bluuebunny/crossref_metadata_2025_split huggingface dataset:
MRI volumetric and 31PMRS metabolic correlates of caudate nucleus in antipsychotic‐naïve schizophrenia
Authors: Jayakumar P. N. , Venkatasubramanian G. , Keshavan M. S. , Srinivas J. S. , Gangadhar B. N. 
Published: June 2006

Objective: To examine the volumetric and metabolic correlates of caudate nucleus in antipsychotic‐naïve schizophrenia patients in comparison with healthy controls.Method: Twelve antipsychotic‐naïve schizophrenia patients and 13 healthy controls underwent31P magnetic resonance spectroscopy of basal ganglia. Magnetic resonance imaging volume of caudate nuclei was measured usingscion imagesoftware.Results: Patients had significantly smaller caudate volume than healthy controls. Phosphocreatine (PCr)/total phosphorous and PCr/total adenosine tri‐phosphate ratios of both caudate nuclei were significantly lower in patients than controls. Significant negative correlation was found between the left caudate volume and left PCr/total phosphorus ratio in the patients. Age at onset of psychosis had i) significant negative correlation with right and left caudate volumes and ii) significant positive correlation with left PCr/total phosphorus ratio.Conclusion: The metabolic and volumetric abnormalities of caudate nucleus in antipsychotic‐naïve schizophrenia patients support neurodevelopmental etiopathogenesis.
Is psychosis in DSM‐IV mania due to severity? The relevance of selected demographic and comorbid social‐phobic features
Authors: Azorin J.‐M. , Akiskal H. , Akiskal K. , Hantouche E. , Châtenet‐Duchêne L. , Gury C. , Lancrenon S. 
Published: June 2006

Objective: We tested whether factors other than episode severity contributed to psychosis in mania.Method: Psychiatrists collected systematic clinical data on 1090 hospitalized DSM‐IV manic patients in France, and completed the Mania Rating Scale (MRS) and the Scale for the Assessment of Positive Symptoms (SAPS).Results: Using DSM‐IV specifiers, 21.9% were non‐severe, 28.2% severe without psychosis, and 49.9% severe with psychosis. On the MRS, patients with psychosis scored significantly higher (P < 0.0001) than non‐severe, but did not differ from the severe without psychosis. We found significant correlations between both the Hallucination and the Delusion subscores of the SAPS and the MRS, as well as correlations between age, single marital status, comorbid social phobia and psychotic mania.Conclusion: Apart from episode severity, social isolation – associated with younger age, single marital status and social phobia – seems to make a contribution to the origin of manic psychosis largely independent from such severity.
Understanding suicidal ideation in psychosis: findings from the Psychological Prevention of Relapse in Psychosis (PRP) trial
Authors: Fialko L. , Freeman D. , Bebbington P. E. , Kuipers E. , Garety P. A. , Dunn G. , Fowler D. 
Published: June 2006

Objective:  To examine the clinically important phenomenon of suicidal ideation in psychosis in relation to affective processes and the multidimensional nature of hallucinations and delusions.Method:  In a cross‐sectional study of 290 individuals with psychosis, the associations between level of suicidal ideation, affective processes, positive symptoms, clinical and demographic variables were examined.Results:  Forty‐one per cent of participants expressed current suicidal ideation. Suicidal ideation was associated with depressed mood, anxiety, low self‐esteem, negative illness perceptions, negative evaluative beliefs about the self and others and daily alcohol consumption. Frequency of auditory hallucinations and preoccupation with delusions were not associated with suicidal ideation; however, positive symptom distress did relate to suicidal thoughts.Conclusion:  Affective dysfunction, including distress in response to hallucinations and delusions, was a key factor associated with suicidal ideation in individuals with psychotic relapse. Suicidal ideation in psychosis appears to be an understandable, mood‐driven process, rather than being of irrational or ‘psychotic’ origin.
The Basel early‐detection‐of‐psychosis (FEPSY)‐study – design and preliminary results
Authors: Riecher‐Rössler A. , Gschwandtner U. , Aston J. , Borgwardt S. , Drewe M. , Fuhr P. , Pflüger M. , Radü W. , Schindler Ch. , Stieglitz R.‐D. 
Published: June 2006

