bluuebunny/crossref_metadata_2025_split huggingface dataset:
Metabolic consequences of susceptibility and resistance (race‐specific and broad‐spectrum) in barley leaves challenged with powdery mildew
Authors: SWARBRICK PHILIP J. , SCHULZE‐LEFERT PAUL , SCHOLES JULIE D. 
Published: April 2006

ABSTRACTIn a compatible interaction biotrophic fungi often lower the yield of their hosts by reducing photosynthesis and altering the fluxes of carbon within the infected leaf. In contrast, comparatively little is known about the metabolic consequences of activating resistance responses. In this study we investigated the hypothesis that the activation of both race‐specific (Mla12) and broad‐spectrum (mlo) resistance pathways in barley leaves infected with Blumeria graminis represents a cost to the plant in terms of carbon production and utilization. We have shown, using quantitative imaging of chlorophyll fluorescence, that during a susceptible interaction, photosynthesis was progressively reduced both in cells directly below fungal colonies and in adjacent cells when compared with uninoculated leaves. The lower rate of photosynthesis was associated with an increase in invertase activity, an accumulation of hexoses and a down‐regulation of photosynthetic gene expression. During both Mla12‐ and mlo‐mediated resistance, photosynthesis was also reduced, most severely inhibited in cells directly associated with attempted penetration of the fungus but also in surrounding cells. These cells displayed intense autofluorescence under ultraviolet illumination indicative of the accumulation of phenolic compounds and/or callose deposition. The depression in photosynthesis was not due only to cell death but also to an alteration in source‐sink relations and carbon utilization. Apoplastic (cell wall‐bound) invertase activity increased more rapidly and to a much greater extent than in infected susceptible leaves and was accompanied by an accumulation of hexoses that was localized to areas of the leaf actively exhibiting resistance responses. The accumulation of hexoses was accompanied by a down‐regulation in the expression of Rubisco (rbcS) and chlorophyll a/b binding protein (cab) genes (although to a lesser extent than in a compatible interaction) and with an up‐regulation in the expression of the pathogenesis‐related protein 1 (PR‐1). These results are consistent with a role for invertase in the generation of hexoses, which may supply energy for defence reactions and/or act as signals inducing defence gene expression.
Cell and leaf size plasticity in Arabidopsis: what is the role of endoreduplication?
Authors: COOKSON SARAH JANE , RADZIEJWOSKI AMANDINE , GRANIER CHRISTINE 
Published: April 2006

ABSTRACTLeaf area expansion is affected by environmental conditions because of differences in cell number and/or cell size. Increases in the DNA content (ploidy) of a cell by endoreduplication are related to its size. The aim of this work was to determine how cell ploidy interacts with the regulation of cell size and with leaf area expansion. The approach used was to grow Arabidopsis thaliana plants performing increased or decreased rounds of endoreduplication under shading and water deficit. The shading and water deficit treatments reduced final leaf area and cell number; however, cell area was increased and decreased, respectively. These differences in cell size were unrelated to alterations of the endocycle, which was reduced by these treatments. The genetic modification of the extent of endoreduplication altered leaf growth responses to shading and water deficit. An increase in the extent of endoreduplication in a leaf rendered it more sensitive to the shade treatment but less sensitive to water deficit conditions. The link between the control of whole organ and individual cell expansion under different environmental conditions was demonstrated by the correlation between the plasticity of cell size and the changes in the duration of leaf expansion.
Multiseismic cycle deformation rates from Holocene normal fault scarps on Crete (Greece)
Authors: Caputo R. , Monaco C. , Tortorici L. 
Published: April 2006

AbstractMorphotectonic features reveal recent seismic activity on normal faults on Crete allowing slip rates, palaeoearthquake magnitudes and earthquake recurrence intervals to be inferred. The studied faults show major escarpments (100s m high, 10s km long), separating uplifted Mesozoic rocks from Quaternary deposits. During the Holocene, slip rates outpaced erosion/sedimentation rates and 5–15 m high fresh scarps formed at the base of the major escarpments. Based on our field observations and following empirical relationships between magnitude, surface rupture length and maximum co‐seismic vertical displacement, it is possible to infer some important seismotectonic parameter relative to the investigated faults. Taking into account the possible sources of error and the corresponding uncertainties, our preferred long‐term slip rates range between 0.5 and 1.3 mm yr−1, the maximum expected magnitudes between 6.3 and 6.6 (or 6.5 and 6.8, considering worst case scenarios), while the mean recurrence intervals range between 260 andc. 840 years. These estimates are in good agreement with the shallow seismicity thus allowing to improve our knowledge on the seismic potential in Crete. Horizontal extension rates could be also inferred from our geological data and compared with the few available GPS data.
A novel R2R3 MYB transcription factor NtMYBJS1 is a methyl jasmonate‐dependent regulator of phenylpropanoid‐conjugate biosynthesis in tobacco
Authors: Gális Ivan , Šimek Petr , Narisawa Tomoko , Sasaki Mami , Horiguchi Tatsuya , Fukuda Hiroo , Matsuoka Ken 
Published: April 2006

