bluuebunny/crossref_metadata_2025_split huggingface dataset:
Outcomes of split versus reduced‐size grafts in pediatric liver transplantation
Authors: OSWARI HANIFAH , LYNCH STEPHEN V , FAWCETT JONATHAN , STRONG RUSSELL W , EE LOOI C 
Published: October 2005

AbstractBackground:  Split‐liver transplantation, where two grafts are created from a single donor organ, is a means of overcoming donor organ scarcity. There are few data comparing outcomes of split with reduced‐size liver grafts, which is the most common type of cadaveric graft in pediatric liver transplantation. The aims of the present paper were to compare survival and complication rates between split and reduced‐size cadaveric grafts in pediatric patients receiving a liver transplant in Brisbane.Methods:  Review of the Queensland Liver Transplant Service database was undertaken. All pediatric patients who received either a cadaveric split or reduced‐size graft between 1985 and 2000 were examined. The incidence of patient and graft survival, vascular complications and biliary complications were identified.Results:  A total of 251 liver transplants were performed of which 138 were reduced‐size grafts and 30 were split grafts. There were no differences in etiology of liver disease, mean age, weight, and urgency of transplant between the two groups. One‐year patient and graft survivals were comparable at 73% and 67%, respectively, in both groups. There was no difference in the incidence of vascular complications between groups. Biliary complications were significantly more common after split grafts when compared with reduced‐size grafts (21%vs 4%, P < 0.0001) but did not affect patient or graft survival.Conclusions:  Survival and vascular complications after split‐liver grafts were comparable to outcomes after reduced‐size grafts. Biliary complications occur more commonly with split‐liver grafts but did not affect patient or graft survival. It is recommended that every pediatric recipient be considered for a split‐liver graft.
Interferon/long‐term lamivudine combination therapy in anti‐HBe positive chronic hepatitis B patients
Authors: NIKOLAIDIS NIKOLAOS L , GIOULEME OLGA I , TZIOMALOS KONSTANTINOS A , SAVERIADIS ADAMOS S , GRAMMATIKOS NIKOLAOS , DOUKELIS PANAGIOTIS , VOUTSAS ANASTASIOS D , VASSILIADIS THEMISTOKLIS , PATSIAOURA KALLIOPI , ORFANOU‐KOUMERKERIDOU ELENI , BALASKA AIKATERINI , EUGENIDIS NIKOLAOS P 
Published: October 2005

AbstractBackground:  Monotherapy with a single antiviral agent is insufficient in controlling hepatitis B virus infection in the majority of patients with anti‐HBe positive chronic hepatitis B. Interferon/long‐term lamivudine combination therapy was evaluated to determine if this strategy would improve treatment efficacy and reduce the emergence of lamivudine resistance.Methods:  In total, 36 consecutive anti‐HBe positive patients were treated with interferon (3 MU subcutaneously three times weekly) and lamivudine (100 mg orally once a day) for 12 months. After completion of the combined treatment, all patients continued to receive lamivudine monotherapy indefinitely.Results:  Overall, 35 patients (97%) showed virological response at 12 months. Four patients (11%) cleared HBsAg and developed anti‐HBs. During the follow‐up time, after the discontinuation of interferon, of 30 ± 12 months (range: 7–57 months), 13 patients (36%) exhibited breakthrough infection. The cumulative rates of breakthrough infection at the end of 1, 2, 3 and 4 years of treatment were 0%, 14%, 32%, and 59%, respectively.Conclusions:  Combination therapy appears to be effective and may also delay the selection of lamivudine‐resistant variants. However, controlled trials are definitely warranted to clarify the potential benefits of combination antiviral treatment over monotherapy.
Pathogens causing community gastroenteritis in Australia
Authors: SINCLAIR MARTHA I , HELLARD MARGARET E , WOLFE RORY , MITAKAKIS TERESA Z , LEDER KARIN , FAIRLEY CHRISTOPHER K 
Published: October 2005

