Ehud Klein
Jerusalem Mental Health Center
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Featured researches published by Ehud Klein.
Biological Psychiatry | 1985
Ricardo Kidron; Ilya Averbuch; Ehud Klein; R.H. Belmaker
Raisman R, Sechter D, Briley MS, et al (1981): High affinity 3H-imipramine binding in platelets from untreated and treated depressed patients compared to healthy volunteers. Psychopharmacology 75:368-371. Raisman R, Briley MS, Bouchani F, Sechter D, Zarifian E, Langer SZ (1982): 3H-imipramine binding and serotonin uptake in platelets from untreated depressed patients and control volunteers. Psychopharmacology 77:332-335. Seeman P (1983): Dopamine receptors in brain. In Marangos PJ, Campbell I, Cohen RM (eds.), Methods in Neurobiology, Vol 1. New York: Academic Press.
Brain Research | 1983
Michael E. Newman; Ehud Klein; Boris Birmaher; Moshe Feinsod; R.H. Belmaker
Lithium at a therapeutically effective concentration of 1 mM caused significant inhibition of the rise in cyclic AMP induced by noradrenaline in fresh surgically-obtained slices of human brain.
Progress in Neuro-psychopharmacology & Biological Psychiatry | 1983
R.H. Belmaker; Bernard Lerer; Ehud Klein; Newman Michael; Dick Earl
Lithium is a unique drug in its clinical profile in psychiatry. Lithium has numerous biochemical effects, but none has yet been proven to be its mode of therapeutic action. Inhibition of noradrenaline-sensitive adenylate cyclase is reviewed as the only biochemical effect of lithium shown to occur in both animals and man at therapeutic lithium concentrations. A tetracycline antibiotic, demeclocycline, also blocks noradrenaline-sensitive adenylate cyclase. A clinical trial of demeclocycline in mania would provide a test of the adenylate cyclase theory of lithium action.
Biological Psychiatry | 1990
Ehud Klein; Thomas Tomai; Thomas W. Uhde
This study was conducted to further evaluate HPA axis activity by the measurement of plasma ACTH and cortisol and ACTH corticotropin-releasing hormone (CRH) in the cerebrospinal fluid (CSF) of nervous and normal dogs
Archive | 1989
Ehud Klein; Thomas W. Uhde
Genetically nervous pointer dogs have been characterized in earlier works as an animal model for pathological anxiety.1–3 Individual differences in fearfulness were initially used to create two lines of pointer dogs.4,5 These lines have been maintained now for more than 20 years with continuous selection for the most fearful dogs in the nervous line and for the least fearful dogs in the normal line. Each line originated from a single male-female pair of each type. The behavioral traits of both fearfulness and normality have bred essentially true since the first generation.2 The nervous dogs begin to demonstrate from the age of 3–9 months a highly characteristic and reproducible pattern of fear-related behaviors to certain exogenous stimuli.6 In the absence of such stimuli, these dogs do not appear to be markedly different from the normal dogs: they move freely, play with other dogs, breed as well as the normal dogs, and adequately rear their pups or foster pups from the normal line.1 In contrast to these normal behaviors, exposure to humans, a sudden blast of a loud noise, and certain other stimuli elicit a dramatic expression of fear-related behaviors such as excessive timidity, hyperstartle, reduced exploratory activity, marked avoidance of the human observer, catatonic freezing cardiovascular changes, urination, and defecation.1,2 The normal dogs behave differently under those conditions as evidenced by friendly play with humans. They are active and inquisitive and comply without protest to experimental tasks,1,3 and despite such tasks they continue to approach man in a friendly fashion.1,3 The phenotypic expression of the nervous behavior in these dogs is not prevented by cross-rearing or by extra home-rearing, which produces only temporary changes compared to kennel rearing.7 Studies done in our group with these dogs included the evaluation of a hearing deficit and its relation to the abnormal behavior.
Archive | 1985
R.H. Belmaker; Ehud Klein; Bernard Lerer
Okuma et al.1,2,3 and Ballenger and Post4,5 have reported antimanic efficacy for carbamazepine. Since antimanic drugs such as lithium (Li)6 and neuroleptics7 are also effective in excited psychoses other than mania, we decided to study carbamazepine in excited schizoaffective illness and excited schizophrenia as well as in mania.
Archives of General Psychiatry | 1984
Ehud Klein; Efraim Bental; Bernard Lerer; R.H. Belmaker
Pharmacology & Toxicology | 2009
Ehud Klein; R.H. Belmaker; Michael E. Newman; Jan Gruszkiewicz
Archive | 2016
Ehud Klein; Isabella Kreinin; Andrei V. Chistyakov; Danny Koren; Lilly Mecz; Sarah Marmur; Dorit Ben-Shachar; Moshe Feinsod
Biological Psychiatry | 1998
Ehud Klein; B. Kreinin; A. Chistyakov; Moshe Feinsod