bluuebunny/crossref_metadata_2025_split huggingface dataset:
Failed takeover attempts, corporate governance and refocusing
Authors: Chatterjee Sayan , Harrison Jeffrey S. , Bergh Donald D. 
Published: December 2002

AbstractHostile takeover attempts oftentimes signal that a target firm has an over‐diversified and ineffective corporate strategy. What does this signal mean when takeover attempts fail? Drawing from agency theory, we argue that target firms managed by independent directory boards are likely to ignore the takeover attempt and not refocus their firms' strategy. Conversely, target firms managed by nonindependent boards are more likely to view the failed takeover attempt as a ‘wake‐up call’ and will refocus their firms' strategy so as to preserve the firm's survival. These arguments are tested using a sample of 76 firms that were targets of failed hostile takeover attempts. Logistic regression analyses confirm the predictions. This study suggests that in the aftermath of a failed takeover attempt board of director characteristics can help predict changes in corporate strategies. Copyright © 2002 John Wiley & Sons, Ltd.
Strategic determinants of decisions not to settle patent litigation
Authors: Somaya Deepak 
Published: December 2002

AbstractSettlement outcomes in patent litigation are modeled as resulting from strategies pursued by firms with their patented technologies. Hypotheses are derived for two types of influences: the use of patents as isolating mechanisms to protect valuable strategic stakes, and their ‘defensive’ role in obtaining access to external technologies through mutual hold‐up. Parameter estimates from a sample selection probit model provide support for the strategic stakes hypotheses, while the evidence for mutual hold‐up is inconclusive. Interindustry comparisons show that nonsettlement of patent suits in both research medicines and computers is increased by strategic stakes and, in addition, mutual hold‐up appears to play an important role in computer patent suits. Copyright © 2003 John Wiley & Sons, Ltd.
D1 dopamine receptors in the mouse prefrontal cortex: Immunocytochemical and cognitive neuropharmacological analyses
Authors: Lidow Michael S. , Koh Phil‐Ok , Arnsten Amy F.T. 
Published: December 2002

AbstractDopamine D1 receptors have critical neuromodulatory influences on the working memory functions of the prefrontal cortex, a brain region affected in many neuropsychiatric disorders. When D1 receptor agents are administered to rats or monkeys performing working memory tasks, an “inverted U” dose/response function is typically observed, whereby either too little or too much D1 receptor stimulation impairs working memory. There are two subtypes of D1 receptors, the D1A and the D1B (also known as the D1 and D5, respectively), but the relative contributions of these subtypes to prefrontal cortical function are not known, as there are no pharmacological agents that can distinguish between these receptors. Thus, genetically altered mice are needed to address this question. However, it is not known whether the mouse prefrontal cortex contains both D1A and D1B receptor subtypes, nor is it known whether mice will exhibit responses to D1 receptor agonists similar to those seen in rats and monkeys. The current study examined these issues by immunostaining the mouse brain with specific antibodies directed at the D1A and D1B receptor subtypes and by assessing the effects of increasing doses of a D1 receptor agonist, SKF81297, on spatial working memory performance in mice. Results indicate that mice are generally similar to monkeys and rats, expressing both D1A and D1B receptors in the prefrontal cortex and exhibiting an inverted “U” dose/response curve when administered SKF81297. Synapse 47:101–108, 2003. © 2002 Wiley‐Liss, Inc.
[11C]‐DASB, a tool for in vivo measurement of SSRI‐induced occupancy of the serotonin transporter: PET characterization and evaluation in cats
Authors: Ginovart Nathalie , Wilson Alan A. , Meyer Jeffrey H. , Hussey Doug , Houle Sylvain 
Published: December 2002

