bluuebunny/crossref_metadata_2025_split huggingface dataset:
When parties matter: A review of the possibilities and limits of partisan influence on public policy
Authors: SCHMIDT MANFRED G. 
Published: May 2006

AbstractThis essay explores the possibilities and limits of partisan influence on public policy in democratic nations. It will be pointed out, that differences in party composition of government, in general, matter in public policy in constitutional democracy. However, the extent to which parties influence public policy is to a significant extent contingent upon the type of democracy and countermajoritarian institutional constraints of central state government. Large partisan effects typify majoritarian democracies and states, in which the legislature and the executive are ‘sovereign’. More complex and more difficult to identify is the partisan influence on public policy in consensus democracies and in states, in which the political‐institutional circumstances allow for co‐governance of the opposition party. Narrowly circumscribed is the room to manoeuvre available to incumbent parties above all in political systems which have been marked by countermajoritarian institutional pluralism or institutional ‘semi‐sovereignty’. The article suggests, that it would be valuable if direct effects and interaction effects of the party composition of government and state structures featured more prominently in future research on comparative public policy.
Effects of Prenatal Ethanol Exposure on Phospholipase C‐β1 and Phospholipase A2 in Hippocampus and Medial Frontal Cortex of Adult Rat Offspring
Authors: Allan Andrea M. , Weeber Edwin J. , Savage Daniel D. , Caldwell Kevin K. 
Published: May 2006

Previous studies in our laboratory using a rat model of fetal alcohol exposure (FAE) suggest that FAE‐induced behavioral deficits are, in part, linked to neurochemical and electrophysiological deficits in long‐term potentiation (LTP) in the entorhinal cortical perforant path projection to the hippocampal formation. Several findings suggest that signal‐activated phospholipase C (PLC) and phospholipase A2 (PLA2) are critical to the induction and maintenance of LTP. Thus, alterations in phospholipid metabolism may play a significant role in the LTP deficits observed in FAE offspring. To test this hypothesis, we measured PLC‐β1 and PLA2 activities in the hippocampus and medial frontal cortex of adult rats prenatally exposed to ethanol.PLC‐β1 activities were significantly decreased by 20 to 30% in both the hippocampus and medial frontal cortex of FAE rats, compared with ad libitum and pair‐fed controls. Total Ca2+‐dependent PLA2 activity was 25% lower in the medial frontal cortex of FAE rats, but did not significantly differ from controls in the hippocampal formation. Approximately 30% of the measured activity in both the medial frontal cortex and hippocampal formation of ad libitum and pair‐fed animals was associated with an 85 kDa cytosolic PLA2 form. Cytosolic PLA2 activities were significantly reduced in both the medial frontal cortex and hippocampal formation of FAE rats, compared with controls. These changes in Ca2+‐dependent PLA2 and PLC‐β1 activities, coupled with reports of FAE‐induced deficits in protein kinase C activity, indicate that prenatal exposure to moderate quantities of ethanol causes profound and long‐lasting deficits in the cellular signaling mechanisms associated with activity‐dependent synaptic plasticity and memory formation.
Increased Circulating Products of Lipid Peroxidation in Patients with Alcoholic Liver Disease
Authors: Aleynik Semyon I. , Leo Maria Anna , Aleynik Maria K. , Lieber Charles S. 
Published: May 2006

F2‐isoprostanes (F2‐IP) and 4‐hydroxynonenal (4‐HNE), peroxidation products of polyunsaturated fatty acids (PUFA), are considered the most reliable indicators of endogenous lipid peroxidation in vivo. To determine to what extent these are also altered in patients with alcoholic liver disease, plasma free and esterified F2‐IP as well as 4‐HNE were measured by GC/MS in 49 fasting subjects who underwent diagnostic percutaneous needle biopsies of the liver. Compared to patients with mild steatosis and no fibrosis, free F2‐IP and 4‐HNE were strikingly increased in individuals with alcoholic hepatitis. There was also a significant but lesser rise of 4‐HNE in patients with perivenular fibrosis. An increase of F2‐IP was also found in subjects with transition to, or complete, alcoholic cirrhosis, with a comparable trend for 4‐HNE. By contrast, in patients who were drinking heavily up to 48 hr before admission, F2‐IP were not abnormal, but they increased later (p < 0.005). Contrasting with plasma free F2‐IP, esterified F2‐IP were not significantly changed with fibrosis. Thus, whereas circulating esterified F2‐IP were unchanged in patients with alcoholic liver disease, there was an increase in free F2‐IP as well as 4‐HNE during recovery from intoxication. The increase was not a result of accompanying hepatitis C but a function of the stage of alcoholic liver injury, possibly reflecting enhanced lipid peroxidation as well as interference with biliary excretion and/or hepatic esterification.Alcohol, Liver Disease, 4‐Hydroxynonenal, F2‐lsoprostanes, Lipid Peroxidation.
Size of Mamillary Bodies in Health and Disease: Useful Measurements in Neuroradiological Diagnosis of Wernicke's Encephalopathy
Authors: Sheedy Donna , Lara Ana , Garrick Therese , Harper Clive 
Published: May 2006