SummaryTarget metabolic and large‐scale transcriptomic analyses of tobacco (Nicotiana tabacum L.) Bright Yellow‐2 (BY‐2) cells were employed to identify novel gene(s) involved in methyl jasmonate (MJ)‐dependent function in plants. At the metabolic level, we describe the specific accumulation of several phenylpropanoid–polyamine conjugates in MJ‐treated BY‐2 cells. Furthermore, global gene expression analysis of MJ‐treated cells using a 16K cDNA microarray containing expressed sequence tags (ESTs) from BY‐2 cells revealed 828 genes that were upregulated by MJ treatment within 48 h. Using time‐course expression data we identified a novel MJ‐inducible R2R3 MYB‐type transcription factor (NtMYBJS1) that was co‐expressed in a close temporal pattern with the core phenylpropanoid genes phenylalanine ammonia‐lyase (PAL) and 4‐coumarate:CoA ligase (4CL). Overexpression of NtMYBJS1 in tobacco BY‐2 cells caused accumulation of specific phenylpropanoid conjugates in the cells. Subsequent microarray analysis of NtMYBJS1 transgenic lines revealed that a limited number of genes, including PAL and 4CL, were specifically induced in the presence of the NtMYBJS1 transgene. These results, together with results of both antisense expression analysis and of gel mobility shift assays, strongly indicate that the NtMYBJS1 protein functions in tobacco MJ signal transduction, inducing phenylpropanoid biosynthetic genes and the accumulation of phenylpropanoid–polyamine conjugates during stress.
Vascular endothelial growth factor secretion from mesenteric adipose tissue and from creeping fat in Crohn’s disease
Authors: Schäffler Andreas , Fürst Alois , Büchler Christa , Paul Gisela , Rogler Gerhard , Schölmerich Jürgen , Herfarth Hans 
Published: April 2006

AbstractBackground:  Creeping fat represents a characteristic feature of Crohn’s disease (CD), and adipose tissue secretes adipocytokines and chemokines/growth factors such as vascular endothelial growth factor (VEGF). Because VEGF serum levels and mucosal VEGF expression is elevated in CD patients, the aim of the present paper was to investigate creeping fat‐derived VEGF secretion in CD.Material and Methods:  Adipose tissue was obtained from creeping fat of 10 patients with CD. Mesenteric adipose tissue was resected from 13 patients with colon cancer (CC) and from seven patients with diverticulitis (DIV). Three fat tissue specimens per well, and several wells (6–8) per patient were incubated ex vivo for 24 h. The release of VEGF into the supernatant was measured by ELISA.Results:  There was stable VEGF secretion from mesenteric adipose tissue of patients with CC or DIV and from creeping fat of patients with CD. Whereas the VEGF secretion rate was not different between patients with CD (465 ± 98 pg/g fat per 24 h) and CC (399 ± 48 pg/g fat per 24 h), VEGF secretion was significantly reduced in patients suffering from DIV (115 ± 41 pg/g fat per 24 h; P < 0.0001 and P = 0.001, respectively). The CD patients treated with steroids had significantly lower VEGF secretion rates (294 ± 42 pg/g fat per 24 h) than CD patients not receiving steroids (607 ± 105 pg/g fat per 24 h; P = 0.001).Conclusions:  Creeping fat is an important source of VEGF secretion. The characteristics of the inflammatory changes in CD might be due to the lack of VEGF downregulation that is seen in DIV.
Characteristics of acute and sub‐acute liver failure in China: nomination, classification and interval
Authors: Liu Qing , Liu Zheng , Wang Tailing , Wang Qingguo , Shi Xiaohong , Dao Wenbin 
Published: April 2006

