Search PubMed⌕ Search

Biomedical subjects

J Martinez

Publications and source records attributed to J Martinez.

At least 163 records · Page 9Linked to original sources
PubMed1999

Heterotopic pregnancy: discovery of ectopic pregnancy after elective abortion.

We report a case of combined intrauterine and tubal pregnancy in a 23-year-old woman. The patient came to the emergency department complaining of lower abdominal pain after having had an elective abortion 2 weeks earlier. Her physician had done pelvic ultrasonography, noting an intrauterine pregnancy before the abortion. Our working diagnosis in the emergency department was retained products of conception versus postabortion endometritis. Pelvic ultrasonography in the emergency department revealed an ectopic pregnancy without evidence of retained products of conception, and the patient had a right salpingotomy with removal of the ectopic fetus without complications.

Abortion, Induced↗
PubMed1999

Identification of synthetic by-products in combinatorial libraries using high performance liquid chromatography-electrospray ionization mass spectrometry.

High performance liquid chromatography (HPLC), electrospray ionization mass spectrometry (ESI) and high performance liquid chromatography coupled to mass spectrometry (LC-MS) were used to analyze randomly chosen samples from parallel syntheses carried out on derivatized polypropylene crowns compatible with a Multipin solid support system. Side-reactions and by-products were clearly identified, and the yields of the expected molecules were unexpectedly low for most samples. LC-MS was superior to HPLC with absorbance detection or electrospray mass spectrometry alone for determining the identity and purity of each desired combinatorial compounds.

Acrylamides↗
PubMed1998

Transplantation rate of the blood group B waiting list is increased by using A2 and A2B kidneys.

BACKGROUND: We have increased the transplantation rate for blood group B cadaveric waiting list candidates by transplanting them with A2 and A2B kidneys. METHODS: Since 1991, five of the seven renal transplant programs in our organ procurement organization service area have preferentially transplanted blood group A2 and A2B cadaveric kidneys to B blood group waiting list candidates with histories of low anti-A isoagglutinin titers. RESULTS: Between 1991 and 1997, these five centers performed transplantations on 71 patients from the B cadaveric waiting list. Of those 71 patients, 29% (21 of 71) underwent transplantation with either A2 (n=18) or A2B (n=3) cadaveric kidneys. In 1997 alone, 48% (11 of 23) of the B patient transplant recipients received A2 or A2B kidneys. CONCLUSIONS: Transplantation of A2 and A2B kidneys into B waiting list patients has successfully increased access of B patients to kidneys. Such an allocation algorithm implemented nationally may similarly increase the transplantation rate of B waiting list candidates.

ABO Blood-Group System↗
PubMed1998

Long-term graft survival is improved in cadaveric renal retransplantation by flow cytometric crossmatching.

BACKGROUND: Cadaveric renal retransplantation is associated with a higher risk of early graft failure than primary grafts. A large proportion of those graft losses is likely attributable to donor-directed HLA class I antibodies, detectable by flow cytometry cross-matching but not by conventional crossmatching techniques. METHODS: Long-term graft survival in a group of 106 recipients of consecutive cadaveric renal regrafts between 1990 and 1997, in whom a negative flow T-cell IgG crossmatch was required for transplantation, was compared with two other groups of cadaveric transplant recipients. The first group consisted of 174 cadaveric regrafts transplanted between 1985 and 1995 using only a negative anti-human globulin (AHG) T-cell IgG crossmatch. The second group was primary cadaveric transplants done concurrently with the flow group (1990 to 1997) using only the AHG T-cell IgG crossmatch. RESULTS: The long-term (7 year) graft survival rate of flow crossmatch-selected regraft recipients (68%; n= 106) was significantly improved over that of regraft recipients who were selected for transplantation by only the AHG crossmatch technique (45%; n=174; log-rank=0.001; censored for patients dying with a functioning graft). Graft outcome for the flow cross-matched regraft recipients was not significantly different from that of primary cadaveric patients (72%; n=889; log-rank=0.2; censored for patients dying with a functioning graft). Finally, a positive B-cell IgG flow cytometric crossmatch had no influence on long-term regraft outcome. CONCLUSIONS: The use of the flow T-cell IgG cross-match as the exclusion criterion for cadaveric renal retransplantation yields an improved long-term graft outcome over that obtained when only the AHG cross-match is used and has improved survival of regraft recipients to the level of our primary cadaveric renal transplant population.