Background: As the resolution of noninvasive neuroimaging techniques improves, small structures such as the mamillary bodies can be visualized and measured. The mamillary bodies are pathologically small in a number of neurological disorders, the most common and important is chronic Wernicke's encephalopathy (WE), or the Wernicke‐Korsakoff syndrome (WKS), as it is often called. This disorder is caused by vitamin B1 deficiency (thiamin) and is seen most commonly in people who drink excessive amounts of alcohol. The disorder is easily preventable by using oral or parenteral thiamin. The aim of this study was to establish a range for the volume of the mamillary bodies in normal and in various disease states, particularly WE. Methods: Brains were taken from 2212 sequential autopsies performed at the New South Wales Institute of Forensic Medicine from 1996 through 1997. After fixation in 10% formalin, the brains were sectioned coronally and a block containing the mamillary bodies was dissected. The maximum vertical and transverse diameters of the mamillary bodies were measured using Mitutoyo vernier callipers and the volume calculated (V = 413 (a2b), where a and b are the vertical and transverse radii, respectively). Results: There were 164 cases with significant pathological changes in the mamillary bodies. These included cases with WE (25), Alzheimer's disease (10), infarction (11), and trauma (55). All but two of the WE cases were chronic or acute on chronic. The mean volume of the mamillary bodies was reduced by 60% in cases with chronic WE and by 25% in cases with Alzheimer's disease. In normal cases, there was a significant age‐related reduction in volume, and males had larger mamillary bodies than females. Cases with alcoholic cirrhosis of the liver had normal mamillary body volumes. Conclusions: There is a gross shrinkage of the mamillary bodies in cases of chronic WE, but clinicians need to consider other diagnoses, such as Alzheimer's disease, which can also result in shrinkage. These quantitative data will be helpful in the neuroradiological diagnosis of some of these disorders, particularly WE.
In Vivo Mammillary Body Volume Deficits in Amnesic and Nonamnesic Alcoholics
Authors: Sullivan E. V. , Lane B. , Deshmukh A. , Rosenbloom M. J. , Desmond J. E. , Lim K. O. , Pfefferbaum A. 
Published: May 2006

Background: Neuropathological studies use the presence of mammillary body (MB) pathology as a cardi nal, diagnostic feature of Wernicke's encephalopathy (WE) in neuropsychiatric diseases, most notably alcoholism. Although Korsakoff's Syndrome (KS), which is marked behaviorally by dense global amnesia, is a typical sequela of WE, it remains controversial whether these two conditions necessarily co‐occur and whether MB pathology is therefore a diagnostic requisite for KS. Methods: We investigated these issues by examining, in vivo, 24 nonamnesic alcoholics (ALC), 5 amnesic alcoholics (KS), and 51 normal controls with three‐dimensional MRI and memory testing. MB volume was dctermined from successive, 1 mm thick slices. Results: The ALC group had significantly smaller MB volumes bilaterally (mean = 54.5 ± 22.0 mm3) than controls (mean = 66.3 ± 17.1 mm3), and the KS group had even smaller MB volumes than the ALC group (mean = 20.7 ± 14.8 mm3). Only 2 ALC patients met historical clinical criteria for past WE, and their MB volumes were well within range of the remaining 22 ALC patients. Although all five KS patients met historical clinical criteria for WE, three KS did not have accompanying dementia and had the same degree of MB volume loss as the ALC; the remaining two KS had accompanying dementia and MB volumes half the volume of the ALC group and of KS patients without dementia. Conclusions: These findings provide volumetric in vivo evidence that: (1) MB volume deficits do occur in alcoholics without amnesia, although these deficits are not present in all such alcoholics; (2) greater MB volume deficits are present in alcoholics with clinically detectable amnesia or dementia; (3) MB shrinkage is related to severity of cognitive and memory dysfunction, which suggests a continuum of MB pathology in chronic alcoholism to KS; and (4) the presence of WE in all of the KS patients and in the two ALC patients with the greatest long‐term declarative memory deficit supports the possibility of an additional and unique pathology distinguishing nonamnesic and amnesic alcoholism.
Purkinje Cell Vulnerability to Developmental Ethanol Exposure in the Rat Cerebellum
Authors: Pierce Dwight R. , Williams D. Keith , Light Kim Edward 
Published: May 2006

