bluuebunny/crossref_metadata_2025_split huggingface dataset:
Difference in localization of esophageal mucosal breaks among grades of esophagitis
Authors: Katsube Tomoko , Adachi Kyoichi , Furuta Kenji , Miki Masaharu , Fujisawa Tomoo , Azumi Takane , Kushiyama Yoshinori , Kazumori Hideaki , Ishihara Shunji , Amano Yuji , Kinoshita Yoshikazu 
Published: April 2006

AbstractBackground:  Gastroesophageal reflux occurs mainly during the daytime in patients with Los Angeles grade A esophagitis, but predominantly during the night in patients with grade C and D esophagitis. The purpose of the present paper was to investigate whether this difference in the pattern of gastroesophageal reflux influences the circumferential localization of erosions in the esophageal wall.Methods:  The subjects were 394 consecutive patients diagnosed endoscopically as having reflux esophagitis (grade A, n = 223; B, n = 93; C, n = 53; D, n = 25 cases). Their endoscopic films were reviewed retrospectively to determine the circumferential location of esophageal mucosal breaks, and also the prevalence and size of hiatal hernia (HH).Results:  The numbers of mucosal breaks analyzed in patients with grade A, B and C esophagitis were 321, 173 and 54, respectively. Patients with grade A and B esophagitis had longitudinal mucosal breaks mainly in the right‐anterior wall of the lower esophagus, whereas patients with grade C esophagitis had transverse mucosal breaks mainly in the posterior wall. The prevalence and size of HH was significantly higher and larger, respectively, in patients with grade C or D esophagitis than in those with grade A and B esophagitis.Conclusion:  The circumferential location of esophageal mucosal breaks differs significantly among different grades of esophagitis.
Treatment effects and predictors of a 24‐week course of interferon α‐2b plus ribavirin combination therapy for patients with chronic hepatitis C
Authors: Tomimatsu Masahiko , Aizawa Yoshio , Chuganji Yoshimichi , Ishizuka Hideo , Fujita Yoshiyuki , Aizawa Ryouichi , Abe Hiroshi , Matsuda Takako , Itou Yumi , Nakanishi Hiroyuki , Ushiyama Hisashi , Higuchi Teruhisa , Fujimoto Tomoko , Endou Hitoshi , Iga Daijiro , Ohta Kazuki , Kuroda Hiroyuki 
Published: April 2006

AbstractBackground and Aims:  In chronic hepatitis C patients with genotype 1b and a high viral load, the sustained virological response (SVR) rate remained as low as 2‐3% with conventional interferon (IFN) monotherapy, but improved to more than 20% with IFN α‐2b plus ribavirin combination therapy. This study examined the therapeutic effects and predictors of this combination therapy.Methods:  Subjects were 105 patients with chronic hepatitis C (73 males, 32 females) with a median age of 53 years (range 19–70 years). Seventy‐two patients had genotype lb and 33 patients had genotype 2 (2a or 2b). Six million units (MU) or 10 MU of IFN α‐2b was administered by intramuscular injection six times a week for the first 2 weeks, and the same amount of IFN was administered three times a week for the following 22 weeks. During the IFN administration period, 600–800 mg of oral ribavirin was administered daily. Patients who were hepatitis C virus (HCV)‐RNA negative 24 weeks after the completion of administration were defined as SVR.Results:  The overall SVR rate was 39%; 22.2% for the genotype 1b group and 75.8% for the genotype 2 group, and the difference between the groups was significant (P < 0.0001). Multivariate logistic regression analysis indicated that the factors that contributed to SVR include genotype 2, age (younger than 53 years), and an increase in Th2 measured by flow cytometry before and 4 weeks after start of treatment.Conclusions:  The overall SVR rate of IFN α‐2b plus ribavirin combination therapy for 24 weeks was 39%, and contributing factors for SVR rate include genotype 2, age younger than 53 years and elevated Th2.
Clinical significance of measuring blood coagulation factor XIIIA regularly and continuously in patients with Crohn’s disease
Authors: Higaki Shingo , Nakano Kaori , Onaka Sachiko , Amano Ayaka , Tanioka Yukari , Harada Katsunori , Hashimoto Shinichi , Sakaida Isao , Okita Kiwamu 
Published: April 2006

