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Biomedical subjects

J Martinez

Publications and source records attributed to J Martinez.

At least 451 records · Page 25Linked to original sources
PubMed1984

Reproductive disorders in dairy cattle. II. Interrelationships between pre-or post-service infectious and functional disorders.

This retrospective study was aimed at investigating the interrelationships between the various post-partum reproductive disorders whose incidence distribution was reported in a previous paper. There were 343 calving cows, and 319 of them were inseminated at least once. Although approximately one-third of the cows suffered from metritis, its influence on subsequent pathology was only minor. No within-animal relationship could be found between post-partum cyclic anestrus and post-AI anestrus. The distribution of repeat breeding cows showed that almost half of them also had post-AI anestrus, and only 17% had no other disorders. Previous metritis accounted for only 10% of these cases. Embryonic mortality was related only to post-partum cyclic anestrus. Finally, it was found that approximately half of the cows suffered from more than one reproductive disorder with many different relations between the disorders within individuals during post partum. In conclusion, optimal efficiency of post-partum reproduction requires careful checking of all possible disorders.

Journal Article↗
PubMed1984

A new class of potent gastrin antagonists.

The hexapeptide Z-Tyr(SO-3)-Met-Gly-Trp-Met-Asp-NH2, from the natural sequence of C-terminal cholecystokinin was found to be a competitive antagonist of cholecystokinin receptors, in vitro. In the present study, we report that this peptide inhibits gastrin-induced acid secretion in vivo, (ED50 = 1.5 mumol . kg-1), without agonist activity. Desulfation of the tyrosine residue slightly altered this effect. The tripeptide Boc-Trp-Met-Asp-NH2 showed similar effects, but had lower potency (ED50 = 12 mumol . kg-1). From these preliminary results, it can be concluded that removal of the phenylalanine residue from the C-terminal sequence of CCK or gastrin, leads to an antagonist of the natural hormones and that C-terminal phenylalanine residue is important for agonist activity. As compared with proglumide, a well known gastrin receptor antagonist, these peptides were 20-200 times more potent as inhibitors on the same model.

Amino Acid Sequence↗
PubMed1984

Synthesis and antitumor evaluation of some nitrosourea and nitrogen mustard amino acid derivatives.

A series of (2-chloroethyl)nitrosourea and nitrogen mustard amino acid derivatives have been synthesized for antitumor evaluation. Reaction of an appropriate N-protected amino acid with 2-chloroethylamine followed by removal of the N-protecting group and condensation with an active (2-chloroethyl)nitrosocarbamate yielded N-[(2-chloroethyl)nitrosocarbamoyl]amino acid (2-chloroethyl)amides. Antitumor evaluation was performed against leukemia L1210, in vivo, in mice. These derivatives exhibited very interesting activities, particularly the sarcosine and gamma-aminobutyric acid derivatives.

Animals↗
PubMed1984

Synthesis and biological activity of new peptide segments of gastrin exhibiting gastrin antagonist property.

A series of C-terminal peptide segments of gastrin, i.e., (tert-butyloxycarbonyl)-L-tryptophyl-L-methionyl-L-aspartic acid amide, (tert-butyloxycarbonyl)-glycyl-L-tryptophyl-L-methionyl-L-aspartic acid amide, (tert-butyloxy-carbonyl)-L-tyrosyl-glycyl-L-tryptophyl-L-methionyl-L-asp artic acid amide, and (benzyloxycarbonyl)-L-glutamyl-L-alanyl-L-tyrosyl-glycyl-L-tryptophyl-L -methionyl-L-aspartic acid amide were prepared and were shown to competitively inhibit the binding of labeled human gastrin to its receptors in an isolated gastric mucosal cell preparation and to antagonize the action of gastrin on gastric acid secretion (ED50 from 1.5 to 7 mg/kg) in vivo in the reperfused rat stomach, determined according to the method of Ghosh and Schild. From these studies, it could be concluded that the C-terminal phenylalanine residue, which is of primary importance for intrinsic biological gastrin-like activity, is not essential for binding to gastrin receptors.

Amino Acid Sequence↗
PubMed1984

Sodium lactate infusion, panic attacks, and ionized calcium.