AbstractBackground and Aim:  Many individuals with gastrointestinal symptoms do not seek medical attention and so there is little known about the pathogens involved in most cases of community gastroenteritis. We aimed to identify the pathogens responsible for community gastroenteritis and to examine the associated symptoms.Methods:  In a prospective study of 2811 subjects over 15 months, fecal pathogens were examined following highly credible gastroenteritis (HCG) events. The population consisted of family units of at least two children (≤15 years‐old) and two adults each. Fecal samples were tested for a range of bacterial, viral and protozoal pathogens. Gastroenteric episode duration and symptoms such as vomiting, nausea and diarrhea were measured.Results:  One or more pathogens were identified in 198 of a total 791 specimens collected. Pathogens detected most often were Norovirus virus (10.7%), pathogenic E. coli (6.7%), Campylobacter spp. (3.0%) and Giardia sp. (2.5%). Children were more prone than adults to all the pathogens tested, except E. coli. Children infected with Campylobacter were 8.3 times more likely (95% CI: 2.7–25.4) to have a longer duration of diarrhea than children with Norovirus (P < 0.001). Similarly, children infected with E. coli had increased persistence of diarrhea compared to Norovirus (OR = 3.5; 95% CI: 1.3–9.5; P = 0.02). Infection with Norovirus in children meant greater persistence of vomiting symptoms than infection with Campylobacter (P = 0.005), E. coli (P = 0.03), or if no pathogen was identified (P = 0.004). Adults usually vomited for fewer days than children while duration of diarrhea was similar to children.Conclusions:  Many of the pathogens responsible for cases of gastroenteritis in the Australian community are likely to go undetected by current surveillance systems and routine clinical practice.
Monitoring and management of antituberculosis drug induced hepatotoxicity
Authors: AGAL SUBHASH , BAIJAL RAJIV , PRAMANIK SNEHANSHU , PATEL NIKHIL , GUPTE PARIJAT , KAMANI PRAFUL , AMARAPURKAR DEEPAK 
Published: October 2005

AbstractBackground:  Hepatotoxicity to antituberculosis therapy (ATT) poses a major challenge. This often results in inadequate therapy. The risk of fulminant hepatic failure and mortality is high once icteric hepatitis develops. There is no consensus on monitoring protocols and for the reintroduction of ATT.Methods:  All patients (from the Department of Internal Medicine and Gastroenterology, Jagjivanram Hospital and the Department of Gastroenterology, Bombay Hospital, Mumbai, India) with a diagnosis of tuberculosis, who were to receive ATT during the study period, were included in the present study for prospective periodic laboratory monitoring for the development of hepatotoxicity. Those patients who developed hepatotoxicity formed Group A (n = 21), whereas those who did not develop hepatotoxicity were included in Group C (n = 179). For the purpose of comparison with Group A, all the patients who presented directly with ATT induced hepatotoxicity during the study period were categorized as Group B (n = 24). Group A and B were further studied after normalization of liver functions for sequential reintroduction with therapeutic doses at a weekly interval.Results:  In Group A, 66.6% (14 patients) of the patients were diagnosed in the asymptomatic period. Seven patients had symptomatic hepatitis, but none had icteric illness. There were no mortalities in Group A. In contrast, all the patients in Group B had symptomatic hepatitis (75% icteric hepatitis). There was a mortality rate of 16.6% (four patients). Of the 41 patients from Groups A and B who survived, reintroduction was successful in 38/39 (97.4%). In the remaining two patients who were in Group B, reintroduction was not attempted because of decompensated liver disease.Conclusions:  Periodic laboratory monitoring is important in detecting hepatotoxicity at an early stage, thereby preventing mortality. Sequential reintroduction is often successful.
Community‐based epidemiology of hepatitis B virus infection in West Bengal, India: Prevalence of hepatitis B e antigen‐negative infection and associated viral variants
Authors: CHOWDHURY ABHIJIT , SANTRA AMAL , CHAKRAVORTY RUNU , BANERJI ARUP , PAL SUPARNA , DHALI GOPAL K , DATTA SIBNARAYAN , BANERJI SOMA , MANNA BYOMKESH , CHOWDHURY SUSANTA ROY , BHATTACHARYA SUJIT K , MAZUMDER DEBENDRANATH GUHA 
Published: October 2005