AbstractBackground:  The aim of the present paper was to determine the mechanism by which the level of coagulation factor XIIIA declines during the active phase of Crohn’s disease.Methods:  The relationship between the activity of Crohn’s disease and factor XIIIA was observed in 31 patients with Crohn’s disease prospectively. The relationship between factor XIIIA and thrombin–antithrombin III complex (TAT), factor XIIIA expressed on the surface of peripheral monocytes, was also evaluated.Results:  During the first year, there were 11 patients with Crohn’s disease in the active phase and 20 patients who remained in remission. The average of the lowest level of factor XIIIA among the patients in the active phase was 60.1%. The average of the lowest level of factor XIIIA in patients who remained in remission was 78.1% (P = 0.049). Among the 20 patients who remained in remission for 1 year, eight patients had factor XIIIA levels below 70%. Six of them required surgical enterectomies, on average 2 years and 1 month later. However, none of the 12 patients who remained in remission for 1 year and who never had factor XIIIA levels <70% had a surgical enterectomy during follow up of 4 years and 6 months (P = 0.002). The decline of factor XIIIA was not due to increased consumption secondary to blood coagulation (TAT), nor was it due to a decline in the function of monocytes that produce factor XIIIA.Conclusion:  Factor XIIIA declines during the active phase of Crohn’s disease because it might be consumed in the repair of injured tissue.
Inhibitory effects of Ligusticum chuanxiong on the proliferation of rat hepatic stellate cells
Authors: Lin Yun‐Lian , Lee Ting‐Fang , Huang Yeh‐Jeng , Huang Yi‐Tsau 
Published: April 2006

AbstractBackground and Aims:  Platelet‐derived growth factor (PDGF) is a very potent mitogen for hepatic stellate cells (HSC) in hepatic fibrogenesis. Ligusticum chuanxiong Hort. (LC), a traditional Chinese herb used for cerebrovascular diseases, has been shown to exert anti‐inflammatory and free radical scavenging effects. The aims of the present study were to investigate the effects of LC extract on the proliferation‐related biomarkers in a rat HSC cell line (HSC‐T6) stimulated with PDGF.Methods:  DNA synthesis via bromodeoxyuridine (BrdU) incorporation, cell cycle related proteins and apoptosis markers were determined to evaluate the inhibitory effects of LC.Results:  The results revealed that LC extract (25–100 µg/mL) concentration‐dependently decreased the PDGF‐induced cell proliferation as well as α‐smooth muscle actin expression in HSC. The inhibitory activity of LC on HSC was associated with: (i) inhibition of BrdU incorporation; (ii) induction of apoptosis with the activation of caspase‐3, up‐regulation of cell cycle inhibitory proteins p21 and p27, and down‐regulation of cell cycle stimulatory proteins cyclins D1 and D2; and (iii) increased phosphorylation of mitogen‐activated protein kinases (JNK). LC at the studied concentrations showed no direct cytotoxicity on primary hepatocytes.Conclusion:  The results suggest that LC significantly inhibited PDGF‐activated HSC proliferation, possibly through apoptotic mechanisms and the potential of LC as an antifibrotic agent warrants further investigation.
Concurrent alterations of O‐GlcNAcylation and phosphorylation of tau in mouse brains during fasting
Authors: Li Xu , Lu Fen , Wang Jian‐Zhi , Gong Cheng‐Xin 
Published: April 2006

AbstractImpaired brain glucose uptake/metabolism precedes the symptoms of Alzheimer disease (AD) and is likely to play a role in the development of the disease, but the mechanism by which it contributes to AD is not understood. Because glucose uptake/metabolism regulates protein O‐GlcNAcylation, and the latter modulates phosphorylation of tau inversely, we investigated, in fasting Kunming mice, whether impaired brain glucose uptake/metabolism causes abnormal hyperphosphorylation of tau and, consequently, facilitates the neurofibrillary degeneration of AD via down‐regulation of tau O‐GlcNAcylation. We found that fasting caused decreased tau O‐GlcNAcylation and concurrent hyperphosphorylation of tau at most of the phosphorylation sites studied. The hippocampus was found more vulnerable to the tau alterations than the cerebral cortex, which is consistent with the fact that it is the hippocampus that is first affected in AD. Furthermore, hyperphosphorylation of tau induced by fasting was reversible in the brain after re‐feeding. These findings provide a novel mechanism explaining how impaired brain glucose uptake/metabolism contributes to AD and suggest that it may be feasible to treat AD by reversing the abnormal hyperphosphorylation of tau at early stages of the disease.
Pro‐opiomelanocortin colocalizes with corticotropin‐ releasing factor in axon terminals of the noradrenergic nucleus locus coeruleus
Authors: Reyes Beverly A. S. , Glaser Julia D. , Magtoto Ronaldo , Van Bockstaele Elisabeth J. 
Published: April 2006

