|1.||Jitrapakdee, Sarawut: 4 articles (01/2015 - 07/2007)|
|2.||MacDonald, Michael J: 4 articles (01/2015 - 10/2008)|
|3.||Wallace, John C: 3 articles (01/2015 - 07/2007)|
|4.||Hasan, Noaman M: 3 articles (04/2013 - 10/2008)|
|5.||Stoker, Scott W: 3 articles (04/2013 - 10/2008)|
|6.||Higashi, Richard M: 2 articles (02/2015 - 01/2009)|
|7.||Lane, Andrew N: 2 articles (02/2015 - 01/2009)|
|8.||Bousamra, Michael: 2 articles (02/2015 - 01/2009)|
|9.||Miller, Donald M: 2 articles (02/2015 - 01/2009)|
|10.||Patel, Anant B: 2 articles (01/2014 - 01/2005)|
08/30/1991 - "13C NMR study of hepatic pyruvate carboxylase activity in tumor rats."
09/01/1973 - "Enzymatic and immunological studies on pyruvate carboxylase in livers and liver tumors."
08/30/1991 - "Although it is well known that hepatic gluconeogenesis from these substrates is increased in tumor hosts, the involvement of pyruvate carboxylase has not been demonstrated. "
08/30/1991 - "In the present study, we examined pyruvate carboxylase activity in the perfused livers of tumor rats using 13C NMR spectroscopy with [3-13C]-alanine as the gluconeogenic substrate. "
05/24/2011 - "Pyruvate carboxylase is required for glutamine-independent growth of tumor cells."
|2.||Leigh Disease (Leigh's Disease)
10/01/1973 - "Renal function studies and kidney pyruvate carboxylase in subacute necrotizing encephalomyelopathy (Leigh's syndrome)."
04/01/1984 - "Pyruvate carboxylase activity in subacute necrotizing encephalopathy (Leigh's disease)."
01/01/1980 - "In a patient with the clinical symptoms of Leigh's disease a partial deficiency of hepatic pyruvate carboxylase and pyruvate decarboxylase was found at necropsy. "
01/01/1980 - "Leigh's disease with decreased activities of pyruvate carboxylase and pyruvate decarboxylase."
03/01/1982 - "Studies on pyruvate carboxylase, pyruvate decarboxylase and lipoamide dehydrogenase in subacute necrotizing encephalomyelopathy."
|3.||Pyruvate Carboxylase Deficiency Disease
03/01/1984 - "We propose that the different clinical presentation of human pyruvate carboxylase deficiency is a manifestation of two different mutations in the pyruvate carboxylase gene, one that results in the synthesis of a relatively inactive pyruvate carboxylase protein CRM(+ve) and one that results in the lack of expression of the gene in the form of a recognizable protein CRM(-ve)."
06/30/1983 - "Pyruvate carboxylase activity was investigated in cultured fibroblasts from a patient shown to have hepatic pyruvate carboxylase deficiency. "
05/25/1983 - "Four out of 5 cell lines from patients with classical pyruvate carboxylase deficiency (less than 5% of normal activity) labeled with this technique displayed a normal band in the position of pyruvate carboxylase while one cell line showed complete absence of any labeled protein in this area. "
01/01/1980 - "The activity of pyruvate carboxylase in the crude homogenate from cultured human fibroblasts was 0.76 +/- 0.12 nmol/min per mg protein, while the activity in cultured amniotic fluid cells was 0.66 +/- 0.17 nmol/min per mg protein, suggesting the possibility of prenatal diagnosis of pyruvate carboxylase deficiency."
04/01/2005 - "Considering that pyruvate carboxylase is a key enzyme for anaplerosis, besides the new perspectives brought by anaplerotic therapies in those rare pyruvate carboxylase deficiencies, this therapeutic trial also emphasizes the possible extended indications of triheptanoin in various diseases where the citric acid cycle is impaired."
|4.||Diffuse Cerebral Sclerosis of Schilder (Alpers' Disease)
01/01/1977 - "The authors describe an anatomical familial case of progressive infantile cerebral poliodystrophy (Alpers disease), in which the study of enzyme kinetics of hepatic pyruvate carboxylase revealed an abnormal graph reflecting a loss of activity of the enzyme with low concentrations of substrate, This is a new feature in the literature on Alpers disease, and possibly indicates one of the pathogenic mechanisms responsible in this disorder which remains mysterious, although its pathology has been clearly described."
06/01/1975 - "[Proceedings: Infantile cerebral poliodystrophy (Alper's disease) in an infant with hyperlactacidemia and hepatic pyruvate carboxylase]."
01/01/2005 - "During seizures the initial rate of Glx(2+3) synthesis (0.069 +/- 0.013 micromol/g/min) was not significantly different (P = 0.68) from that of the controls (0.059 +/- 0.010 micromol/g/min), indicating that anaplerotic flow through pyruvate carboxylase was unaltered. "
01/01/2005 - "Cerebral pyruvate carboxylase flux is unaltered during bicuculline-seizures."
01/01/2005 - "Intense neuronal activation of seizures did not seem to increase anaplerosis through pyruvate carboxylase, despite the substantial increase in neuronal activity and glutamate/glutamine cycling shown in a previous study (Patel et al., 2004b)."
01/01/2005 - "In this study, pyruvate carboxylase flux was assessed during intravenous infusion of [2-(13)C]glucose using localized (1)H-[(13)C] NMR spectroscopy at 7 Tesla in vivo in halothane-anesthetized and ventilated adult Wistar rats during 85 min of bicuculline-induced seizures (1 mg/kg, intravenously) and in nontreated controls. "
|3.||Glutamic Acid (Glutamate)
|4.||Pyruvate Decarboxylase (Decarboxylase, Pyruvate)
|5.||Dihydrolipoamide Dehydrogenase (Lipoamide Dehydrogenase)
|10.||Biotin (Vitamin H)
|3.||Drug Therapy (Chemotherapy)