Background: Ethanol cxposure is a consistent and reliable producer of neuronal toxicity, especially during periods of enhanced neuronal vulnerability. For rat cerebellar Purkinje cells, the postnatal period during the time of the brain growth spurt exhibits the greatest vulnerability to ethanol. Analyses of studies completed over more than 20 years provides sufficient detail to allow for the determination of the specific vulnerable window for ethanol‐induced loss of Purkinje cells. Methods: Data reporting Purkinje cell counts after ethanol exposure were compiled from 18 studies published since 1975. We conducted linear regression analysis between peak blood ethanol concentration (BEC) and percent reduction in Purkinje cells for the following individual postnatal (PN) days: PN4, PN5, PN6, PN7, and PN8 or beyond (+). The slope of the regression and the coefficients of determination (r2) were the primary factors of interest. Analysis of variance of the regressions was conducted to identify whether the slopes were significantly different from zero, or from each other. Results: Exposures involving the PN4‐6 period demonstrated the greatest significance in the relationship between BEC and reduction of Purkinje cell number. No significant differences were identified between different ethanol exposure techniques or for different Purkinje cell counting techniques. In addition, the initial day of exposure and the duration of exposure were not identified as critical variables. Conclusions: The literature database, developed over the past 20 years is clear in its direction that studies designed to identify the ethanol‐specific mechanisms of Purkinje cell death are best designed to involve ethanol exposure during the vulnerable window of postnatal days 4‐6.
Ethanol Feeding Selectively Impairs the Spreading of Rat Perivenous Hepatocytes on Extracellular Matrix Substrates
Authors: Tuma Dean J. , Smith Teresa E. , Schaffert Courtney S. , Kharbanda Kusum K. , Sorrell Michael F. 
Published: May 2006

Background: Hepatocytes require attachment and subsequent spreading on an extracellular matrix for their proper growth, function and survival. Our previous studies have shown that ethanol feeding selectively impairs perivenule hepatocyte attachment to various extracellular matrices. This study was undertaken to determine whether zonal differences in hepatocyte spreading in response to ethanol feeding occurs and to ascertain the influence of ethanol consumption on the zonal expression of the β1, subunit of integrins, which are the major surface receptors responsible for matrix binding and subsequent interactions.Methods: Hepatocytes from the perivenous and periportal regions of the liver were isolated by digitonin/collagenase perfusion from rats that were pair‐fed for 2 to 3 weeks with a liquid diet containing either ethanol or isocaloric carbohydrate. The ability of perivenous and periportal hepatocytes to spread on plates coated with either type IV collagen, laminin, fibronectin or polylysine was determined. In addition, the isolated cells were used for the analysis of total cellular and surface β1integrin expression.Results: With all of the matrix substrates tested, the spreading of perivenous hepatocytes isolated from the ethanol‐fed animals was markedly impaired, while the spreading of periportal hepatocytes was essentially unaffected by ethanol feeding. Both the total cellular as well as the surface expression of the β1integrin subunit in perivenous cells from the ethanol‐fed rats were significantly higher than from the perivenous control cells, whereas the total and surface expression of the β1integrin in periportal cells isolated from ethanol‐fed and control rats were not significantly different.Conclusions: The results indicated that in addition to impairing hepatocyte attachment, ethanol feeding also impairs another critical step of the adhesion process, that of hepatocyte spreading on extracellular matrix substrates. This defect occurred preferentially in perivenous cells and not periportal cells and was associated with an increase in β1integrin expression, suggesting that a compensatory mechanism occurs as an attempt by the perivenous cells to overcome impaired cell‐matrix interactions caused by ethanol. Overall, these alterations in extracellular matrix‐hepatocyte interactions could lead to alterations of hepatocyte structure and function and potentially play a role in alcoholic liver injury.
Effects of Benzodiazepines on Acute and Chronic Ethanol‐Induced Nociception in Rats
Authors: Gatch Michael B. 
Published: May 2006

