bluuebunny/crossref_metadata_2025_split huggingface dataset:
Marked pneumoperitoneum 3 weeks after percutaneous endoscopic gastrostomy
Authors: Chen Wunbill , Kawahara Hiromu , Takahasi Masakatsu , Matsushima Akihiro , Takase Shujiro 
Published: May 2006

AbstractIn November 2001, a 29‐year‐old woman was admitted to the hospital because of dysphagia due to an apallic state caused by cerebral anoxia. Nutritional support was maintained by nasogastric tube feeding for approximately 3 months. For improvement of the body state maintenance and quality of life, a percutaneous endoscopic gastrostomy (PEG) was performed. Three weeks after the PEG, the patient had a wound infection and abdominal distension appeared. Marked pneumoperitoneum was confirmed by radiological examination. No signs or symptoms of peritoneal inflammation developed. A gastrografin study showing that the PEG tube was in the stomach appropriately was checked, and it was noted to be firmly in place without extravasation of contrast. After suspension of the tube feeding and tube opening to decrease intragastric pressure, intravenous hyperalimentation was performed. The pneumoperitoneum resolved within 7 days. Forty days after the PEG, tube feeding was resumed successfully. No recurrence of pneumoperitoneum developed and the patient has remained stable until the present time. The etiology of this finding probably occurs by insufficient fixation of the PEG, causing leakage of air through the gastric wall which enters the free peritoneal space. We recommend that the external binder should be kept 1 cm away from the abdominal skin after the gastrostomy fistula has formed and matured, and periodic rotation of the tube to verify that the internal bumper is free and sufficiently fixed to the gastric wall. In the case of abdominal distension after PEG placement, a X‐ray examination and computed tomography (CT) scan with contrast medium would be helpful to ascertain pneumoperitoneum.
An investigation into signal transduction mechanisms involved in insulin‐induced long‐term depression in the CA1 region of the hippocampus
Authors: Huang Chiung‐Chun , Lee Cheng‐Che , Hsu Kuei‐Sen 
Published: May 2006

AbstractRecent work has demonstrated that brief application of insulin to hippocampal slices can induce a novel form of long‐term depression (insulin‐LTD) in the CA1 region of the hippocampus; however, the molecular details of how insulin triggers LTD remain unclear. Using electrophysiological and biochemical approaches in the hippocampal slices, we show here that insulin‐LTD (i) is specific to 3‐hydroxy‐5‐methylisoxazole‐4‐propionic acid (AMPA) receptor‐ but not NMDA receptor‐mediated synaptic transmission; (ii) is induced and expressed postsynaptically but does not require the activation of ionotropic and metabotropic glutamate receptors; (iii) requires a concomitant Ca2+ influx through l‐type voltage‐activated Ca2+ channels (VACCs) and the release of Ca2+ from intracellular stores; (iv) requires the series of protein kinases, including protein tyrosine kinase (PTK), phosphatidylinositol 3‐kinase (PI3K), and protein kinase C (PKC); (v) is mechanistically distinct from low‐frequency stimulation‐induced LTD (LFS‐LTD) and independent on protein phosphatase 1/2 A (PP1/2 A) and PP2B activation; (vi) is dependent on a rapamycin‐sensitive local translation of dendritic mRNA, and (vii) is associated with a persistent decrease in the surface expression of GluR2 subunit. These results suggest that a PI3K/PKC‐dependent insulin signaling, which controls postsynaptic surface AMPA receptor numbers through PP‐independent endocytosis, may be a major expression mechanism of insulin‐LTD in hippocampal CA1 neurons.
Exogenous, but not endogenous nociceptin modulates mesolimbic dopamine release in mice
Authors: Koizumi Miwako , Midorikawa Naoko , Takeshima Hiroshi , Murphy Niall P. 
Published: May 2006

