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J Prieto

Publications and source records attributed to J Prieto.

At least 271 records · Page 15Linked to original sources
PubMed1992

Induction of intercellular adhesion molecule-1 (CD54) on isolated mouse pancreatic beta cells by inflammatory cytokines.

Insulin-dependent diabetes mellitus (IDDM) results from a T cell-dependent autoimmune destruction of insulin-producing pancreatic beta cells. In the present study, expression of adhesion molecule ICAM-1 (CD54) on pancreatic beta cells was studied in normal, obese hyperglycemic (ob/ob), and nonobese diabetic (NOD) mice. Freshly isolated pancreatic beta cells from ob/ob mice did not express ICAM-1, but treatment of the cells with IL-1-beta, TNF-alpha, or INF-gamma strongly induced its expression as measured by immunofluorescence flow cytometry. The cytokines acted in a dose- and time-dependent manner. Maximal induction by either cytokine occurred at 24 hr and thereafter expression decreased, except for INF-gamma. Immunoprecipitation from IL-1-beta-treated beta cells demonstrated a cell-surface glycoprotein with an apparent molecular weight of 95 kDa. ICAM-1 expression was undetectable on pancreatic beta cells of normal and ob/ob mice as measured by immunohistochemistry. In NOD mice at different ages (1 to 6 months) ICAM-1 was also undetectable on beta cells, in contrast to the strong expression on infiltrating mononuclear cells. The present study indicates that mouse pancreatic beta cells, under certain conditions, can express ICAM-1.

Animals↗
PubMed1992

Detection of hepatitis C virus antibodies with new recombinant antigens: assessment in chronic liver diseases.

A new serological assay to detect antibodies against hepatitis C, based on a recombinant protein (BHC10) which incorporates structural and non-structural viral antigens, was tested in 67 healthy subjects and 409 patients with various forms of liver disease. Results were compared with the current assay based on the recombinant non-structural viral antigen c100 and with the recently introduced second-generation assay, Ortho2. None of the healthy subjects was positive by any of the assays. In patients with chronic non-A, non-B hepatitis the prevalence of anti-BHC10 was 96.8%, higher than anti-c100 (83.3%, p less than 0.001) and similar to Ortho2 (94.3%). False-positive results were less frequently found when BHC10 was used. These findings show that assays incorporating structural and non-structural antigens provide higher sensitivity to detect hepatitis C virus infection and they define an almost exclusive role of hepatitis C virus in the genesis of chronic non-A, non-B hepatitis.

Adolescent↗
PubMed1992

Splenic embolization prior to myelosuppressive treatment in hepatocarcinoma and active chronic hepatitis.

In the treatment of active chronic hepatitis and hepatocellular carcinoma some effective drugs can produce myelosuppression. Hypersplenism may considerably limit the dosage of such drugs. Splenectomy is an effective treatment for hypersplenism, although it is not without complications. Partial splenic embolization is a good and safe procedure; 15 patients were treated in order to achieve higher platelet and leukocyte counts. Embolization has been performed with gelfoam with local and systemic antibiotics (Spigos' protocol) and 50-75% of the splenic parenchyma was infarcted. All patients could be treated for the underlying hepatopathy with adequate dosages of interferon or chemotherapeutic drugs.

Aged↗
PubMed1992

Replication of hepatitis C virus in peripheral blood mononuclear cells. Effect of alpha-interferon therapy.

Hepatitis C virus (HCV) is a positive-stranded RNA virus which replicates through a negative-stranded RNA intermediate. Using a PCR procedure to detect positive and negative strands, we investigated the existence of HCV replication in lymphoid cells. Both positive and negative strands were found in the peripheral blood mononuclear cells (PBMC) of all patients (n = 10) with untreated chronic hepatitis C. No HCV sequences were detected in PBMC in any of the 8 healthy controls. Fifteen patients with chronic hepatitis C were studied at the end of a 12-month course of alpha-interferon therapy. The positive strand was detected in PBMC in all 9 non-responder patients, and the negative strand in 7. In contrast, in PBMC from responder patients (n = 6) the positive strand was found in 4 and the negative strand in only 2 cases. These results demonstrate that HCV can infect PBMC and replicate in these cells and that interferon seems to exert an inhibitory effect on this process. Persistence of HCV-RNA in PBMC may help explain disease relapse after successful interferon therapy.