Background: Acute and chronic ethanol produces antinociception, and ethanol withdrawal induces hyperalgesia.Methods: A radiant heat tail‐flick assay was used to assess the effects of benzodiazepine ligands on ethanol‐induced changes in nociception in rats. Acute activity of cumulative doses of ethanol (0.5–2.0 g/kg) and diazepam (0.1–10 mgkg), a benzodiazepine agonist, was tested alone and after pretreatment with flumazenil (1.0–10 mg/kg), a benzodiazepine antagonist. Chronic effects of ethanol were tested in three groups of rats that received a liquid diet for 10 days. One group received ethanol alone; one group received ethanol and twice‐daily injections of flumazenil (10 mg/kg); and one received a dextrin control diet. Acute withdrawal was tested at 12 hr after removal of the liquid diet. Effects of cumulative doses of diazepam (1.0–10 mg/kg) were tested during withdrawal (12 hr) in the ethanol‐alone group.Results: Acute doses of ethanol produced a small but significant degree of antinociception, which was fully suppressed by flumazenil. Acute doses of diazepam did not produce antinociception. Chronic exposure to ethanol produced antinociception on days 2 through 8. Tolerance developed by day 10, and hyperalgesia was seen 12 hr after removal of ethanol. Administration of diazepam or ethanol during withdrawal reversed the hyperalgesia induced by ethanol withdrawal. However, flumazenil (10–50 mg/kg) failed to reverse the antihyperalgesic effect of either diazepam or ethanol. No antinociception was seen in either the ethanoliflumazenil or dcxtrin control groups.Conclusions:These results suggest that the antinociceptive effects of both acute and chronic ethanol are at least partially mediated by GABA receptors, and that diazepam's antihyperalgesic effects may not be mediated by the GABA acid receptor.
Mismatch Negativity and Auditory Sensory Memory in Chronic Alcoholics
Authors: Polo M. Dolores , Escera Carles , Gual Antoni , Grau Carles 
Published: May 2006

Background & Methods: Preattentive auditory processing and sensory memory were investigated by means of mismatch negativity (MMN) in a sample of 22 middle‐aged abstinent chronic alcoholics and 25 age‐matched healthy controls. Stimuli were presented at two inter‐stimulus intervals (ISIs, 0.75 sec and 2.0 sec) in separate blocks.Results: No significant differences in amplitude or latency of MMN were found between aicoholic and control subjects in either of the two ISI conditions. However, when age was included as a factor in the analysis, MMN amplitude was attenuated in chronic alcoholics who were older than 40 years of age.Conclusions: These results indicate that the automatic stimulus‐change detector mechanism associated with MMN gencration is impaired in chronic alcoholics over the age of 40, suggesting that the neurotoxic effects of chronic consumption of alcohol are more prone to appear after a critical age.
Suppression of Alcohol Intake by Chronic Naloxone Treatment in P Rats: Tolerance Development and Elevation of Opiate Receptor Binding
Authors: Overstreet David H. , Kampov‐Polevoy Alexey B. , Rezvani Amir H. , Braun Chris , Bartus Raymond T. , Crews Fulton T. 
Published: May 2006

Background: This study was planned to determine the feasibility of using a slow release naloxone preparation to treat alcoholism, because compliance with medication is a significant problem in alcoholics.Methods: Experiments were performed in alcohol‐preferring P rats maintained either on continuous access or on limited access (1 hr/day) to alcohol with water and food provided ad libitum. Naloxone (Nx) was administered either by twice daily subcutaneous injections or by slow release (1.1 mg/kg/hr) osmotic minipump. In limited access experiments, Nx was injected immediately before access to alcohol.Results: An initial experiment estimated the dose‐effect curve for Nx subcutaneous suppression on alcohol intake. Nx (2.5–20 mgkg) had a stronger effect during the first 2 hr after injection (ED50= 2.1 mgkg); however, the effect was more modest on 24‐hr consumption. Similar results were found with chronic Nx treatment. Low doses of Nx (0.5 and 2.0 mgkg) injected immediately before limited access to alcohol produced almost complete suppression of alcohol intake for at least 14 consecutive days. However, 14 days of treatment with 26 mg/kg/day by minipump or injection produced an initial 50% suppression of 24‐hr alcohol intake with the gradual development of tolerance. An acute challenge with Nx immediately after the pumps were scheduled to be empty provided additional evidence of tolerance development in chronically Nx‐treated rats. Brain μ‐opiate receptors, estimated autoradiographically by using the ligand [3H][D‐Ala2,N‐Me‐Phe4, Gly‐015][tyrosyl‐3,5‐3H]‐enkephalin, showed that rats chronically exposed to Nx and showing tolerance to Nx suppression of drinking exhibited 17% to 250% increases in [3H][D‐Ala2, N‐Me‐Phe4, Gly‐ol5][tyrosyl‐3,5‐3H]‐enkephalin binding.Conclusions: High doses of Nx are required to suppress continuous access alcohol consumption in P rats, and tolerance develops to the ethanol consumption‐suppressing effect of Nx that may be related to increases in μ‐opiate receptors.
Ethanol Consumption, Amino Acid and Glutathione Blood Levels in Patients With and Without Chronic Liver Disease
Authors: Loguercio C. , Del Vecchio Blanco F. , De Girolamo V. , Disalvo D. , Nardi G. , Parente A. , Del Vecchio Blanco C. 
Published: May 2006