AbstractThe effect of nociceptin (an endogenous ligand of the ORL1 receptor) on mesolimbic dopamine release and simultaneous horizontal locomotion was studied in freely moving mice undergoing microdialysis of the nucleus accumbens. Intracerebroventricular (i.c.v.) administration of nociceptin (7 nmol) induced a long‐lasting suppression of mesolimbic dopamine release and horizontal locomotion in wild‐type but not ORL1 knockout mice. I.c.v. administration of the recently reported peptide nociceptin antagonist [Nphe1, Arg14, Lys15] nociceptin‐NH2(known also as UFP‐101, 5 nmol) completely abolished the suppressive effect of nociceptin on mesolimbic dopamine release. However, UFP‐101 administration alone induced a mild and lasting suppression of mesolimbic dopamine release in both wild‐type and ORL1 knockout mice that was magnified in ORL1 knockout mice by coadministration of nociceptin. UFP‐101 administration alone suppressed locomotion in both genotypes. These results confirm that the suppressive action of nociceptin on mesolimbic dopamine release is mediated entirely by the ORL1 receptor, and that UFP‐101 effectively antagonizes this action. However, the lack of a stimulatory effect of UFP‐101 in wild‐type mice indicates that despite being sensitive to exogenous nociceptin action, basal mesolimbic dopaminergic activity is not determined by endogenous nociceptin in mice.
Identification of GABAAreceptor subunit variants in midbrain dopaminergic neurons
Authors: Okada Hideki , Matsushita Natsuki , Kobayashi Kenta , Kobayashi Kazuto 
Published: May 2006

AbstractModulation of the activity of dopamine (DA)‐producing neurons by GABA plays an important role in the control of DA‐mediated brain functions. Ionotropic GABAAreceptors exist as heteropentametric structures assembling different subunits composed of various subtypes. However, the expression pattern of these subunits in DA neurons in the ventral midbrain has not been fully defined. In the present study, we investigated the subunit composition of GABAAreceptors in DA neurons in the substantia nigra pars compacta (SNc) and the ventral tegmental area (VTA). We isolated DA neurons from the ventral midbrain of transgenic mice that express green fluorescent protein under the control of the tyrosine hydroxylase (TH) gene promoter and analyzed expression of various GABAAreceptor subunits in single cells by using the reverse transcription‐polymerase chain reaction. This analysis showed the presence of the transcripts encoding α2, α3, α4, β1, β3 and γ2 subunits in the isolated DA neurons. Double fluorescencein situhybridization with probes for TH and GABAAreceptor subunit mRNAs revealed the expression of these six subunits in the majority of DA neurons in the SNc and the VTA.
Involvement of ERK MAP kinase in endoplasmic reticulum stress in SH‐SY5Y human neuroblastoma cells
Authors: Arai Ken , Lee Sun‐Ryung , Van Leyen Klaus , Kurose Hitoshi , Lo Eng H. 
Published: May 2006

AbstractEndoplasmic reticulum (ER) stress has increasingly come into focus as a factor contributing to neuronal injury. Although caspase‐dependent mechanisms have been implicated in ER stress, the signaling pathways involved remain unclear. In this study, we examined the role of the extracellular signal‐regulated kinase (ERK), a mitogen‐activated protein (MAP) kinase pathway that is highly conserved in many systems for balancing cell survival and death. Prolonged treatment of the human neuroblastoma cell line SH‐SY5Y with thapsigargin, an inducer of ER stress, increased cell death over 24–48 h, as measured by LDH release. Caspases were involved; increased levels of active caspase‐3 and cleaved caspase substrate PARP were detected, and treatment with Z‐VAD‐FMK reduced thapsigargin‐induced cytotoxicity. In contrast, inhibition of calpain was not protective, although calpain was activated following thapsigargin treatment. An early and transient phosphorylation of ERK1/2 occurred after thapsigargin‐induced ER stress, and targeting this pathway with the MEK inhibitors U0126 or PD98059 significantly reduced cell death. Similar cytoprotection was obtained against brefeldin A, another ER stress agent. However, protection against ER stress via ERK inhibition was not accompanied by amelioration of caspase‐3 activation, PARP cleavage, or DNA laddering. These data indicate that ERK may contribute to non‐caspase‐dependent pathways of injury after ER stress.
Differential Regulation of the Alcohol Dehydrogenase 1B (ADH1B) and ADH1C Genes by DNA Methylation and Histone Deacetylation
Authors: Dannenberg Luke O. , Chen Hui‐Ju , Tian Huijun , Edenberg Howard J. 
Published: May 2006