AbstractBackground and Aims:  There is a paucity of population‐based epidemiological information regarding hepatitis B virus (HBV) infection in India. The present study was planned to outline the magnitude and pattern of HBV infection, hepatitis B e antigen (HBeAg)‐negative infection and the associated viral mutants in India.Methods:  A community‐based epidemiological study of HBV infection was carried out in West Bengal, India. Serological markers of infection and potential risk factors for HBV transmission were determined. Among the infected individuals, HBV‐DNA, genotypes and mutations in the precore (PC) stop codon and basal core promoter (BCP) regions were determined by DNA sequencing and polymerase chain reaction (PCR) restriction fragment length polymorphism methods.Results:  Of the 7653 people included in the study, 227 (2.97%) tested positive for hepatitis B surface antigen (HBsAg), of whom 204 (90%) were HBeAg‐negative and hepatitis B e antibody (anti‐HBe)‐positive, and 78% had normal alanine aminotransferase (ALT) levels. HBV‐DNA could be detected by PCR in only 32% of people. G1896A PC stop codon mutants were present in 12% of people, BCP mutants in 18% and the remainder (70%) of the HBeAg‐negative infections were associated with wild type sequences in these regions.Conclusions:  This first general population‐based epidemiological study of HBV infection from India suggests that HBV acquisition starts in early childhood and peaks in adulthood. Most infections in the community are e‐negative and inactive. The point prevalence of PC stop codon and BCP mutants is low in this primarily inactive and asymptomatic HBV‐infected population sample in eastern India.
Dynamics of directional selectivity in MT receptive field centre and surround
Authors: Perge János A. , Borghuis Bart G. , Bours Roger J. E. , Lankheet Martin J. M. , Van Wezel Richard J. A. 
Published: October 2005

AbstractWe studied receptive field organization of motion‐sensitive neurons in macaque middle temporal cortical area (MT), by mapping direction selectivity in space and in time. Stimuli consisted of pseudorandom sequences of single motion steps presented simultaneously at many different receptive field locations. Spatio‐temporal receptive field profiles were constructed by cross‐correlating stimuli and spikes. The resulting spike‐triggered averages revealed centre‐surround organization. The temporal dynamics of the receptive fields were generally biphasic with increased probability for the preferred direction at short latency (50–70 ms) and decreased probability at longer latency (80–100 ms). The response latency of the receptive field surround was on average 16 ms longer than that of the centre. Our results show that surround input and biphasic behaviour reflect two different mechanisms, which make MT cells specifically sensitive to motion contrast in space and time.
Cognitive disorders and neurogenesis deficits in Huntington's disease mice are rescued by fluoxetine
Authors: Grote Helen E. , Bull Natalie D. , Howard Monique L. , Van Dellen Anton , Blakemore Colin , Bartlett Perry F. , Hannan Anthony J. 
Published: October 2005

AbstractHuntington's disease (HD) is a neurodegenerative disorder caused by an expanded CAG trinucleotide repeat encoding an extended polyglutamine tract in the huntingtin protein. Affected individuals display progressive motor, cognitive and psychiatric symptoms (including depression), leading to terminal decline. Given that transgenic HD mice have decreased hippocampal cell proliferation and that a deficit in neurogenesis has been postulated as an underlying cause of depression, we hypothesized that decreased hippocampal neurogenesis contributes to depressive symptoms and cognitive decline in HD. Fluoxetine, a serotonin‐reuptake inhibitor commonly prescribed for the treatment of depression, is known to increase neurogenesis in the dentate gyrus of wild‐type mouse hippocampus. Here we show that hippocampal‐dependent cognitive and depressive‐like behavioural symptoms occur in HD mice, and that the administration of fluoxetine produces a marked improvement in these deficits. Furthermore, fluoxetine was found to rescue deficits of neurogenesis and volume loss in the dentate gyrus of HD mice.
Striatal dopaminergic responses observed in latent inhibition are dependent on the hippocampal ventral subicular region
Authors: Peterschmitt Y. , Hoeltzel A. , Louilot A. 
Published: October 2005

AbstractWe showed recently that behavioural and striatal dopaminergic (DA) responses obtained in latent inhibition are crucially dependent on the parahippocampal region, the entorhinal cortex. In the present study, we investigated the influence exerted by the hippocampal ventral subicular region (SUB) on the DA responses in the anterior part of the dorsal striatum using in vivo voltammetry in freely moving rats and the same latent inhibition paradigm. To that end, the left SUB was temporarily blocked with tetrodotoxin (TTX) during pre‐exposure to a new olfactory stimulus (banana odour). During the second session the animals were aversively conditioned to banana odour. With respect to the results obtained during the test session (third presentation of banana odour), similar changes in behaviour and DA levels were obtained in control and conditioned rats microinjected with the solvent, phosphate‐buffered saline (PBS), in the SUB, consistently with a latent inhibition phenomenon. In contrast, after reversible inactivation of the SUB during the pre‐exposure session, TTX‐pre‐exposed conditioned animals displayed aversive behaviour in the test session, and anterior striatal DA variations in these animals differed significantly from those obtained in pre‐exposed rats injected locally with PBS. Striatal DA variations obtained in conditioned animals microinjected with TTX were also significantly different from those observed in conditioned non‐pre‐exposed animals. The present data suggest that, in parallel to the entorhinal cortex, the SUB regulates the latent inhibition‐related behavioural and DA responses in the anterior part of the dorsal striatum. These data may provide new insight into the pathophysiology of schizophrenic psychoses.
Time‐sensitive enhancement of motor learning with the less‐affected forelimb after unilateral sensorimotor cortex lesions in rats
Authors: Hsu J. Edward , Jones Theresa A. 
Published: October 2005