Background: Ethanol abuse and liver cirrhosis cause a reduction of glutathione blood levels; liver cirrhosis induces an alteration of the plasma amino acid pattern. We evaluated whether or not ethanol abuse affects amino acid levels, particularly those that are involved in metabolizing glutathione in the plasma and erythrocytes of chronic alcohol abusers with or without liver cirrhosis.Methods:. We studied 10 chronic alcohol abusers without liver cirrhosis, 10 with alcoholic cirrhosis, 10 affected by hepatitis C virus‐related cirrhosis, and 10 healthy subjects. Glutathione, γ‐glutamyl‐cysteine, and cysteine were determined by fluorescent HPLC, glutamic acid, glycine, and other free amino acids by cation exchange chromatography both in the plasma and erythrocytes of all studied subjects.Results and Conclusions: In both alcoholics and cirrhotics, we found a significant increase of plasma‐aromatic amino acid and methionine levels, whereas glutathione was significantly reduced. The erythrocytes of these patients showed a significant increase of cysteine, glutamic acid, and glycine; γ‐glutamyl‐cysteine was normal; and glutathione and other free amino acids were significantly decreased. Data suggest that, independent of liver cirrhosis, ethanol abuse affects the metabolism of amino acids and glutathione in both the plasma and the erythrocytes.
Prenatal Ethanol Reduces the Activity of Adult Midbrain Dopamine Neurons
Authors: Shen Roh‐Yu , Hannigan John H. , Kapatos Gregory 
Published: May 2006

Background: Prenatal ethanol exposure has been demonstrated to reduce dopamine (DA) neurotransmission in the forebrain area, which could be contributed by altered electrical activity in midbrain DA neurons. This hypothesis was tested in the present study.Methods: The effects of prenatal ethanol exposure on the spontaneous activity of DA neurons in the substantia nigra and ventral tegmental area were investigated with extracellular single‐unit recording techniques in adult male rats. Pregnant rats were administered single daily doses of 0, 3, or 5 g/kg ethanol via intragastric intubation from gestation day 8 through 20. An additional control group did not receive the intubation procedure.Results: Prenatal ethanol treatment significantly reduced the number of spontaneously active DA neurons in the substantia nigra and ventral tegrnental area in 3‐ to 5‐month‐old male offspring. The firing rate and firing pattern of the remaining spontaneously active DA neurons were not altered. There were no differences in the spontaneous activity of DA neurons between the nonintubated and 0 g/kg control groups, indicating possible intubation‐induced stress did not influence the activity of DA neurons in adult offspring. Similar prenatal ethanol effects were also determined from older animals (14–16 months old), suggesting that the reduction in the spontaneous activity of DA neurons is a persistent phenomenon in adulthood after prenatal ethanol exposure. Furthermore, the reduction in the number of spontaneously active DA neurons was not the result of a loss in DA neurons per se, as revealed by the results of tyrosine hydroxylase immunohistochemistry. The prenatal ethanol exposure‐induced reduction in DA neuronal activity may result from depolarization inactivation, because systemically administered apomorphine (20 μg) increased the spontaneous activity of DA neurons.Conclusions: Prenatal ethanol exposure induced a long‐lasting reduction in the activity of midbrain DA neurons in adult animals. The effect was not the result of cell loss but possible changes in the electrical properties of DA neurons. The decreased electrical activity in midbrain DA neurons could contribute to the prenatal ethanol exposure‐induced reduction in DA content and metabolites observed in previous studies and the attention/hyperactivity problems reported in children with fetal alcohol effects/fetal alcohol syndrome.