Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0155339 (Brown)
12,436 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

3':5'-Cyclic-AMP phosphodiesterase (EC 3.1.4.17) and the activating factor of cyclic nucleotide phosphodiesterase were detected in cultured human cell lines from patients with lymphoblastic leukemia and retinoblastoma and in the Brown-Pearce (rabbit) carcinoma. The homogenate of lymphoblasts contained levels of the activating factor in excess of that required to produce maximal activation of the endogenous phosphodiesterase. The activating factor found in these malignant cells appears to be similar to the calcium-binding protein activator of bovine brain phosphodiesterase on the basis of the molecular weight obtained from gel filtration, electrophoretic patterns, calcium requirement for the activity, and the effect of calcium on the proteolysis. In addition, the tumor-derived activator was able to restore the activity of activator-deficient phosphodiesterase from the bovine brain.
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PMID:Cyclic nucleotide phosphodiesterase and protein activator in human cancer cell lines and Brown-Pearce carcinoma. 20 Jul 56

Ultrastructurally identified inhibitory synapses in layer II of rat sensorimotor cortex decline between middle and old age [Poe, B.H., Linville, C., Brunso-Bechtold, J., 2001. Age-related decline of presumptive inhibitory synapses in the sensorimotor cortex as revealed by the physical disector. J. Comp. Neurol. 439, 65-72]. The current study investigated whether a loss or shrinkage of gamma-aminobutyric acid (GABA)ergic interneurons contribute to that decline. Coronal sections from middle-aged (15-17 months) and old (25-29 months) Fischer 344 X Brown Norway male rats were immunoreacted with antibodies to the GABA synthesizing enzyme glutamic acid decarboxylase (GAD); the calcium-binding protein parvalbumin (PV), or the neuronal marker NeuN. The number of GAD-immunoreactive (IR), PV-IR, and NeuN-IR cells were determined stereologically using the optical disector technique and the cross-sectional areas of GAD-IR cells were measured in layers II/III, IV, V and VI of sensorimotor cortex. Neither the number of GAD-IR or NeuN-IR cells, nor the size of GAD-IR cells, declined significantly between middle and old age. A modest decline in the PV-IR subset of inhibitory interneurons was observed, predominantly due to changes in layers V and VI. Stereological analysis of layer II/III GAD-IR boutons revealed a stability of immunocytochemically identified inhibitory terminals. Taken together, these results indicate a general maintenance of overall GABAergic neurons in sensorimotor cortex between middle and old age and the loss of ultrastructurally identified inhibitory synapses may be due to the decline of a subset of GABAergic terminals.
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PMID:Maintenance of inhibitory interneurons and boutons in sensorimotor cortex between middle and old age in Fischer 344 X Brown Norway rats. 1672 92