Adult↗
PubMed1998

Proteolysis of cell adhesion molecules by serine proteases: a role in long term potentiation?

Tissue plasminogen activator (tPA), a serine protease endogenous to hippocampal neurons, is shown to recognize a highly conserved sequence in the extracellular domain of cell adhesion molecules (CAMs). When added to brain homogenates, tPA generated a CAM fragment similar in size to that produced in hippocampal slices by brief periods of NMDA receptor stimulation. The serine protease inhibitor 4-(2-Aminoethyl)-benzenesulfonyl fluoride blocked the effects of tPA with an approximately 50% suppression at 250 microM. The inhibitor at this concentration had no evident effect on synaptic responses but caused long term potentiation to decay back to baseline over a 1 h period. These results suggest that extracellular breakdown of cell adhesion molecules initiated by NMDA receptors and mediated by serine proteases contributes to the formation of stable potentiation.

Animals↗
PubMed1998

Endothelial cell VE-cadherin functions as a receptor for the beta15-42 sequence of fibrin.

The contact of fibrin with the apical surface of human umbilical vein endothelial cells (HUVEC) can induce capillary tube formation via the interaction of fibrin beta15-42 with a putative cell receptor (Chalupowicz, D. G., Chowdhury, Z. A., Bach, T. L., Barsigian, C., and Martinez, J. (1995) J. Cell Biol. 130, 207-215). To characterize this interaction, we studied the binding of the thrombin-cleaved N-terminal disulfide knot of fibrin (NDSK II), a dimeric fragment with exposed beta15-42, to HUVEC in three separate assay systems. Time-course binding of 125I-NDSK II to HUVEC monolayers or suspensions revealed that binding was specific at 50-60%, as determined by the addition of unlabeled NDSK II. Specific binding of 125I-NDSK II to HUVEC was 70% reversible by dilution or by competition, and was found to be divalent cation-independent. Binding plateaued after 10 min at a saturation of 15-20 nM. Scatchard analysis using the LIGAND computer program defined a single population of receptors with a KD of 7.7 +/- 1.6 nM and approximately 21,000 +/- 7000 binding sites/cell. N-terminal disulfide knot derivatives in which beta15-42 was absent (NDSK 325) or unexposed (NDSK, NDSK I) did not show specific binding. Specific binding of 125I-NDSK II could not be inhibited by RGDS or by antibodies to the alphavbeta3 or beta1 integrins, PECAM-1, ICAM-1, or N-cadherin. In contrast, a synthetic beta15-42/ovalbumin conjugate inhibited total 125I-NDSK II binding by 47 +/- 19% (corresponding to 95% of specific 125I-NDSK II bound) and a monoclonal antibody to vascular endothelial cadherin (VE-cadherin) inhibited binding by 35 +/- 8% (corresponding to 70% of specific 125I-NDSK II bound). Another assay was based on the capture of cadherins from HUVEC lysates by a polyclonal pan-cadherin antibody immobilized on plastic dishes. Binding of NDSK II to the captured cadherins was 89 +/- 5% specific, while specific binding of NDSK 325 and NDSK was negligible. An immortalized line of human adipose-derived microvascular endothelial cells, which express N-cadherin but not VE-cadherin, demonstrated no specific binding of NDSK II by the capture assay. These data define a novel interaction of fibrin with VE-cadherin, which is mediated by the fibrin N-terminal beta15-42 sequence, and may contribute to the mechanism through which fibrin induces angiogenesis.

Antigens, CD↗
PubMed1998

A man with vague rheumatic complaints.

A 52-year-old man presented with a four-month history of malaise, low-grade fever, decreased appetite, and a 20-pound weight loss. He complained of joint pain and swelling, proximal muscle weakness, exertional dyspnea, and a dry cough. He also noted that his fingers had turned white and then blue when chilled and red when rewarmed. He had not had pleuritic chest pain, dysphagia, dry eyes or mouth, rash, or skin photosensitivity.

Connective Tissue Diseases↗
PubMed1998

An inflamed elbow after an insect sting.

