bluuebunny/crossref_metadata_2025_split huggingface dataset:
Quality of life in acute and maintenance treatment of non‐erosive and mild erosive gastro‐oesophageal reflux disease
Authors: PACE F. , NEGRINI C. , WIKLUND I. , ROSSI C. , SAVARINO V. ,   THE ITALIAN ONE INVESTIGATORS STUDY GROUP
Published: August 2005

SummaryBackground:  Quality of life has been assessed in a large, multicentre randomized, open label study.Aim:  To evaluate the economic and clinical consequences of two different maintenance treatment modalities, administered to 6017 gastro‐oesophageal reflux disease patients at 451 gastroenterological centres in Italy.Methods:  Adult gastro‐oesophageal reflux disease patients received, at enrolment, an acute treatment of esomeprazole 40 mg/day for 4 weeks and, if successfully treated, were randomized into two maintenance treatment strategies: esomeprazole 20 mg/day or esomeprazole on demand for 6 months. A baseline endoscopy allowed the exclusion of grade II–IV oesophagitis according to Savary–Miller's classification. Burden of gastro‐oesophageal reflux disease was measured at baseline by the generic questionnaire Short‐Form 36 and by a disease specific instrument, quality of life in reflux and dyspepsia (QOLRAD), also administered at start and conclusion of maintenance period. Investigators were required to collect patient judgement about the degree of satisfaction with treatment effect on heartburn, with a 7‐point scale.Results:  A comparison between Short‐Form 36 scores and the normative source of the Italian general population suggested that symptomatic gastro‐oesophageal reflux disease patients experience a worse quality of life than the general population. At the end of the 4‐week treatment with esomeprazole 40 mg all (QOLRAD) dimensions showed a statistically significant (P < 0.0001) and clinically meaningful improvement.Satisfaction level towards treatment was reported high in the total enrolled population after acute treatment with esomeprazole 40 mg/day (96.2% satisfied and 64.4% very satisfied). A statistically significant difference in (QOLRAD) scores was registered at the end of maintenance phase in favour of the continuous regimen, nevertheless the size of this difference was very small in all dimensions; similarly, the proportion of patients very satisfied was slightly higher in the continuous treatment arm (64.5%) than in the on‐demand arm (59.7%).Conclusions:  Gastro‐oesophageal reflux disease can significantly impair health‐related quality of life and esomeprazole therapy allows immediate relief in the acute phase of the disease. Quality of life improvement was maintained during the 6‐month follow‐up with a slight difference in term of quality of life in reflux and dyspepsia scores and patients’ satisfaction in favour of the continuous treatment strategy.
Impact of precore and core promoter mutations on hepatic histology in patients with chronic hepatitis B
Authors: YUAN H.‐J. , YUEN M.‐F. , KA‐HO WONG D. , SUM S.‐M. , SABLON E. , OI‐LIN NG I. , LAI C.‐L. 
Published: August 2005

SummaryBackground:  The details of liver histology of patients with precore and core promoter mutations are still not clear.Aim:  To determine the role of precore and core promoter mutations in liver histology in Chinese patients with chronic hepatitis B.Patients and methods:  Intrahepatic hepatitis B virus DNA (by COBAS Amplicor hepatitis B virus Monitor test) and precore and core promoter mutations (by a line probe assay) were measured in 54 chronic hepatitis B patients. Expression of hepatitis B core antigen, hepatitis B e antigen and hepatitis B surface antigen was determined by immunohistological staining. Histological activity index was scored according to Knodell's criteria.Results:  Compared with patients without core promoter mutations, patients with core promoter mutations had more severe intrahepatic inflammation and fibrosis, and more cytoplasmic expression of hepatitis B core antigen (P = 0.028). No such differences were found in patients with and without precore mutations. Logistic regression showed that core promoter mutations were independently associated with cytoplasmic expression of hepatitis B core antigen (P = 0.026). Intrahepatic hepatitis B virus DNA levels correlated with serum hepatitis B virus DNA levels (r = 0.71, P < 0.001) and the percentage of hepatitis B core antigen‐positive hepatocytes (r = 0.37, P = 0.047), but had no correlation with serum alanine aminotransferase levels nor the degree of inflammation and fibrosis.Conclusions:  Patients with core promoter mutations had more severe inflammation and fibrosis, and more frequent cytoplasmic expression of hepatitis B core antigen. This suggested that core promoter mutations might cause more serious liver disease.
Is coeliac disease screening in risk groups justified? A fourteen‐year follow‐up with special focus on compliance and quality of life
Authors: VILJAMAA M. , COLLIN P. , HUHTALA H. , SIEVÄNEN H. , MÄKI M. , KAUKINEN K. 
Published: August 2005

