bluuebunny/crossref_metadata_2025_split huggingface dataset:
Bupropion and thiothixene versus placebo and thiothixene in the treatment of depression in schizophrenia
Authors: Dufresne Robert L. , Kass David J. , Becker Robert E. 
Published: January 2005

AbstractThe authors performed a double‐blind study in which 38 inpatients diagnosed as schizophrenic with depressive symptoms were treated with either bupropion and thiothixene or placebo and thiothixene. Of the 36 patients who completed 4 weeks of study treatment, the placebo‐thiothixene treated patients did significantly better than the bupropion‐thiothixene treated patients on BPRS total scores as well as anxiety and depression items. The bupropion‐thiothixene treated patients reported significantly more dry mouth and constipation than the placebo‐thiothixene treated group, whereas the placebo‐thiothixene treated group reported more frequent occurrences of increased appetite, menstrual disturbance, and decreased sex drive. Neither group differed on ratings of pseudoparkinson or dyskinetic signs. The antidepressant bupropion as an adjunct to thiothixene was less effective in the treatment of depressed schizophrenic patients than the antipsychotic alone and appeared to inhibit the therapeutic effects of thiothixene primarily in the depressive symptoms of the syndrome.
Calcium channel antagonists modulate calcium by increasing magnesium influx: A hypothesis
Authors: Singh R. B. 
Published: January 2005

AbstractMg2+ and Ca2+ ‐channel blockers exert similar effects on the cardiovascular system. These agents have been successfully used for treating hypertension and for protecting against myocardial ischaemia. The exact mechanism of action of Ca2+ ‐blocking drugs, including verapamil, is unknown. It is proposed that Ca2+ ‐blockers stimulate the Mg2+ transport system and Mg2+ diffusion into the cell, thereby enhancing Mg2+ influx. This, in turn, causes suppression of the slow inward Ca2+ current and fast inward Na+ current, resulting in decreased transport of Ca2+ and Na+. Ca2+ ‐blockers might also influence outward K+ and Mg2+ currents, thereby altering the shape and duration of the action potential. Since Mg2+ is involved in maintaining the structural and functional integrity of the cardiovascular system, Mg2+ ‐mediated mechanisms of action for Ca2+ ‐antagonists appear possible.
Effect of luteinizing hormone releasing hormone (LHRH) agonists on body weight in rats
Authors: Ataya Khalid , Weintraub Alan , Dunbar Joseph , Zimniski Stephen , Puett David , Lemaire William 
Published: January 2005

AbstractAs the potential clinical applications of LHRH agonists increase, the issue of side effects on nonreproductive organ systems assumes greater significance. LHRH agonists administered continuously or in twice‐daily injections accelerated body weight gain in female rats. Two different LHRH agonists produced similar effects on body weight in female rats. When Leuprolide (LHRHa) was given to female rats in twice‐daily injections, the adrenal weight increased after 21 days of treatment, whereas administration by osmotic minipumps produced no significant effect on adrenal weight. When another agonist, Zoladex (LHRHz), was given continuously for 52 and 229 days to female rats, the adrenal weight decreased. No change was noted in adrenal weight or body‐weight gain of male rats given LHRHz continuously for 51 and 62 days. Reproductive‐organ weights were significantly reduced in all LHRH‐agonist‐treated animals. Serum progesterone in female rats and testosterone in male rats were significantly decreased following treatment with LHRHz. No significant differences were noted in serum prolactin, growth hormone, or corticosterone. The mechanisms and significance of these findings are discussed.
Antiamnesic effects of magnesium pyrrolidone carboxylate (MAG 2) in three models of amnesia in the mouse
Authors: Porsolt Roger D. , Lenègre Antoine , Avril Isabelle , Parot Philippe , Tran Gilles 
Published: January 2005

