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Biomedical subjects

V Ruiz

Publications and source records attributed to V Ruiz.

At least 19 recordsLinked to original sources
PubMed2006

Dynamics of a hepatitis B virus e antigen minus population ascribed to genotype F during the course of a chronic infection despite the presence of anti-HBs antibodies.

The in vivo evolution of genotype F HBV variants was recorded in a chronically infected patient throughout a 3-year observation period. Fluctuating levels of HBs Ag and anti-HBs antibodies were recorded, both of them cocirculating in peripheral blood samples at given times. Fifty S gene derived clones were sequenced and phylogenetically analyzed. As expected, some amino acid replacements within the S ORF were also observed within the P ORF while others were silent for the former. Such change was statistically significant for both S and P overlapping genes, which clearly indicates the appearance of a positive selection pressure. Supporting this notion, amino acid replacements were documented at both B and T cell epitopes in samples from 1997 and 1998. Several mutations were documented within and outside the "a" determinant in the major hydrophilic region. Such substitutions might have resulted from the attempt of HBV to evade both humoral and/or cellular immune response. To the best of our knowledge this unusual profile of HBV variants in presence of usually "neutralizing" anti-HBs antibodies was examined in vivo for the first time.

Amino Acid Sequence↗
PubMed2005

Risk stratification of patients with acute chest pain and normal troponin concentrations.

OBJECTIVE: To investigate the outcome of patients with acute chest pain and normal troponin concentrations. DESIGN: Prospective cohort design. SETTING: Single centre study in a teaching hospital in Spain. PATIENTS: 609 consecutive patients with chest pain evaluated in the emergency department by clinical history (risk factors and a chest pain score according to pain characteristics), ECG, and early (< 24 hours) exercise testing for low risk patients with physical capacity (n = 283, 46%). All had normal troponin concentrations after serial determination. MAIN OUTCOME MEASURES: Myocardial infarction or cardiac death during six months of follow up. RESULTS: 29 events were detected (4.8%). No patient with a negative early exercise test (n = 161) had events versus the 6.9% event rate in the remaining patients (p = 0.0001). Four independent predictors were found: chest pain score > or = 11 points (odds ratio (OR) 2.4, 95% confidence interval (CI) 1.1 to 5.5, p = 0.04), diabetes mellitus (OR 2.3, 95% CI 1.1 to 4.7, p = 0.03), previous coronary surgery (OR 3.1, 95% CI 1.3 to 7.6, p = 0.01), and ST segment depression (OR 2.8, 95% CI 1.3 to 6.3, p = 0.003). A risk score proved useful for patient stratification according to the presence of 0-1 (2.7% event rate), 2 (10.2%, p = 0.008), and 3-4 predictors (29.2%, p = 0.0001). CONCLUSIONS: A negative troponin result does not assure a good prognosis for patients coming to the emergency room with chest pain. Early exercise testing and clinical data should be carefully evaluated for risk stratification.

Acute Disease↗
PubMed2003

Hepatitis B virus S gene mutants in a patient with chronic active hepatitis with circulating Anti-HBs antibodies.

An adult male farmer with chronic active hepatitis and cirrhosis despite previous circulating anti-HBs antibodies was studied. No markers of other hepatotropic viral infection were observed. HBV DNA was detected in serum by PCR and was characterized further by restriction fragment length polymorphism (RFLP) and sequencing of cloned PCR products derived from the S gene. The HBV DNA was ascribed to genotype F, and single-strand conformational polymorphism (SSCP) demonstrated the co-circulation of multiple quasispecies. Some of the variants exhibited changes located within the neutralizing "a" determinant, located between amino acids 124-147 of the S protein. Within this region, two clones showed either C124R or C124Y mutations. Other mutations were Q129R, C138R, C139R, and S140T (one clone each). Outside the "a" determinant several substitutions were documented. The high degree of the quasispecies variability was probably linked to the severity of the infection. Most members of the patient's family were infected with HBV, all with genotype F.

Amino Acid Substitution↗
PubMed2003

Angiogenesis in hypersensitivity pneumonitis.