A 63-year-old man presented with fever and a painfully swollen right elbow and forearm. He had been stung by a yellow jacket two weeks earlier and had since found it increasingly difficult to bend his arm.

Animals↗
PubMed1998

Budesonide epimer R or dexamethasone selectively inhibit platelet-activating factor-induced or interleukin 1beta-induced DNA binding activity of cis-acting transcription factors and cyclooxygenase-2 gene expression in human epidermal keratinocytes.

To further understand the molecular mechanism of glucocorticoid action on gene expression, DNA-binding activities of the cis-acting transcription factors activator protein 1 (AP1), AP2, Egr1 (zif268), NF-kappaB, the signal transducers and activators of transcription proteins gamma interferon activation site (GAS), Sis-inducible element, and the TATA binding protein transcription factor II D (TFIID) were examined in human epidermal keratinocytes. The cytokine interleukin 1beta (IL-1beta) and platelet-activating factor (PAF), both potent mediators of inflammation, were used as triggers for gene expression. Budesonide epimer R (BUDeR) and dexamethasone (DEX) were studied as potential antagonists. BUDeR or DEX before IL-1beta- or PAF-mediated gene induction elicited strong inhibition of AP1-, GAS-, and in particular NF-kappaB-DNA binding (P < 0.001, ANOVA). Only small effects were noted on AP2, Egr1 (zif268), and Sis-inducible element-DNA binding (P > 0.05). No significant effect was noted on the basal transcription factor TFIID recognition of TATA-containing core promoter sequences (P > 0.68). To test the hypothesis that changing cis-acting transcription factor binding activity may be involved in inflammatory-response related gene transcription, RNA message abundance for human cyclooxygenase (COX)-1 and -2 (E.C.1.14.99.1) was assessed in parallel by using reverse transcription-PCR. Although the COX-1 gene was found to be expressed at constitutively low levels, the TATA-containing COX-2 gene, which contains AP1-like, GAS, and NF-kappaB DNA-binding sites in its immediate promoter, was found to be strongly induced by IL-1beta or PAF (P < 0.001). BUDeR and DEX both suppressed COX-2 RNA message generation; however, no correlation was associated with TFIID-DNA binding. These results suggest that on stimulation by mediators of inflammation, although the basal transcription machinery remains intact, modulation of cis-activating transcription factor AP1, GAS, and NF-kappaB-DNA binding by the glucocorticoids BUDeR and DEX play important regulatory roles in the extent of specific promoter activation and hence the expression of key genes involved in the inflammatory response.

Anti-Inflammatory Agents↗
PubMed1998

VE-Cadherin mediates endothelial cell capillary tube formation in fibrin and collagen gels.

Various cell adhesion molecules mediate the diverse functions of the vascular endothelium, such as cell adhesion, neutrophil migration, and angiogenesis. In order to identify cell adhesion molecules important for angiogenesis, we used an in vitro model (Chalupowicz, Chowdhury, Bach, Barsigian, and Martinez, J. Cell Biol. 130, 207-215, 1995) in which human umbilical vein endothelial cell monolayers are induced to form capillary-like tubes when a second gel, composed of either fibrin or collagen, is formed overlying the apical surface. In the present investigation, we observed that a monoclonal antibody directed against the first extracellular domain of human vascular endothelial cadherin (VE-cadherin, cadherin 5) inhibited the formation of capillary tubes formed between either fibrin or collagen gels. Moreover, when added to preformed capillary tubes, this antibody disrupted the capillary network. In contrast, monoclonal antibodies directed against the extracellular domain of N-cadherin, the alphavbeta3 integrin, and PECAM-1 failed to inhibit capillary tube formation. During capillary tube formation, Western blot and RT-PCR analysis revealed no marked change in VE-cadherin expression. Immunocytochemical studies demonstrated that VE-cadherin was concentrated at intercellular junctions in multicellular capillary tubes. Thus, VE-cadherin plays a specific role in fibrin-induced or collagen-induced capillary tube formation and is localized at areas of intercellular contact where it functions to maintain the tubular architecture. Moreover, its function at tubular intercellular junctions is distinct from that at intercellular junctions present in confluent monolayers, since only the former was inhibited by monoclonal antibodies.

Animals↗
PubMed1998

Synthesis and biological activity of glutamic acid derivatives.