AbstractThe effects of magnesium pyrrolidone carboxylate (MAG 2) on the amnesias induced by scopolamine, diazepam, and electroconvulsive shock (ECS) were studied in a passive avoidance procedure in the mouse and compared with the effects of a standard dose of piracetam. Amnesia was induced by injecting scopolamine or diazepam (1 mg/kg intraperitoneally [i.p.]) 30 min before or ECS administered immediately after the first session (S1) of the passive avoidance task. MAG 2 was studied in a dose range of 128 to 1,024 mg/kg and compared with piracetam (2,048 mg/kg), both drugs being administered orally (p.o.) 60 min before S1. Retention was measured 24 hr later (S2) in the absence of any treatment. Further experiments investigated the effects of repeated administration of MAG 2 (twice daily for 3 days) on diazepam‐induced amnesia. Additional experiments investigated the interactions of the compound with the major behavioral effects of the amnesic treatments, namely scopolamine‐induced hyperactivity, diazepam‐induced release of punished behavior (four plates test), and ECS‐induced convulsions. MAG 2 dose‐dependently attenuated the memory deficits induced by the three amnesic treatments after acute treatment and more effectively antagonized diazepam‐induced amnesia after repeated than after acute treatment. It did not affect either scopolamine‐induced hyperactivity, diazepam‐induced release of punished behavior or ECS‐induced convulsions. These results point to the specificity of MAG 2′s antiamnesic activity and suggest that it might be a useful agent for the treatment of memory deficits of different origins in man.
Acne: Androgens and microbiology
Authors: Pochi Peter E. 
Published: January 2005

AbstractAcne, the most prevalent disease of the skin, is a multifactorial follicular disorder in which androgens and microbiology are essential for the occurrence of the pathogenic events that characterize it. The role of the androgen is to stimulate the development and secretory activity of the sebaceous gland, which performs several important actions in the etiopathogenesis of acne. The anaerobic diphtheroid Propionibacterium acnes, a resident organism in acne‐susceptible follicles, is directly responsible for much of the inflammation in acne. This review deals with a description of these events and the therapeutic modalities that have been developed in an attempt to counteract them.
Antagonism of diazepam hyperphagia by propranolol in rats
Authors: Kamatchi G. Lenin , Chandra Dinesh , Rajasekaran M. , Rao K. Madhusudana , Venkatadri N. , Bapna J. S. 
Published: January 2005

AbstractThe effects of adrenergic beta‐receptor blockers on the hyperphagia produced by diazepam were studied in free‐feeding rats. The hyperphagia produced by 1.0 mg/kg subcutaneous (s.c.) diazepam, was antagonised by dl‐propranolol (6.0 mg/kg s.c.) and 1‐propranolol (6.0 mg/kg s.c.), but not by d‐propranolol (6.0 mg/kg s.c.). Intracerebroventricular administration of dl‐propranolol (50, 100, and 200 μg) failed to antagonise this hyperphagia. Other specific β1 and β2 blockers, metoprolol (10.0 mg/kg s.c.), and butoxamine (10.0 mg/kg s.c.) also did not antagonise this hyperphagia. It is suggested that some intrinsic property other than β‐blockade, tranquilising, or local anesthetic activity is responsible for this antagonism caused by s.c. administration of dl‐ or l‐propranolol.
Partial and complete blockade of 5‐hydroxytrytophan (5‐HTP)‐induced head twitches in the rat: A study of ritanserin (R 55 667), risperidone (R 64 766), and related compounds
Authors: Meert Theo F. , Niemegeers Carlos J. E. , Awouters Frans , Janssen Paul A. J. 
Published: January 2005

AbstractA series of test compounds were studied for their ability to inhibit and block the head‐twitch response to either intraperitoneal (i.p.) 5‐hydroxytryptophan (5‐HTP) or intravenous (i.v.) mescaline in rats. Both responses were found to be sensitive to serotonin S2 antagonists, and there was very good agreement between the inhibitory doses in both tests, particularly for the selective serotonin S2 antagonists ritanserin and seganserin. However, these two compounds did not block the 5‐HTP response, although they completely abolished the mescaline response. In contrast, the mixed serotonin‐dopamine‐norepinephrine antagonist risperidone was a potent blocker of both responses. The use of various antagonists and the combination treatments of ritanserin with haloperidol or prazosin indicated that the 5‐HTP response is abolished when potent serotonin S2 antagonism is associated with antagonistic activity on either dopamine D2 or α1 receptors.
Tazadolene: A centrally‐acting, non‐narcotic analgesic
Authors: Piercey Montford F. 
Published: January 2005