Angiogenesis is an essential process required for growth and tissue repair after injury, but it may also contribute to the pathology of a number of human disorders including neoplasias, atherosclerosis and inflammatory diseases. Vascular endothelial growth factor (VEGF) is a potent angiogenic peptide upregulated by many cytokines and endothelium shear stresses. Lung is a highly vascular tissue with finely organized and regulated microvascular beds, and its inflammation may lead to dysregulated angiogenesis. Hypersensitivity pneumonitis (HP) is a lung disorder characterized by chronic lymphocytic inflammation and endothelial damage. However, neovascularization has not been previously explored. In this study, we examined the expression and localization of VEGF in 38 patients with HP and 14 healthy control subjects (CS). VEGF levels in bronchoalveolar lavage fluid (BALF) were measured by ELISA, and cellular lung localization was determined by immunohistochemistry. In addition, VEGF expression was analyzed in lung tissue by RT-PCR. Our results showed sera levels significantly increased in HP patients compared with CS (209.3 +/- 189.3 vs. 55.3 +/- 31.4 pg/ml; p = 0.004). By contrast, BALF levels of VEGF were significantly decreased in HP patients compared with CS (35.3 +/- 51.5 pg/ml vs. 185.1 +/- 191.4 pg/ml; p < 0.001). VEGF was primary expressed by epithelial cells, smooth muscle cells, and interstitial macrophages in HP tissue. Flt-1 and Flk-1 receptors were highly expressed by endothelial cells from medium and small vessels in HP tissue. By RT-PCR the VEGF RNA was increased compared with those in normal lung. Our results suggest that abnormal expression of VEGF may contribute to impair the lung repair in HP.

Alveolitis, Extrinsic Allergic↗
PubMed2002

Fluid secretion in Rhodnius upper malpighian tubules (UMT): water osmotic permeabilities and morphometric studies.

We have measured the osmotic permeability of the basolateral cell membrane (Poscb) and compared it with the transepithelial permeability (Poste) to calculate the paracellular (Posp) permeability of the upper malpighian tubules (UMT) of the 5th instar of Rhodnius prolixus under several experimental conditions, namely, at rest and after stimulation to secrete with 5-HT, each under control conditions (no treatment), after treatment with pCMBS, and after addition of pCMBS and DTT. Secretion rate is negligible at rest. During stimulation mean secretion rate is 43.5 nl/cm2 sec. Secretion is severely curtailed by pCMBS and fully restored by DTT. Poscb = 9.4 (resting, control); 5.8 (control + pCMBS); 10.7 (control + pCMBS + DTT); 20.6 (stimulated, control); 14.7 (stimulated + pCMBS); 49.1 (stimulated + pCMBS + DTT) (x10?4 cm3/cm2 sec Osm). Calculated Posp are higher than the transcellular permeability, Posc, at rest and after stimulation. Electron micrograph morphometry of UMT sections show that cells significantly decrease their volume after stimulation. Lateral intercellular space (LIS) and basolateral extracellular labyrinth (BEL) are barely discernible at rest. LIS and BEL are widely dilated in stimulated UMT. Thus, ions have restricted access to the deep and narrow basolateral cell membrane indentations at rest, but they have ready access to cell membrane indentations after stimulation, because of the opening of LIS and BEL. These findings are discussed in relation to isosmotic secretion. The rate-limiting step for paracellular movement is located at the smooth septate junctions.

4-Chloromercuribenzenesulfonate↗
PubMed2002

Vascular endothelial growth factor plasma levels in patients with systemic lupus erythematosus and primary antiphospholipid syndrome.

The objective of this study was to assess the possible role of vascular endothelial growth factor (VEGF) in the pathogenesis of systemic lupus erythematosus (SLE) and primary antiphospholipid syndrome (PAPS). We studied 28 patients with SLE, 10 patients with PAPS, and 24 healthy controls. VEGF plasma levels were measured by ELISA. Immunolocalization of VEGF was done in renal tissue from SLE patients and cadaveric controls. Our results showed that VEGF plasma levels were increased in SLE patients compared with PAPS and controls. The correlation between clinical manifestations and VEGF levels revealed that SLE patients with renal failure had significantly increased plasma VEGF levels (134.1 + 91.0 pg/ml) compared with SLE patients with normal renal function (42.9 + 19.0 pg/ml), PAPS patients (41.9 + 26.6 pg/ml), and controls (36.2 + 27.0 pg/ml; P < 0.01). Immunostaining showed a strong expression of VEGF in SLE renal tissue samples. Our preliminary results indicate that VEGF is increased in plasma from patients with lupus nephritis and a moderate degree of renal failure and is overexpressed in renal tissue from these patients.