Objective:  Early detection and therapy of schizophrenic psychoses have become broadly accepted aims in psychiatry, recently even in very early stages of the disorder when clear diagnostic criteria are not yet fulfilled. However, reliable and widely applicable methods do not yet exist. This study aims at contributing to the improvement of the early assessment of psychosis.Method:  Individuals potentially at risk are identified by a newly developed stepwise screening procedure. Identified subjects are then examined extensively and followed‐up for at least 5 years to detect actual transition to psychosis.Results:  Of 50 subjects who have been followed up for 1–5 years by now, 16 have progressed to frank psychosis, 12 of them during the first 12 months of follow‐up.Conclusion:  At this stage, our approach seems to be promising for the early detection of psychosis. Further results from this ongoing study will hopefully permit us to optimize the assessment procedure.
A double‐blind, placebo‐controlled trial of sibutramine for clozapine‐associated weight gain
Authors: Henderson D. C. , Fan X. , Copeland P. M. , Borba C. P. , Daley T. B. , Nguyen D. D. , Zhang H. , Hayden D. , Freudenreich O. , Cather C. , Evins A. E. , Goff D. C. 
Published: June 2006

Objective: This study sought to examine the effectiveness of sibutramine, a weight loss agent, on clozapine‐associated weight gain.Method: This was a 12‐week double‐blind, placebo controlled, randomized trial of sibutramine for weight loss in obese clozapine‐treated schizophrenia or schizoaffective disorder subjects.Results: Ten patients were enrolled into the placebo group and 11 patients into the sibutramine group. There were no significant baseline differences between the two groups on age, gender, education, ethnicity, diagnosis, weight, body mass index (BMI), and blood pressure. At week 12, there were no significant differences in changes in weight, BMI, abdominal and waist circumferences, Hba1c, fasting glucose, or cholesterol levels.Conclusion: Sibutramine treatment did not show significant weight loss compared with placebo in clozapine‐treated patients with schizophrenia or schizoaffective disorder. Further research with a larger sample size and longer follow‐up duration is warranted.
Type 2 diabetes and periodontal indicators: epidemiology in France 2002–2003
Authors: Mattout C. , Bourgeois D. , Bouchard P. 
Published: June 2006

Background and Objective:   Diabetes and periodontal disease have been associated in the literature. In the present study, the periodontal heath of noninsulin‐dependent diabetic adults was compared with that of a general population of nondiabetic patients.Material and Methods:  In France, 2144 adults (age: 35–65 years) were examined for life habits (tobacco, alcohol), biological diagnosis (type II diabetes, arterial hypertension), biometry (weight, size) and biochemistry. Dental and periodontal data included plaque index, gingival index, probing depth, and clinical attachment loss.Results:  Descriptive and multifactorial analysis evidenced a more severe periodontal disease in diabetic patients. Moreover, when the plaque index was held constant, the gingival index was more elevated in diabetics. In nondiabetics, age, gender, glycemia, alcohol, and tobacco smoking were identified as significant risk factors for periodontal disease. In contrast, in diabetic subjects, only tobacco smoking was a significant risk factor.Conclusion:  In type II diabetics, the diabetes factor is probably more significant than periodontal risk factors, age, and gender.
Synergism between nifedipine and cyclosporine A on the incorporation of [35S]sulfate into human gingival fibroblast cultures in vitro
Authors: Flynn J. C. , Henderson J. S. , Johnson R. B. 
Published: June 2006

