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Biomedical subjects

J Montes

Publications and source records attributed to J Montes.

At least 55 records · Page 3Linked to original sources
PubMed1990

Ascitic fluid polymorphonuclear cell count and serum to ascites albumin gradient in the diagnosis of bacterial peritonitis.

The analysis of ascitic fluid has been complicated by several recently reported new tests. To simplify this assessment, we evaluated nine parameters prospectively and simultaneously in blood and ascitic fluid from 285 patients with ascites to determine which were the most reliable for immediate diagnosis of the etiology of the ascites and of its complications. Subjects were first divided into four groups: sterile cirrhotic ascites (n = 201), spontaneous bacterial peritonitis (n = 41), malignant ascites (n = 34), and miscellaneous ascites (n = 9). An ascitic fluid polymorphonuclear count greater than 500/microliters was the test with the greatest accuracy (96%) for the diagnosis of spontaneous bacterial peritonitis. Neither the most precise cutoff values for ascitic fluid pH (less than 7.32) and ascitic fluid lactate (greater than 32 mg/dl), nor their respective blood-ascitic fluid gradients (greater than 0.11 and less than -20 mg/dl) were more reliable indexes of spontaneous bacterial peritonitis, mainly due to the decreased ascitic fluid pH and increased ascitic fluid lactate observed in malignant ascites, tuberculous peritonitis, and pancreatic ascites. A blood-ascitic fluid albumin gradient less than 1.1 g/dl was the most accurate parameter for the diagnosis of malignant ascites (diagnostic efficacy, 93%). Therefore, the etiologic analysis of ascitic fluid might be simplified and the single practice of two tests, ascitic fluid polymorphonuclear cell count and blood-ascitic fluid albumin gradient, provides immediately useful information.

Adult↗
PubMed1982

Further evidence that ultraviolet radiation-enhanced reactivation of simian virus 40 in monkey kidney cells is not accompanied by mutagenesis.

Can simian virus 40 (SV40) be used to detect mutagenic DNA repair in cultured mammalian cells? The published evidence from different laboratories are in direct conflict. In order to decide between the conflicting evidence, we conducted experiments in two separate laboratories using experimental protocols similar to those previously used to investigate mutagenic repair with viral probes. Mutagenesis in SV40 virus stocks obtained by infecting ultraviolet (UV)-irradiated or unirradiated CV-1 monkey kidney cells with UV-irradiated or unirradiated temperature-sensitive SV40 mutant tsB201 was investigated. The frequency of reversion of the ts mutant to phenotypically wild-type virus was determined by assaying the virus stocks at permissive (33 degrees) and non-permissive (39 degrees) temperatures. These data show that (a) the reversion frequency for unirradiated virus propagated in irradiated cells was more than that in unirradiated cells; (b) irradiated virus gave more reversion than unirradiated virus in unirradiated and irradiated cells; and (c) irradiated virus had a lower reversion frequency in irradiated cells than in unirradiated cells. Reactivation experiments carried out in parallel; with the mutagenesis showed enhanced reactivation in UV-irradiated SV40 in UV-irradiated CV-1 cells. We conclude that enhanced reactivation of UV-irradiated SV40 was not mutagenic in monkey kidney cells.

Animals↗
PubMedDate not supplied

Identification of immunogenic epitopes of the 170-kDa subunit adhesin of Entamoeba histolytica in patients with invasive amebiasis.

Entamoeba histolytica causes amebic dysentery (AD) and liver abscess (ALA). Little is known about protective immunity to amebiasis, and studies in this area have been complicated by the paucity of defined ameba antigens. We examined the proliferative responses of peripheral blood mononuclear cells (PBMC) from patients with AD and ALA to a recombinant protein containing a portion of the 170 kDa adhesin of E. histolytica (170CR), and to two synthetic peptides (1 and 2) derived from the 170 kDa sequence that were predicted to contain T cell epitopes. A significant number of patients with AD and ALA had PBMC that proliferated to 170CR molecule, and several individuals with ALA and AD had T cells that recognized one or both peptides. Contrarily, individuals from a non-endemic region for amebiasis did not respond to 170CR protein, or to both peptides. In regard to antibody response, nine of fifteen patients with ALA showed antibodies to 170CR protein. These same patients had antibodies to peptide 2. We identified peptides from 170-kDa adhesin that may contain both T and B cell epitopes recognized by some patients with invasive amebiasis. These peptides may be valuable reagents in studies of the immune response to amebiasis.

Adolescent↗