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PubMed1953

Role playing.

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Humans↗
PubMed1979

Lack of evidence for an inhibitory role played by tuberoinfundibular dopaminergic neurons on TSH secretion in the rat.

The role of dopamine (DA) in the control of thyroid stimulating hormone (TSH) secretion in basal or cold stimulated conditions was investigated by using pharmacological or neurosurgical tools. The intraventricular injection of DA (5 micrograms/animal) or the subcutaneus (s.c.) injection of a dopaminomimetic agent failed to induce changes of TSH plasma levels in normal or in cold stimulated conditions. The same results were obtained by intraperitoneal (i.p.) administration of haloperidol, a blocker of dopaminergic receptors. The complete deafferentation of hypothalamus, which causes degeneration of norepinephrinergic nerve endings and leaves the DA tuberoinfundibular system unaffected, prevented the TSH release evoked by cold exposure. alpha-Methyl-p-tyrosine (alpha-MpT) (250 mg/kg i.p.), which causes a remarkable reduction of DA in the median eminence (ME) of deafferented animals, was unable to restore the TSH response to cold. Collectively these results seem to suggest that DA does not play a significative role in the control of TSH secretion in the rat.

Animals↗
PubMed1994

Tissue and epithelial cell-specific expression of chicken proto-oncogene c-ros in several organs suggests that it may play roles in their development and mature functions.

Proto-oncogene c-ros codes for a receptor-type protein tyrosine kinase (PTK) sharing high homology with the Drosophila sevenless protein. Recent studies of c-ros expression in mouse by in situ hybridization showed that c-ros was expressed specifically and transiently in the epithelial cells of late embryonic kidney collecting duct and intestine villi. Those investigators suggested that c-ros may play a role in the development of those organelles. In the present study, we have examined the expression profile of c-ros in chicken by RNAase protection and in situ hybridization with riboprobes. Our results showed that in addition to kidney and intestine, low levels of c-ros mRNA could also be detected in lung, testis, thymus and bursa. Expression of c-ros commences during middle to late embryonic stages in those organs and persists into the adult life. In situ hybridization revealed that expression of c-ros was restricted to the epithelial cells of all the tissues examined including kidney, intestine, bursa, thymus and testis. In kidney c-ros was detected in all the epithelial cells of the collecting ducts, in intestine it was detected in the epithelial cells of villi and the underneath crypts. Our finding of c-ros expression in chicken differs from those in mouse in (1) instead of transient expression during the embryonic stage, expression of c-ros in chicken kidney and intestine persists into the adult life and (2) expression of c-ros in renal collecting ducts is not restricted to its growing tips, instead it is expressed in the entire epithelial layer of the ducts. Our results suggest that c-ros may play a role not only in the initial induction events in the organogenesis, but also in the mature function of those organs.

Animals↗
PubMedDate not supplied

The use of role play.

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Education, Nursing, Diploma Programs↗
PubMed2006

[The role played by calcium in neuronal injury following neonatal hypoxia or convulsions].

AIM: Calcium plays a complex and pivotal role both in neuronal development and function, and in hypoxia/ ischemia-induced cell death. In this paper, we review current concepts of calcium function emphasizing the neonatal period. DEVELOPMENT: Calcium enters the neuron through glutamate receptors (NMDA and AMPA) located on the neuronal membrane. After hypoxia or seizures, there is a conformational change of the receptors, with increased flow of calcium into the cytoplasm. Cytoplasmatic calcium triggers activation of several free-radical generation pathways, including the nitric oxide pathway, with a deleterious effect upon the neuron. Calcium then enters the neuronal nucleus, through specific receptors on the nuclear membrane. In our experience, hypoxia and neonatal seizures create nuclear membrane dysfunction, increasing the nitric-oxide-dependent flow of calcium into the nucleus. Nuclear calcium increase is critical for genetic transcription, pro-apoptotic gene activation and a cascade of biochemical and molecular events that lead to an increase of caspases and apoptotic neuronal death. CONCLUSIONS: Calcium has a crucial role in neuronal damage after neonatal hypoxia or seizures. A better knowledge of the pathogenic mechanisms that lead to neuronal damage after neonatal hypoxia or seizures will assist in future development of efficacious neuroprotective therapies.

Calcium↗