Background: The human class I alcohol dehydrogenase (ADH) genes (ADH1A, ADH1B, and ADH1C) differ in expression during development and in various tissues. They are repressed in the HepG2 human hepatoma cell line. We hypothesized that epigenetic modifications play a role in this repression and that class I ADH gene expression would be enhanced upon global inhibition of DNA methylation and histone deacetylation.Methods: Southern blotting was used to assess the methylation status of each class I ADH gene. HepG2 and HeLa cells were treated with either the DNA methylation inhibitor 5‐aza‐2′‐deoxycytidine (5‐aza‐dC), the histone deacetylase inhibitor Trichostatin A (TSA), or both in combination, and class I ADH gene expression was analyzed. Chromatin immunoprecipitation assays were performed to analyze histone H3 acetylation. Transient transfections and gel mobility shift assays were used to analyze the role that methylation plays in inhibiting transcription factor binding and promoter function.Results: We show that the upstream regions of ADH1A, ADH1B, and ADH1C are methylated in HepG2 cells. 5‐Aza‐2′‐deoxycytidine treatment enhanced expression of both ADH1B and ADH1C. Trichostatin A treatment elevated expression of ADH1C. ADH1A expression was not stimulated by either 5‐aza‐dC or TSA. H3 histones associated with a methylated upstream region of ADH1B were hyperacetylated in TSA‐treated, but not in 5‐aza‐dC–treated, HepG2 cells. A methylated upstream region of ADH1C achieved histone H3 hyperacetylation upon either 5‐aza‐dC or TSA treatment. Methylation of the ADH1B proximal promoter in vitro decreased its activity to 54% and inhibited the binding of the upstream stimulatory factor.Conclusions: These findings suggest that the class I ADH genes are regulated by epigenetic mechanisms in human hepatoma cells. The temporal and tissue‐specific expression of these genes may in part result from differences in epigenetic modifications and the availability of key transcription factors.
Effects of Chronic Alcohol Dependence and Chronic Cigarette Smoking on Cerebral Perfusion: A Preliminary Magnetic Resonance Study
Authors: Gazdzinski Stefan , Durazzo Timothy C. , Jahng Geon‐Ho , Ezekiel Frank , Banys Peter , Meyerhoff Dieter J. 
Published: May 2006

Background: Although approximately 80% of individuals with alcohol use disorders are chronic smokers and despite reported associations between chronic cigarette smoking and lower cerebral perfusion in nonalcoholics, previous brain perfusion studies with alcoholics did not account for the potential effects of concurrent chronic cigarette smoking.Methods: One‐week‐abstinent alcohol‐dependent individuals in treatment (ALC) [19 smokers (sALC) and 10 nonsmokers (nsALC)] and 19 healthy light drinking, nonsmoking control participants (nsLD) were scanned with a pulsed arterial spin labeling method to measure cerebral perfusion without an exogenous contrast agent. Studies were performed with 2 different postlabeling delay times (time from labeling pulse to the excitation pulse; PLD=1,500 ms and PLD=1,200 ms) to assess the potential effect of arterial blood transit time on the perfusion. Average gray matter (GM) and white matter (WM) perfusion for the frontal and parietal lobes were calculated for each hemisphere from voxels containing at least 90% GM and 100% WM.Results: At PLD=1,500 ms, multivariate analyses compared ALC (combined sALC and nsALC) with nsLD (p=0.04) and contrasted sALC, nsALC, and nsLD (p=0.006). ALC, as a group, showed 13% lower frontal GM perfusion (p=0.005) and 8% lower parietal GM perfusion than nsLD (p=0.03). With ALC separated into smokers and nonsmokers, sALC showed 19% lower frontal GM perfusion (p=0.001) and 12% lower parietal GM perfusion than nsLD (p=0.004). In sALC, a higher number of cigarettes smoked per day was associated with lower perfusion. Overall, regional perfusion did not differ significantly between nsALC and nsLD. Results obtained with PLD=1,200 ms generally confirmed the 1,500 ms findings.Conclusions: This study provides preliminary evidence that chronic cigarette smoking adversely affects cerebral perfusion in frontal and parietal GM of 1‐week‐abstinent alcohol‐dependent individuals. These results are in line with our spectroscopic and structural magnetic resonance studies that suggest chronic cigarette smoking compounds the detrimental effects of alcohol dependence on brain neurobiology.
Effects of Alcohol on Sleep and the Sleep Electroencephalogram in Healthy Young Women
Authors: Van Reen Eliza , Jenni Oskar G. , Carskadon Mary A. 
Published: May 2006