Adult↗
PubMed1992

[Computed tomography guided fine needle aspiration biopsies].

Computed tomography (CT) allows the performance of fine needle aspiration biopsies in situations in which ultrasound or conventional X rays do not correctly visualize the lesion or the needle tract. One hundred four patients with a clinical suspicion of neoplasia were subjected to CT guided percutaneous aspiration biopsies in a lapse of 6 years. The most frequently biopsied organs were the lung (39.5%), liver and gallbladder (20.2%) and pancreas (15.4%). Forty nine percent of procedures were performed in the thorax and 51% in the abdomen. Of 51 patients with suspicion of thoracic cancer, there was only one false negative and no false positive results, with an overall accuracy of 98%. For abdominal procedures, there were no false positive results, although there were 6 false negative results, specially for pancreatic or retroperitoneal lesions. Overall accuracy for abdominal procedures was 88%. It is concluded that CT guided fine needle biopsy is a safe and accurate method for the diagnosis of thoracic and abdominal lesions.

Abdominal Neoplasms↗
PubMed1991

Dictyostelium discoideum acidic ribosomal phosphoproteins: identification and in vitro phosphorylation.

Four acidic phosphoproteins from the ribosomes of the slime mold Dictyostelium discoideum have been identified and partially characterized. These proteins are selectively released from ribosomal particles by salt/ethanol washes, have low molecular weight and acidic pI, and tend to aggregate in solution to form homodimers. These features correspond to proteins of different origins that have been included in the conserved family of eukaryotic A-ribosomal proteins, and, therefore, we have named them Dictyostelium ribosomal proteins A1, A2, A3 and A4. We also demonstrate that Dictyostelium ribosomal A-proteins are specifically phosphorylated in vitro by a type II casein kinase previously identified in Dictyostelium. Isoelectric focusing separation has permitted us to identify four proteins (or P-proteins) that may consist of the phosphorylated forms of A-proteins. A-proteins from Dictyostelium and yeast do not present immunological cross-reactivity. Dictyostelium A-proteins contain, therefore, some specific features in their amino acid sequence that distinguish them from other members of the conserved eukaryotic A-protein family; this conclusion is coherent with data deduced from the nucleotide sequence of cDNA clones encoding two Dictyostelium A-proteins (P1 and P2) which we have recently reported.

Animals↗
PubMed1991

Transforming growth factors beta 1 and alpha in chronic liver disease. Effects of interferon alfa therapy.

BACKGROUND: Cirrhosis is a diffuse process of hepatic fibrosis and regenerative nodule formation of unknown pathogenesis. Transforming growth factor (TGF) beta 1 induces the production of extracellular matrix proteins by liver cells and has been implicated in the pathogenesis of hepatic fibrosis in laboratory animals. TGF alpha is a hepatocyte mitogen that participates in liver regeneration. METHODS: Using Northern blot analysis, we studied the expression of TGF beta 1 messenger RNA (mRNA) in liver specimens from 42 patients with chronic hepatitis and cirrhosis and 12 subjects with either normal or fatty livers. The results were correlated with measurements of procollagen Type I mRNA in liver tissue, procollagen Type III peptide in serum, and the degree of histologic injury. We also investigated whether TGF alpha mRNA would be detectable in biopsy specimens of livers with proliferative activity. RESULTS: TGF beta 1 mRNA expression correlated closely with the expression of procollagen Type I mRNA (r = 0.94) and serum procollagen Type III peptide (r = 0.89) and with the histologic activity index (r = 0.73). All patients with increased fibrogenic activity (serum procollagen Type III peptide level, greater than 11.9 micrograms per liter) had increased levels of TGF beta 1 mRNA (2 to 14 times the levels in the control group or in patients with normal fibrogenic activity), and both TGF alpha and H3 histone (a marker of DNA synthesis) mRNAs were detectable in patients with regenerative nodules. Six of eight patients with hepatitis C treated with interferon alfa for one year had sustained clinical responses with normalization of serum procollagen Type III peptide and aminotransferase activity. All these patients had normal levels of TGF beta 1 mRNA in liver specimens obtained at the end of the year. CONCLUSIONS: TGF beta 1 may have an important role in the pathogenesis of fibrosis in patients with chronic liver disease, and TGF alpha expression may be associated with liver regeneration in these patients.

