bluuebunny/crossref_metadata_2025_split huggingface dataset:
Antiviral maintenance treatment with interferon and ribavirin for recurrent hepatitis C after liver transplantation: Pilot study
Authors: Kornberg Arno , Küpper Bernadett , Tannapfel Andrea , Bärthel Erik , Thrum Katharina , Settmacher Utz 
Published: July 2006

AbstractBackground:  The aim of this pilot study was to evaluate efficacy of a long‐term antiviral maintenance therapy (AMT) with interferon‐α2b and ribavirin in liver transplant recipients with recurrent hepatitis C.Methods:  Twenty‐one patients with recurrent hepatitis C after liver transplantation received AMT with interferon and ribavirin, following 12 months of a basic antiviral combination treatment. Allograft function, viremia loads and allograft morphology were evaluated continuously.Results:  After 12 months of basic antiviral therapy, 14 patients (66.6%) had achieved initial clearance of viremia levels, and 17 recipients (81%) demonstrated normalization of allograft function, respectively. Inflammation score declined significantly (6.0 vs 3.9; P = 0.002), while stage of fibrosis remained unchanged. In virological responders maintenance therapy led to further regression of inflammation score (4.0 at baseline vs 3.1 at 24 months AMT) and fibrosis score (1.6 at baseline vs 1.1 at 24 months AMT). Despite persistence of viremia levels, continued antiviral therapy prevented progression to severe allograft inflammation in virological non‐responders. Hematologic adverse effects resulted in treatment discontinuation in seven patients (33.3%).Conclusion:  Long‐term AMT, if tolerable, might be an effective approach for preventing progression to severe allograft fibrosis and thereby improving long‐term survival in liver transplant recipients with recurrent hepatitis C.
Is aperistalsis with complete lower esophageal sphincter relaxation an early stage of classic achalasia?
Authors: Kim Jeong Hwan , Rhee Poong‐Lyul , Lee Sang Soo , Lee Hyuk , Choi Yong Sung , Son Hee Jung , Kim Jae J , Rhee Jong Chul 
Published: July 2006

AbstractBackground:  Aperistalsis with complete lower esophageal sphinter (LES) relaxation, characterized by the complete relaxation of the LES and aperistalsis of the esophageal body on manometry, has been considered by some authors to be an early manifestation of classic achalasia, which is defined as incomplete relaxation of the LES and aperistalsis of the esophageal body. The aim of the present study was to compare the clinical features of patients with aperistalsis with complete LES relaxation, with those of patients with classic achalasia.Methods:  Eighteen patients with aperistalsis with complete LES relaxation and 53 patients with classic achalasia were analyzed with regard to clinical history, the maximal diameter of the esophageal body on barium esophagogram, LES resting pressure and the duration of LES relaxation on manometric recordings, and the selected treatment and its efficacy.Results:  The aperistalsis with complete LES relaxation group had distinctly different features compared to those of the classic achalasia group including older age, more frequent association with non‐cardiac chest pain, less frequent association with dysphagia and weight loss, lower LES resting pressures, and longer duration of LES relaxation. However, the two groups were similar in terms of maximal diameter of the esophageal body, and efficacy associated with pneumatic dilation.Conclusions:  Aperistalsis with complete LES relaxation on manometry is not necessarily an early manifestation of classic achalasia. However, this condition does not preclude a diagnosis of achalasia or a good response to achalasia therapy.
Prevalence and determinants of SENV viremia among adolescents in an endemic area of chronic liver diseases
Authors: Wang Li‐Yu , Ho Tzu‐Ying , Chen Ming‐Che , Yi Chi‐Shun , Hu Chi‐Tan , Lin Hans Hsienhong 
Published: July 2006