SummaryBackground:  The benefits of serologic screening for coeliac disease in asymptomatic individuals are debatable.Aim:  To investigate dietary compliance, quality of life and bone mineral density after long‐term treatment in coeliac disease patients found by screening in risk groups.Methods:  The study comprised 53 consecutive screen‐detected coeliac patients diagnosed 14 years (median) ago. Dietary compliance was assessed by interview, 4‐day food record and serology. Quality of life was evaluated by the Psychological General Well‐Being and SF‐36 questionnaires, gastrointestinal symptoms by the Gastrointestinal Symptom Rating Scale and bone mineral density by dual‐energy x‐ray absorptiometry. Comparisons were made to 44 symptom‐detected‐treated coeliac patients, 110 non‐coeliac subjects and the general population.Results:  A total of 96% of screen‐detected and 93% of symptom‐detected coeliac patients adhered to a strict or fairly strict gluten‐free diet. In screen‐detected patients, quality of life and gastrointestinal symptoms were similar to those in symptom‐detected patients or non‐coeliac controls and bone mineral density was similar to that in the general population.Conclusions:  Long‐term dietary compliance in screen‐detected patients was good. Quality of life and bone mineral density were comparable with those in non‐coeliac subjects and the general population. Active screening in coeliac disease risk groups seems to be reasonable rather than harmful.
Is a long‐term ranitidine‐based triple therapy against Helicobacter pylori only a heritage of the past? A prospective, randomized clinicopharmacological study
Authors: PELLEGRINI M. , URSO R. , GIORGI G. , BAYELI P. F. , MARZOCCA G. , CERRETANI D. 
Published: August 2005

SummaryBackground:  Acid suppression plus two antibiotics is currently considered the gold standard anti‐Helicobacter pylori treatment, but the effective role of gastric antisecretory drugs is still poorly understood.Aims:  To compare a 14‐day ranitidine‐based triple regimen against Helicobacter pylori with one based on omeprazole, and to study the influence of antisecretory drugs on metronidazole pharmacokinetics in human plasma.Methods:  A total of 150 dyspeptic H. pylori‐infected patients were randomized for ranitidine 300 mg b.d. (RCM group) or omeprazole 20 mg b.d. (OCM group) 14‐day triple therapy, with clarithromycin 500 mg b.d. and metronidazole 500 mg b.d. On the eighth day of therapy, metronidazole pharmacokinetics was studied in plasma by high‐performance liquid chromatography. The pharmacokinetic parameters (terminal half‐life, area under the curve, peak‐plasma level, peak time) of metronidazole were computed using standard non‐compartmental methods. H. pylori status was monitored before and 4 weeks after the end of therapy by histology, serology and rapid urease test.Results:  On an intention‐to‐treat basis, eradication rates were 91 and 76% for the RCM and OCM groups respectively (P < 0.02). Significantly different pharmacokinetic parameters of metronidazole were found between the groups: peak‐plasma level (P < 0.01) and area under the curve (P < 0.02).Conclusion:  Our results show that the RCM regimen was more effective than that based on OCM and that the antisecretory drugs affected metronidazole availability, increasing the efficacy of ranitidine‐based regimens.
Retrograde cerebral perfusion of oxygenated, compacted red blood cells attenuates brain damage after hypothermia circulation arrest of rat
Authors: Su D. S. , Wang X. R , Zheng Y. J. , Zhao Y. H. , Zhang T. J. 
Published: August 2005