Adult↗
PubMed1991

Induction of antibodies against a peptide hapten does not require covalent linkage between the hapten and a class II presentable T helper peptide.

Following immunization with a complex antigen, a B cell internalizes this antigen through an interaction between its surface immunoglobulins and an epitope of the antigen. Enzymatic processing of the antigen frees one or more short peptide determinants (TD) which bind to class II molecules of the B cell. If the complex TD-MHC II is recognized by the receptor of a T helper cell, T cell help is provided leading to the expansion of an antibody-producing B cell clone specific for the epitope. We present experimental evidence proving that the induction of anti-peptide hapten antibodies does not require covalent linkage between the peptide hapten and the peptide behaving as TD. Indeed, high anti-peptide hapten antibody titers are induced if an emulsion of TD and hapten are injected in the same immunization site. This result suggests a way to manipulate antibody production with useful applications to research and therapy.

Animals↗
PubMed1991

The expression of human intercellular adhesion molecule-2 is refractory to inflammatory cytokines.

The beta 2-integrin CD11a/CD18 binds to the intercellular adhesion molecules (ICAM)-1 (CD54) and ICAM-2. ICAM-1 has a wide distribution, and its expression is up-regulated by various cytokines. In contrast, ICAM-2 has a more restricted distribution, and is mainly expressed on endothelial cells. In the present study we show that it is not induced by inflammatory cytokines or other treatments on any of several cells studied. Moreover, antibodies to the intercellular adhesion ligands were not able to block all CD11a/CD18-dependent adhesion, indicating the presence of additional CD11a/CD18 ligands.

Antigens, CD↗
PubMed1991

Abnormal sympathetic and renal response to sodium restriction in compensated cirrhosis.

It has been proposed that in liver cirrhosis portal hypertension causes splanchnic vasodilation and this induces blood volume expansion to maintain blood pressure. The current study was designed to explore the homeostatic response to sodium restriction, a maneuver aiming to contract blood volume, in compensated cirrhosis. Mean blood pressure, sympathetic nervous activity, and proximal sodium reabsorption were evaluated in 16 healthy control and 21 nonazotemic cirrhotic patients (11 without ascites and 10 with ascites) under two experimental conditions: after 4 days on a free sodium diet (basal condition) and after 4 days on a restricted sodium diet (40 mmol/day). No differences were observed in basal conditions in the above parameters between control and cirrhotic patients without ascites. However, cirrhotic patients with ascites showed lower basal values of mean blood pressure and higher basal levels of both plasma norepinephrine and fractional proximal sodium reabsorption than controls. Neither control nor cirrhotic patients with ascites showed significant changes in the measured parameters after sodium restriction. In contrast, in nonascitic patients, this maneuver induced an elevation in plasma norepinephrine concentration (164.4 +/- 24.6 vs. 270.1 +/- 24.9 pg/mL; mean +/- SEM; P less than 0.005) and in fractional proximal sodium reabsorption (86.4 +/- 2.1 vs. 91.8% +/- 0.5%; P less than 0.01). In addition, the nonascitic cirrhotic patients became hypotensive compared with controls (80.9 +/- 1.6 vs. 88.5 +/- 4.8 mm Hg; P less than 0.05) when subjected to the low-sodium diet. In patients without ascites, under conditions of sodium restriction, the decrease in mean arterial pressure correlated inversely with the increase in plasma norepinephrine concentration (r = -0.713; P less than 0.05), whereas the levels of plasma norepinephrine correlated directly with fractional proximal sodium reabsorption (r = 0.893; P less than 0.01). These findings suggest that ineffective circulatory volume is detected in nonascitic cirrhotic patients only under conditions of sodium restriction, but it is always present in cirrhotic patients with ascites, irrespectively of the amount of sodium in the diet. These results are compatible with the existence of fixed arterial vasodilation in cirrhosis.

Adult↗
PubMed1991

Inhibitors of the lipoxygenase arachidonic acid pathway impair glycocholate efflux in isolated rat hepatocytes.