AbstractBackground:  SENV is a potential causative agent responsible for chronic liver diseases (CLDs) that are precipitated in early life. SENV prevalence in adolescents is unknown and its transmission route is uncertain.Methods:  We randomly selected 824 serum samples from a cohort of 2383 adolescents aged 15–17 years who resided in Hualien County, an endemic area of liver diseases. Serum SENV genotype‐D and genotype‐H DNA were assayed by seminested polymerase chain reaction.Results:  The positive rates for SENV‐D and SENV‐H DNA were 25.1% and 30.6%, respectively. Amis adolescents had a significantly higher rate of SENV‐D viremia than Han Chinese adolescents (31.0%vs 22.2%; P = 0.025). Adolescents residing in rural or mountainous areas had significantly higher rates of SENV‐H viremia than those residing in urban areas. There was no difference in the positive rates of SENV‐D and SENV‐H DNA among adolescents with or without hepatitis B virus (HBV) or hepatitis C virus (HCV) infection or history of hospitalization, surgery or blood transfusion. In multivariate analyses, males and adolescents residing in rural or mountainous areas had significantly higher risks of SENV‐H viremia. As compared with those residing in urban areas, the multivariate‐adjusted odds ratio (OR) for rural and mountainous areas were 1.49 (95% confidence interval [CI], 1.08–2.07) and 2.16 (95% CI, 1.32–3.53), respectively.Conclusion:  SENV‐D and SENV‐H infection were frequent among adolescents in eastern Taiwan. SENV was unlikely to be transmitted via the parenteral route and factors associated with level of urbanization were probably the major determinants of SENV infection.
Long‐term depression activates transcription of immediate early transcription factor genes: involvement of serum response factor/Elk‐1
Authors: Lindecke Antje , Korte Martin , Zagrebelsky Marta , Horejschi Volker , Elvers Margitta , Widera Darius , Prüllage Maria , Pfeiffer Julia , Kaltschmidt Barbara , Kaltschmidt Christian 
Published: July 2006

AbstractLong‐term depression (LTD) is one of the paradigms used in vivo or ex vivo for studying memory formation. In order to identify genes with potential relevance for memory formation we used mouse organotypic hippocampal slice cultures in which chemical LTD was induced by applications of 3,5‐dihydroxyphenylglycine (DHPG). The induction of chemical LTD was robust, as monitored electrophysiologically. Gene expression analysis after chemical LTD induction was performed using cDNA microarrays containing >7000 probes. The DHPG‐induced expression of immediate early genes (c‐fos, junB, egr1 and nr4a1) was subsequently verified by TaqMan polymerase chain reaction. Bioinformatic analysis suggested a common regulator element [serum response factor (SRF)/Elk‐1 binding sites] within the promoter region of these genes. Indeed, here we could show a DHPG‐dependent binding of SRF at the SRF response element (SRE) site within the promoter region of c‐fos and junB. However, SRF binding to egr1 promoter sites was constitutive. The phosphorylation of the ternary complex factor Elk‐1 and its localization in the nucleus of hippocampal neurones after DHPG treatment was shown by immunofluorescence using a phosphospecific antibody. We suggest that LTD leads to SRF/Elk‐1‐regulated gene expression of immediate early transcription factors, which could in turn promote a second broader wave of gene expression.
Erythropoietin and GDNF enhance ventral mesencephalic fiber outgrowth and capillary proliferation following neural transplantation in a rodent model of Parkinson's disease
Authors: McLeod M. , Hong M. , Mukhida K. , Sadi D. , Ulalia R. , Mendez I. 
Published: July 2006

AbstractLow dopaminergic cell survival and suboptimal fiber reinnervation are likely major contributing factors for the limited benefits of neural transplantation in Parkinson's disease (PD) patients. Glial cell lined‐derived neurotrophic factor (GDNF) has been shown to enhance dopaminergic cell survival and fiber outgrowth of the graft site as well as promote behavioral recovery in rodent models of PD, while erythropoietin (EPO) can produce dopaminergic neuroprotective effects against 6‐hydroxydopamine (6‐OHDA) exposure on cultured neurons and 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine‐treated mice. The aim of this study was to determine if fetal ventral mesencephalic (FVM) tissue exposed to hibernation media containing a combination of GDNF and EPO could enhance dopaminergic graft survival, striatal reinnervation and functional recovery in a 6‐OHDA rodent model of PD. FVM tissue was dissected from 14‐day‐old rat fetuses and placed for 6 days in hibernation media alone, and in hibernation media that received either a daily administration of GDNF, EPO or a combination of GDNF and EPO. Following hibernation, FVM cells were transplanted as a single cell suspension into the striatum of unilateral 6‐OHDA‐lesioned rats. Rotational behavioral assessment revealed animals that received FVM tissue exposed to GDNF, EPO or the combination of both drugs had accelerated functional recovery. Immunohistochemical and stereological assessment revealed a significant increase in graft fiber density and angiogenesis into the graft when compared with control. These findings suggest that the hibernation of FVM tissue in a combination of GDNF and EPO can enhance graft efficacy and may have important implications for tissue preparation protocols for clinical neural transplantation in PD.
Chronic cocaine exposure impairs progenitor proliferation but spares survival and maturation of neural precursors in adult rat dentate gyrus
Authors: Domínguez‐Escribà L. , Hernández‐Rabaza V. , Soriano‐Navarro M. , Barcia J. A. , Romero F. J. , García‐Verdugo J. M. , Canales J. J. 
Published: July 2006

