Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0406810 (NAME)
 13,345 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report a case of paraneoplastic retinopathy in a patient who was found to have small cell carcinoma of the lung and was shown to have serum antibody against retinal soluble 70 kDa protein. A 71-year-old woman visited her ophthalmologist for gradual visual loss in both eyes. Although she underwent uncomplicated cataract surgery in her left eye, she was referred to our hospital because of progressive visual deterioration in November 1994. On admission, her corrected visual acuity was 0.3 OD and hand motion OS. Funduscopic examination showed narrowing retinal arteries, pigment epithelial mottling in the posterior retina bilaterally, and optic disc pallor in the left eye. An electroretinogram demonstrated marked reduction in the a and b waves. Bilateral central scotomas were detected by kinetic perimetry. We pursued further examination for systemic disease, and identified increased serum level of neuron specific enolase and radiographically abnormal shadow in the chest. Transcutaneous needle biopsy of the mediastinum confirmed small cell carcinoma. In western blot analysis the patient's serum reacted strongly with soluble retinal proteins of 70 kDa molecular weight, although the 26 kDa CAR antigen was not labeled. This patient was diagnosed as having paraneoplastic retinopathy due to small cell carcinoma and unusual serum protein which responded to an antigen with a molecular weight of 70 kilodaltons.
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PMID:[A case of paraneoplastic retinopathy with serum antibody against retinal soluble 70 kDa protein]. 902 14

Using an in vitro primary cell culture model in which cortical neurons undergo a gradual and delayed neuronal death after a brief (5 min) challenge with glutamate receptor agonist N-methyl-D-aspartate (NMDA, 300 microM), the neuroprotective effects of various nitric oxide synthases (NOS) inhibitors were compared with that of the NMDA receptor antagonist dizocilpine maleate (MK-801). Our rat cortical cultures consisted of approximately 80-96% neurons and 5-20% astroglia as determined by immunocytochemical staining with antibodies against glial fibrillary acidic protein (GFAP) or neuron specific enolase (NSE). The delayed type of NMDA-induced neurotoxicity was examined by the morphological estimate of cell injury and was further confirmed by the activity of lactate dehydrogenase (LDH) in the extracellular fluid measured 24 hrs after the 5-min NMDA exposure. The accumulation of nitrite, the stable metabolite of nitric oxide (NO), was also measured 24 hrs after the 5-min NMDA exposure. The brief NMDA exposure caused about 60% neuronal death, as compared with persist (24 hr) NMDA exposure at 24 hr after NMDA exposure. Effects of drugs were studied by pretreating the cultures for 10 mins prior to the induction of NMDA neurotoxicity. Both the nonselective NOS inhibitor N alpha-nitro-L-arginine methyl ester (L-NAME, 100 microM) and the selective neuronal nitric oxide synthase (nNOS) inhibitor 7-nitroindozale (7-NI, 100 microM) suppressed nitrite accumulation and attenuated neuronal damage induced by NMDA. However, the selective inducible nitric oxide synthase (iNOS) inhibitor aminoguanidine (AG, 100 microM) exhibited no neuroprotective effects and no reduction in the nitrite production. The NMDA-induced neurotoxicity and nitrite production was abolished by pretreatment with the NMDA receptor antagonist MK-801 (100 microM). Thus the results indicate that a brief NMDA exposure leads to delayed neuronal damage with concomitant increase in NO production in cortical neuronal cultures. We suggest that the NO may originate primarily from nNOS. The neuroprotective effects of NOS inhibitors are weaker than that of MK-801.
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PMID:Effects of various nitric oxide synthase inhibitors on NMDA-induced neuronal injury in rat cortical neurons. 905 7

SUMMARY We investigated the in vitro effect of total excretory/secretory and somatic antigens from Ascaris suum adults (ESA and SA) and larvae 3 (ESL3 and SL3), and of 10 purified protein fractions from ESA components on rat alveolar macrophage nitric oxide (NO) production. Our results showed that in vitro incubation of macrophages with SA and SL3 antigens of A. suum did not result in NO release from cells, whereas incubation with ESA or ESL3 antigens resulted in the stimulation of NO production by these cells, both in a specific (inhibited by L-NAME and L-canavanine) and dose-dependent manner. In addition, we could demonstrate that a purified ESA fraction consisting of three Coomassie-stained bands of approximately 37, 44 and 46 kDa is involved in the in vitro triggering of NO production by host cells. These three bands were subjected to MALDI-peptide mass fingerprint, showing similarities with phosphoglycerate kinase, elongation factor Tu and enolase molecules, respectively. Future studies will focus on the characterization of these parasite-derived molecules.
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PMID:Antigens from Ascaris suum trigger in vitro macrophage NO production. 1604 43