Background and Objective:  We assessed the effects of cyclosporine A and nifedipine on the in vitro incorporation of [35S]sulfate into gingival fibroblast cell cultures derived from responder and nonresponder subjects who had received an organ transplant followed by a therapeutic regimen using a combination of those drugs.Material and Methods:   Gingival fibroblasts were isolated from responder and nonresponder subjects and maintained in vitro. Prior to cell harvest, gingival interleukin‐1β concentrations were determined by enzyme‐linked immunosorbent assay (ELISA). Cells were untreated or exposed to either 10−7−10−10 m nifedipine or 100–500 ng/ml cyclosporine A. Incorporation of [3H]proline or [35S]sulfate into the cell cultures was determined by liquid scintillation analysis. In addition, the effects of 400 ng/ml cyclosporine A + 10−7 m nifedipine and 400 ng/ml cyclosporine A + 10−10 m nifedipine on incorporation of [35S]sulfate into the cell cultures was determined. Data were compared by factorial analysis of variance (anova) and a posthoc Tukey's test.Results:   Gingiva from responders contained significantly more interleukin‐1β than gingiva from nonresponders (p < 0.01). The cell cultures derived from responders incorporated significantly more [35S]sulfate than those derived from nonresponders following exposure to either cyclosporine A or 10−7 m nifedipine. In addition, the exposure of fibroblasts derived from gingival overgrowth to either 400 ng/ml cyclosporine A + 10−7 m nifedipine or 400 ng/ml cyclosporine A + 10−10 m nifedipine significantly increased or decreased, respectively, the incorporation of [35S]sulfate into the cultures.Conclusion:   The therapeutic combination of cyclosporine A and nifedipine could be a significant risk factor for gingival overgrowth in subjects susceptible to either agent. The mechanism for overgrowth could include edema secondary to increased sulfated‐glycosaminoglycan (sGAG) synthesis by fibroblasts, but further investigation is required.
An immunohistochemical study of the attachment mechanisms in different kinds of adhesive interfaces in teeth and alveolar bone of the rat
Authors: Arambawatta A. K. S. , Yamamoto T. , Wakita M. 
Published: June 2006

Background and Objective:  This study was designed to examine the histological and immunohistochemical nature of different kinds of adhesive interfaces in the rat molar region under identical experimental conditions and to discuss the structural and functional similarities between these adhesive interfaces.Material and Methods:  Four kinds of adhesive interfaces – an initial attachment layer for principal fibers on the developing alveolar bone surface, a reattachment layer for principal fibers on resorbed alveolar bone surface, cement lines on the alveolar bone surface unrelated to the principal fibers, and the cemento–dentinal junction – were examined in 25‐d‐old male Wistar rats. Routine histological staining, immunohistochemical staining for bone sialoprotein and osteopontin, and digestion tests with trypsin were conducted.Results:  The adhesive interfaces showed very similar histological and immunohistochemical features: they were intensely hematoxylin‐stainable, deficient in collagen fibrils, and rich in bone sialoprotein and osteopontin. After trypsin treatment the four adhesive interfaces had lost immunoreactivity to bone sialoprotein and osteopontin, and the two adjacent tissue parts held together finally separated at the adhesive interfaces.Conclusion:  The above findings suggest that (i) the different types of adhesive interfaces in the rat molar region have a common structure in that they are filled with highly accumulated bone sialoprotein and osteopontin and deficient in collagen fibrils; (ii) accumulated bone sialoprotein and osteopontin are closely associated with the adhesion at the interfaces; and (iii) the adhesive interfaces have a similar developmental process.
Periodontal healing may be affected by aging: a histologic study in rats
Authors: Benatti B. B. , Neto J. B. C. , Casati M. Z. , Sallum E. A. , Sallum A. W. , Nociti F. H. 
Published: June 2006

