of more than 15 mmol/h whose results are compared with those in 10 male Zollinger–Ellison syndrome patients with intact stomachs reported in detail in an accompanying paper. Results: All 19 subjects, except one Zollinger–Ellison syndrome patient who had gastric and oesophageal ulcers, had a history of duodenal ulcers; 22% of those with gastric acid hypersecretion had oesophagitis compared with 60% of those with Zollinger–Ellison syndrome. Each subject had the dose of lansoprazole adjusted to give a BAO of less than 5 mmol/h. At 3‐month intervals to 1 year, and then at 6‐monthly intervals, basal and pentagastrin stimulated secretions were studied, in addition to gastroscopy with biopsy for gastric mucosal morphology. Basal and maximal acid and pepsin secretions were not different between gastric acid hypersecretion and Zollinger–Ellison syndrome patients before treatment. During treatment, BAO was reduced by over 90% to less than 2 mmol/h, while peak acid output was reduced by 70% in those with gastric acid hypersecretion and 90% in Zollinger–Ellison syndrome patients. Four gastric acid hypersecretion patients had relapses during treatment, three times in one patient and twice in another patient, but all responded to continued treatment with lansoprazole. Of the seven ulcer‐related relapses in the gastric acid hypersecretion patients, four occurred with a BAO of less than 2 mmol/h and three with a BAO of 7.1–7.3 mmol/h; five of the seven relapses occurred in the absence of Helicobacter pylori. Lansoprazole remained effective at an average dose of ≈70 mg/day, without causing any side‐effects. Conclusion: Lansoprazole is apparently safe and effective for treating hypersecretion, whether due to hypergastrinaemia (Zollinger–Ellison syndrome) or not (non‐Zollinger–Ellison syndrome hypersecretors).
Prescriptions for mesalazine and sulphasalazine: a prevalence estimate of patients treated for inflammatory bowel disease in Rome
Authors: TEBANO M. T. , TRAVERSA G. , DA CAS R. , LOIZZO A. 
Published: October 2003

Background: Sulphasalazine and 5‐amino salicyclic acid drugs are specifically indicated for the treatment of inflammatory bowel disease. Aim: To use drug consumption by a given population as a marker to estimate the number of patients with inflammatory bowel disease. Methods: Prescriptions for sulphasalazine and mesalazine were identified for the 133000 inhabitants of a local health unit in Rome. Other prescriptions received by the patients, who were users of sulphasalazine or mesalazine, were also studied. Results: 99465 patients received at least one prescription for any drug in 1991. Three hundred and seventy‐six patients were prescribed sulphasalazine and/or mesalazine, an average of 3.8 prescriptions per patient. These patients were exposed more frequently than the general population to other drugs often used in inflammatory bowel disease treatment, for example, corticosteroids, anti‐diarrhoeal drugs and intestinal anti‐infectives. We identified that 258 of 100000 inhabitants were prescribed either sulphasalazine or mesalazine; 127 of 100000 inhabitants received full‐dose treatment for at least 30 days, and 42.8 of 100000 inhabitants received prescriptions of either drug, also associated with systemic corticosteroids. Conclusion: The consumption of drugs used specifically for inflammatory bowel disease may act as a marker for the prevalence of the condition in a community.
Systemic availability of 5‐aminosalicylic acid: comparison of delayed release and an azo‐bond preparation
Authors: GIONCHETTI P. , CAMPIERI M. , VENTURI A. , RIZZELLO F. , FERRETTI M. , BRIGNOLA C. , MIGLIOLI M. 
Published: October 2003

Aim: To determine the systemic uptake of 5‐aminosalicylic acid (5‐ASA) and acetyl‐5‐ASA (Ac‐5‐ASA) at steady state during treatment with either an azo‐bond preparation, olsalazine, or a delayed‐release mesalazine. Methods: In an open cross‐over trial with randomized sequence, 15 patients with ulcerative colitis in remission were given 7‐day courses of olsalazine (Dipentum 1.0 g daily) and of mesalazine (Asacol 1.6 g daily). Plasma and urine were collected on days 6 and 7 of each course and concentrations of 5‐ASA and Ac‐5‐ASA were determined by high‐performance liquid chromatography (HPLC). Results: Mean steady‐state plasma concentrations of 5‐ASA and Ac‐5‐ASA were significantly higher after treatment with mesalazine than with olsalazine (P< 0.0001). Total urinary excretion of 5‐ASA and Ac‐5‐ASA as a percentage of the given dose was significantly higher on mesalazine than on olsalazine (P<0.01).Only two patients experienced, during the first 3 days of treatment with olsalazine, transient watery diarrhoea which resolved spontaneously. No unexpected or major changes in haematology or biochemistry were detected during the study. Conclusion: As 5‐ASA acts locally, the lower systemic load provided by olsalazine may increase efficacy and reduce the potential risk of nephrotoxicity during long‐term maintenance treatment of ulcerative colitis.
Antral gastrin cell hyperfunction and Helicobacter pylori infection
Authors: ANNIBALE B. , RINDI G. , D'AMBRA G. , MARIGNANI M. , SOLCIA E. , BORDI C. , DELLE FAVE G. 
Published: October 2003

Background: Antral gastrin cell hyperfunction (AGCH), is a rare cause of duodenal ulcer associated with non‐tumour hypergastrinaemia and acid hypersecretion. Aim: To investigate the role of Helicobacter pylori in AGCH. Patients: Twelve AGCH patients and eight H. pylori‐positive non‐hypergastrinaemic duodenal ulcer patients were compared. Methods: Basal and peak acid outputs, gastrin‐stimulation (meal and bombesin) tests, and immunohistochemistry for antral G and D cells were performed. One year after H. pylori eradication, six AGCH patients were again investigated with the same tests. Results: Significantly more basal, and stimulated gastrin and acid secretion, were found in AGCH compared to the H. pylori‐positive duodenal ulcer patients (P<0.01). G cell counts were significantly higher in AGCH than in duodenal ulcer patients (118.8, range 58–192.4, vs. 86.1, range 49–184; P<0.05), and the resulting G/D cell ratio was also higher in AGCH patients (4.2, range 2.6–5.6, vs. 3.3, range 1.9–4.3; P<0.05). H. pylori was present in the gastric mucosa of all 12 AGCH patients. Cure of infection in six AGCH individuals resulted in marked a decrease of gastrin levels associated with a significant (23.7%; P<0.05) decrease of G cell count and an increase (12%; P<0.05) of D cell count. Conclusions: The results indicate that AGCH may result from H. pylori overstimulation of gastrin cell function in patients with some presently undefined, familial predisposition and that an imbalance of the G/D cell ratio may have a role in the genesis of hypergastrinaemia.