AbstractThe in vivo pharmacological profile of [11C]‐DASB, a new radioligand developed for in vivo imaging of the serotonin transporter (SERT), was evaluated in the cat brain using positron emission tomography (PET). The in vivo distribution of [11C]‐DASB binding was consistent with the known distribution of SERT sites in the cat brain in vitro with high uptakes of radioactivity in the midbrain and thalamus, intermediate levels in striatum, and modest to low levels of radioactivity in the neocortex and cerebellum, respectively. [11C]‐DASB binding potential (BP) values ranged from about 0.2 in the neocortex to 2.2 in the midbrain. Radioligand binding in all brain regions except cerebellum was markedly reduced following pretreatment with fluoxetine and citalopram, but was unaffected by pretreatment with GBR12909, maprotiline, and haloperidol, indicating specificity of [11C]‐DASB binding to the SERT. Two cats were each examined using PET and [11C]‐DASB in a longitudinal fashion (from 30 min and up to 24 days) following a single i.v. dose of: 1) fluoxetine, and 2) citalopram at different dosages. Both drugs induced similar degrees of SERT occupancy at 30 min postinjection (∼90%). A comparison of citalopram and fluoxetine pharmacokinetics in the same animal and at the same dosage (1 mg/kg) showed that citalopram SERT occupancy and plasma half‐lives were 9 times and 14 times shorter, respectively, than those of fluoxetine and norfluoxetine. In addition, studies performed after injection of the monoamine oxidase inhibitor tranylcypromine suggested that high levels of synaptic serotonin may compete with [11C]‐DASB for binding on the SERT. These studies indicate that [11C]‐DASB is a suitable PET radioligand for measuring drug occupancy of the SERT in vivo and has potential for monitoring in vivo changes in serotonin levels. Synapse 47:123–133, 2003. © 2002 Wiley‐Liss, Inc.
Short‐term intravaginal maximal electrical stimulation for refractive detrusor instability
Authors: Yalcin O.T. , Hassa H. , Sarac I. 
Published: December 2002

AbstractObjectives: To determine the efficacy of intravaginal maximal electrical stimulation for the treatment of refractive detrusor instability. Methods: Thirty‐five consecutive patients, treated by maximal electrical stimulation for pure refractive detrusor instability were evaluated subjectively by patient's questionnaires and 24‐h urinary diary and objectively by 1‐h standardized pad test and subtracted cystometry before and 1 week after the treatment. Paired‐t and χ2‐tests were used for the statistical analysis of the data. Results: Thirty‐one (88.6%) of the 35 patients were found to be either cured or improved, subjectively. The overall objective success rates based on the 1‐h pad test and subtracted cystometry were 80.0% and 74.3%, respectively. The results of all subjective and objective assessment tests, except postvoiding residual urine volume, improved significantly after the treatment (P<0.01). No significant adverse effect related to the treatment was observed, except vaginal irritation noted only by 5 (14.3%) patients. Conclusion: Maximal electrical stimulation could offer a safe, non‐invasive and effective treatment for patients with detrusor instability who respond poorly to other conservative therapies.
F3/contactin, a neuronal cell adhesion molecule implicated in axogenesis and myelination
Authors: Falk Julien , Bonnon Carine , Girault Jean‐Antoine , Faivre‐Sarrailh Catherine 
Published: December 2002

AbstractA general feature of the cell adhesion molecules belonging to the immunoglobulin family (Ig‐CAMs) is to display a modular structure that provides a framework for multiple binding sites for other recognition molecules. Among this family, F3/contactin is a glycan phosphatidyl‐inositol (GPI)‐anchored molecule expressed by neurons that displays the distinctiveness to exert heterophilic but no homophilic binding activities. The Ig domains of F3/contactin were shown to interact with the L1 family of Ig‐CAMs, including L1, NrCAM, and neurofascin. Binding between F3/contactin and NrCAM is known to modulate axonal elongation of the cerebellar granule cells and to control sensory axon guidance. F3/contactin mediates neuron—glial contacts through its association with extracellular matrix components (tenascin‐R, tenascin‐C) and RPTPβ/phosphacan, influencing axonal growth and fasciculation. Another major role of F3/contactin is to organize axonal subdomains at the node of Ranvier of myelinated fibers in interplay with other Ig‐CAMs, through its binding with caspr/paranodin at paranodes and the voltage‐gated sodium channels in the nodal region. The F3/contactin deficient mice display a severe ataxia correlated with defects in axonal and dendritic projections in the cerebellum. These mice also display defects in nerve influx conduction due to the disruption of the axo‐glial contacts at paranodes. Finally, the recent identification of a Drosophila homologue of F3/contactin indicated that this family of GPI‐anchored CAMs plays a conserved function in axonal insulation.
Expression of slow skeletal myosin heavy chain 2 gene in Purkinje fiber cells in chick heart
Authors: Machida Shuichi , Noda Setsuko , Takao Atsuyoshi , Nakazawa Makoto , Matsuoka Rumiko 
Published: December 2002

