Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:6.3.5.5 (CPS)
 1,262 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

'77orn', a derivative of the Morris rat hepatoma 7777, stably expresses high levels of ornithine transcarbamoylase (OTC) and carbamoylphosphate synthetase I (CPS-I), and is able to grow indefinitely in ornithine-medium (medium with ornithine in place of arginine). Variants that have lost this ability are isolated from 77orn by a 'suicide' selective technique dependent on the cellular incorporation of [3H]ornithine. These variants, which have reduced levels of CPS-I, or of both CPS-I and OTC, are shown to have developed multiple hormonal requirements; their enzyme deficiencies can be reversed by use of an appropriately supplemented medium. In particular, CPS-I is inducible by dexamethasone and dibutyryl-cyclic-AMP in combination. Cholera toxin can be used instead of cyclic-AMP, but then butyrate is additionally required if the induction is to be maintained in the long term. The use of these agents in excess can depress OTC. Several other hepatomas, and alos explanted foetal rat liver cells, have similar requirements for CPS-I expression. It is argued that multiple hormonal requirements for CPS-I production are normal in liver cells in vitro, and that hormone-independent hepatomas should be regarded as abnormal. The implications of this for the somatic cell genetic investigation of differentiation are briefly discussed.
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PMID:Arginine synthesis by hepatomas in vitro. II. Isolation and characterization of Morris hepatoma variants unable to convert ornithine to arginine, and modulation of urea-cycle enzymes by dexamethasone and cyclic-AMP. 609 98

We conducted a retrospective longitudinal self-controlled study of 124 adult patients treated with resective surgery for medically uncontrolled partial epilepsy from 1949 to 1988. Approximately 65% of the patients experienced > 95% reduction in seizure frequency, and 75% had worthwhile improvement of at least 75% seizure reduction. Significant reductions were noted in all major seizure types treatable with resective surgery; complex partial (CPS), simple partial (SPS), and secondarily generalized tonic-clonic seizures (GTC) (all p < 0.05). Tissue pathology and region of resection did not provide significant information with respect to seizure outcome. EEG in the first postoperative year was an important predictor of long-term seizure outcome (p = 0.03). One third of the temporal lobe resected patients had neurologic deficits as a consequence of the resection as compared with 14% of patients with frontal resections (p = 0.03). One third of the deficits among the temporal lobe resected patients were considerable, with possible social implications. Half of the patients with preoperative focal spike activity had a normal EEG postoperatively. One fifth of patients maintained their preoperative epileptic focus after the operation, and about one fifth displayed new foci. Approximately one fourth of the patients were free of medication for a median of 16 years postoperatively, and 60% of patients who were seizure-free were still receiving medication. There was no operative mortality, but the late mortality, as expected, was higher than that of the general population. Two male patients (1.6%) committed suicide.
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PMID:Surgical treatment for partial epilepsy among Norwegian adults. 802

Programmed cell death is an integral component of C. elegans development. Genetic studies in C. elegans have led to the identification of more than two dozen genes that are important for the specification of which cells should live or die, the activation of the suicide program, and the dismantling and removal of dying cells. Molecular and biochemical studies have revealed the underlying conserved mechanisms that control these three phases of programmed cell death. In particular, an interplay of transcriptional regulatory cascades and networks involving CES-1, CES-2, HLH-1/HLH-2, TRA-1, and other transcriptional regulators is crucial in activating the expression of the key death-inducing gene egl-1 in cells destined to die. A protein interaction cascade involving EGL-1, CED-9, CED-4 and CED-3 results in the activation of the key cell death protease CED-3. The activation of CED-3 initiates the cell disassembly process and nuclear DNA fragmentation, which is mediated by the release of apoptogenic mitochondrial factors (CPS-6 and WAH-1) and which involves multiple endo- and exo-nucleases such as NUC-1 and seven CRN nucleases. The recognition and removal of the dying cell is mediated by two partially redundant signaling pathways involving CED-1, CED-6 and CED-7 in one pathway and CED-2, CED-5, CED-10, CED-12 and PSR-1 in the other pathway. Further studies of programmed cell death in C. elegans will continue to advance our understanding of how programmed cell death is regulated, activated, and executed in multicellular organisms.
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PMID:Programmed cell death. 1806 82