AbstractIntravenous tazadolene elevated the threshold stimulus for rabbits to respond to electrical tooth‐pulp stimulation. Systemic tazadolene also increased the latency for mice to lick their paws in the hot‐plate analgesic test. However, tazadolene did not alter the mouse tail flick, a spinal reflex most sensitive to analgesics acting at spinal sites. Tazadolene analgesia was not antagonized by naloxone. Intracranial (i.c.), but not intraspinal (i.s.), injections of tazadolene were more effective than systemic injections in producing analgesic effects in the hot‐plate test. It is concluded that tazadolene is a centrally‐acting, non‐narcotic analgesic.
Mutagenicity evaluation of tetrahydro‐amino acridine by the Salmonella/microsome mutagenicity ames test
Authors: Townsend Steven E. , Sehgal Suren N. 
Published: January 2005

Abstract1,2,3,4‐tetrahydro‐5‐amino acridine (THA), a cholinesterase inhibitor currently under investigation for use in the treatment of senile dementia, exhibited mutagenic activity with and without metabolic microsomal S‐9 activation against tester strain TA97a in the Salmonella typhimurium incorporation assay. The mutagenic response was concentration‐dependent within the dose range of 500 to 2,500 μg/plate.
GABA agonists enhance morphine and fentanyl antinociception in rabbit tooth pulp and mouse hot plate assays
Authors: Bergman Stewart A. , Wynn Richard L. , Peterson Michael D. , Rudo Frieda G. 
Published: January 2005

AbstractParallel experiments in the rabbit tooth pulp and mouse hot plate paradigms were performed to elucidate the effect of pretreatment with the GABA mimetic compound muscimol (M) and diazepam (DZ) on the antinociceptive effect of both morphine sulfate (MS) and fentanyl citrate (F). The ED50 values for F in both rabbits and mice were lowered significantly (p ≤ 0.05) by pretreatment with either i.v. DZ or M in rabbits or i.p DZ or i.v. M in mice. There was a significant 7‐fold shift of the F dose‐response curve after pretreatment with M in rabbits and a 3‐fold shift in mice compared to controls; a 10‐fold shift after pretreatment with i.v. DZ in rabbits and a 2‐fold shift after i.p DZ in mice. The ED50 values for MS in both rabbits and mice were lowered significantly (p ≤ 0.05) by pretreatment with i.v. muscimol but not DZ (p ≤ 0.18). Similarly, pretreatment with i.v. M, in rabbits and mice, but not i.v DZ in rabbits or i.p DZ in mice, significantly shifted the dose‐response curves of MS to the left compared to controls. DZ and M i.v. significantly prolonged the duration of antinociception (rabbit) of an ED98 dose of MS and ED90 dose of F. Time to 50% maximal possible antinociceptive effect (MPE) increased from 240 min for MS + vehicle to 425 min for MS + DZ, and over 450 min for MS + M. Time to 50% MPE increased from 25 min for F + vehicle to 38 min for F + DZ. Similar results were observed for F + M. DZ pretereatment enhances the antinociceptive potency of 2X ED50 of F. In general, the average % MPE of F + DZ was twice tha tof F + vehicle over the first 20 min postopioid injection. A similar trend was noted following 2 × ED50 pf MS, whereas scopolamine had no significant effect. These results suggest that GABAA agonists, both direct M and indirect DZ enhance the antinociceptive effect of the opioids F and MS. since naloxone completely reversed this effect and scopolamine had no significant effect, this implies that GABAA agonists enhance opioid antinociception by an opioid and not a cholinergic mechanism.
Pyrazoloquinolines and zolpidem: Effects on hypertonic saline consumption in rehydrating rats
Authors: Cooper Steven J. , Desa Asmawati 
Published: January 2005

AbstractMale rats were adapted to a 22‐hr‐daily water‐deprivation schedule and to consuming an aversive 2.7% NaCl solution in a 30‐min period. Previous reports had shown that benzodiazepines and other anxiolytics stimulate ingestion of hypertonic saline under these conditions; however, two pyrazoloquinolines, CGS 9895 and CGS 9896, failed to do so [Cooper, 1987]. The present experiments were designed to investigate possible antagonist properties of CGS 9895 and CGS 9896 in this model and also to characterize the effects of a newly described pyrazoloquinoline, CGS 17867A, on saline drinking. In addition, a novel sedative‐hypnotic, zoloidem, and a benzodiazepine peripheral‐type receptor compound, Ro5‐4864, were treated. The results indicate that CGS 9895 and CGS 9896 exhibited antagonistic activity in this model, that CGS 17867A increased salt drinking without displaying antagonist activity, and that neither zolpidem nor Ro5‐4864 affected drinking responses.
Efficacy of denbufylline in patients with multi‐infarct dementia
Authors: O'Connolly M. , Dierdorf D. , Greb W. H. , Mayer M.‐E. R. , Wolf D. 
Published: January 2005

