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  • 1
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Scandinavian journal of immunology 8 (1978), S. 0 
    ISSN: 1365-3083
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Simultaneous determination of CEA, AFP and ALP4 was made in patients with various gynecological malignancies. CEA was positive in 65%, AFP was positive in 1.8% of 55 cases with cervical carcinoma stage 0—-II. ALP4 was positive in one patient in these stages. In the group of cervical carcinoma stage III, stage IV and recurrence, CEA and AFP were positive in 100% and in 8.6% of 35 cases respectively. ALP4 was positive in 14.3%. High levels and/or progressively increasing CEA with positive ALP4 were found to be significant in poor prognostic patients in whom ALP4 was not always found positive. Out of 17 cases with endometrial carcinoma, CEA was positive in 12 patients. AFP and ALP4 were each positive in one case. Of 30 cases with ovarian carcinoma, CEA was positive in 70%, AFP in 23% and ALP4 in 14%. Increasing CEA and/or increasing AFP appeared to be correlated with poor prognosis. In the group of 5 vulvar carcinoma, only CEA was positive in 80% of the patients. Of 19 cases of choriocarcinoma, CEA was positive in 11%, AFP was positive in 5.3% and ALP4 was positive in 5.6%. There existed reverse-correlation between serum CEA and AFP in some cases.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-2072
    Keywords: Key words Carteolol hydrochloride ; Catalepsy ; Neuroleptics ; Akathisia ; Extrapyramidal side effects
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract It is known that β-adrenoceptor antagonists are effective in the treatment of akathisia, one of the extrapyramidal side effects that occur during neuroleptic treatment. Neuroleptic-induced catalepsy, a model of neuroleptic-induced extrapyramidal side effects, was considered suitable as a model for predicting neuroleptic-induced akathisia in humans, although neuroleptic-induced catalepsy was not considered a specific test for neuroleptic-induced akathisia. Therefore, the effects of carteolol, a β-adrenoceptor antagonist, on haloperidol-induced catalepsy in rats were behaviorally studied and compared with those of propranolol and biperiden, a muscarinic receptor antagonist. Carteolol, as well as propranolol and biperiden, inhibited the haloperidol-induced catalepsy. The inhibitory effect of carteolol was almost comparable to that of propranolol, but was weaker than that of biperiden. Carteolol did not evoke postsynaptic dopamine receptor-stimulating behavioral signs such as stereotypy and hyperlocomotion in rats. Carteolol did not antagonize the inhibitory effects of haloperidol on apomorphine-induced stereotypy and locomotor activity in rats. In addition, carteolol did not evoke 5-HT1A receptor-stimulating behavioral signs such as flat body posture and forepaw treading and did not inhibit 5-hydroxytryptophan-induced head twitch in rats. Finally, carteolol did not inhibit physostigmine-induced lethality in rats. These results strongly suggest that carteolol improves haloperidol-induced catalepsy via its β-adrenoceptor antagonistic activity and is expected to be effective in the treatment of akathisia without attenuating neuroleptic-induced antipsychotic effects due to its postsynaptic dopamine receptor antagonistic activity.
    Type of Medium: Electronic Resource
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