Background: Although the association between sleep and alcohol has been of interest to scientists for decades, the effects of alcohol on sleep and sleep electroencephalogram (EEG) have not been extensively studied in women. Our specific aim was to determine whether sleep stage variables and/or spectral characteristics of the sleep EEG are altered by alcohol administration in women.Methods: Changes of sleep and the sleep EEG were investigated after administration of a moderate dose of alcohol (0.49 g/kg) in the hour before bedtime compared with placebo in young healthy women. After approximately 2 weeks at home on a fixed 8.5‐ or 9‐hour stabilization sleep schedule, sleep was continuously recorded by polysomnography for 3 consecutive nights [adaptation, placebo, alcohol (mean breath alcohol concentration 0.043 g/% before bedtime)] in the laboratory in 7 women (ages 22–25, mean=23.5, SD=1 year). Sleep stages were scored according to conventional criteria. Electroencephalogram power spectra of the bipolar derivations Fz/Cz (anterior) and Pz/Oz (posterior) were calculated using a fast Fourier transform routine.Results: Only few changes in sleep and the sleep EEG were observed. Across the entire night rapid eye movement (REM) sleep decreased, while minutes of stage 4 sleep were increased in the first 2‐hour interval on alcohol nights compared with placebo nights. Spectral analysis of the EEG showed increased power in the α range (9–11 Hz) during all‐night non‐REM (NREM) sleep in anterior derivations after alcohol compared with placebo. Differences in spectral EEG power were also present in 2‐hour intervals of NREM sleep; in particular, EEG power was increased on the alcohol night for frequency bins within the α range in anterior derivations and within the δ range (3–4 Hz) in posterior derivations during the initial part of the night.Conclusions: A moderate dose of alcohol just before bedtime resulted in a short‐lived increase in sleep intensity. A limitation of the study, however, was that only a single dose of alcohol was used to examine the effects of alcohol on sleep.
The Epidemiology of Drinking Among Women of Child‐Bearing Age
Authors: Caetano Raul , Ramisetty‐Mikler Suhasini , Floyd Louise R. , McGrath Christine 
Published: May 2006

Objectives:To estimate the prevalence of drinking, binge drinking (4 or more drinks), and alcohol abuse and dependence and to identify predictors of heavier drinking among women of child‐bearing age (18–44 years).Methods:Subjects are part of a national multistage random sample from the 2002 National Epidemiologic Survey on Alcohol and Related Conditions (NESARC).Results:Binge drinking, abuse, and dependence are higher in younger (<30 years) pregnant and nonpregnant women. Among pregnant women, binge drinking is highest among Whites; alcohol abuse and dependence rates are relatively low and similar in all racial/ethnic groups. Among nonpregnant women, Whites and mixed race women have the highest rates of binge drinking. Alcohol abuse and dependence are highest among Native Hawaiian/Pacific Islanders, followed by Native American/Alaska Native women. Women who are White, younger (21–29 years), single, or cohabiting and with a higher income (>$40,000) are at a higher risk for heavier drinking.Conclusions:Drinking and heavier drinking remain at high levels among women of child‐bearing age. Prevention efforts must be comprehensive and should target pregnant women who are drinking and those who could become pregnant and are drinking at high‐risk levels.
Both Global Gray Matter Volume and Regional Gray Matter Volume Negatively Correlate with Lifetime Alcohol Intake in Non–Alcohol‐Dependent Japanese Men: A Volumetric Analysis and a Voxel‐Based Morphometry
Authors: Taki Yasuyuki , Kinomura Shigeo , Sato Kazunori , Goto Ryoi , Inoue Kentaro , Okada Ken , Ono Shuichi , Kawashima Ryuta , Fukuda Hiroshi 
Published: May 2006