Background:  It was proved that higher haematocrit (Hct) might improve the function of brain after hypothermia circulation arrest (HCA). In the present study we established a new rat HCA model and investigated whether retrograde cerebral perfusion of oxygenated, compacted red blood cells (RBC) could attenuate brain injury after HCA.Methods:  A new rat HCA model was developed and rats were randomly distributed into three groups: HCA group, HCA combined with retrograde cerebral perfusion of oxygenated, compacted red blood cell group (HCArcp group), and sham operation group (sham op. group). Animals both in the HCA group and in the HCArcp group underwent HCA 90 min at 18°C. Brain damage after HCA was evaluated with light microscopy and electron microscopy. Immunohistochemistry and RT‐PCR techniques were used to measured the different expressions of the C‐Fos, Bcl‐2, Bax mRNA and protein among the groups. Additionally we measured the wet/dry ratio of the brain in order to evaluate the oedema degree after HCA.Results:  The new HCA model of rat we developed was comparable to the clinical setting not only in terms of the intubation, anaesthesia method and materials employed but also in terms of the priming volume in relation to body weight. The number of injured neurones in the hippocampus CA1 and parietal cortex, but not in the thalamus of the HCA group, was significantly greater than that of the HCArcp group (P < 0.05). The mean score of mitochondrion of the hippocampus CA1 in the HCA group was significantly higher than in the HCArcp group (P < 0.05). The expression of C‐Fos, Bax mRNA and protein in the hippocampus CA1 and/or parietal cortex area was higher in the HCA group than in the HCArcp group (P < 0.05). Expression of the mRNA and protein of Bcl‐2 was higher in the HCArcp group than in the HCA group (P < 0.05). The degree of oedema after HCA between the HCA group and HCArcp group had no significant difference (P > 0.05).Conclusions:  We established a new rat model of HCA comparable to the clinical setting. Retrograde cerebral perfusion of oxygenated, compacted RBC is a simple, effective, and safe method to protect the brain during HCA. Adjusting the gene expression in relation to apoptosis might contribute to the neuroprotective effects of a retrograde cerebral infusion of oxygenated, compacted RBC.
Glycine – an important neurotransmitter and cytoprotective agent
Authors: Gundersen R. Y. , Vaagenes P. , Breivik T. , Fonnum F. , Opstad P. K. 
Published: August 2005

Background:  Glycine, the simplest of the amino acids, is an essential component of important biological molecules, a key substance in many metabolic reactions, the major inhibitory neurotransmitter in the spinal cord and brain stem, and an anti‐inflammatory, cytoprotective, and immune modulating substance.Material and methods:  Based on available literature, we discuss some of the important biological properties of glycine. In addition, we describe some clinical disorders where glycine plays a central role, either as an essential structural element, or through its metabolism or receptors.Results:  The past few years have witnessed a broadening of glycine research. The traditional prime interest in aspects related to its role as an inhibitory neurotransmitter in the central nervous system has been expanded to equally emphasize other organs and tissues. With the demonstration of glycine‐gated chloride channels on neurons in the central nervous system, on most leukocytes, and subsequently on other cells as well, a unifying mechanism of action accounting for many of the widespread effects of glycine has been found.Conclusions:  Glycine is a simple, easily available, and inexpensive substance with few and innocuous side‐effects. The diversity of biological activities is well documented in the literature. Despite this, glycine has only gained a modest place in clinical medicine.
Loss of connexin36 increases retinal cell vulnerability to secondary cell loss
Authors: Striedinger Katharine , Petrasch‐Parwez Elisabeth , Zoidl Georg , Napirei Markus , Meier Carola , Eysel Ulf T. , Dermietzel Rolf 
Published: August 2005

AbstractAccruing evidence indicates that gap junctions are involved in neuronal survival after brain injury. The present study was aimed at clarifying the contribution of the neuronal gap‐junction protein connexin36 (Cx36) to secondary cell loss after injury in the mouse retina. A focal retinal lesion was induced by infrared laser photocoagulation. Remarkably, this model allowed spatial and temporal definition of the lesion with high reproducibility. Moreover, Cx36 is abundantly expressed in the retina and plays an essential role in the visual transmission process. Taking advantage of these features, cell death was assessed using TUNEL assay and light and electron microscopy, and the extent of Cx36 expression was studied by immunohistochemistry, Western blot, in situ hybridization and real‐time RT‐PCR. Secondary cell loss was most prominent between 24 and 48 h after lesioning. This peak was accompanied by an increase in Cx36 expression. When cultured explanted retinas were subjected to gap‐junction blockers a significant increase in the extent of secondary cell loss after laser photocoagulation became evident. Using the same experimental paradigm we compared the incidence of cell death in wild‐type and Cx36–/– mice. A significant increase in total number of TUNEL‐positive cells occurred in the Cx36–/– mice compared to controls. From these data we conclude that Cx36 contributes to the survival and resistance against damage of retinal cells and thus constitutes a protective factor after traumatic injury of the retina.
The unilateral 6‐OHDA rat model of Parkinson's disease revisited: an electromyographic and behavioural analysis
Authors: Metz Gerlinde A. , Tse Arthur , Ballermann Mark , Smith Lori K. , Fouad Karim 
Published: August 2005