AbstractWe previously demonstrated that the opioid peptide enkephalin and corticotropin‐releasing factor (CRF) are occasionally colocalized in individual axon terminals but more frequently converge on common dendrites in the locus coeruleus (LC). To further examine potential opioid cotransmitters in CRF afferents we investigated the distribution of pro‐opiomelanocortin (POMC), the precursor that yields the potent bioactive peptide β‐endorphin, with respect to CRF immunoreactivity using immunofluorescence and immunoelectron microscopic analyses of the LC. Coronal sections were collected through the dorsal pontine tegmentum of rat brain and processed for immunocytochemical detection of POMC and CRF or tyrosine hydroxylase (TH). POMC‐immunoreactive processes exhibited a distinct distribution within the LC as compared to the enkephalin family of opioid peptides. Specifically, POMC fibers were enriched in the ventromedial aspect of the LC with fewer fibers present dorsolaterally. Immunofluorescence microscopy showed frequent coexistence of POMC and CRF in varicose processes that overlapped TH‐containing somatodendritic processes in the LC. Ultrastructural analysis showed POMC immunoreactivity in unmyelinated axons and axon terminals. Axon terminals containing POMC were filled with numerous large dense‐core vesicles. In sections processed for POMC and TH, ∼ 29% of POMC‐containing axon terminals (n = 405) targeted dendrites that exhibited immunogold–silver labeling for TH. In contrast, sections processed for POMC and CRF showed that 27% of POMC‐labeled axon terminals (n = 657) also exhibited CRF immunoreactivity. Taken together, these data indicate that a subset of CRF afferents targeting the LC contain POMC and may be positioned to dually impact LC activity.
Delayed ischemic electrocortical suppression during rapid repeated cerebral ischemia and kainate‐induced seizures in rat
Authors: Ilie Andrei , Spulber Stefan , Avramescu Sinziana , Nita Dragos Alexandru , Zagrean Ana‐Maria , Zagrean Leon , Moldovan Mihai 
Published: April 2006

AbstractGlobal cerebral ischemia induces, within seconds, suppression of spontaneous electrocortical activity, partly due to alterations in synaptic transmission. In vitro studies have found that repeated brief hypoxic episodes prolong the persistence of synaptic transmission due to weakened adenosine release. The aim of this study was to investigate in vivo whether the time to ischemic electrocortical suppression (TES) could be altered during energy stress conditions such as rapid repeated global cerebral ischemia and kainate‐induced seizures. Experiments were carried out in adult rats under chloral hydrate anaesthesia. Repeated episodes of 1 min of ischemia were induced by transiently clamping the carotid arteries in a ‘four‐vessel occlusion’ model. We devised an automatic method of TES estimation based on the decay of the root mean square of two‐channel electrocorticographic recordings. To distinguish the alterations in spontaneous electrocortical activity we compared TES with the ischemic suppression of visual evoked potentials (VEP). During the first ischemic episode, TES was ∼ 15 s and remained unchanged when five ischemic episodes were separated by 10‐min reperfusion intervals. When ischemia was repeated after 2 min of reperfusion TES progressively increased, reaching a plateau value of ∼ 24 s. A similar plateau was reached during kainate‐induced seizures. The TES plateau occurred prior to ischemic suppression of VEP. Our data suggest that, under conditions of acute metabolic stress in vivo, the ischemic suppression of spontaneous electrocortical activity may be delayed up to a plateau value. These findings are consistent with the hypothesis of a depletable adenosine pool; however, the restoration of synaptic transmission may be faster in vivo than in vitro.
Multiple isoforms of the tumor protein p73 are expressed in the adult human telencephalon and choroid plexus and present in the cerebrospinal fluid
Authors: Cabrera‐Socorro Alfredo , Morlans Mercedes Pueyo , Sola Maria Luisa Suarez , Delgado Francisco J. Gonzalez , Castañeyra‐Perdomo Agustin , Marin Maria C. , Meyer Gundela 
Published: April 2006