AbstractThe efficacy and tolerance of denbufylline (25 and 50 mg tid for three months) were investigated in 20 inpatients with cerebrovascular disease in a placebo‐controlled, doubleblind parallel study. Denbufylline at 50 mg tid significantly improved the mental, emotional, and social capabilities of the patients; tolerance was acceptable.
Correlation between cerebral circulation and intellectual impairment in patients with “aging brain,” and the effect of vinpocetine on cerebral circulation
Authors: Miyazaki Manabu 
Published: January 2005

AbstractThe Doppler ultrasonic technique is useful for the examination of cerebral circulation as well as for the evaluation of cerebral circulation‐improving drugs. This study deals with a correlation of cerebral circulation with intellectual impairment in subjects with aging brain syndrome and with measuring the effect of vinpocetine on cerebral circulation, using the Doppler technique.The correlatiion between cerebral circulation and intellectual impairment was first studied in 48 patients with aging brain and intellectual impairment. As a parameter for cerebral ciruclation, the Continuous Index (CI), as calculated from the blood flow pattern recorded at the internal carotid artery, was used together with Hasegawa's Dementia Scale (HDS) for intellectual impairment.Second, blood flow change of the internal carotid and vertebral artery was measured after a single oral dose of 5 mg vinpocetine and after multiple oral doses of 5 mg vinpocetine three times daily for 7 days in six patients with aging brain.The mean correlation coefficient (r) between CI and HDS was 0.391 (P < 0.01) in 48 patients. It was 0.612 (P < 0.01) in 27 patients with moderate to severe intellectual impairment, 0.735 (P < 0.01) in 14 patients with vascular type impairment, and 0.443 (not significant) in 10 patients with the Alzheimer type. The results suggest some correlation between cerebral circulation and intellectual impairment in the aging brain, especially in patients with the vascular type.An increase of blood flow was recognizable after a single oral dose of 5 mg vinpocetine and was more conspicuous after multiple oral doses. Thus, the effect of vinpocetine in improving cerebral circulation was evident, suggesting its clinical efficacy in improving intellectual impairment in patients with aging brain.
Multicenter clinical placebo‐controlled study with acetyl‐l‐carnitine (LAC) in the treatment of mildly demented elderly patients
Authors: Cucinotta Domenico , Passeri Mario , Ventura Sandro , Lannuccelli Maurizio , Senin Umberto , Bonati Piero Angelo , Parnetti Lucilla 
Published: January 2005

AbstractAcetyl‐l‐carnitine (LAC) was administered for 3 months, 2 g/daily, to 30 elderly patients with mild mental deterioration. Results were compared to those of a homogeneous control group of 28 patients treated with placebo. The study was carried out according to a double‐blind, randomized methodology. A complete battery of rating scales and psychometric tests was used for for evaluating the modifications induced by either drug or placebo. The statistical evaluation of results showed a sufficient clear efficacy of the drug studied: results from patients on LAC were frequently different from those receiving placebo. Therefore, LAC must be taken into consideration as a useful drug for the global treatment of demented elderly patients.
Computed tomography study of cerebral infarctions treated with vinpocetine
Authors: Kalvach Pavel , Bauer Jiří , Vymazal Josef 
Published: January 2005

AbstractA group of 20 persons with cerebral infarctions who had been treated with vinpocetine was compared with a group of 20 similar patients who had been treated with other vasoregulative drugs. Two computed tomography (CT) examinations were evaluated for each patient. The initial scan was done during the first ten days, and the second between the 20th and 50th day after the stroke. Three parameters were studied: extension of the lesion, intensity of hypodensity, and presence of postcontrast enhancement. In the first and second criteria, the vinpocetine‐treated patients exhibited better results, whereas the third did not yield any explicit data.
Strategies and new aspects in the pharmacology of drugs for the treatment of senile dementia
Authors: Schmidt Joachim , Fischer Hans‐Dieter , Wustmann Christian 
Published: January 2005