AbstractRecent observations indicate that drugs of abuse, including alcohol and opiates, impair adult neurogenesis in the hippocampus. We have studied in rats the impact of cocaine treatment (20 mg/kg, daily, i.p.) on cell proliferation, survival and maturation following short‐term (8‐day) and long‐term (24‐day) exposure. Using 5′‐bromo‐2‐deoxyuridine (BrdU) and Ki‐67 as mitotic markers at the end of the drug treatments, we found that both short‐ and long‐term cocaine exposures significantly reduced cell proliferation in the dentate gyrus (DG) of the hippocampus. By labelling mitotic cells with BrdU pulses before or during the early stages of the drug treatment, we determined that long‐term cocaine exposure did not affect the survival of newly generated cells. In register with this finding, cocaine chronic exposure did not increase the number of apoptotic cells labelled by TUNEL (terminal deoxynucleotidyl transferase‐mediated dUTP nick‐end labelling). Using doublecortin (DCX) immunocytochemistry and electron microscopy, we next examined the effects of cocaine exposure on the maturation of the neural precursors and on synaptic output to CA3. DCX immunocytochemistry showed that immature hippocampal cells of rats exposed to cocaine displayed normal arborization patterns and similar degrees of colocalization with BrdU at two different developmental stages. Moreover, cocaine did not produce significant morphological alterations of the mossy fibre projection system to stratum lucidum in the CA3 area of the hippocampus. The results presented demonstrate that chronic cocaine exposure impairs proliferation dynamics in the DG without significantly altering either the survival and growth of immature cells or the structural features of terminal projections to CA3.
Galanin–neuropeptide Y (NPY) interactions in central cardiovascular control: involvement of the NPY Y1 receptor subtype
Authors: Díaz‐Cabiale Zaida , Parrado Concepción , Rivera Alicia , De La Calle Adelaida , Agnati Luigi , Fuxe Kjell , Narváez José A. 
Published: July 2006

AbstractThe interactions between neuropeptide Y (NPY), specifically through NPY Y1 and Y2 receptor subtypes, and galanin [GAL(1–29)] have been analysed at the cardiovascular level. The cardiovascular effects of intracisternal coinjections of GAL(1–29) with NPY or NPY Y1 or Y2 agonists, as well as quantitative receptor autoradiography of the binding characteristics of NPY Y1 and Y2 receptor subtypes in the nucleus of the solitary tract (NTS), in the presence or absence of GAL(1–29), have been investigated. The effects of coinjections of GAL(1–29) and the NPY Y1 agonist on the expression of c‐FOS immunoreactivity in the NTS were also studied. The coinjection of NPY with GAL(1–29) induced a significant vasopressor and tachycardic action with a maximum 40% increase (P < 0.001). The coinjection of the NPY Y1 agonist and GAL(1–29) induced a similar increase in mean arterial pressure and heart rate as did NPY plus GAL(1–29), actions that were not observed with the NPY Y2 agonist plus GAL(1–29). GAL(1–29), 3 nm, significantly and substantially (by ∼ 40%) decreased NPY Y1 agonist binding in the NTS. This effect was significantly blocked (P < 0.01) in the presence of the specific galanin antagonist M35. The NPY Y2 agonist binding was not modified in the presence of GAL(1–29). At the c‐FOS level, the coinjection of NPY Y1 and GAL(1–29) significantly reduced the c‐FOS‐immunoreactive response induced by either of the two peptides. The present findings suggest the existence of a modulatory antagonistic effect of GAL(1–29) mediated via galanin receptors on the NPY Y1 receptor subtype and its signalling within the NTS.
Neonatal nicotine exposure impairs nicotinic enhancement of central auditory processing and auditory learning in adult rats
Authors: Liang Kevin , Poytress Bonnie Sue , Chen Yiling , Leslie Frances M. , Weinberger Norman M. , Metherate Raju 
Published: July 2006