Abstractp73, a homolog of the p53 tumor suppressor, codes for full‐length transactivating (TA) and N‐terminally truncated (ΔN) isoforms, with pro‐ and anti‐apoptotic activities, respectively. We examined the expression of the main p73 isoforms in adult human and mouse telencephalon and choroid plexus by immunohistochemistry on paraffin sections, and immunoblotting (IB) of tissue extracts and cerebrospinal fluid (CSF), using antibodies against different protein domains. Cortical neurons expressed TAp73 predominantly in the cytoplasm and ΔNp73 mainly in the nucleus, with partial overlap in the cytoplasm. Highest expression was found in the hippocampus. IB showed an array of TAp73 variants in adult human cortex and hippocampus. IB of human choroid plexus and CSF using TAp73‐specific antibodies revealed the presence of a ∼90‐kDa protein whose molecular weight was reduced after N‐deglycosylation, suggesting that glycosylated TAp73 is exported into the CSF. In the mouse, high expression of TAp73 was also detected in the subcommissural organ (SCO), an ependymal gland absent in adult humans. TAp73 colocalized with anti‐fibra‐Reissner‐antibody (AFRU), which is a marker of Reissner's fiber, the secreted SCO product. p73‐deficient mice had generalized cortical hypoplasia and hydrocephalus; in addition, we observed a dramatic size reduction of the choroid plexus. However, the SCOs were apparently unaltered and continued to secrete Reissner's fiber. Our findings point to complex and widespread p73 activities in the maintenance of adult cortical neurons and in brain homeostasis. TAp73 in the CSF may play important roles in the maintenance of the adult ventricular wall as well as in the development of the proliferating neuroepithelium.
Muscarinic autoreceptors modulate transmitter release through protein kinase C and protein kinase A in the rat motor nerve terminal
Authors: Santafé Manel M. , Lanuza M. Angel , Garcia Neus , Tomàs Josep 
Published: April 2006

AbstractWe have used intracellular recording to investigate the existence of a functional link between muscarinic presynaptic acetylcholine (ACh) autoreceptors, the intracellular serine‐threonine kinases‐mediated transduction pathways and transmitter release in the motor nerve terminals of adult rats. We found the following. (1) Transmitter release was reduced by the M1 muscarinic acetylcholine receptor (mAChR) blocker pirenzepine and enhanced by the M2 blocker methoctramine. The unselective mAChR blocker atropine increased ACh release, which suggests the unmasking of another parallel release‐potentiating mechanism. There are therefore two opposite, though finely balanced, M1–M2 mAChR‐operated mechanisms that tonically modulate transmitter release. (2) Both M1 and M2 mechanisms were altered when protein kinase C (PKC), protein kinase A (PKA) or the P/Q‐type calcium channel were blocked. (3) Both PKC and PKA potentiated release when they were specifically stimulated [with phorbol 12‐myristate 13‐actetate (PMA) and Sp‐8‐Br cAMPs, respectively], and both needed the P/Q channel. (4) In normal conditions PKC seemed not to be directly involved in transmitter release (the PKC blocker calphostin C did not reduce release), whereas PKA was coupled to potentiate release (the PKA blocker H‐89 reduced release). However, when an imbalance of the M1–M2 mAChRs function was experimentally produced with selective blockers, an inversion of the kinase function occurred and PKC could then stimulate transmitter release, whereas PKA was uncoupled. (5) The muscarinic function may be explained by the existence of an M1‐mediated increased PKC activity‐dependent potentiation of release and an M2‐mediated PKA decreased activity‐dependent release reduction.These findings show that there is a precise interrelation pattern of the mAChRs, PKC and PKA in the control of the neurotransmitter release.
Effects of lesions to the dorsal and ventral hippocampus on defensive behaviors in rats
Authors: Pentkowski Nathan S. , Blanchard D. Caroline , Lever Colin , Litvin Yoav , Blanchard Robert J. 
Published: April 2006