Adult↗
PubMed2001

Bidimensional spectroelectrochemistry.

A new methodology is presented to offer the possibility of simultaneously obtaining two different spectroscopic signals in a single spectroelectrochemical experiment. Taking the plane of the electrode surface as a spatial reference, normal-beam and parallel-beam UV-vis absorbance signals are jointly analyzed, revealing important experimental differences between the two kinds of signals. Two different chemical systems are selected to show the possibilities of the bidimensional spectroelectrochemistry: a simple diffusive process and an adsorptive electrode reaction. Comparative results show clearly that the two kinds of spectroscopic signals, both normal and parallel to the electrode surface, have to be used together in the study of any electrode reaction scheme.

Journal Article↗
PubMed2001

Hepatitis C virus and GBV-C/hepatitis G virus in Argentine patients with porphyria cutanea tarda.

To investigate hepatitis C virus (HCV) and GBV-C/hepatitis G virus (HGV) genotype prevalence among HCV-infected porphyria cutanea tarda (PCT) patients, 19 HCV-infected patients with associated PCT were studied. A control group of 53 age-matched HCV-infected patients without associated PCT was selected. Eighteen of the 19 serologically positive HCV-PCT patients showed HCV RNA in serum. Genotype 1b was the most prevalent among both HCV-PCT patients (72.2%; 13/18) and age-matched HCV controls (50.9%; 27/53). Such different genotypic prevalence failed to reach statistical significance (chi(2) with Yates' correction, p = 0.19). The single HCV-PCT patient without detectable HCV RNA was also infected with genogroup 3 GBV-C/HGV. This GBV-C/HGV RNA prevalence (5.3%) among HCV-PCT patients is not statistically different from that observed among Argentine blood donors (5.5%; 11/200). To our knowledge, these results show for the first time the molecular epidemiology of both HCV and GBV-C/HGV associated to PCT in America.

Adult↗
PubMed2001

Tumor necrosis factor receptor deficiency alters matrix metalloproteinase 13/tissue inhibitor of metalloproteinase 1 expression in murine silicosis.

Murine exposure to silica is associated with enhanced tumor necrosis factor alpha (TNF-alpha) expression and matrix deposition. The regulation of TNF is mediated through TNF receptor (TNFR) activation of transcription factors. In the present work we have studied the importance of the individual TNFR in silica-induced lung inflammation and matrix deposition in mice. We studied RNA expression of TNF, alpha1(I) collagen, interstitial collagenase (MMP-13), and its inhibitor (TIMP-1) in the lungs of silica-treated mice. Furthermore, we correlated MMP-13/TIMP-1 RNA abundance with activation of the transcription factors AP-1 and NF-kappaB in the lungs of C57BL/6 mice, and of mice deficient in one of the two types of TNFR (p55(-/-) or p75(-/-)), exposed to silica (0.2 g/kg) or saline by intratracheal instillation. Animals were killed 28 d after exposure and lung hydroxyproline (HP), TNF, alpha1(I) collagen, MMP-13, and TIMP-1 RNA abundance was measured. AP-1 and NF-kappaB activation was studied by gel-shift assays. Compared with C57BL/6 mice, p55(-/-) and p75(-/-) mice significantly (*p < 0.05) decreased lung HP accumulation in response to silica. All murine strains enhanced TNF and alpha1(I) collagen mRNA in response to silica. Enhanced (p < 0.05) MMP-13 RNA expression was also observed in all murine strains in response to silica. Enhanced (p < 0.05) TIMP-1 RNA expression was observed in C57BL/6 mice, but not in p55(-/-) or p75(-/-) mice, in response to silica. NF-kappaB activation was observed in all murine strains, whereas AP-1 activation was observed only in C57BL/6 mice after silica treatment. These data suggest that TNFR deletion modifies MMP-13/ TIMP-1 expression in favor of matrix degradation.