AbstractBackground and Aims: Unlike most other countries, in China, liver failure is termed as severe hepatitis. However, there are two differences between liver failure and severe hepatitis: the interval of acute and sub‐acute severe hepatitis and the etiology. The aims of this study were to assess the best cutoff time‐point to distinguish between acute and sub‐acute severe hepatitis caused mainly by hepatitis B virus (HBV; 67.5%) in China and to determine whether the Chinese classifications of severe hepatitis can meet the international criteria based on pathological features and clinical characteristics.Methods: A total of 157 patients with acute, sub‐acute and chronic severe hepatitis were involved in the study. Their clinical findings, laboratory data and liver biopsies were retrospectively analyzed.Results: The different incidences of complications between acute and sub‐acute severe hepatitis were significant if the cutoff point was set at 15 days or 4 weeks (P < 0.01), but there is no significant differences if the cutoff was 8 weeks. Identifying the better cutoff point with a receiver–operator characteristic curve showed that 28 days was better than 15 days (sensitivity 100%vs92%; specificity 75%vs53%). The major differences in histopathology between acute and sub‐acute severe hepatitis were: (i) there was a single hepatic necrosis in acute severe hepatitis, but repeated and continuous hepatic necrosis in sub‐acute severe hepatitis; and (ii) survivors of acute severe hepatitis had full hepatocyte regeneration in the native liver architecture. Regeneration in survivors with sub‐acute severe hepatitis indicated the destruction of nodular architecture; new and old necrosis appeared at the same time. When the cutoff point for acute and sub‐acute severe hepatitis was set at 15 days, some sub‐acute severe hepatitis cases (full hepatocyte regeneration and one massive necrosis) had an overlap in pathological features with acute severe hepatitis. If the cutoff time‐point was set at 4 weeks, the clinical features between acute and sub‐acute, as well as the pathological changes, were clearly distinguished.Conclusion: The best cutoff time‐point to distinguish between acute and sub‐acute severe hepatitis is 4 weeks. This classification meets the international criteria based on the present clinical and pathological results.
Effect of hepatitis C virus core shadow protein expressed in human hepatoma cell line on human gene expression profiles
Authors: Dou Jun , Liu Pengbo , Wang Jing , Zhang Xinjian 
Published: April 2006

AbstractBackground and Aims:  The hepatitis C virus (HCV) C region has been reported to have overlapping genes or regions, and may encode a core shadow protein that has a role in HCV self‐replication, pathogenesis and carcinogenesis. The aim of this study was to identify the effect of HCV core shadow protein expressed in a human hepatoma (Huh‐7) cell line on human gene expression profiles.Methods:  Recombinants for expression of HCV genotype 1b core shadow protein and genotype 1b core protein were constructed, and an Huh‐7 cell line was established that could express the shadow protein and the core protein constitutively. Affymetrix human gene chip, HG‐U133 A and B microarray analysis and semiquantitative RT‐PCR were employed to identify the expression profiles of two kinds of core proteins in the Huh‐7 cell line.Results:  The microarray analysis showed that the core shadow protein caused expression of more genes to be up/down‐regulation than the core protein, including signal transduction, protease activity, molecular transport and, particularly, immune responses genes. Surprisingly, the core shadow protein could increase/decrease expression of apoptosis and anti‐apoptosis genes simultaneously. The expression profiles of three up‐regulated genes were confirmed by semiquantitative RT‐PCR, with results similar to the microarray analysis.Conclusions:  Hepatitis C virus core shadow protein may play an important role in inhibiting or stimulating host cells apoptosis processing and carcinogenesis, which is useful for the understanding of HCV core shadow protein biological functions in vivo and in vitro.
Profile of chronic hepatitis B virus in children in India: Experience with 116 children
Authors: Satapathy SK , Garg S , Chauhan R , Malhotra V , Sakhuja P , Sharma B C , Sarin SK 
Published: April 2006

AbstractBackground:  Hepatitis B virus (HBV) infection in children is mostly asymptomatic and therefore the disease burden is likely to be under appreciated. There is limited information on the profile of chronic HBV infection in children from the Indian subcontinent.Method:  In 116 (male : female 89:27) children, aged <15 years, with persistent HBsAg positivity for more than 6 months, a clinical, biochemical, virological and histological assessment was carried out.Results:  At presentation, 21.6% of children were symptomatic, with icterus in 12%. Features of decompensation such as ascites (7%) and gastrointestinal (GI) bleed (5%) were noted uncommonly. Five (4.3%) children had hepatocellular carcinoma (HCC) at presentation. Elevated alanine aminotransferase (ALT) was observed in 76% of subjects (median 61; range 14–815). A significantly higher proportion of children with hepatitis B early antigen (HbeAg) positive status had higher histological activity index (HAI) (84%vs 16%, P < 0.001) and fibrosis score (80%vs 20%, P = 0.007). A strong positive correlation was noted between aspartate aminotransferase (AST), ALT, HBV‐DNA and histological severity of the disease (HAI ≥4, fibrosis ≥2). Median HBV‐DNA levels were significantly higher in the HBeAg positive compared to the HBeAg negative group (25.6 vs 0.7 pg/mL, P = 0.004). Seventy‐four percent of the mothers had evidence of past or present HBV infection.Conclusions:  Majority of the children with chronic HBV infection are asymptomatic at presentation. HBeAg positive status reflects histologically more severe disease, and a higher level of HBV‐DNA. Almost two‐thirds of the children may have acquired their HBV infection perinataly.
Cardiac involvement in Crohn’s disease: Echocardiographic study
Authors: Bragagni Gianpaolo , Brogna Raffaele , Franceschetti Paola , Zoli Giorgio 
Published: April 2006

