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Biomedical subjects

J Perez

Publications and source records attributed to J Perez.

At least 163 records · Page 9Linked to original sources
PubMed1992

Roles of manganese and organic acid chelators in regulating lignin degradation and biosynthesis of peroxidases by Phanerochaete chrysosporium.

We studied the effect of manganese and various organic chelators on the distribution, depolymerization, and mineralization of synthetic 14C-labeled lignins (DHP) in cultures of Phanerochaete chrysosporium. In the presence of high levels of manganese [Mn(II) or Mn(III)], along with a suitable chelator, lignin peroxidase (LiP) production was repressed and manganese peroxidase (MnP) production was stimulated. Even though partial lignin depolymerization was observed under these conditions, further depolymerization of the polymer to smaller compounds was more efficient when low levels of manganese were present. LiPs were prevalent under these latter conditions, but MnPs were also present. Mineralization was more efficient with low manganese. These studies indicate that MnP performs the initial steps of DHP depolymerization but that LiP is necessary for further degradation of the polymer to lower-molecular-weight products and mineralization. We also conclude that a soluble Mn(II)-Mn(III) organic acid complex is necessary to repress LiP.

Basidiomycota↗
PubMed1992

Development and validation of prognostic models in metastatic breast cancer: a GOCS study.

The significance of several prognostic factors and the magnitude of their influence on response rate and survival were assessed by means of uni- and multivariate analyses in 362 patients with stage IV (UICC) breast carcinoma receiving combination chemotherapy as first systemic treatment over an 8-year period. Univariate analyses identified performance status and prior adjuvant radiotherapy as predictors of objective regression (OR), whereas the performance status, prior chemotherapy and radiotherapy (adjuvants), white blood cells count, SGOT and SGPT levels, and metastatic pattern were significantly correlated to survival. In multivariate analyses favorable characteristics associated to OR were prior adjuvant radiotherapy, no prior chemotherapy and postmenopausal status. Regarding survival, the performance status and visceral involvement were selected by the Cox model. The predictive accuracy of the logistic and the proportional hazards models was retrospectively tested in the training sample, and prospectively in a new population of 126 patients also receiving combined chemotherapy as first treatment for metastatic breast cancer. A certain overfitting to data in the training sample was observed with the regression model for response. However, the discriminative ability of the Cox model for survival was clearly confirmed.

Analysis of Variance↗
PubMed1992

Transcranial color-coded real-time sonography in the evaluation of intracranial neoplasms and arteriovenous malformations.

Transcranial color-coded real-time sonography (TCCS) was performed in 57 patients with primary intracranial brain tumors (n = 49) or arteriovenous malformations (n = 8) to evaluate its diagnostic potential. In 46 patients (81%), lesions could be identified employing this technique. In 7 patients, transcranial ultrasound examination was not feasible because of bone thickness; in the remaining 4 patients, the tumor was indistinguishable from adjacent brain tissue despite sufficient insonation, suggesting that these neoplasms are isoechogenic. The sonographic features of brain tumors were very similar: a hyperechogenic matrix of the lesion was interspersed by hypoechogenic pixels. Larger hypoechogenic areas (0.5-1 cm) gave evidence of tumor necrosis. Differences between the findings of TCCS and computed tomography concerning tumor size were found in 7 patients, in whom TCCS revealed an area of smaller extension within the corresponding hypodense area on the computed tomographic scan. Perifocal brain edema could not be detected by ultrasound examination. In 13 patients, a thin, hypoechogenic peritumoral halo was disclosed that did not correlate with perifocal brain edema identified by computed tomography and that may have been due to compression of adjacent parenchyma. In patients with arteriovenous malformations, TCCS permitted the identification of the main feeders, the nidus, and the draining venous system by color-coded depiction of intravascular blood flow. In conclusion, TCCS is an additional method for initial diagnosis and highly suitable for follow-up in tumor patients and provides valuable information about tissue characteristics and blood flow.

Adult↗
PubMed1992

Detection of African swine fever viral antigens in paraffin-embedded tissues by use of immunohistologic methods and polyclonal antibodies.

Tissues obtained from pigs inoculated with African swine fever virus (ASFV), fixed by vascular perfusion using glutaraldehyde, and embedded in paraffin or araldite were used for an immunohistologic electron microscopic study. To detect ASFV antigens, 4 methods were used on paraffin sections with or without pretreatment of the tissues. Use of biotinylated anti-ASFV antiserum combined with avidin-biotin complex and peroxidase proved to be the most suitable method, and antigen was detected in tissues infected with 2 ASF viruses of different virulence. Use of the glutaraldehyde fixation method should ensure optimal morphologic (structural and ultrastructural) data while allowing an immunohistologic study, and add to knowledge of the pathogenesis of ASF.