Animals↗
PubMed2001

Fibroblasts from idiopathic pulmonary fibrosis and normal lungs differ in growth rate, apoptosis, and tissue inhibitor of metalloproteinases expression.

Idiopathic pulmonary fibrosis (IPF) is a chronic lung disorder characterized by fibroblast proliferation and extracellular matrix accumulation. However, studies on fibroblast growth rate and collagen synthesis have given contradictory results. Here we analyzed fibroblast growth rate by a formazan-based chromogenic assay; fibroblast apoptosis by in situ end labeling (ISEL) and propidium iodide staining; percent of alpha-smooth muscle actin (alpha-SMA) positive cells by fluorescence-activated cell sorter; and alpha1-(I) collagen, transforming growth factor (TGF)-beta1, collagenase-1, gelatinases A and B, and tissue inhibitor of metalloproteinase (TIMP)-1, -2, -3, and -4 expression by reverse transcriptase/polymerase chain reaction in fibroblasts derived from IPF and control lungs. Growth rate was significantly lower in IPF fibroblasts compared with controls (13.3 +/- 38.5% versus 294.6 +/- 57%, P < 0.0001 at 13 d). Conversely, a significantly higher percentage of apoptotic cells was observed in IPF-derived fibroblasts (ISEL: 31.9 +/- 7.0% versus 15.5 +/- 7.6% from controls; P < 0.008). alpha-SMA analysis revealed a significantly higher percentage of myofibroblasts in IPF samples (62.8 +/- 25.2% versus 14.8 +/- 11.7% from controls; P < 0.01). IPF fibroblasts were characterized by an increase in pro-alpha1-(I) collagen, TGF-beta1, gelatinase B, and all TIMPs' gene expression, whereas collagenase-1 and gelatinase A expression showed no differences. These results suggest that fibroblasts from IPF exhibit a profibrotic secretory phenotype, with lower growth rate and increased spontaneous apoptosis.

Apoptosis↗
PubMed2001

[Tropical endomyocardial fibrosis or Davies disease. A case report].

Endomyocardial fibrosis is a restrictive endomyocardial myocardiopathy of unclear etiology, it is an endemic disease in tropical and subtropical countries. The patients are usually young and the disease has an insidious onset and poor prognosis. Surgery may lead to clinical improvement and prolong life expectancy, although it is only a palliative treatment and does not stop disease progression. We present a case of endomyocardial fibrosis from Equatorial Guinea with severe clinical involvement and clear improvement following surgery. The current etiopathogenic hypothesis, the results obtained and the management of these cases, which are infrequent in Spain, are discussed. We also comment upon the differences with the historically related Loeffler syndrome according to one of the etiopathogenic hypotheses.

Adult↗
PubMed2000

TIMP-1, -2, -3, and -4 in idiopathic pulmonary fibrosis. A prevailing nondegradative lung microenvironment?

Fibroblast proliferation and extracellular matrix accumulation characterize idiopathic pulmonary fibrosis (IPF). We evaluated the presence of tissue inhibitor of metalloproteinase (TIMP)-1, -2, -3, and -4; collagenase-1, -2, and -3; gelatinases A and B; and membrane type 1 matrix metalloproteinase (MMP) in 12 IPF and 6 control lungs. TIMP-1 was found in interstitial macrophages and TIMP-2 in fibroblast foci. TIMP-3 revealed an intense staining mainly decorating the elastic lamina in vessels. TIMP-4 was expressed in IPF lungs by epithelial and plasma cells. TIMP-2 colocalized with Ki67 in fibroblasts, whereas TIMP-3 colocalized with p27 in inflammatory and epithelial cells. Collagenase-1 was localized in macrophages and alveolar epithelial cells, collagenase-2 was localized in a few neutrophils, and collagenase-3 was not detected. MMP-9 was found in neutrophils and subepithelial myofibroblasts. Myofibroblast expression of MMP-9 was corroborated in vitro by RT-PCR. MMP-2 was noticed in myofibroblasts, some of them close to areas of basement membrane disruption, and membrane type 1 MMP was noticed in interstitial macrophages. These findings suggest that in IPF there is higher expression of TIMPs compared with collagenases, supporting the hypothesis that a nondegrading fibrillar collagen microenvironment is prevailing.