AbstractBackground:  Crohn’s Disease (CD) commonly presents extra‐intestinal manifestations, but cardiac involvement is considered rare. The aim of the present study was to assess cardiac involvement in CD and its possible correlation with activity, duration, localization and therapy.Patients and Methods:  A group of 68 patients with CD and a control group of 60 healthy subjects were subjected to a transthoracic echocardiogram with Doppler study.Results:  The study found overall morphologic alterations in 47/68 CD patients (69.11%) versus 12/60 controls (20.0%; P < 0.01); mitral valve prolapse in 20/68 CD patients (29.4%) versus 4/60 controls (6.6%; P < 0.01); and pericardial effusion in 13/68 CD patients (19.1%)versus 1/60 controls (1.6%; P < 0.01). The following findings were frequent, but without statistical significance: mitral insufficiency, 9/68 CD (13.2%) versus 3/60 controls (5.0%); tricuspidalic insufficiency, 8/68 CD (11.7%) versus 3/60 controls (5%); aortic insufficiency, 3/68 CD (4.4%) versus none in the control group; and decreased left ventricle ejection fraction, 5/68 CD (7.3%) versus none in the control group. Pericardial effusion was found to be related to CD activity (r = 0.375; P = 0.002) as well as decreased ejection fraction (r = 0.358; P = 0.003). No correlation with age, sex, duration, therapy or localization of disease was found.Conclusions:  These findings suggest that CD frequently determines cardiac involvement, although it is usually subclinical. The alteration of cytokine network, especially the elevated levels of tumor necrosis factor‐α, could be implicated in the cardiac alterations because it was observed, as for raised oxidative stress, in other heart diseases.
Mice lacking L1 cell adhesion molecule have deficits in locomotion and exhibit enhanced corticospinal tract sprouting following mild contusion injury to the spinal cord
Authors: Jakeman Lyn B. , Chen Ying , Lucin Kurt M. , McTigue Dana M. 
Published: April 2006

AbstractL1 is a member of the immunoglobulin superfamily of cell adhesion molecules that is associated with axonal growth, including formation of the corticospinal tract (CST). The present study describes the effects of L1 deletion on hindlimb function in locomotion, and examines the role of L1 in recovery and remodeling after contusive spinal cord injury (SCI) in mice. Uninjured adult L1 knockout (Y/–) mice had impaired performance on locomotor tests compared with their wild‐type littermates (Y/+). Anterograde tracing demonstrated that CST axons project to thoracic, but not lumbar, levels of the spinal cord of Y/– mice, and revealed a diversion of these fibers from their position in the base of the dorsal columns. Retrograde tracing also revealed reduced numbers of descending projections from paraventricular hypothalamus and red nuclei to the lumbar spinal cord in Y/– mice. SCI at the mid‐thoracic level produced a lesion encompassing the center of the spinal cord, including the site of the dorsal CST and surrounding gray matter (GM). The injury caused lasting deficits in fine aspects of locomotion. There was no effect of genotype on final lesion size or the growth of axons into the lesion area. However, injured Y/– mice demonstrated a robust expansion of CST projections throughout the GM of the cervical and thoracic spinal cord rostral to the lesion compared with Y/+ littermates. Thus, L1 is important for the development of multiple spinal projections and also contributes to the restriction of CST sprouting rostral to the site of a SCI in adults.
l‐Glutamate activates RhoA GTPase leading to suppression of astrocyte stellation
Authors: Chen Chun‐Jung , Ou Yen‐Chuan , Lin Shih‐Yi , Liao Su‐Lan , Huang Yong‐San , Chiang An‐Na 
Published: April 2006