AbstractThis study investigated the role of the hippocampus in both unconditioned and conditioned defensive behaviors by examining the effects of pretraining ibotenic acid lesions to the dorsal and ventral hippocampus in male Long–Evans hooded rats exposed to three types of threat stimuli: cat‐odor, a live cat and footshock. Defensive behaviors were assessed during exposure to cat‐odor and a live cat, and immediately following the presentation of footshock. Conditioned defensive behaviors were also assessed in each context 24 h after initial threat exposure. During both unconditioned and conditioned trials, dorsal hippocampal lesions failed to significantly alter any behavioral measure in each test of defense. In contrast, ventral hippocampal lesions significantly reduced unconditioned defensive behaviors during exposure to cat‐odor without producing any observable effects during cat exposure. Furthermore, ventral lesions significantly attenuated conditioned defensive behaviors following the administration of footshock and during re‐exposure to each context. These results suggest a specific role for the ventral, not dorsal, hippocampus in modulating anxiety‐like behaviors in certain animal models of defense.
Temperature‐dependence of biomass accumulation rates during secondary succession
Authors: Anderson Kristina J. , Allen Andrew P. , Gillooly James F. , Brown James H. 
Published: April 2006

AbstractRates of ecosystem recovery following disturbance affect many ecological processes, including carbon cycling in the biosphere. Here, we present a model that predicts the temperature dependence of the biomass accumulation rate following disturbances in forests. Model predictions are derived based on allometric and biochemical principles that govern plant energetics and are tested using a global database of 91 studies of secondary succession compiled from the literature. The rate of biomass accumulation during secondary succession increases with average growing season temperature as predicted based on the biochemical kinetics of photosynthesis in chloroplasts. In addition, the rate of biomass accumulation is greater in angiosperm‐dominated communities than in gymnosperm‐dominated ones and greater in plantations than in naturally regenerating stands. By linking the temperature‐dependence of photosynthesis to the rate of whole‐ecosystem biomass accumulation during secondary succession, our model and results provide one example of how emergent, ecosystem‐level rate processes can be predicted based on the kinetics of individual metabolic rate.
Implications of hyperglycaemia and ethnicity in patients with acute coronary syndromes in New Zealand
Authors: Scott A. R. , Cheng A. , Greenacre M. , Devlin G. 
Published: April 2006

Background:  Admission blood glucose (ABG) is an independent predictor of death in patients with acute ST elevation myocardial infarction (STEMI). In New Zealand, mortality following myocardial infarction is disproportionally higher in Maori. Little information, however, exists concerning the predictive value of ABG in non‐ST elevation acute coronary syndromes (NSTEACS) events or indeed if similar ethnic differences exist in outcome in this patient population.Aim:  To assess the predictive value of ABG and ethnicity in individuals admitted with acute coronary syndromes (ACS) on mortality.Methods:  A retrospective analysis of hospital discharge diagnosis of all ACS between 1 January 1999 and 31 December 2002 at Waikato hospital, Hamilton, New Zealand. The primary outcome was all‐cause mortality.Results:  There were 4408 episodes of ACS with 1091 (25%) due to STEMI. There were 806 (18%) deaths. The presence of diabetes mellitus (DM) or an elevated ABG, in the absence of a history of DM, was associated with poor patient outcome. Early mortality is seen in individuals presenting with STEMI. People in the highest glucose category were older, more likely to be Maori, had a higher percentage of people with diabetes and remained in hospital longer, regardless of ACS type, than those in the lowest glucose category. Diabetes was more common in Maori (33%) than in Europeans (17.5%); p < 0.001. Significant risk factors for mortality were age, gender, diabetes, ethnicity, glucose and STEMI. For each mmol/l increase in glucose there is a 4.3% increase risk of dying. Adjusting for age and gender, Maori have a much higher mortality than Europeans (RR 2.12; p < 0.00001) regardless of ACS type (STEMI or NSTEACS).Conclusions:  Our study confirms the higher mortality following ACS, of Maori compared to New Zealanders of European origin. A raised ABG is a marker of this increased risk in all patients with ACS.