Aged↗
PubMed1998

Gelatinases A and B are up-regulated in rat lungs by subacute hyperoxia: pathogenetic implications.

Subacute hyperoxia may cause basement membrane disruption and subsequent fibrosis. To test the role of extracellular matrix degradation in hyperoxic damage, we analyzed the expression of gelatinases A and B and tissue inhibitors of metalloproteinases (TIMP)-1 and TIMP-2 in rats exposed to 85% O2. Oxygen-exposed rats were studied at 1, 3, 5, and 7 days, and compared with air-breathing rats. Lung mRNAs assayed by Northern and in situ hybridization showed an up-regulation of lung gelatinases A and B from the 3rd day on. Gelatinase A was localized in alveolar macrophages and in interstitial and alveolar epithelial cells. Gelatinase B mRNA and protein were localized in macrophages and bronchiolar and alveolar epithelial cells. Increased gelatinase A and B activities were demonstrated in bronchoalveolar lavage. TIMP-1 and TIMP-2 were constitutively expressed, and only TIMP-1 displayed a moderate increase with hyperoxia. To elucidate transcriptional mechanisms for increased gelatinase B expression after hyperoxia, nuclear transcription factor-kappabeta activation was explored. Oxidative stress significantly increased the lung expression of nuclear transcription factor-kappabeta (p65) protein, and nuclear transcription factor-kappabeta activation and increased levels of gelatinases A and B were found in isolated type II alveolar cells obtained from hyperoxic rats. Conceivably, subacute hyperoxia induces excessive gelatinase activity, which may contribute to lung damage.

Acute Disease↗
PubMed1998

Use of transesophageal echocardiography to predict significant coronary artery disease in aortic stenosis.

STUDY OBJECTIVES: This study was conducted to examine if the use of multiplane transesophageal echocardiography (TEE) could predict the absence or the presence of significant coronary artery disease (CAD) in patients with aortic stenosis. DESIGN: Prospective study. SETTING: University hospital. PATIENTS: Clinical, angiographic features and TEE findings were prospectively analyzed in 132 consecutive patients with aortic stenosis. MEASUREMENTS AND RESULTS: In 63 patients with significant CAD, 57 had thoracic aortic plaque on TEE studies. In contrast, aortic plaque existed in only 19 of the remaining 69 patients with normal or mildly abnormal coronary arteries. Therefore, the presence of aortic plaque on the TEE identified significant CAD with a sensitivity of 90.5%, a specificity of 72.5%, and with positive and negative predictive values of 75.0% and 89.3%, respectively. There was a significant relation between the severity of thoracic aortic atherosclerosis and the severity of CAD (p<0.0001). Multivariate logistic regression analysis revealed that aortic plaque, angina, and age were independent predictors of CAD. Aortic plaque was the most significant independent predictor. CONCLUSION: This prospective study indicates that TEE examination of thoracic atherosclerotic plaque is a powerful predictor of absence of significant CAD in patients with aortic stenosis.

Adult↗
PubMed1998

[The incidence of intraoperative conciousness in emergency surgery and its possible relation to the post-traumatic stress syndrome. Presentation of three cases].

Intraoperative awakening and recall of specific events is a rare complication (0.2 to 1.3%) of surgery. The possibility of developing serious psychiatric complications, such as posttraumatic stress disorder (PTSD) makes the prevention and detection of intraoperative awareness a subject of special interest. We describe our experience with three patients in whom awareness was detected during emergency surgery under general anesthesia. We conducted two structured interviews with the patients three months after surgery in order to detect the possible development of psychiatric complications. One patient suffered insomnia and reexperience of the event during the first two weeks after surgery. Improvement was spontaneous. None of the patients suffered PTSD. Efforts to decrease the incidence of episodes of intraoperative awakening with specific recall must be based on clinical observation and exhaustive monitoring of the patient, including anesthetic gases, given that no ideal method of monitoring depth of anesthesia exists. Cases should be detected in the first few days after surgery by means of a specific test. Likewise, possible causes for the episode should be explained to the patient, who should be followed for six months so that early diagnosis of PTSD or other psychiatric complications can be made.

Adult↗