AbstractUnilateral damage to the forelimb region of the sensorimotor cortex (FLsmc) results in time‐dependent changes in neuronal activity, structure and connectivity in the contralateral motor cortex of adult rats. These changes have been linked to facilitation of motor skill learning in the less‐affected/ipsilesional forelimb, which is likely to promote its use in the development of behavioral compensation. The goal of this study was to determine whether an early post‐lesion‐sensitive time period exists for this enhanced learning and whether it is linked to synaptogenesis in the contralesional motor cortex. Rats were trained for 21 days on a skilled reaching task with the ipsilesional forelimb beginning 4 or 25 days after unilateral ischemic (endothelin‐1‐induced) FLsmc lesions or sham operations. As found previously, reaching performance was significantly enhanced in rats trained early post‐lesion compared with sham‐operates. In rats trained later post‐lesion, performance was neither significantly different from time‐matched sham‐operates nor strikingly different from animals trained earlier post‐lesion. In layer V of the contralesional motor cortex, stereological methods for light and electron microscopy revealed significantly more total, multisynaptic bouton and perforated synapses per neuron compared with sham‐operates, but there were no significant differences between early‐ and late‐trained lesion groups. Thus, there appears to be a sensitive time window for the maximal expression of the enhanced learning capacity of the less‐affected forelimb but this window is broadly, rather than sharply, defined. These results indicate that relatively long‐lasting lesion‐induced neuronal changes are likely to underlie the facilitation of learning with the less‐affected forelimb.
Species divergence and trait convergence in experimental plant community assembly
Authors: Fukami Tadashi , Martijn Bezemer T. , Mortimer Simon R. , van der Putten Wim H. 
Published: October 2005

AbstractDespite decades of research, it remains controversial whether ecological communities converge towards a common structure determined by environmental conditions irrespective of assembly history. Here, we show experimentally that the answer depends on the level of community organization considered. In a 9‐year grassland experiment, we manipulated initial plant composition on abandoned arable land and subsequently allowed natural colonization. Initial compositional variation caused plant communities to remain divergent in species identities, even though these same communities converged strongly in species traits. This contrast between species divergence and trait convergence could not be explained by dispersal limitation or community neutrality alone. Our results show that the simultaneous operation of trait‐based assembly rules and species‐level priority effects drives community assembly, making it both deterministic and historically contingent, but at different levels of community organization.
Effects of organism size and community composition on ecosystem functioning
Authors: Long Zachary T. , Morin Peter J. 
Published: October 2005

AbstractWe tested (1) if the size of dominant species influenced ecosystem functioning in food webs consisting of bacteria, algae, and protozoa; (2) whether those effects changed in importance through time; and (3) how those effects compared with differences in diversity among experimental food webs. We constructed food webs using two size fractions of organisms that differed in individual mass by approximately two orders of magnitude. We measured total biomass and respiration (total CO2production) as two aspects of ecosystem functioning. We also compared these size‐dependent patterns in functioning across two levels of species richness. Initially, organism size strongly influenced total community biomass. With time, however, biomass and respiration eventually converged in communities dominated by large or small species. We conclude that after sufficient time for community development any differences in ecosystem functioning resulted from differences in community composition, including species richness, but not the size of the dominant organisms.
Mass spectrometric analysis reveals changes in phospholipid, neutral sphingolipid and sulfatide molecular species in progressive epilepsy with mental retardation, EPMR, brain: a case study
Authors: Hermansson Martin , Käkelä Reijo , Berghäll Maria , Lehesjoki Anna‐Elina , Somerharju Pentti , Lahtinen Ulla 
Published: October 2005