Background: Non–alcohol‐dependent heavy drinkers, as well as alcohol‐dependent individuals, show brain atrophy. The purpose of this study was to evaluate whether there are correlations between global and regional gray matter volumes and the lifetime alcohol intake using volumetric analysis and voxel‐based morphometry (VBM) among Japanese non‐alcohol–dependent male individuals.Methods: High‐resolution three‐dimensional magnetic resonance images were acquired from 405 Japanese non‐alcohol–dependent male individuals. The collected images were normalized, segmented for volumetric analysis, and additionally smoothed for VBM. For volumetric analysis, the partial correlation coefficient was estimated between the gray matter ratio, which represents the percentage of gray matter volume in the intracranial volume, and the lifetime alcohol intake adjusted for the age of each subject. Multiple regression analysis was performed among regional gray matter volume, lifetime alcohol intake, and age using VBM.Results: Volumetric analysis revealed that gray matter ratio showed a negative correlation with the lifetime alcohol intake adjusted for age (p=0.059, partial correlation coefficient=−0.091). The VBM revealed that the gray matter volumes of the bilateral middle frontal gyri showed a significant negative correlation with the lifetime alcohol intake adjusted for age and systolic blood pressure (left side, p=0.006, Z=4.77; right side, p=0.023, Z=4.45, and p=0.046, Z=4.27).Conclusions: Our study suggests that non‐alcohol–dependent Japanese male individuals show that both global gray matter volume and regional gray matter volume have negative correlations with the lifetime alcohol intake. Our study may contribute to clarifying the mechanism underlying the brain structural changes because of alcohol influence in healthy non‐alcohol–dependent individuals.
Cost effectiveness of brace, physiotherapy, or both for treatment of tennis elbow
Authors: Struijs P A A , Korthals-de Bos I B C , van Tulder M W , van Dijk C N , Bouter L M , Assendelft W J J 
Published: May 2006

Background:The annual incidence of tennis elbow in the general population is high (1–3%). Tennis elbow often leads to limitation of activities of daily living and work absenteeism. Physiotherapy and braces are the most common treatments.Objectives:The hypothesis of the trial was that no difference exists in the cost effectiveness of physiotherapy, braces, and a combination of the two for treatment of tennis elbow.Methods:The trial was designed as a randomised controlled trial with intention to treat analysis. A total of 180 patients with tennis elbow were randomised to brace only (n  =  68), physiotherapy (n  =  56), or a combination of the two (n  =  56). Outcome measures were success rate, severity of complaints, pain, functional disability, and quality of life. Follow up was at six, 26, and 52 weeks. Direct healthcare and non-healthcare costs and indirect costs were measured. Mean cost differences over 12 months were evaluated by applying non-parametric bootstrap techniques.Results:No clinically relevant or statistically significant differences were found between the groups. Success rate at 12 months was 89% in the physiotherapy group, 86% in the brace group, and 87% in the combination group. Mean total costs per patient were €2069 in the brace only group, €978 in the physiotherapy group, and €1256 in the combination group. The mean difference in total costs between the physiotherapy and brace group was substantial (€1005), although not significant. Cost effectiveness ratios and cost utility ratios showed physiotherapy to be the most cost effective, although this also was not statistically significant.Conclusion:No clinically relevant or statistically significant differences in costs were identified between the three strategies.
The fading of reported effectiveness. A meta-analysis of randomised controlled trials
Authors: Gehr Bernhard T , Weiss Christel , Porzsolt Franz 
Published: May 2006

Abstract

Background
The "real" effect size of a medical therapy is constant over time. In contrast, the effect size reported in randomised controlled trials (RCTs) may change over time because the sum of all kinds of bias influencing the reported effectiveness is not necessarily constant. As this would affect the validity of meta-analyses, we tested the hypothesis that the reported effect size decreases over time. Furthermore, we tested three hypotheses that would explain a possible change.

Methods
Because of well established outcome measures, the lipid-lowering drugs Pravastatin and Atorvastatin (serum low-density lipoprotein cholesterol, LDL-C) and the anti-glaucoma drugs Timolol and Latanoprost (intraocular pressure, IOP) were chosen for this investigation. Studies were identified by a standardized MEDLINE search. RCTs investigating the above identified medications administered as monotherapy, and in defined dosages, were included. Publication year, baseline (= pre-treatment value in the treatment group of interest) and post intervention means, number of patients and the assignment to experimental or control group were extracted for each study.

Results
A total of 625 citations were screened; 206 met the inclusion criteria. The reported effect size of Pravastatin (change of reported effect size in five years: -3.22% LDL-C, P < .0001), Timolol (-0.56 mmHg, P < .0001) and Latanoprost (-1.78 mmHg, P = .0074) decreased over time, while there was no significant change for Atorvastatin (+0.31% LDL-C, P = .8618). Multiple regression analysis showed that baseline values were the most important influencing factor; study size or treatment group did not play a significant role.

Conclusion
The effectiveness of medical therapies reported in RCTs decreases over time in three of the four investigated pharmaceuticals, caused mainly by baseline differences. We call this phenomenon "fading of reported effectiveness". Under this condition the validity of a meta-analysis may be impaired. Therefore we propose to observe this phenomenon in future meta-analyses in order to guarantee a maximum of transparency.