AbstractRational therapeutic strategies can be derived only from an understanding of the etiopathogenetic processes leading to dysfunction in the demented brain. Senile dementias (SD) of different origins are associated with biochemical changes in functionally important transmission systems, in energy metabolism, and in synthesis of macromolecules. Much evidence supports a particularly important role of dysfunction in central cholinergic mechanisms. Recent results have furnished encouraging indications that changes in synaptic efficiency and plasticity are integrated to a considerable degree. At present, the pharmacological manipulation of clinical symptoms and impaired functions is the basis for rational strategies in the development of drugs for the treatment of SD. On the basis of present knowledge, the following strategies can be considered: (1) drugs to prevent underlying etiopathogenetic processes (antioxidants, aluminium chelating agents, etc.); (2) enhancers of cerebral neurotransmission; (3) cerebral metabolic enhancers (nootropics and related drugs); (4) modulators of synaptic efficiency and plasticity; (5) nooanaleptics; (6) regulators of cerebral circulation; and (7) symptomatic therapy of associated functional mental disorders. The improvement of neuronal metabolism and synaptic transmission are presently the most important strategies in drug development. Nootropics and related drugs fulfill two aspects in the pharmacotherapy of SD: they are cerebral metabolic enhancers and they improve cerebral synaptic transmission processes. In eight of these functions, the relationship between lipid metabolism and cellular Ca++ homeostasis also may be of special functional importance. For the development of further strategies, more detailed knowledge about the pathogenesis of SD and further experimental modeling of the etiopathogenetic and neuropathological processes underlying SD of different origins are required.
Vinpocetine facilitates noradrenaline release in rat brain cortex slices
Authors: Schlicker E. , Betz R. , Göthert M. 
Published: January 2005

AbstractRat brain cortex slices preincubated with 3H‐noradrenaline were superfused with physiological salt solution, and the effect of vinpocetine on the electrically (3 Hz) evoked 3H overflow was studied. Vinpocetine at 10–100 μmol/liter facilitated the evoked overflow; at 32 and 100 μmol/liter, basal efflux was slightly increased. The facilitatory effect of vinpocetine on the evoked overflow was not altered by desipramine, rolipram (an inhibitor of cAMP phosphodiesterase), or ICS 205‐930 ([3α‐tropanyl]‐1H‐indole‐3‐carboxylic acid ester; an antagonist at 5‐HT3 (M) receptors); it was strongly attenuated by phentolamine. In turn, vinpocetine moderately decreased the facilitatory effect of phentolamine on the evoked overflow. The concentrationresponse curve of noradrenaline (obtained in the presence of desipramine) for its inhibitory effect on the evoked overflow was not shifted to the right by vinpocetine at 32 and 100 μmol/liter. The present results show that vinpocetine facilitates noradrenaline release. This effect may be related to the blockade of presynaptic α2‐adrenoceptors (although evidence is not unequivocal), but does not appear to involve inhibition of noradrenaline uptake or cAMP phosphodiesterase nor activation of 5‐HT3 (M) receptors. The facilitatory effect of vinpocetine on noradrenaline release occurs at concentrations higher than those obtained under treatment with this drug.
Immune dysfunctions: New targets of drug discovery for alzheimerapos;s disease and other cognitive disorders
Authors: Lal Harbans , Forster Michael J. , Retz Konrad C. , Reisberg Barry 
Published: January 2005

AbstractThe development of treatments applicable to Alzheimerapos;s disease and other age‐associated dementias represents a serious challenge to biomedical research. It is suggested that advances in the understanding of basic etiologic mechanisms in these disorders would provide the most direct avenues to discovery of preventive and arrestive treatments. An overview of research relating to the potential involvement of immune dysfunctions in the etiology of Alzheimerapos;s and other central nervous system (CNS) diseases is reviewed as this was presented and discussed in a recent satellite symposium, “Autoimmunity: Its Role in Alzheimerapos;s Disease and Other Behavioral Dysfunctions,” held at the 17th Annual Meeting of The Society for Neuroscience. It is predicted that some future research may focus on immunological dysfunctions as targets for the discovery and development of drugs for treatment of Alzheimerapos;s dieseas and other cognitive disorders.