AbstractChildren of women who smoke cigarettes during pregnancy display cognitive deficits in the auditory–verbal domain. Clinical studies have implicated developmental exposure to nicotine, the main psychoactive ingredient of tobacco, as a probable cause of subsequent auditory deficits. To test for a causal link, we have developed an animal model to determine how neonatal nicotine exposure affects adult auditory function. In adult control rats, nicotine administered systemically (0.7 mg/kg, s.c.) enhanced the sensitivity to sound of neural responses recorded in primary auditory cortex. The effect was strongest in cortical layers 3 and 4, where there is a dense concentration of nicotinic acetylcholine receptors (nAChRs) that has been hypothesized to regulate thalamocortical inputs. In support of the hypothesis, microinjection into layer 4 of the nonspecific nAChR antagonist mecamylamine (10 µm) strongly reduced sound‐evoked responses. In contrast to the effects of acute nicotine and mecamylamine in adult control animals, neither drug was as effective in adult animals that had been treated with 5 days of chronic nicotine exposure (CNE) shortly after birth. Neonatal CNE also impaired performance on an auditory‐cued active avoidance task, while having little effect on basic auditory or motor functions. Thus, neonatal CNE impairs nicotinic regulation of cortical function, and auditory learning, in the adult. Our results provide evidence that developmental nicotine exposure is responsible for auditory–cognitive deficits in the offspring of women who smoke during pregnancy, and suggest a potential underlying mechanism, namely diminished function of cortical nAChRs.
Partial depletion of dopamine in substantia nigra impairs motor performance without altering striatal dopamine neurotransmission
Authors: Andersson Daniel R. , Nissbrandt Hans , Bergquist Filip 
Published: July 2006

AbstractPrevious data indicate that the release of somatodendritic dopamine in substantia nigra influences motor activity and coordination, but the relative importance of somatodendritic dopamine release vs. terminal striatal dopamine release remains to be determined. We utilized simultaneous measurement of dopamine neurotransmission by microdialysis and motor performance assessment by rotarod test to investigate the effects of local dopamine depletion in rats. The vesicular monoamine transporter inhibitor tetrabenazine (100 µm) was administered locally in substantia nigra as well as in striatum. Nigral tetrabenazine administration decreased nigral dopamine dialysate concentrations to 7% of baseline and whole‐tissue dopamine content by 60%. Nigral dopamine depletion was associated with a reduction in motor performance to 73 ± 6% of pretreatment value, but did not alter dialysate dopamine concentrations in the ipsilateral striatum. Striatal tetrabenazine administration decreased striatal dopamine dialysate concentrations to 5% of baseline and doubled the somatodendritic dopamine response to motor activity, but it was not associated with changes in motor performance or dopamine content in striatal tissue. Simultaneous treatment of substantia nigra and striatum reduced motor performance to 58 ± 5% of the pretreatment value. The results of this study indicate that partial depletion of nigral dopamine stores can significantly impair motor functions, and that increased nigral dopamine release can counteract minor impairments of striatal dopamine transmission.
Glutamate enhances proliferation and neurogenesis in human neural progenitor cell cultures derived from the fetal cortex
Authors: Suzuki Masatoshi , Nelson Aaron D. , Eickstaedt Joshua B. , Wallace Kyle , Wright Lynda S. , Svendsen Clive N. 
Published: July 2006

AbstractExcitatory amino acids such as glutamate play important roles in the central nervous system. We previously demonstrated that a neurosteroid, dehydroepiandrosterone (DHEA), has powerful effects on the cell proliferation of human neural progenitor cells (hNPC) derived from the fetal cortex, and this effect is modulated through NMDA receptor signaling. Here, we show that glutamate can significantly increase the proliferation rates of hNPC. The increased proliferation could be blocked by specific NMDA receptor antagonists, but not other glutamate antagonists for kainate–AMPA or metabotropic receptors. The NR1 subunit of the NMDA receptor was detectable in elongated bipolar or unipolar cells with small cell bodies. These NR1‐positive cells were colocalized with GFAP immunoreactivity. Detection of the phosphorylation of cAMP response element‐binding protein (pCREB) revealed that a subset of NR1‐positive hNPC could respond to glutamate. Furthermore, we hypothesized that glutamate treatment may affect mainly the hNPC with a radial morphology and found that glutamate as well as DHEA selectively affected elongated hNPC; these elongated cells may be a type of radial glial cell. Finally we asked whether the glutamate‐responsive hNPC had an increased potential for neurogenesis and found that glutamate‐treated hNPC produced significantly more neurons following differentiation. Together these data suggest that glutamate stimulates the division of human progenitor cells with neurogenic potential.
Multi‐sited mutations of beta‐tubulin are involved in benzimidazole resistance and thermotolerance of fungal biocontrol agent Beauveria bassiana
Authors: Zou Gen , Ying Sheng‐Hua , Shen Zhi‐Chen , Feng Ming‐Guang 
Published: July 2006