In order to develop new specific glutamate analogues at metabotropic glutamate receptors, Diels-Alder, 1-4 ionic and radical reactions were performed starting from (2S)-4-methyleneglutamic acid. Preliminary pharmacological evaluation by measuring IP accumulation using rat forebrain synaptoneurosomes has shown that (2S)-4-(2-phthalimidoethyl)glutamic acid (3a), (2S)-4-(4-phthalimidobutyl)glutamic acid (3b) and 1-[(S)-2-amino-2-carboxyethyl]-3,4-dimethylcyclohex-3-ene-1-carbox ylic acid (8) presented moderate antagonist activities.

Animals↗
PubMed1998

Immunohistochemical demonstration of tissue transglutaminase in amyloid plaques.

The brain of Alzheimer's disease patients contains deposits of the 39-42-amino acid (approximately 4 kDa) amyloid beta-peptide, which is derived from the beta-amyloid precursor protein. These pathological deposits have been shown to consist in part of insoluble 8- and 16-kDa aggregates of the amyloid beta-peptide. This report confirms that the amyloid beta-peptide is a substrate for tissue transglutaminase (TGase) and demonstrates that human brain preparations from Alzheimer's disease patients and control patients form cross-linked dimers from added iodinated amyloid beta-peptide. Immunohistochemical staining for TGase revealed its presence in tissue sections and isolated amyloid plaque cores obtained from brains of patients diagnosed as having Alzheimer's disease. These results provide evidence that the previously described insoluble amyloid deposits in Alzheimer's disease may involve TGase-mediated cross-linked amyloid beta-peptide polymers, and suggest a potential role for TGase in the pathogenesis of this disease.

Aged↗
PubMed1998

Differential expression of systemic cytokine profiles in Chagas' disease is associated with endemicity of Trypanosoma cruzi infections.

Chagas' disease is a serious public health problem in Paraguay, however, the immunoepidemiology of the disease has not been well documented. A preliminary cross-sectional survey was carried out in two villages of the Paraguayan Chaco region and in five villages of the Oriental region to assess the endemicity of Trypanosoma cruzi infections. Thereafter, a subset of individuals (ages ranging from 23 to 65 years) participated in a follow-up study to evaluate clinical and parasitological parameters. Physical examinations and electrocardiograms (ECG) were conducted and blood samples collected for parasite detection and serology. The most frequent ECG abnormalities which were observed among chagasic individuals were left anterior hemifascicular block and right bundle branch block. Thirty-two of these subjects, seropositive and non-parasitemic from the high endemic Chaco (n = 16) and low endemic Oriental (n = 16) regions, were randomly selected for an analysis of T. cruzi-induced expression of cytokines IL-2, IFN-gamma, IL-4 and IL-10 by RT-PCR. The individuals were grouped (n = 8) according to the presence or absence of abnormal ECG. In subjects that exhibited abnormal ECG profiles, five of eight (63%) individuals from the high endemic area showed a dominant type 2 (IL-4) response, whereas a comparable number (63%) of subjects from the low endemic area expressed a strong type 1 (IFN-gamma) response; the remainder (37%) presented a Th0-type (IFN-gamma, IL-4) response. Subjects with normal ECG showed a defined cytokine profile according to endemicity. All subjects from the high endemic region showed a Th0 response, whereas 100% of the individuals from the low endemic area demonstrated a type 1 response. In most chagasic patients regardless of ECG profile and endemicity, IL-2 expression was depressed, while IL-10 mRNA transcripts were consistently elevated. Taken together, these data indicate that chronic human chagasic disease is associated with increased systemic production of type 2 cytokines in response to T. cruzi infection and may be involved in the reciprocal down-regulation of IL-2 production.

Adult↗
PubMed1998

Platelet kinetics in autosomal dominant macrothrombocytopenia.

A family with autosomal dominant macrothrombocytopenia is described. Despite severe thrombocytopenia, only a moderate hemorrhagic tendency was observed. Kinetic studies revealed a normal platelet survival, normal megakaryocytic numbers, and normal bone marrow responsiveness. The rate of platelet production was set low, despite moderately impaired hemostasis and thrombocytopenia; it apparently was set to maintain another platelet parameter at an optimal level. Measurements of total circulating platelet mass and platelet surface suggested that the platelet production was set to maintain the platelet surface rather than the platelet mass at a normal value.