AbstractIn avian, there are three slow skeletal myosin heavy chain (MHC) isoforms, slow skeletal MHC 1, 2, and 3. While slow skeletal MHC 3 has been characterized, slow skeletal MHC 1 and 2 are not yet fully studied. To determine the complete sequence of slow skeletal MHC 2, we isolated six overlapping cDNA clones, each encoding a portion of chick slow skeletal MHC 2, using the reverse transcription polymerase chain reaction (RT‐PCR). The entire slow skeletal MHC 2 cDNA consisted of 5927 nucleotides including a 104 bp 3’‐untranslated region and encoded 1941 amino acids. Using one of the cDNA clones, we made a probe for in situ hybridization. We also used immunohistochemistry to localize slow skeletal MHC 2 in skeletal and cardiac tissues. These studies showed that in addition to its expected expression in the adult chicken slow skeletal muscle, slow skeletal MHC 2 was expressed in the subendocardial cluster of cells and around the blood vessels within the ventricle of late embryos and adults. This isoform was not expressed in the myocardium throughout the life of the chicken. Based on morphological criteria as well as rich desmin expression, we concluded that the subendocardial cluster of cells were Purkinje cells. Although the physiological significance of the slow skeletal MHC expression remains elusive at this time, this MHC isoform may be used as a specific marker for Purkinje cells.
Arachidonic acid cytotoxicity in leukocytes: implications of oxidative stress and eicosanoid synthesis
Authors: Pompeia Celine , Freitas Jofre J.S , Kim Jung S. , Zyngier Szulim B. , Curi Rui 
Published: December 2002

AbstractArachidonic acid (AA)‐induced cytotoxicity was evaluated in leukocytes: the human leukemia cell lines HL‐60, Jurkat and Raji and in rat lymphocytes. Such cytotoxicity was dose‐ and time‐dependent. At concentrations below 5 μM, AA was not toxic; at 10–400 μM, AA induced apoptosis and at concentrations beyond 400 μM, necrosis. The minimum exposure time to trigger cell death was of around 1 h, but the effect was increased by longer exposure times until 6–24 h. Apoptosis was morphologically characterized by a decrease in cell and nuclear volume, chromatin condensation and DNA fragmentation and the presence of lipid bodies, without changes in organelle integrity. Biochemically, AA‐induced apoptosis was associated with internucleosomal fragmentation and caspase activation, evaluated by PARP cleavage and the use of a caspase inhibitor. Necrosis was characterized by increased cell volume, presence of loose chromatin, appearance of vacuoles, loss of membrane integrity and of the definition of organelles. The apoptotic effect of AA was studied as to oxidative—reductive imbalance and the participation of eicosanoids. Apoptotic AA treatment was accompanied by an increase in the quantity of thiobarbituric acid reactive substances (TBARS), low‐level chemiluminescence and in the glutathione disulfide/reduced glutathione ratio, indicating oxidative stress. The addition of tocopherol, ascorbate, prostaglandin E2 and lipoxygenase inhibitors delayed cell death, whereas the inhibition of cyclooxygenase promoted AA‐induced cell death. Cell treatment with AA was accompanied by increased cellular production of LTB4. AA, therefore, is cytotoxic at physiological and supraphysiological concentrations, causing apoptosis and necrosis. Cell treatment with apoptotic concentrations of AA involves oxidative stress and changes in eicosanoid biosynthesis.
The relationship between predisposing factors, premorbid function and symptom dimensions in psychosis: an integrated approach
Authors: Guerra Almudena , Fearon Paul , Sham Pak , Jones Peter , Lewis Shon , Mata Ignacio , Murray Robin 
Published: December 2002

SummaryBackground.Increasing evidence suggests psychosis may be more meaningfully viewed in dimensional terms rather than as discrete categorical states and that specific symptom clusters may be identified. If so, particular risk factors and premorbid factors may predict these symptom clusters.Aims.(i) To explore, using principal component analysis, whether specific factors for psychotic symptoms can be isolated. (ii) To establish the predictors of the different symptom factors using multiple regression techniques.Method.One hundred and eighty-nine inpatients with psychotic illness were recruited and information on family history, premorbid factors and current symptoms obtained from them and their mothers.Results.Seven distinct symptom components were identified. Regression analysis failed to identify any developmental predictors of depression or mania. Delusions/hallucinations were predicted by a family history of schizophrenia and by poor school functioning in spite of normal premorbid IQ (F = 6.5; P < 0.001); negative symptoms by early onset of illness, developmental delay and a family history of psychosis (F = 4.1; P = 0.04). Interestingly disorganisation was predicted by the combination of family history of bipolar disorder and low premorbid IQ (F = 4.9; P = 0.003), and paranoia by obstetric complications (OCs) and poor school functioning (F = 4.2; P = 0.01).Conclusion.Delusions and hallucinations, negative symptoms and paranoia all appeared to have a developmental origin though they were associated with different childhood problems. On the other hand, neither mania nor depression was associated with childhood dysfunction. Our most striking finding was that disorganisation appeared to arise when a familial predisposition to mania was compounded by low premorbid IQ.
The Impact of Inflation on ROE, Growth and Stock Prices
Authors: Reilly Frank K. 
Published: December 2002