SummaryFungicide resistance and thermotolerance of biocontrol agents in mitosporic fungi are of merits for enhancing fungal formulations against insect pests in the field. Among 20 wild strains of Beauveria bassiana (a well‐known fungal biocontrol agent) tested in this study, 19 were sensitive or highly sensitive to carbendazim (methyl 2‐benzimidazole carbamate), a typical benzimidazole fungicide, despite low resistance found in one strain. Sequential mutagenesis of a carbendazim‐sensitive wild strain [minimal inhibitory concentration (MIC) = 1.32 µg ml−1] under artificial selection pressure generated 11 mutants sharing a common MIC of > 1000 µg ml−1 without visible variation in colony growth and conidiation capacity. This represents at least 758‐fold enhancement of the resistance among the mutants. However, accompanied with the enhanced resistance, all the mutants became less thermotolerable. Stressed at 48°C, conidial LT50s of the mutants varied from 1.8 to 9.6 min and were lower than the parental LT50 (36 min). Moreover, the contents of hydrophobin‐like proteins in conidial walls declined significantly among the mutants compared with that of the wild parent. Mutations commonly relating to benzimidazole resistance in fungi were located at Q134, F167 and/or E198 around the taxol‐binding site of beta‐tubulin by sequencing the beta‐tubulin of the mutants. Also, mutations of other 37 amino acid residues in the sequences (each having one to five residues mutated) were found for the first time and they were diverse in spatial structure. All mutations restricted to the half of beta‐tubulin close to alpha‐tubulin were likely involved in variation in each of the traits concerned but their interactions were complicated.
Criblamydia sequanensis, a new intracellular Chlamydiales isolated from Seine river water using amoebal co‐culture
Authors: Thomas Vincent , Casson Nicola , Greub Gilbert 
Published: July 2006

SummaryAccumulating evidence supports a role for Chlamydia‐related organisms as emerging pathogens for human and animals. Assessment of their pathogenicity requires strain availability, at least for animal models and serological studies. As these obligate intracellular species are able to grow inside amoebae, we used co‐culture with Acanthamoeba castellanii in an attempt to recover new Chlamydia‐related species from river water. We isolated two strains from eight water samples. The first strain is a new Parachlamydia acanthamoebae strain that differs from previously described isolates by only two bases in the complete 16S rRNA gene sequence. The second isolate is the first representative of a new Chlamydiales family, as demonstrated by genetic and phylogenetic analyses of the 16S rRNA, 23S rRNA, ADP/ATP translocase and RnpB encoding genes. Using fluorescent in situ hybridization and electron microscopy, we demonstrated that it grows in high numbers in amoebae, where it exhibits a Chlamydia‐like developmental cycle with reticulate bodies and star‐like elementary bodies. Based on these results, we propose to name this new species ‘Criblamydia sequanensis’. This work confirmed that amoebal co‐culture is a relevant method to isolate new chlamydiae, and that it can be successfully applied to ecosystems colonized with a complex microbial community.
Obesity and disability – a short review
Authors: Ells L. J. , Lang R. , Shield J. P. H. , Wilkinson J. R. , Lidstone J. S. M. , Coulton S. , Summerbell C. D. 
Published: July 2006

SummaryThe prevalence of both obesity and disability is increasing globally and there is now growing evidence to suggest that these two health priorities may be linked. This paper explores the evidence linking obesity to muscular‐skeletal conditions, mental health disorders and learning disabilities in both adult and child populations. The impact of obesity on the four most prevalent disabling conditions in the UK (arthritis, mental health disorders, learning disabilities and back ailments) has been examined through novel data analysis of the 2001 Health Survey for England and UK Back Exercise And Manipulation trial data. Together these analyses strongly suggest that whether the cause or result of disability, obesity is undeniably implicated, thus presenting a serious public health priority. Future research efforts are required to strengthen the evidence base examining obesity in back disorders, mental health and learning disabilities, in order to improve current clinical management.