Adult↗
PubMed1998

Comparative study of in vitro and in vivo activities of bombesin pseudopeptide analogs modified on the C-terminal dipeptide fragment.

Analogs of bombesin in which the peptide bond between the two last amino acid residues were replaced by a pseudopeptide bond mimicking the transition state analog were evaluated. These compounds were able to recognize the bombesin receptor on isolated rat pancreatic acini with high potency (Ki from 0.60 +/- 0.27 nM to 4.3 +/- 2.3 nM). Although they were devoid of agonist activity, they were able to antagonize bombesin-induced amylase secretion in this model, with potencies in accordance with their affinities (IC50 from 1.6 +/- 0.3 nM to 10.0 +/- 1.7 nM). When tested in vivo in the anesthetized rat, these bombesin receptor antagonists exhibited high potency in inhibiting bombesin-induced pancreatic secretion (H-DPhe-Gln-Trp-Ala-Val-Gly-His-NH-CH[CH2-CH(CH3)2]-CHOH-(CH 2)3-CH3, JMV845, was among the most potent compounds with ED50 of 7.82 +/- 2.89 nM in inhibiting bombesin-induced protein secretion). The results of this study showed that replacing the peptide bond between the two last amino acid residues in bombesin by mimicking the transition state analog resulted in in vitro and in vivo potent bombesin receptor antagonists.

Amylases↗
PubMed1998

Symptomatic venous hypertension because of occult iliofemoral deep vein thrombosis: a report of two cases.

Two 25-year-old males with symptomatic venous hypertension (venous claudication, n = 1; swollen leg, n = 1) were evaluated for iliofemoral venous occlusive disease. One patient had a common femoral vein/external iliac vein occlusion with no history of deep vein thrombosis or trauma. The second patient had an acute deep vein thrombosis superimposed on a chronic external iliac vein stenosis. No source of extrinsic venous compression was identified in either patient. Venous reconstruction with vein bypass (patient no. 1) and vein patch angioplasty (patient no. 2) led to resolution of their hypertensive symptoms. Intraoperative examination of the involved vein segments revealed chronic changes consistent with a prior occult deep vein thrombosis in both patients. Occult iliofemoral deep vein thrombosis in young healthy males is rarely seen. The acute deep vein thrombosis may manifest minimal or no symptoms but it can lead to chronic venous occlusive disease and serious post-phlebitic morbidity. In this context, these two cases are discussed with a review of the pertinent literature.

Adult↗
PubMed1998

Oxyntomodulin reduces hydromineral transport through rat small intestine.

Glicentin (GLIC) and oxyntomodulin (OXM) are released from the ileum and colon during digestion. Both hormones reduce fluid and proton secretion in the stomach. The luminal concentration of sodium and chloride underlying the nutrient absorption, the effect of OXM on electrolyte transport through the small intestine, was assessed in vivo using ligated loops and in vitro using Ussing chambers. In vivo, a zero transport state, estimated by the net water, chloride, and sodium fluxes, was observed when an 80 mM NaCl normoosmolar solution (274 mosm) was administered intraluminally. Active secretion was observed with hyperosmotic challenge (474 mosm). The amplitude of this active secretion increased 2.5- to 3-fold when an electrogenic challenge (NaCl 40 mM) was substituted to the hyperosmotic one. OXM (800 fmol/ml plasma) did not modify the basal transport in the duodenum or in the jejunum (t = 45 min). When active secretion was induced by the hyperosmotic challenge, OXM (200 fmol/ml plasma) had no effect on duodenal or jejunal transport (t = 50 min). When active secretion was induced by an electrogenic challenge, OXM (300 fmol/ml plasma) preferentially reduced the hydromineral transport in jejunum. In vitro, OXM also induced a reduction in the ion transport towards the jejunal lumen (EC50 = 20 pM), the amplitude of which depended upon the integrity of the tetrodotoxin-sensitive neurons. In conclusion, OXM was able to reduce the large secretion induced in rat jejunum in vivo by an electrogenic gradient. In vitro, the antisecretory effect of OXM was partly mediated by the neurons present in the intrajejunal wall.

Animals↗