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)

The aim of the present study is to demonstrate the sensitivity, specificity and applicability of several tissue markers in the determination of the primary sites of metastatic tumors. The immunoperoxidase technique was used in 19 metastatic tumors from breast (6), gastrointestinal tract (6), thyroid (3), prostate (1), ovary (1), pancreas (1) and melanoma (1). Polyclonal antisera against thyroglobulin and prostatic specific antigen were used. The following monoclonal antibodies were employed: BRST-1, BRST-2, CAR-3, BD-5 and HMB-45. BRST-1 and BRST-2 are considered to be breast cancer markers, while CAR-3 and BD-5 gastrointestinal markers. HMB-45 was described as a melanoma marker. Breast markers were positive for 3 out of 6 breast metastases. BRST-1 was also positive for metastases from melanoma and prostate. CAR-3 and BD-5 were positive for 5 out of 6 gastrointestinal metastases. CAR-3 also presented focal positivity for 4 out of 6 breast metastasis, 1 out of 3 thyroid metastasis and for metastasis from ovary, prostate, pancreas and melanoma. BD-5 was also positive for prostate metastasis. Thyroglobulin and prostatic specific antigen were only positive for thyroid and prostate metastasis, respectively. In conclusion, immunocytochemistry and monoclonal antibodies are useful tools in the detection of the primary sites of metastatic tumors of unknown origin. In some of the fields, the results are already satisfactory. Nevertheless, further studies should be carried out to improve this promising technique.
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PMID:[Use of immunohistochemistry in detecting the primary site in neoplasm metastasis]. 269 78

The roles of VIP and NO in vagally mediated relaxations of the gastric corpus were investigated in the anaesthetized ferret. Intracorpus pressure was recorded manometrically during electrical stimulation of the cervical vagus nerve in three groups of animals: one control group (n = 6), one group treated with an inhibitor of NO synthesis (NG-nitro-L-arginine methyl ester (L-NAME), 1.6 mg/kg); and a third group which had been immunized, prior to the experiment, with a VIP-thyroglobulin conjugate (25 nmol equivalent) in Freund's complete adjuvant. In control animals, following treatment with atropine (100 micrograms/kg), vagal stimulation resulted in a frequency dependent fall in intracorpus pressure with the maximum response at 5 Hz of 2.2 +/- 0.3 cm H2O. Two components of the response could be observed: an initial rapid fall over the first 10 s of stimulation followed by a slower decline over the remainder of the stimulation period. In animals treated with L-NAME (n = 6) the initial rapid response was significantly reduced at all frequencies of stimulation (P < 0.05 - P < 0.005, Mann-Whitney U-test) leaving only the slower second component. In immunized animals (n = 6) the initial rapid response to vagal stimulation was not different from control but the slower second component was significantly reduced at 1 Hz (P < 0.005). We conclude that the response to vagal stimulation appears to consist of two components which can be differentiated using L-NAME and autoimmunization to VIP.
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PMID:Role of nitric oxide and vasoactive intestinal polypeptide in vagally mediated relaxation of the gastric corpus in the anaesthetized ferret. 836 53

Nitric oxide (NO) is a free radical that mediates a wide array of cell functions. It is generated from l-arginine by NO-synthase (NOS). Expression of NOS isoforms has been demonstrated in thyroid cells. Previous reports indicated that NO donors induce dedifferentiation in thyrocytes. However, the functional significance of endogenous thyrocyte-produced NO has not been explored. This work aimed to study the influence of endogenous NO on parameters of thyroid cell function and differentiation in FRTL-5 cells. We observed that treatment with the NOS inhibitor, Nomega-nitro-L-arginine methyl ester (L-NAME), increased the TSH-stimulated iodide uptake. The TSH-induced sodium iodide symporter (NIS) and thyroglobulin (TG) mRNA expressions were increased after incubation with L-NAME. In transient transfection assays, TSH-stimulated transcriptional activities of NIS and TG promoters were increased by L-NAME. An increment of the TSH-stimulated cell proliferation was observed after NOS inhibition. Similar results were obtained when the action of another NOS inhibitor, N(g)-monomethyl-L-arginine, was analysed for most of these studies. The production of NO, which was not detectable in basal conditions, was increased by TSH. Our data provide strong evidence that endogenous NO could act as a negative signal for TSH-stimulated iodide uptake and thyroid-specific gene expression as well as proliferation in thyrocytes. These findings reveal a possible new inhibitory pathway in the regulation of thyroid cell function.
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PMID:Endogenous thyrocyte-produced nitric oxide inhibits iodide uptake and thyroid-specific gene expression in FRTL-5 thyroid cells. 1733 30