AbstractThe characteristic locomotor disturbances of Parkinson's disease (PD) include shuffling gait, short steps and low walking velocity. In this study we investigated features of walking and turning in a rat model of PD caused by unilateral infusion of the neurotoxin 6‐hydroxydopamine (6‐OHDA). We assessed gait and electromyographic (EMG) patterns of the ankle flexor tibialis anterior and the knee extensor vastus lateralis of the hindlimb, and triceps brachii of the forelimb, during overgound locomotion, spontaneous rotation (turning) and apomorphine‐induced rotation. When compared with control rats, rats with unilateral dopamine depletion displayed a shuffling gait and short stride lengths. This locomotor pattern was accompanied by prolonged ankle flexor activity on the ipsilateral side, and prolonged activity of knee extensors on the contralateral side. The dopamine depletion also led to enhanced contraversive rotations after an apomorphine challenge. The EMG recordings during drug‐induced rotation suggested that hindlimb stepping was a reflective response to an active drive produced by forelimbs. The EMG recordings of the contralateral side during rotation were marked by reduced ankle flexor activity and increased knee extensor activity. Furthermore, EMG recordings indicated that dopamine‐agonists induce rotational bias by altering the coupling between ipsi‐ and contralateral hindlimbs, and between forelimbs. In straight walking, however, the gait of 6‐OHDA lesion animals reflected normal, coupled hindlimb stepping as controlled by spinal pattern generators. The data suggest that the unilateral rat model of PD resembles key features of human parkinsonian gait, and that asymmetric descending input may underlie the observed changes in gait patterns.
Transient maternal hypothyroxinemia at onset of corticogenesis alters tangential migration of medial ganglionic eminence‐derived neurons
Authors: Cuevas Estela , Ausó Eva , Telefont Martin , De Escobar Gabriella Morreale , Sotelo Constantino , Berbel Pere 
Published: August 2005

AbstractCorrect positioning of cortical neurons during development depends on the radial migration of the projection neurons and on the coordinated tangential and radial migrations of the subcortically generated interneurons. As previously shown, a transient and moderate maternal deficiency in thyroxin during early corticogenesis alters the radial migration of projection neurons. To determine if a similar effect might also affect tangential migration of medial ganglionic eminence (MGE)‐derived neurons at the origin of cortical interneurons, explants of MGE from green fluorescent protein (GFP)‐transgenic embryos were implanted into flat cortical mounts from wild‐type embryos. The distances covered and the preferential migration (medially) of GFP‐MGE neurons from embryos of hypothyroxinemic dams are not affected in their tangential migration into wild‐type control cortices. In contrast, when GFP‐MGE neurons from embryos of control or hypothyroxinemic dams migrate within cortices from embryos of hypothyroxinemic dams, the GFP‐MGE‐derived neurons lose their preferential direction of migration, although they still migrate for long distances throughout the cortex. Our results show that maternal hypothyroxinemia alters the tangential migration of GFP‐MGE‐derived neurons in the neocortex of the progeny and suggest that this alteration is not derived from the migratory neurons themselves but through undefined short‐ and long‐range cues responsible for the guidance of their migration.
Transcriptional involvement of protein kinase C‐alpha isozyme in amphetamine‐mediated appetite suppression
Authors: Hsieh Yih‐Shou , Yang Shun‐Fa , Chiou Hui‐Ling , Kuo Dong‐Yih 
Published: August 2005

AbstractAmphetamine (AMPH) is known as an anorectic agent. The anorectic action of AMPH has been attributed to its inhibitory action on hypothalamic neuropeptide Y (NPY), an appetite stimulant in the brain. The molecular mechanisms behind this anorectic action of AMPH are still unclear. This study investigated the possible role of protein kinase C (PKC) isotypes in this anorectic action. Results revealed that most PKC isotypes (α, βII, γ, δ, η, λ and ζ), except βI and ε isotypes, were stimulated during a repeated treatment of AMPH. Among these stimulated isotypes, three isotypes (α, δ, λ) were activated and expressed in a similar manner, while the other isotypes were expressed differently and specifically. To determine if PKCα was involved in the anorectic response of AMPH, the infusions of antisense oligonucleotide into the brain were performed 1 h before daily AMPH treatment in freely moving rats, and the results showed that PKCα knock down could block the anorectic response and restore NPY mRNA levels in AMPH‐treated rats. These results suggest that PKC isotypes‐ (at least the α isotype), related modification of NPY gene expression in hypothalamus might play an essential role in the central regulation of AMPH‐mediated feeding suppression.
Individual differences in male rat ejaculatory behaviour: searching for models to study ejaculation disorders
Authors: Pattij Tommy , De Jong Trynke R. , Uitterdijk Andre , Waldinger Marcel D. , Veening Jan G. , Cools Alexander R. , Van Der Graaf Piet Hein , Olivier Berend 
Published: August 2005