Using the constant growth dividend discount model (DDM), it can be shown that the critical factor which determines whether common stocks will be able to be an inflation hedge is the growth rate of dividends. In turn, the growth of dividends is mainly impacted by the aggregate return on equity (ROE). Using the DuPont formula, it is clear that the main variable that drives the aggregate ROE in an inflationary environment is the profit margin.
Following from this background, this article updates and extends an earlier analysis that involves an analysis ofROE and its componentsfor the 40-yearperiod 1956-1995. The analysis demonstrates that the aggregate ROE is currently at about the same level as in the 1960's, but the components have changed, that is, there has been a decline in total asset turnover and profit margin, but a significant increase in financial leverage that has compensated for the declines in turnover and profit margin. It is further shown that there have been periods of high and low inflation since 1956, and the negative impact of inflation of the implied growth rate is confirmed, which helps explain why investigators find consistent empirical results that common stocks are poor inflation hedges.
Effects of carvedilol on left ventricular remodeling and systolic function in elderly patients with heart failure
Authors: Palazzuoli A. , Bruni F. , Puccetti L. , Pastorelli M. , Angori P. , Pasqui A.L. , Auteri A. 
Published: December 2002

AbstractBackground:Recent studies have shown that carvedilol therapy in patients with heart failure improves clinical outcome and survival, however, the effects of such treatment on left cardiac morphology and function in elderly patients with severe heart failure has not been widely studied.Aim:The purpose of this study was to establish the effect of carvedilol at short‐ and long‐term on left ventricular size and performance with mono‐ and two‐dimensional echocardiography, in subjects with dilated cardiomyopathy, NYHA III functional class, low LV ejection fraction (EF<35%) and mean age of >70 years.Methods:We studied 48 patients, previously randomized to treatment with either carvedilol or placebo, and we performed echocardiographic evaluation at the start, and after 3 and 12 months. Left ventricular diameters, LV mass and fractional shortening were calculated by Deveraux formula; left ventricular volumes and ejection fraction were measured by area–length formula; pulmonary pressure was calculated by tricuspid reflow.Results:After 3 months, only LV end‐diastolic diameter was lower in the carvedilol group compared to the placebo group. Nevertheless, after 12 months, patients on carvedilol treatment showed a LV geometric and functional improvement compared to placebo. We found significant differences in: diastolic (P<0.01) and systolic diameters (P<0.001); on LV mass (P<0.002); on LV systolic volume (P<0.03); and on LV ejection fraction (P<0.01). Pulmonary pressure was also reduced in beta‐blocker subjects (P<0.001).Conclusions:Carvedilol therapy for 12 months reduced LV diameters and volumes. Thus, improving cardiac remodeling and LV systolic function in elderly patients with severe heart failure. Several months of therapy are required for these favorable effects to occur, as these changes do not occur in the short term.
Heart failure in primary care: qualitative study of current management and perceived obstacles to evidence‐based diagnosis and management by general practitioners
Authors: Khunti Kamlesh , Hearnshaw Hilary , Baker Richard , Grimshaw Gill 
Published: December 2002