Background and Objective:  Although wound healing has been reported to be impaired with aging, very little is known about its effect on periodontal tissues. Therefore, the aim of this study was to evaluate, histologically in rats, the influence of aging on a spontaneous periodontal healing model.Material and Methods:  Twenty‐four male Wistar rats were used and assigned to the following groups: control (n = 12; 2 mo old) and aged (n = 12; 18 mo old). Fenestration defects (4 × 3 × 1 mm) were created bilaterally at the buccal aspect of the distal root of the first mandibular molars, and the mandibulae were retrieved 3 and 6 wk postoperatively. The percentage of bone fill and density of newly formed bone, new cementum formation (NC), and the extension of the remaining defect (ERD) were histometrically obtained.Results:  Intragroup analysis demonstrated that, except for cementum, all histological parameters significantly improved over time (p < 0.05). Intergroup analysis additionally showed that the defects were initially similar in size, and that at 3 wk aging negatively influenced newly formed bone (86.38 ± 2.99% and 73.06 ± 3.21%, p < 0.001, for groups control and aged, respectively), BF (75.84 ± 16.53% and 57.70 ± 22.28%, p = 0.014) and ERD (0.41 ± 0.20 mm and 1.17 ± 0.37 mm, p < 0.001). At 6 wk, aging negatively influenced newly formed bone (88.12 ± 2.90% and 78.19 ± 5.35%, p < 0.001, for groups control and aged, respectively) and ERD (0.01 ± 0.006 mm and 0.34 ± 0.18 mm, p = 0.003), but not BF (98.15 ± 2.43% and 87.87 ± 11.63%, p > 0.05). No new cementum was formed along the root surface in the above groups.Conclusion:  Within the limits of the present study, data analysis suggests that aging may impair, but not prevent, periodontal healing.
Regulation of epithelial cell growth factor receptor protein and gene expression using a rat periodontitis model
Authors: Ekuni D. , Firth J. D. , Putnins E. E. 
Published: June 2006

Background and Objective:  Regulation of epithelial cell behavior associated with periodontitis is not well elucidated but many responses will ultimately be regulated by growth factor receptors. Using a rat experimental periodontitis model, protein and gene expression of select growth factor receptors in junctional and pocket epithelium were examined.Material and Methods:  Periodontal disease was induced by daily topical application of lipopolysaccharide using an established protocol. Animals were killed at time 0 (control), and at 2 and 8 wk. Frozen tissue samples were collected from the right palatal gingival soft tissue, and the left periodontal tissues were decalcified and embedded in paraffin. Laser microdissection and quantitative reverse transcription–polymerase chain reaction (qRT–PCR) was used to quantify keratinocyte growth factor receptor (KGFR), hepatocyte growth factor receptor (HGFR), epidermal growth factor receptor (EGFR) and fibroblast growth factor receptor 1 (FGFR1) gene expression, and in situ RT–PCR localized these increases to specific epithelial cells. Receptor protein expression was examined immunohistochemically. In cell culture, induction of HGFR and KGFR protein expression by serum, lipopolysaccharide and pro‐inflammatory cytokines were examined using flow cytometry.Results:  Eight‐week tissue samples exhibited histological changes consistent with periodontitis. KGFR and HGFR gene and protein expression were significantly induced at the 8 wk time point. KGFR expression was significantly up‐regulated in basal and parabasal pocket epithelial cells, but HGFR was up‐regulated throughout the pocket epithelium. In cell culture serum, lipopolysaccharide and pro‐inflammatory cytokines, interleukin‐1β and tumour necrosis factor‐α significantly induced KGFR protein receptor expression, but HGFR expression was only induced by serum.Conclusion:  KGFR and HGFR are highly up‐regulated in this model of periodontal disease and may play a significant role in regulating the proliferation and migration of pocket epithelium.
Helicobacter pylori infection induces accumulation of Vδ1 T cells via CCR2 upregulation
Authors: FUTAGAMI S. , HIRATSUKA T. , SHINDO T. , HAMAMOTO T. , UEKI N. , SUZUKI K. , KUSUNOKI M. , WADA K. , MIYAKE K. , OHASHI K. , GUDIS K. , TSUKUI T. , SAKAMOTO C. 
Published: June 2006