African Swine Fever↗
PubMed1991

Estradiol increases the number of nuclear pores in the arcuate neurons of the rat hypothalamus.

Freeze-fracture replicas of hypothalamic arcuate neurons and of Purkinje and granule cells of the cerebellar cortex from adult female rats were assessed in order to test the possible influence of estradiol on nuclear pores. Rats were ovariectomized and injected either with estradiol or with vehicle. An additional group of rats in proestrus was also studied. Pore diameter was not affected by ovariectomy or estrogen treatment. In arcuate neurons, the number of nuclear pores per nuclear membrane area, the total number of pores per nucleus, and the percentage of nuclear pores arranged in clusters were decreased by ovariectomy and increased within 30 minutes after estradiol administration to ovariectomized rats. The effect of estradiol on nuclear pores was sustained for several days; the number of pores and the percentage of pores in clusters reverted to control values by 1 month after the hormonal treatment. None of the above mentioned changes was observed in Purkinje and granule cells of the cerebellar cortex. These results indicate that estradiol may modulate the number and distribution of nuclear pores in arcuate neurons and suggest that the modification of the ultrastructure of the nuclear envelope may be one of the first effects of gonadal steroids on target cells.

Animals↗
PubMed1991

Altered growth hormone response after growth hormone releasing hormone administration in chronic renal failure.

Eleven chronic renal failure patients and 11 matched controls, received growth hormone GHRH (1 microgram/kg iv) or TRH (400 microgram iv) on separate occasions, immediately before undergoing hemodialysis. GHRH-induced GH peak in uremics (22.7 +/- 5.2 micrograms/l) was not different from that obtained in control subjects (16.0 +/- 4.3 micrograms/l). However, the uremic patients did not show the habitual post-peak fall, remaining GH levels over 10 micrograms/l till the end of the test. Differences between the two groups were significant (p less than 0.05). Uremic patients showed PRL values higher than in controls, however their TRH-induced PRL peak (20.6 +/- 6.6 micrograms/l) was not different from that of controls (26.5 +/- 3.0 micrograms/l). Again chronic renal failure patients showed PRL plasma values abnormally elevated till the end of the test. Differences between the two groups were significant (p less than 0.05). Administration of placebo to a different group of seven uremic patients did not alter GH and PRL plasma levels. This sustained secretion of both GH and PRL in uremia could be attributed to reduced kidney clearance. However, when subjects were examined individually both the GHRH- and the TRH-induced hormonal peaks and the subsequent fall were not different in both groups. Unlike with controls, in uremic patients GHRH-stimulated GH and TRH-stimulated PRL/GH peaks were dispersed throughout the 120 min period. In controls GH and PRL peaks clustered around 15-30 min. The peak dispersion created a false impression of flattened curves or sustained hypersecretion in uremia.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

Loss of sexual dimorphism in rat arcuate nucleus neuronal membranes with reproductive aging.

Arcuate neurons of the rat hypothalamus have a sexual dimorphic membrane phenotype: quantitative analysis of freeze-fracture replicas has revealed that a population of intramembrane protein particles (IMP) of small size (less than 10 nm) is enriched in the plasma membrane of perikarya and dendritic shafts of cycling females compared to males, whereas a population of large IMPs (greater than 10 nm) is enriched in the membrane of dendritic shafts of males. This different membrane organization is associated with a sex dimorphic synaptic connectivity. To determine whether sex differences in neuronal membrane are affected by reproductive senescence, IMPs were assessed in freeze-fracture replicas of arcuate neuronal plasma membranes of male and female Sprague-Dawley rats aged 3, 15, and 18 months. Three-month-old cycling females were studied on the morning of estrus. Senescent females were in constant estrus (15 months old) or in constant diestrus (18 months old). Young females had more IMPs with diameters under 10 nm in the inner and outer leaflets of the plasma membrane of the perikarya and dendritic shafts compared to males of the same age. In addition, young males showed an increased number of large (greater than 10 nm) IMPs in the outer membrane leaflet of dendritic shafts. No sex differences were detected in the membrane of dendritic spines. In senescent females the number of small IMPs was decreased in the perikarya and dendritic shafts compared to young females while the number of large particles was increased in the outer leaflet of the membrane of dendritic shafts, reaching values similar to those observed in males. IMP counts were not modified with aging in males and in dendritic spines of females. These results indicate that reproductive aging in female rats is associated with a remodeling of neuronal plasma membranes in arcuate neurons.

Aging↗
PubMed1991

Desferrioxamine regulates tumor necrosis factor release in mesangial cells.

