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Biomedical subjects

M D Gomes

Publications and source records attributed to M D Gomes.

7 recordsLinked to original sources
PubMed1994

Structural requirements of bioactive peptides for interaction with endopeptidase 22.19.

A series of biologically active peptides and related compounds (opioid peptides, neurotensin, and bradykinin) were used as substrates or competitive inhibitors to study the structural requirements for peptide interaction with endopeptidase 22.19. The kinetics of hydrolysis of these peptides indicated that, in contrast to other proteases, the substrate specificity of endopeptidase 22.19 is not determined by the amino acids flanking the sensitive bonds of the substrates. The competition between bioactive peptide analogues and the quenched fluorescence substrate of endopeptidase 22.19 indicated that their length and their flexibility may be the dominant factors to explain their binding specificities. These peculiar features of endopeptidase 22.19 may be of importance to understand the physiological processes of conversion and inactivation of biologically active peptides.

Amino Acid Sequence↗
PubMed1993

Dynorphin-derived peptides reveal the presence of a critical cysteine for the activity of brain endo-oligopeptidase A.

Brain endo-oligopeptidase A, a neuropeptide-metabolizing endopeptidase, has been considered a cysteine-endopeptidase because it is activated by thiols and inhibited by phydroxymercuribenzoate or 5,5'-dithiobis-(2-nitrobenzoic acid). The understanding of the unique specificity of endo-oligopeptidase A was useful for the synthesis of affinity labeling compounds containing as a thiol reactive group the Cys-(3-nitro-2-pyridinesulfenyl) group into dynorphin-derived peptides which are among the best substrates and competitive inhibitor of endopeptidase 22.19. Of the ten compounds tested, only peptides containing 8 to 13 amino acid residues caused irreversible inhibition. The fact that the most effective inhibitors had the reactive group either at the P'1 or at P'3 position [nomenclature of Schechter and Berger] would seem to argue that the reactive cysteine is in the vicinity of the active site, or actually involved in the catalytic step.

Amino Acid Sequence↗
PubMed1993

Characterization of foot-and-mouth disease virus by monoclonal antibodies.

Monoclonal antibodies (MAbs) were produced against foot-and-mouth disease (FMD) virus types O1 Campos Br1/58, A24 Cruzeiro Br1/55, and C3 Indaial Br1/71, which are the strains used for production of FMD vaccines in the majority of South American countries. Within the library of MAbs produced, a group was selected on the basis of their neutralizing titer in cell culture, protective titer in suckling mice, sensitivity to trypsin, and specificity for virus structural proteins. The MAbs were utilized in an ELISA test format to compare European and South American representative field isolates with vaccine production strains in their r1 relationship as obtained by 50% complement fixation (CF50) with polyclonal antibodies (PAb) and their virus neutralization (VN) relationship obtained with sera from one-time-vaccinated and from revaccinated cattle, respectively. The MAbs selected varied in their reactivity against the different strains and, therefore, enabled us to compare field FMDV strains to those against which the MAbs were produced, with definite advantages over the r1 and VN ratios. Thus, panels of MAb produced with the vaccine strains and appropriately selected are significantly useful for the FMD-control programs because they serve to provide guidance on the immunological coverage provided by the vaccines against FMDV strains circulating in the field. The MAbs are also useful for the differentiation of FMD virus strains.

Animals↗
PubMed1984

Optimal dose of oral omeprazole for maximal 24 hour decrease of intragastric acidity.

In a series of 59 experiments in nine duodenal ulcer patients, 24 hour intragastric acidity was measured before, during, and after treatment with daily oral omeprazole. Omeprazole 10, 20, and 30 mg/day for one week caused a 37, 90, and 97% decrease of 24 hour intragastric acidity, respectively. No further decrease of acidity was observed when the dose of omeprazole was doubled to 60 mg/day, or after a second week of treatment with 30 mg/day. One week after stopping treatment with omeprazole (14 doses) there was a significant 26% decrease of 24 hour intragastric acidity, with full recovery seven weeks later. Fasting plasma gastrin concentration was significantly raised during treatment with all doses of omeprazole. Omeprazole 30 mg/day is the optimal dose for a maximal decrease of 24 hour intragastric acidity in duodenal ulcer patients.

Adult↗
PubMed1983

Effect of daily oral omeprazole on 24 hour intragastric acidity.

Twenty four hour intragastric acidity was measured in nine patients with duodenal ulcer before and after one week of treatment with oral omeprazole 30 mg daily, a drug that inhibits gastric secretion by inhibition of parietal cell H+K+ adenosinetriphosphatase (ATPase). Omeprazole virtually eliminated intragastric acidity in all patients: the median 24 hour intragastric pH rose from 1.4 to 5.3 and the mean hourly hydrogen ion activity fell from 38.50 to 1.95 mmol(mEq)/1 (p less than 0.001). This inhibition of 24 hour intragastric acidity is more profound than that previously reported with either cimetidine 1 g daily or ranitidine 300 mg daily.

Administration, Oral↗
PubMed1982

[Locked-in syndrome. Report of a case and review of the literature].

The case of a 46 year-old man who had a locked-in syndrome is reported. The patient had a haemorragic vascular accident with tetraplegia, anartria, vertical ocular movements and preservation of the consciousness. The EEG showed a projected disturbance possibly caused by a brain-stem lesion, that was confirmed by the CAT SCAN. Cerebral angiography showed high level of aterosclerosis. The lesion is located in the ventral part of the pons above the nucleus of the abducent nerve, without damaging the substantia reticularis of the mesencephalon and can be caused by thrombosis of the basilar artery and tumor, myastenia gravis, polyneurites, heroin overdose, after swine-flu inoculation and post-infectious polyneurites. The patient is still alive 2 years after the stroke with a good recovery. He can walk and speak fluently, but with cordonal ataxy of the limbs.

Cerebrovascular Disorders↗