Lipoxygenase arachidonic acid metabolites mediate secretory processes in several tissues, but their possible involvement in liver transport functions is still unknown. This study evaluated the influence of the lipoxygenase inhibitor nordihydroguayaretic acid (NDGA), the cyclooxygenase inhibitor indomethacin (INDO), and the dual cyclo and lipoxygenase inhibitors 3-amino-1-[m-(trifluoromethyl)-phenyl]-2-pyrazoline (BW 755c) and eicosatetraynoic acid (ETYA) on the handling of glycocholic acid (GC) by isolated rat hepatocytes. No drug modified cell viability or oxygen consumption in hepatocytes. In 30-min incubations with 50 microM GC the initial rate of GC uptake (V0) in control hepatocytes was 1.15 +/- 0.09 nmol.mg protein-1.min-1. The cellular GC content remained constant from 10 to 30 min (steady-state phase), the 30-min value being 6.63 +/- 0.35 nmol.mg protein-1. NDGA (10-50 microM), BW 755c (25-200 microM) and ETYA (5-100 microM), prevented the steady-state phase occurring, thus determining a progressive accumulation of GC in cells with time. As compared to controls, 50 microM NDGA (+37%, p less than 0.01), 200 microM BW 755c (+39%, p less than 0.01) and 5 microM ETYA (+19%, p less than 0.05) induced the highest increases in the amount of GC in cells at 30 min, in all cases V0 being unchanged. Concentrations of BW 755c and ETYA above those indicated also decreased V0. Both V0 and the amount of cellular GC in the steady-state phase were proportionally decreased by high INDO concentrations (25-100 microM) which did not modify the morphology of the uptake curve. Since experiments with dual and lipoxygenase inhibitors suggested an impairment of GC efflux, the initial rate of GC efflux (V0ef) was measured in hepatocytes preloaded with 50 microM GC and transferred to a GC-free medium. In controls, V0ef was 1.12 +/- 0.12 nmol.mg protein-1.min-1. BW 755c (200 microM) and NDGA (50 microM) reduced V0ef by 45 and 38%, respectively. The kinetic analysis of the effect of 200 microM BW 755c on the efflux process using hepatocytes preloaded with GC from 5 to 200 microM disclosed a non-competitive inhibition. Vmax was reduced from 1.37 +/- 0.15 to 0.89 +/- 0.10 (p less than 0.01), whereas Km was unchanged (3.79 +/- 0.33 vs. 4.25 +/- 0.54, N.S.). In summary, inhibitors of the lipoxygenase arachidonic acid pathway impaired the efflux of GC from isolated rat hepatocytes. The hypothesis is raised that oxidized metabolites of arachidonic acid may participate on the secretion of bile salts in these cells.

4,5-Dihydro-1-(3-(trifluoromethyl)phenyl)-1H-pyraz↗
PubMed1991

Renal prostacyclin influences renal function in non-azotemic cirrhotic patients treated with furosemide.

The influence of prostaglandins on renal function changes induced by furosemide was analyzed in 21 non-azotemic cirrhotic patients with ascites. Patients were studied in two periods of 120 min immediately before and after furosemide infusion (20 mg, ev). Furosemide caused an increase in creatinine clearance in 15 patients (group A: 99 +/- 7 vs. 129 +/- 5 ml/min; mean +/- S.E.) and a reduction in the remaining six (group B: 102 +/- 13 vs. 71 +/- 9 ml/min). Parallel changes were observed in the urinary excretion of 6-Keto-prostaglandin-F1 alpha (metabolite of renal prostacyclin) which augmented after furosemide in 14 of the 15 patients from group A (478 +/- 107 vs. 1034 +/- 159 pg/min, p less than 0.001) and decreased in all patients from group B (1032 +/- 240 vs. 548 +/- 136 pg/min, p less than 0.05). In contrast, the urinary excretion of prostaglandin E2 was stimulated by furosemide in all patients (group A, 92 +/- 19 vs. 448 +/- 60 pg/min, p less than 0.001; and group B, 209 +/- 63 vs. 361 +/- 25 pg/min, p less than 0.05). In all of the patients furosemide-induced changes (post- minus pre-furosemide values) in creatinine clearance were closely correlated in a direct and linear fashion with those in 6-Keto-prostaglandin-F1 alpha (r = 0.74; p less than 0.001). These changes were associated with a higher furosemide-induced natriuresis in group A than in group B (641 +/- 68 vs. 302 +/- 46 mumol/min, p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

6-Ketoprostaglandin F1 alpha↗