AbstractIn addition to investigating sexual function in rats that display normal ejaculatory behaviour, studying rats that are either ‘hyposexual’ or ‘hypersexual’ may provide important insights into the aetiology of ejaculatory dysfunctions in men, such as premature and retarded ejaculation. To this end, rats were matched into groups of ‘sluggish’, ‘normal’ and ‘rapid’ ejaculators based on their ejaculation frequencies displayed in a series of weekly sexual behaviour tests. Selecting rats on this parameter revealed large and stable differences in other parameters of sexual behaviour as well, including ejaculation latency and mount frequency but not intromission frequency and mount latency, putative indices of sexual motivation. Neuroanatomically, Fos immunoreactivity as a measure of neuronal activation was increased in rapid ejaculators compared with sluggish ejaculators in ejaculation‐related brain areas, presumably associated with the differences in ejaculatory behaviour. Although the total number of oxytocin neurones within subregions of the hypothalamus did not differ between groups, in the supraoptic nucleus of the hypothalamus more oxytocin neurones were activated in rapid ejaculators compared with the other groups. Apart from the differences observed in ejaculatory behaviour, groups did not differ with respect to their locomotor activity and approach‐avoidance behaviour as measured in the elevated plus‐maze. Finally, apomorphine‐induced stereotypy was similar in sluggish and rapid ejaculators, suggesting no large differences in dopamine susceptibility. Altogether, the present results suggest stable differences in male rat ejaculatory behaviour. Further exploring the neurobiological mechanisms underlying these differences may be a promising approach to gain insights into the aetiology of sexual dysfunctions such as premature, retarded or an‐ejaculation.
Dietary n‐3 polyunsaturated fatty acid depletion activates caspases and decreases NMDA receptors in the brain of a transgenic mouse model of Alzheimer's disease
Authors: Calon Frédéric , Lim Giselle P. , Morihara Takashi , Yang Fusheng , Ubeda Oliver , Salem Norman , Frautschy Sally A. , Cole Greg M. 
Published: August 2005

AbstractEpidemiological data indicate that low n‐3 polyunsaturated fatty acids (PFA) intake is a readily manipulated dietary risk factor for Alzheimer's disease (AD). Studies in animals confirm the deleterious effect of n‐3 PFA depletion on cognition and on dendritic scaffold proteins. Here, we show that in transgenic mice overexpressing the human AD gene APPswe (Tg2576), safflower oil‐induced n‐3 PFA deficiency caused a decrease in N‐methyl‐d‐aspartate (NMDA) receptor subunits, NR2A and NR2B, in the cortex and hippocampus with no loss of the presynaptic markers, synaptophysin and synaptosomal‐associated protein 25 (SNAP‐25). n‐3 PFA depletion also decreased the NR1 subunit in the hippocampus and Ca(2+)/calmodulin‐dependent protein kinase (CaMKII) in the cortex of Tg2576 mice. These effects of dietary n‐3 PFA deficiency were greatly amplified in Tg2576 mice compared to nontransgenic mice. Loss of the NR2B receptor subunit was not explained by changes in mRNA expression, but correlated with p85α phosphatidylinositol 3‐kinase levels. Most interestingly, n‐3 PFA deficiency dramatically increased levels of protein fragments, corresponding to caspase/calpain‐cleaved fodrin and gelsolin in Tg2576 mice. This effect was minimal in nontransgenic mice suggesting that n‐3 PFA depletion potentiated caspase activation in the Tg2576 mouse model of AD. Dietary supplementation with docosahexaenoic acid (DHA; 22 : 6n‐3) partly protected from NMDA receptor subunit loss and accumulation of fodrin and gelsolin fragments but fully prevented CaMKII decrease. The marked effect of dietary n‐3 PFA on NMDA receptors and caspase/calpain activation in the cortex of an animal model of AD provide new insights into how dietary essential fatty acids may influence cognition and AD risk.