The ability of sodium lactate to precipitate panic attacks in vulnerable individuals has been repeatedly demonstrated, although its mechanism of action is unknown. Pitts and McClure hypothesized that the panicogenic effect of sodium lactate was due to its induction of a peripheral hypocalcemia via the complexing of infused lactate ions with extracellular ionized calcium. In the current study, serial ionized calcium measurements during lactate infusion are assessed for 22 panic patients who panicked during infusion, 11 panic patients who did not panic during the procedure, and 6 normal controls. Intravenous sodium lactate infusion was found to be associated with a significant decrease in ionized calcium in all groups. No specific association was found between the rate or magnitude of decrease in ionized calcium and the occurrence of a panic attack during the infusion.

Agoraphobia↗
PubMed1983

Cholecystokinin-27-32-amide. A member of a new class of cholecystokinin receptor antagonists.

In dispersed acini from guinea pig pancreas, cholecystokinin-27-32-amide (CCK-27-32-NH2) did not alter amylase secretion but was able to antagonize the stimulation caused by cholecystokinin-related agonists. CCK-27-32-NH2 caused a parallel rightward shift in the dose-response curve for the stimulation of amylase secretion caused by cholecystokinin and inhibited binding of 125I-labeled cholecystokinin to pancreatic acini. These results indicate that CCK-27-32-NH2 is a fully competitive cholecystokinin receptor antagonist. CCK-27-32-NH2 did not alter the rate of dissociation of bound 125I-cholecystokinin from pancreatic acini but was able to reverse the residual stimulation of enzyme secretion caused by first incubating pancreatic acini with a relatively high concentration of cholecystokinin. Compared to other cholecystokinin receptor antagonists, CCK-27-32-NH2 is the most potent antagonist described to date, i.e. 30 times more potent than N2,O2-dibutyryl guanosine 3':5'-monophosphate. These results also indicate that the COOH-terminal phenylalanine residue of cholecystokinin is essential for intrinsic cholecystokinin-like activity but is not essential for binding of the peptide to cholecystokinin receptors in pancreatic acini.

Animals↗
PubMed1983

The role of the Asp-32 residue of cholecystokinin in gastric acid secretion and gastrin receptor recognition.

The aspartic acid residue at the penultimate position is known to be essential for the hormonal activity of CCK and gastrin on gastric acid secretion. This residue was successively replaced by beta-aspartic acid, beta-alanine, and glutamic acid in the C-terminal heptapeptide of CCK 27-33. The analogues obtained were tested on rat gastric acid secretion and for recognition by gastrin receptors. The replacement by beta-aspartic or beta-alanine decreased gastric secretion and gastrin receptor recognition. In contrast, replacement by glutamic acid affected these two parameters less. The nature of the N-blocking group (Boc or Z) also influenced these activities, Boc derivatives being more potent than Z derivatives. The results were compared to those previously obtained on pancreatic secretion and on stimulation of gall bladder contraction where the modifications were found capable of differentiating between cholecystokinin, pancreozymin and gastrin activities.

Animals↗
PubMed1983

Solitary metastasis to the medulla oblongata.

Of 40 reported cases of solitary brain stem metastasis, only two patients had medullary lesions. We have presented a third case, suggesting that this infrequent occurrence may be due to the mid-brain and pons having a more abundant blood supply, with increased potential for metastatic deposits, and being larger targets for metastases than the medulla.

Adenocarcinoma↗
PubMed1983

Synthesis of an IgG fragment decapeptide exhibiting phagocytosis stimulating activity of polymorphonuclear leucocytes.

Fragment 335-344 of human IgG was synthesized stepwise, using active esters of N-protected amino acids and benzotriazolyloxytris (dimethylamino)phosphonium hexafluorophosphate for coupling. This fragment could be liberated from the carrier molecule by the two specific enzymes responsible for the release of tuftsin from the same carrier molecule: tuftsin endocarboxy-peptidase cleaves at the Arg-Glu bond and leukokininase at the Lys-Thr bond. This decapeptide fragment, Thr-Ile-Ser-Lys-Ala-Lys-Gly-Gln-Pro-Arg showed significant activity in stimulating phagocytosis of human polymorphonuclear leucocytes.

Immunoglobulin G↗
PubMed1983

New synthetic and natural tuftsin-related compounds and evaluation of their phagocytosis-stimulating activity.

The preparation of large amounts of tuftsin (50 g) as well as purification by preparative HPLC are presented. Synthesis of several analogues exhibiting significant phagocytosis-stimulating activity of human PMN are described and discussed. On the other hand, the synthesis of a natural human IgG decapeptide fragment 335-344 that could be liberated from the same carrier molecule is presented. This decapeptide fragment, Thr-Ile-Ser-Lys-Ala-Lys-Gly-Gln-Pro-Arg, showed interesting activity in stimulating phagocytosis of human polymorphonuclear leukocytes.