Cultured rat mesangial cells have been demonstrated to express tumor necrosis factor alpha (TNF alpha) mRNA and to release TNF activity into the medium upon stimulation by bacterial lipopolysaccharide (LPS). The present study was undertaken to determine whether TNF was only secreted by mesangial cells or was also present as a cell-associated molecule. LPS-activated mesangial cells which had been fixed in paraformaldehyde lysed the TNF-sensitive L-929 fibroblasts, as assessed by 51Cr release. This cytotoxic activity was inhibited by anti-TNF alpha antiserum. Cell-associated TNF expression was demonstrable after less than one hour of exposure to LPS, peaked at two hours and decreased progressively thereafter, while TNF activity increased in the medium. Mesangial cell-associated TNF was localized at the cell surface, as shown by immunohistochemical demonstration and by the ability of plasma membranes purified from LPS-activated mesangial cells to lyse L-929 fibroblasts. Flow cytometry experiments revealed that two-thirds of LPS-activated mesangial cells were stained by anti-TNF alpha antiserum. The major part of these cell-associated TNF molecules persisted after low pH treatment, indicating that they were integral membrane proteins. As assessed by immunoprecipitation analysis, these proteins were 26 kDa molecules, whereas the released forms of TNF were 17 kDa molecules. Pretreatment of mesangial cells with desferrioxamine (DFX), an iron chelator preventing the synthesis of hydroxyl radicals (OH.), delayed the release of TNF from the membranes into the medium, and enhanced its cell surface expression. It also subsequently accelerated its decay in the medium.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

cAMP binding proteins in the rat cerebral cortex after administration of selective 5-HT and NE reuptake blockers with antidepressant activity.

This study was undertaken to evaluate the cyclic adenosine monophosphate (cAMP) binding proteins in the cerebral cortex of rat after short- and long-term administration with antidepressants. Prolonged treatment with different antidepressants that inhibit serotonin or norepinephrine uptake such as fluoxetine and the (+) enantiomer of oxaprotiline, respectively, was able to induce an increase in the photoactivated incorporation of 8-N3-[32P]cAMP into a protein band with apparent molecular weight of 52,000 in both soluble and crude microtubule fraction. On the contrary, chronic treatment with the (-) enantiomer of oxaprotiline, which does not affect monoamine uptake, failed to produce this effect. Moreover, no changes were observed after acute or in vitro addition of antidepressants, suggesting that modification in the cAMP binding may be related to adaptive changes elicited by prolonged antidepressants treatment. In conclusion, our studies indicate that the cAMP binding protein associated with the crude microtubule fraction could be an intracellular target for the action of antidepressant drugs.

Affinity Labels↗
PubMed1990

Reduction in tumor necrosis factor binding and cytotoxicity by hydrogen peroxide.

The regulatory effect of H2O2 on both the cytotoxic activity and the specific binding of TNF-alpha was studied by using TNF-alpha-sensitized murine L929 cells. When these cells were exposed simultaneously to TNF-alpha and H2O2 (100 to 500 microM), the cytotoxic activity of TNF-alpha was inhibited by up to 66.6%. This inhibition was also effective when the cells were pretreated by H2O2, but not when TNF-alpha alone was preexposed to H2O2. These data suggest that H2O2 altered the cell sensitivity to TNF-alpha, without modifying the activity of the TNF-alpha molecule. Maximum loss of cell sensitivity to TNF-alpha occurred after 30-min preexposure to 500 microM H2O2. Complete restoration of TNF-alpha sensitivity was obtained within 12 h after H2O2 removal. It required protein synthesis as demonstrated by the suppressive effect of actinomycin D. The inhibitory effect of H2O2 was suppressed by catalase, but was unaffected by the scavengers of hydroxyl radical and hypochlorous acid, suggesting that H2O2 but not one of its metabolites was responsible for this inhibition. H2O2 inhibitory effect did not implicate any change in prostaglandin production or in PKC activity. In contrast, H2O2 effect was associated with an about 50% loss of the density of cell membrane 125I-TNF-alpha receptors (2949 vs 5620 binding sites per cell), without change in their affinity (3.9 vs 3.4 nM). Moreover H2O2 did not affect the rate of degradation of TNF-alpha, and only slightly increased the degree of internalization of 125I-TNF-alpha receptors. These findings indicate that H2O2 can down-regulate the cellular response to TNF-alpha, possibly by reducing the TNF-alpha-binding capacity.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1990

Gap junctions in the hypothalamic arcuate neurons of ovariectomized and estradiol-treated rats.

Freeze-fracture methodology was used to study the organization of the neuronal plasma membrane in the rat arcuate nucleus, an estrogen sensitive area of the hypothalamus. Freeze-fracture replicas were prepared from 6 adult ovariectomized rats injected with a single dose of 17 beta-estradiol and from 6 ovariectomized littermates injected with vehicle. Rats were sacrificed 2 days after the injection. Occasional gap junctions were observed in freeze-fractured neuronal membranes from both groups of animals and their incidence was increased (P less than 0.01) in estradiol treated rats. This study demonstrates gap junctions in arcuate neurons and suggests that these structures may be affected by gonadal hormones.