AbstractProgressive epilepsy with mental retardation, EPMR, belongs to a group of inherited neurodegenerative disorders, the neuronal ceroid lipofuscinoses. The CLN8 gene that underlies EPMR encodes a novel transmembrane protein that localizes to the endoplasmic reticulum (ER) and ER–Golgi intermediate compartment. Recently, CLN8 was linked to a large eukaryotic protein family of TLC (TRAM, Lag1, CLN8) domain homologues with postulated functions in lipid synthesis, transport or sensing. By using liquid chromatography/mass spectrometry we analysed molecular species of major phosholipid and simple sphingolipid classes from cerebral samples of two EPMR patients representing a progressive and advanced state of the disease. The progressive state brain showed reduced levels of ceramide, galactosyl‐ and lactosylceramide and sulfatide as well as a decrease in long fatty acyl chain containing molecular species within these classes. Among glycerophospholipid classes, an increase in species containing polyunsaturated acyl chains was detected especially in phosphatidylserines and phosphatidylethanolamines. By contrast, saturated and monounsaturated species were overrepresented among phosphatidylserine, phosphatidylethanolamine and phosphatidylinositol classes in the advanced state sample. The observed changes in brain sphingo‐ and phospholipid molecular profiles may result in altered membrane stability, lipid peroxidation, vesicular trafficking or neurotransmission and thus may contribute to the progression of the molecular pathogenesis of EPMR.
Amyloid β‐peptide(1–42) and hydrogen peroxide‐induced toxicity are mediated by TRPM2 in rat primary striatal cultures
Authors: Fonfria E. , Marshall I. C. B. , Boyfield I. , Skaper S. D. , Hughes J. P. , Owen D. E. , Zhang W. , Miller B. A. , Benham C. D. , McNulty S. 
Published: October 2005

AbstractAmyloid β‐peptide (Aβ) is the main component of senile plaques which characterize Alzheimer's disease and may induce neuronal death through mechanisms which include oxidative stress. To date, the signalling pathways linking oxidant stress, a component of several neurodegenerative diseases, to cell death in the CNS are poorly understood. Melastatin‐like transient receptor potential 2 (TRPM2) is a Ca2+‐permeant non‐selective cation channel, which responds to increases in oxidative stress levels in the cell and is activated by oxidants such as hydrogen peroxide. We demonstrate here that Aβ and hydrogen peroxide both induce death in cultured rat striatal cells which express TRPM2 endogenously. Transfection with a splice variant that acts as a dominant negative blocker of TRPM2 function (TRPM2‐S) inhibited both hydrogen peroxide‐ and Aβ‐induced increases in intracellular‐free Ca2+ and cell death. Functional inhibition of TRPM2 activation by the poly(ADP‐ribose)polymerase inhibitor SB‐750139, a modulator of intracellular pathways activating TRPM2, attenuated hydrogen peroxide‐ and Aβ‐induced cell death. Furthermore, a small interfering RNA which targets TRPM2, reduced TRPM2 mRNA levels and the toxicity induced by hydrogen peroxide and Aβ. These data demonstrate that activation of TRPM2, functionally expressed in primary cultures of rat striatum, contributes to Aβ‐ and oxidative stress‐induced striatal cell death.
Genomic profiling of the neuronal target genes of the plasticity‐related transcription factor – Zif268
Authors: Allan B.  , James  , Ann‐Marie  , Conway  , Brian J.  , Morris  
Published: October 2005

AbstractThe later phases of neuronal plasticity are invariably dependent on gene transcription. Induction of the transcription factor Zif268 (Egr‐1) in neurones is closely associated with many forms of functional plasticity, yet the neuronal target genes modulated by Zif268 have not been characterized. After transfection of a neuronal cell line with Zif268 we identified genes that show altered expression using high density microarrays. Although some of the genes identified have previously been associated with forms of neuronal plasticity, the majority have not been linked with neuronal plasticity or Zif268 action. Altered expression of a representative sample of the novel target genes was confirmed in Zif268‐transfected PC12 neurones, and in in vitro and in vivo models of Zif268‐associated neuronal plasticity. In particular, altered expression of the protease inhibitor Cystatin C and the chemokine Cxcl10 was observed in striatal tissue after haloperidol administration. Surprisingly, the group of identified genes is enriched for components of the proteasome and the major histocompatibility complex. Our findings suggest that altered expression of these genes following Zif268 induction may be a key component of long lasting plasticity in the CNS.