SummaryBackgroundWe investigated factors that impact γδ T‐cell phenotype accumulation in Helicobacter pylori‐infected gastric mucosa and peripheral blood.AimTo determine whether H. pylori infection induces accumulation of Vδ1 T cells via CC chemokine receptor 2 (CCR2) upregulation.MethodsMucosal biopsy samples from 22 H. pylori‐free and 75 H. pylori‐infected patients were classified into grades I–III gastritis groups as per our previous study. The number of γδ, Vδ1 and Vδ2 T cells was evaluated by immunostaining and then compared with counts in 17 patients after H. pylori eradication. TGF‐β, IFN‐γ and CCR2 mRNA expression levels in Vδ1 T cells stimulated by H. pylori component were also evaluated.Results γδ T‐cell count was significantly higher in grade III gastritis patients, who exhibited strong IgA and IgG responses to H. pylori urease, than in other groups. Vδ1 T cells were found dominantly residing in H. pylori‐infected gastric mucosa, whereas Vδ2 T cells were mainly found in peripheral blood. Vδ1 T‐cell count was significantly reduced after H. pylori eradication therapy. In in vitro studies, H. pylori component stimulation significantly upregulated both TGF‐β and IFN‐γ production in supernatant from stimulated Vδ1 T cells. Moreover, CCR2 mRNA expression in Vδ1 T cells stimulated with H. pylori components was significantly increased.ConclusionAccumulation of Vδ1 T cells may occur through the upregulation of CCR2 expression.
Comparison of efficacies of dual therapy and triple therapy using rabeprazole in second‐line eradication of Helicobacter pylori in Japan
Authors: KAWAI T. , KAWAKAMI K. , KATAOKA M. , TAIRA S. , ITOI T. , MORIYASU F. , TAKAGI Y. , AOKI T. , RIMBARA E. , NOGUCHI N. , SASATSU M. 
Published: June 2006

SummaryBackgroundThe only authorized second‐line Helicobacter pylori regimen in Japan is proton pump inhibitor + amoxycillin + clarithromycin. However, it has been reported that this second‐line regimen is not effective. In this study, we evaluated the efficacy of dual and triple eradication therapies using rabeprazole as second‐line H. pylori eradication regimens.AimTo evaluate the efficacy of dual and triple eradication therapies using rabeprazole as second‐line H. pylori eradication therapy.MethodsSixty‐two H. pylori‐positive patients with first‐line eradication failure were randomly assigned to two groups. The RAM group was administered rabeprazole 20 mg + amoxycillin 1500 mg + metronidazole 500 mg daily for 1 week. The RA group was administered rabeprazole 40 mg + amoxycillin 2000 mg daily for 2 weeks. Eradication of H. pylori infection was determined by 13C‐urea breath testing at 8 weeks after completion of treatment. Prior to treatment, amoxycillin, clarithromycin and metronidazole susceptibility, and CYP2C19 phenotype status were determined.ResultsEradication rates for the RAM and RA groups were 97% and 74%, respectively. Eradication rates were not influenced by CYP2C19 phenotype in either group. Eradication rates for clarithromycin‐resistant patients were 100% in the RAM group and 77% in the RA group.ConclusionsOne week with RAM therapy and 2 weeks with RA therapy were effective as second‐line eradication therapy for H. pylori infection; moreover, RAM was more effective than RA therapy.
Review article: is there a common principle in the development of gastrointestinal cancers? Stem cells in the origin of cancer
Authors: WRIGHT N. A. 
Published: June 2006