AbstractBackground:Chronic heart failure is a common clinical condition with high morbidity and mortality. Despite the evidence that appropriate treatment with angiotensin‐converting enzyme inhibitors can improve morbidity, primary care studies show that patients with heart failure are incorrectly diagnosed and inadequately treated.Aim:To explore general practitioners' accounts of their management of patients with heart failure and identify the perceived obstacles to diagnosis and management.Methods:We conducted this qualitative study using semi‐structured interviews in 18 general practices. The practices were stratified on the basis of size, location, and the level of practice development. The interviews were based on a schedule of open questions based on the literature on diagnosis and management of patients with heart failure. Transcriptions of the audiotaped interviews were independently analysed by two researchers and analysis was based on open coding using a constant comparative approach. Categories were reduced to major themes.Results:General practitioners suspect heart failure when patients present with breathlessness or ankle oedema. Many general practitioners reported that they would diagnose heart failure after respiratory examination and a positive finding of basal crepitations. Many general practitioners arrange a chest X‐ray to establish the diagnosis and some arrange an electrocardiogram. A few general practitioners mentioned that they diagnosed heart failure with a trial of diuretics. Obstacles to diagnosis were mentioned by most general practitioners and included lack of facilities for appropriate investigations (especially echocardiography) and lack of time and expertise. Obstacles to management included lack of time, high cost of drugs, difficulty with diagnosis, selection bias towards younger patients and not having the confidence to initiate angiotensin‐converting enzyme inhibitors. Many general practitioners were unaware of the impact angiotensin‐converting enzyme inhibitors can have on morbidity and mortality.Conclusions:Although symptoms of heart failure are not sufficiently specific for diagnosing patients with heart failure, many general practitioners in European countries treat people with suspected heart failure on the basis of symptoms and signs alone. This study has identified many obstacles to the diagnosis and management of heart failure that may explain why patients are inadequately managed in primary care. Specific implementation strategies need to be tailored to overcome these obstacles.
Effects of the calcineurin dependent signaling pathway inhibition by cyclosporin A on early and late cardiac remodeling following myocardial infarction
Authors: Youn Tae‐jin , Piao Hainan , Kwon Jin‐sook , Choi So‐young , Kim Hyung‐sam , Park Dae‐gyun , Kim Dong‐woon , Kim Young‐gyu , Cho Myeong‐chan 
Published: December 2002

AbstractBackground:The calcineurin‐mediated signaling pathway has been implicated as one of the crucial pathways in cardiac hypertrophy. However, the role of calcineurin pathway on cardiac remodeling after myocardial infarction (MI) has not been well defined.Methods:Infarcted rats (n=45) were randomized into calcineurin inhibitor, cyclosporin A (CsA) or vehicle groups, 3 days after MI and treated for 2 weeks (early post‐MI cardiac remodeling stage), or randomized 17 days after MI and treated for 2 weeks (late remodeling stage).Results:Calcineurin pathway inhibition during the early cardiac remodeling stage attenuated the myocardial hypertrophy after MI (P<0.05). However, left ventricular dimensions were further increased and fractional shortening deteriorated with calcineurin inhibition during this stage (P<0.05, each). During late remodeling stage, CsA treatment did not affect myocardial hypertrophy and cardiac dilation following MI.Conclusion:Our results strongly support the hypothesis that calcineurin pathway mediates compensatory myocardial hypertrophy during the early remodeling stage after MI. However, the calcineurin pathway does not seem to affect the late remodeling after MI.
Morphine for the relief of breathlessness in patients with chronic heart failure—a pilot study
Authors: Johnson M.J. , McDonagh T.A. , Harkness A. , McKay S.E. , Dargie H.J. 
Published: December 2002

AbstractBackground:Chronic heart failure (CHF) patients can experience significant breathlessness despite maximum medication for their heart failure. Morphine has long been used to relieve symptoms in acute failure, but there is little evidence about this potentially useful palliative therapy in CHF.Aims:To determine the efficacy of morphine for the relief of breathlessness in patients with CHF.Method:Ten out‐patients with NYHA III/IV CHF entered a randomised, double‐blind, placebo controlled, crossover pilot study. The active arm was 4 days of 5 mg oral morphine four times daily (2.5 mg morphine if creatinine >200 μmol/l). There were 2 days wash‐out between active and placebo arms.Results:6/10 patients indicated that morphine improved their breathlessness. On morphine, the median breathlessness score fell by 23 mm (P=0.022) by day 2. The improvement was maintained. Sedation scores increased until day 3 (P=0.013), reducing on day 4. Four patients developed constipation (P=0.026). On placebo, there was no significant difference in breathlessness or sedation. One patient had constipation. There were no significant differences in either arm in nausea, quality of life scores, blood pressure, pulse, respiratory rate, or catecholamines. Brain natriuretic peptide fell in both arms; significantly in the morphine arm.Conclusion:Morphine relieves breathlessness due to CHF. A larger study is indicated.