Animals↗
PubMed1990

African green monkeys have sexually dimorphic and estrogen-sensitive hypothalamic neuronal membranes.

Previous studies have shown sex differences in intramembrane particle content in the arcuate neurons of the rat hypothalamus. In this study, freeze-fracture replicas were prepared from the infundibular hypothalamus of adult African green monkeys (Cercopithecus aethiops) in order to determine whether primates also have sexual dimorphism in neuronal membranes. Intramembrane particles (IMP) were quantitatively assessed in the perikaryal plasma membranes of infundibular neurons. Four groups of monkeys were studied: intact males, intact females, ovariectomized females injected with 20 mg of estradiol valerate over 10 days and ovariectomized females injected with vehicle (castor oil). Membranes from females showed an increased numerical density of IMPs when compared to males. Ovariectomy of females did not affect IMP content, while estrogen administration resulted in a significant decrease in IMP numerical density to reach male values. These findings indicate a sex difference in neuronal membranes in the hypothalamus of monkeys and suggest that as in rodents, neuronal plasma membrane organization in higher primates may be modulated by gonadal steroids.

Animals↗
PubMed1990

In vitro production of tumour necrosis factor and prostaglandin E2 by peripheral blood mononuclear cells from tuberculosis patients.

We investigated the production of tumour necrosis factor-alpha (TNF-alpha) and prostaglandin E2 (PGE2) by peripheral blood mononuclear cells (PBMC) from tuberculosis patients and healthy controls. PBMC from tuberculosis patients generated constitutively more TNF-alpha than did control PBMC. This production was significantly higher for patients with high-grade fever and cachexia. The increase of TNF-alpha production by PBMC from tuberculosis patients was associated with a comparatively weaker elevation of PGE2 synthesis which did not parallel fever or weight loss. In vitro treatment of control PBMC with the tuberculin purified protein derivative (PPD) promoted an increased TNF-alpha production which was similar to that of untreated PBMC from tuberculosis patients. Thus, the increased TNF-alpha production in tuberculosis could be explained by the in vivo exposure of PBMC to mycobacterial antigens. In contrast, the concentration of PGE2 was weaker in the medium of untreated PBMC from tuberculosis patients than in the medium of PPD-treated control PBMC, suggesting that PGE2 synthesis by PBMC was limited in tuberculosis by unidentified factors.

Adult↗
PubMed1990

Mineralization of C-Ring-Labeled Synthetic Lignin Correlates with the Production of Lignin Peroxidase, not of Manganese Peroxidase or Laccase.

Recently, Mn(II) has been shown to induce manganese peroxidases (MnPs) and repress lignin peroxidases (LiPs) in defined liquid cultures of several white rot organisms. The present work shows that laccase is also regulated by Mn(II). We therefore used Mn(II) to regulate production of LiP, MnP, and laccase activities while determining the effects of Mn(II) on mineralization of ring-labeled synthetic lignin. At a low Mn(II) level, Phanerochaete chrysosporium and Phlebia brevispora produced relatively high titers of LiPs but only low titers of MnPs. At a high Mn(II) level, MnP titers increased 12- to 20-fold, but LiPs were not detected in crude broths. P. brevispora formed much less LiP than P. chrysosporium, but it also produced laccase activity that increased more than sevenfold at the high Mn(II) level. The rates of synthetic lignin mineralization by these organisms were similar and were almost seven times higher at low than at high Mn(II). Increased synthetic lignin mineralization therefore correlated with increased LiP, not with increased MnP or laccase activities.

Journal Article↗
PubMed1990

Hepatic alcohol dehydrogenase activity in alcoholic subjects with and without liver disease.

Alcohol dehydrogenase activity was measured in samples of liver tissue from a group of alcoholic and non-alcoholic subjects to determine whether decreased liver alcohol dehydrogenase activity is a consequence of ethanol consumption or liver damage. The alcoholic patients were classified further into the following groups: control subjects with no liver disease (group 1), subjects with non-cirrhotic liver disease (group 2), and subjects with cirrhotic liver disease (group 3). The non-alcoholic subjects were also divided, using the same criteria, into groups 4, 5, and 6, respectively. The analysis of the results showed no significant differences when mean alcohol dehydrogenase activities of alcoholic and non-alcoholic patients with similar degrees of liver pathology were compared (groups 1 v 4, 2 v 5, and 3 v 6. Alcohol dehydrogenase activity was, however, severely reduced in patients with liver disease compared with control subjects. Our findings suggest that alcohol consumption does not modify hepatic alcohol dehydrogenase activity. The reduction in specific alcohol dehydrogenase activity in alcoholic liver disease is a consequence of liver damage.

Alcohol Dehydrogenase↗