AbstractThe actin cytoskeleton is known to support cellular morphological changes. Rho family small GTPases function as switching molecules to promote the convergence of both extracellular and intracellular signals in regulating cytoskeletal organization. Evidence indicates that l‐glutamate suppresses morphological changes of astrocytes over a broad spectrum. To test the possibility that l‐glutamate affects cytoskeletal reorganization, we investigated its effect on morphological changes induced by manganese exposure. l‐Glutamate concentration‐dependently prevented and reversed manganese‐induced astrocyte stellation and cytoskeletal disruption. The suppressive effect of l‐glutamate on manganese‐induced stellation was mediated by the activation of the glutamate transporter rather than ionotropic or metabotropic glutamate receptors. Pharmacological and biochemical approaches revealed the involvement of Ras homolog gene family, member A (RhoA) activation in l‐glutamate‐mediated suppression of manganese‐induced stellation. The activation of RhoA by l‐glutamate was partly through the up‐regulation of guanine nucleotide exchange factor phosphorylation and was abrogated by competitive nonsubstrate inhibitors. Furthermore, the hyperphosphorylation of myosin light chain and cofilin through the activation of RhoA following l‐glutamate treatment synergistically stabilized actin stress fibres. These results suggest that manganese‐induced stellation is suppressed by a mechanism involving glutamate transporters. Our in vitro findings also strongly indicate that astrocyte morphological plasticity is under the control of RhoA and that manganese and l‐glutamate regulate astrocyte morphology by modulating this switching molecule under culture conditions.
Nitric oxide regulation of calcitonin gene‐related peptide gene expression in rat trigeminal ganglia neurons
Authors: Bellamy Jamie , Bowen Elizabeth J. , Russo Andrew F. , Durham Paul L. 
Published: April 2006

AbstractCalcitonin gene‐related peptide (CGRP) and nitric oxide are involved in the underlying pathophysiology of migraine and other diseases involving neurogenic inflammation. We have tested the hypothesis that nitric oxide might trigger signaling mechanisms within the trigeminal ganglia neurons that would coordinately stimulate CGRP synthesis and release. Treatment of primary trigeminal ganglia cultures with nitric oxide donors caused a greater than four‐fold increase in CGRP release compared with unstimulated cultures. Similarly, CGRP promoter activity was also stimulated by nitric oxide donors and overexpression of inducible nitric oxide synthase (iNOS). Cotreatment with the antimigraine drug sumatriptan greatly repressed nitric oxide stimulation of CGRP promoter activity and secretion. Somewhat surprisingly, the mechanisms of nitric oxide stimulation of CGRP secretion did not require cGMP or PI3‐kinase signaling pathways, but rather, nitric oxide action required extracellular calcium and likely involves T‐type calcium channels. Furthermore, nitric oxide was shown to increase expression of the active forms of the mitogen‐activated protein kinases Jun amino‐terminal kinase and p38 but not extracellular signal‐related kinase in trigeminal neurons. In summary, our results provide new insight into the cellular mechanisms by which nitric oxide induces CGRP synthesis and secretion from trigeminal neurons.
Neural progenitor cells engineered to secrete GDNF show enhanced survival, neuronal differentiation and improve cognitive function following traumatic brain injury
Authors: Bakshi Asha , Shimizu Saori , Keck Carrie A. , Cho Sean , LeBold David G. , Morales Diego , Arenas Ernest , Snyder Evan Y. , Watson Deborah J. , McIntosh Tracy K. 
Published: April 2006

AbstractWe sought to evaluate the potential of C17.2 neural progenitor cells (NPCs) engineered to secrete glial cell line‐derived neurotrophic factor (GDNF) to survive, differentiate and promote functional recovery following engraftment into the brains of adult male Sprague–Dawley rats subjected to lateral fluid percussion brain injury. First, we demonstrated continued cortical expression of GDNF receptor components (GFRα‐1, c‐Ret), suggesting that GDNF could have a physiological effect in the immediate post‐traumatic period. Second, we demonstrated that GDNF over‐expression reduced apoptotic NPC death in vitro. Finally, we demonstrated that GDNF over‐expression improved survival, promoted neuronal differentiation of GDNF‐NPCs at 6 weeks, as compared with untransduced (MT) C17.2 cells, following transplantation into the perilesional cortex of rats at 24 h post‐injury, and that brain‐injured animals receiving GDNF‐C17.2 transplants showed improved learning compared with those receiving vehicle or MT‐C17.2 cells. Our results suggest that transplantation of GDNF‐expressing NPCs in the acute post‐traumatic period promotes graft survival, migration, neuronal differentiation and improves cognitive outcome following traumatic brain injury.