SummaryBackgroundAccumulating evidence, outlined in this review, at last provides some elucidation of the orgin of gastrointestinal epithelial tumours.MethodsNew techniques, such as following the process of crypt or gastric gland purification following mutation in genes encoded by the mitochondrial genome, have shown that mutations spead within the proliferative unit, either gastric gland or intestinal crypt, by clonal purification or monoclonal conversion. Spreading otside the crypt or gland then takes place by fission.ResultsFuture research should focus on the mecanisim by which mutated stem cells colonize crypts, and on the mechanisms of crypt fission itself.
Efficacy of proton pump inhibitors for cellular proliferation and apoptosis in Barrett's oesophagus with different mucin phenotypes
Authors: AMANO Y. , CHINUKI D. , YUKI T. , TAKAHASHI Y. , ISHIMURA N. , KAZUMORI H. , KUSHIYAMA Y. , KARIM RUMI M. A. , ISHIHARA S. , KINOSHITA Y. 
Published: June 2006

SummaryBackgroundControversy exists concerning the efficacy of acid suppressants in the regression of Barrett's oesophagus.AimTo evaluate the effect of proton pump inhibitors on cyclooxygenase‐2 expression, cellular proliferation and apoptosis in Barrett's oesophagus with different mucin phenotypes.MethodsFour hundred and sixty‐six biopsy samples of Barrett's oesophagus from 358 non‐treatment patients and 81 from 61 chronic proton pump inhibitor users were immunohistochemically examined using anti‐cyclooxygenase‐2 protein, anti‐proliferating cell nuclear antigen and anti‐single stranded DNA antigens in both mucin phenotypes of Barrett's oesophagus.ResultsPrevalence of the cyclooxygenase‐2 expression pattern did not significantly differ between the non‐treatment and proton pump inhibitor users. In those using proton pump inhibitors, significant suppression of the proliferating cell nuclear antigen index was found in Barrett's oesophagus with the gastric‐predominant mucin phenotype, but not with the intestinal‐predominant mucin phenotype. Apoptosis indices in chronic proton pump inhibitor users did not significantly differ between the two mucin phenotypes.ConclusionsProton pump inhibitors suppress cellular proliferation in Barrett's oesophagus with the gastric‐predominant mucin phenotype but not in that with the intestinal‐predominant mucin phenotype. This finding may at least partly explain the ongoing controversy surrounding the notion that all cases of Barrett's oesophagus respond to acid‐suppressive therapy.
Interactions between the grading of gastric atrophy associated with Helicobacter pylori infection and the severity of clinical symptoms and delay in gastric emptying in patients with functional dyspepsia
Authors: KADOUCHI K. , TOMINAGA K. , OCHI M. , KAWAMURA E. , SASAKI E. , SHIBA M. , WATANABE T. , FUJIWARA Y. , OSHITANI N. , HIGUCHI K. , SHIOMI S. , ARAKAWA T. 
Published: June 2006

SummaryBackgroundAtrophic and inflammatory changes in the gastric mucosa are commonly observed in Japanese patients with functional dyspepsia. However, detailed data regarding the correlation between the severity of these changes and the symptoms of functional dyspepsia are not available.AimTo evaluate grading scales of gastric atrophy and inflammation, severity of clinical symptoms, and gastric emptying in patients with functional dyspepsia.MethodsNinety‐three patients with dyspepsia were enrolled. The severity of gastric atrophy was graded through serological and histological examination, and gastric inflammation was evaluated histologically. Clinical symptoms were evaluated on the Gastrointestinal Symptoms Rating Scale, including subscales for abdominal pain, acid reflux, diarrhoea, indigestion and constipation. Gastric emptying half‐time was measured using a radioisotope technique.Results Helicobacter pylori infection and gastric inflammation influenced neither clinical symptoms nor gastric emptying time. However, a correlation was observed between gastric atrophy as graded by serological examination and indigestion (R = 0.31, P = 0.01). Histological examination also showed a correlation between gastric atrophy and abdominal pain and indigestion (R = 0.31, P = 0.04 and R = 0.35, P = 0.02 respectively).ConclusionGastric atrophy associated with H. pylori infection may be partly responsible for the clinical symptoms experienced by patients with functional dyspepsia.