Amino Acid Sequence↗
PubMed1983

Control of catalase and peroxidase biosynthesis by carbon source and oxygen in the yeast Saccharomyces cerevisiae.

The effect of carbon source and oxygen tension on catalase and peroxidase levels and on the intermediates of the biosynthesis of the prosthetic group of both enzymes has been studied. Oxygen produces an increase of both enzymatic activities, even in presence of glucose. On the other hand it seems probable that glucose does not have a direct inhibitory effect on the biosynthesis of 5-aminolevulinic acid (ALA) and porphyrins.

Aerobiosis↗
PubMed1983

Exposure of platelet fibrinogen-binding sites by collagen, arachidonic acid, and ADP: inhibition by a monoclonal antibody to the glycoprotein IIb-IIIa complex.

Following stimulation with adenosine diphosphate (ADP), collagen, or arachidonic acid, unstirred human platelet suspensions bind 125I-fibrinogen in a reaction that reaches completion within 30 min. Scatchard analysis of these binding data reveals two sets of binding sites with all 3 agents: a high affinity site (Kd 0.029-0.045 microM) binding 1000-1600 fibrinogen molecules per platelet, and a lower affinity site (Kd 1.2-2.0 microM) binding 46,000-76,000 fibrinogen molecules per platelet. At a concentration of apyrase that inhibited ADP-induced fibrinogen binding by greater than 85%, fibrinogen binding induced by collagen and arachidonic acid was only partially affected. This suggests that fibrinogen binding induced by collagen or arachidonic acid does not require released ADP. We isolated a monoclonal antibody, B59.2, which precipitated the glycoprotein IIb-IIIa complex from solubilized platelet membranes. Binding of labeled antibody to platelets before or after exposure to ADP, collagen, or arachidonic acid showed a single class of approximately 22,000 binding sites with Kd 0.019 microM. Binding of B59.2 was complete within 1 min and was not inhibited by EDTA. Preincubation of platelet suspensions with a 2.1 microM concentration of B59.2 caused inhibition of secretion and aggregation, but not of thromboxane-B2 synthesis, in response to 1 microgram/ml collagen, 40 microM arachidonic acid, or 4 microM ADP, concentrations of aggregating agents that produced complete aggregation and secretion in the absence of B59.2. At this concentration of B59.2, fibrinogen binding to stimulated platelets was inhibited by approximately 45%-55%. These data demonstrate that collagen and arachidonic acid can expose fibrinogen binding sites independently of released ADP; and that the glycoprotein IIb-IIIa complex is involved in secretion, aggregation, and fibrinogen binding, but not in thromboxane synthesis occurring in response to collagen, arachidonic acid, or ADP.

Adenosine Diphosphate↗
PubMed1983

Exposure of fibrinogen receptors on fresh and stored platelets by ADP and epinephrine as single agents and as a pair.

Platelet concentrates stored at 22 degrees C have a marked decrease in their aggregation response to adenosine diphosphate (ADP) or epinephrine but a normal response to these agents when used as a pair. Since platelet stimulation involves exposure of receptors for fibrinogen, we studied fibrinogen binding to platelets from fresh and stored concentrates. Following stimulation with 10 microM ADP or 20 microM epinephrine, platelet suspensions from fresh concentrates bound 125I-fibrinogen in a reaction that reached completion within 30 min. Significantly less binding occurred in suspensions from platelet concentrates that had been stored for 5 days at 22 degrees C. When stimulated by ADP and epinephrine as a pair (2 microM each), binding of fibrinogen to platelets was complete within 10-15 min and was not significantly decreased in suspensions from stored concentrates. We also investigated the effect of storage on the glycoprotein IIb-IIa complex, thought to be a specific receptor for fibrinogen on the platelet surface. Binding of a monoclonal antibody specific for this complex (B59.2) to platelet suspensions was unaffected by 5 days of storage. Furthermore, B59.2 inhibited aggregation, secretion, and fibrinogen binding of fresh and stored platelets stimulated with the pair of agents just as it did with single agents. We conclude that storage for 5 days at 22 degrees C impairs the exposure of fibrinogen receptors on platelets in response to ADP or epinephrine when used as single agents, without affecting the glycoprotein IIb-IIIa complex quantitatively. The function of the receptor is normal in response to the pair of agents.

Adenosine Diphosphate↗