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Biomedical subjects

A Pardo

Publications and source records attributed to A Pardo.

At least 19 recordsLinked to original sources
PubMed2006

Insulin-like growth factor I improves intestinal barrier function in cirrhotic rats.

BACKGROUND AND AIMS: In liver cirrhosis, disruption of the intestinal barrier facilitates bacterial translocation and spontaneous bacterial peritonitis. Insulin-like growth factor I (IGF-I) is an anabolic hormone synthesised by hepatocytes that displays hepatoprotective activities and trophic effects on the intestine. The aim of this study was to investigate the effect of IGF-I on intestinal barrier function in cirrhotic rats. METHODS: In rats with carbon tetrachloride induced cirrhosis, we investigated the effect of IGF-I therapy on: (a) portal pressure; (b) intestinal histology and permeability to endotoxin and bacteria; (c) intestinal expression of cyclooxygenase 2 (COX-2) and tumour necrosis factor alpha (TNF-alpha), two factors that influence in a positive and negative manner, respectively, the integrity of the intestinal barrier; (d) intestinal permeability to 3H-mannitol in rats with bile duct ligation (BDL); and (e) transepithelial electrical resistance (TER) of polarised monolayers of rat small intestine epithelial cells. RESULTS: IGF-I therapy reduced liver collagen expression and portal pressure in cirrhotic rats, induced improvement in intestinal histology, and caused a reduction in bacterial translocation and endotoxaemia. These changes were associated with diminished TNF-alpha expression and elevated COX-2 levels in the intestine. IGF-I reduced intestinal permeability in BDL rats and enhanced barrier function of the monolayers of epithelial intestinal cells where lipopolysaccharide (LPS) caused a decrease in TER that was reversed by IGF-I. This effect of IGF-I was associated with upregulation of COX-2 in LPS treated enterocytes. CONCLUSIONS: IGF-I enhances intestinal barrier function and reduces endotoxaemia and bacterial translocation in cirrhotic rats. IGF-I therapy might be useful in the prevention of spontaneous bacterial peritonitis in liver cirrhosis.

Animals↗
PubMed2005

Self-reported skin disease in hydrotherapists working in swimming pools.

The aim of our study was to investigate the risk and characteristics of self-reported skin diseases among hydrotherapists. We attempted to contact 400 adults who participated in 1 of 2 training courses. 248 were reached and 190 of them (76.6%) completed the questionnaires. The data were collected by means of a telephone interview and a detailed questionnaire sent by mail. Statistical analysis included descriptive statistics, univariate and multifactorial analysis. Of those completing the questionnaire (75.8% females and 24.2% males), 44.4% of the hydrotherapists reported on the development of skin disease for the first time after the beginning of work at the swimming pool. The most common symptoms included pruritus and erythematous patches affecting mainly the extremities and trunk. Both smoking and increased exposure hours to pool water were independently associated with skin disease, suggesting a dose-response relationship. We conclude that contact dermatitis should be recognized as an occupational disease in hydrotherapists.

Adult↗
PubMed2005

Expression of insulin-like growth factor I by activated hepatic stellate cells reduces fibrogenesis and enhances regeneration after liver injury.

BACKGROUND/AIM: Hepatic stellate cells (HSCs) express alpha-smooth muscle actin (alphaSMA) and acquire a profibrogenic phenotype upon activation by noxious stimuli. Insulin-like growth I (IGF-I) has been shown to stimulate HSCs proliferation in vitro, but it has been reported to reduce liver damage and fibrogenesis when given to cirrhotic rats. METHODS: The authors used transgenic mice (SMP8-IGF-I) expressing IGF-I under control of alphaSMA promoter to study the influence of IGF-I synthesised by activated HSCs on the recovery from liver injury. RESULTS: The transgene was expressed by HSCs from SMP8-IGF-I mice upon activation in culture and in the livers of these animals after CCl4 challenge. Twenty four hours after administration of CCl4 both transgenic and wild type mice showed similar extensive necrosis and increased levels of serum transaminases. However at 72 hours SMP8-IGF-I mice exhibited lower serum transaminases, reduced hepatic expression of alphaSMA, and improved liver morphology compared with wild type littermates. Remarkably, at this time all eight CCl4 treated wild type mice manifested histological signs of liver necrosis that was severe in six of them, while six out of eight transgenic animals had virtually no necrosis. In SMP8-IGF-I mice robust DNA synthesis occurred earlier than in wild type animals and this was associated with enhanced production of HGF and lower TGFbeta1 mRNA expression in the SMP8-IGF-I group. Moreover, Colalpha1(I) mRNA abundance at 72 hours was reduced in SMP8-IGF-I mice compared with wild type controls. CONCLUSIONS: Targeted overexpression of IGF-I by activated HSCs restricts their activation, attenuates fibrogenesis, and accelerates liver regeneration. These effects appear to be mediated in part by upregulation of HGF and downregulation of TGFbeta1. The data indicate that IGF-I can modulate the cytokine response to liver injury facilitating regeneration and reducing fibrosis.

Actins↗
PubMed2004

[Genotype and phenotypic expression of hereditary hemochromatosis in Spain].

INTRODUCTION: The prevalence of C282Y homozygosity in patients with hereditary hemochromatosis (HH) has been reported to be markedly lower in the Mediterranean Basin than in northern Europe. In Spain, the available data are contradictory and limited to small series in specific regions. The objective of this study is to determine the prevalence of the 2 main HFE gene mutations in a large series of unrelated Spanish patients with HH from different geographical origins. PATIENTS AND METHOD: The criteria for HH diagnosis were: repeat serum transferrin saturation index (> 45% plus C282Y homozygosity and/or hepatic iron index (> 1.9 of dry liver weight in non-cirrhotic patients or (> 4.1 in patients with liver cirrhosis. Cases in related individuals were excluded. Demographic data, clinical expression, iron parameters and HFE gene mutations (C282Y and H63D) were assessed in 222 patients. RESULTS: A total of 83.3% of patients were C282Y homozygous and 5% were compound heterozygous (C282Y/H63D). No significant differences in phenotypic expression or in the frequency of C282Y homozygosity were observed between patients born in the North and South of Spain. CONCLUSION: The genotypic and phenotypic expression of HH in Spain is very similar to that reported in Northern Europe. Thus, the genetic heterogeneity described in some Southern European regions cannot be considered a common feature to all countries of the Mediterranean Basin.

Female↗
PubMed2004

Promoter variants in tissue inhibitor of metalloproteinase-3 (TIMP-3) protect against susceptibility in pigeon breeders' disease.

BACKGROUND: Tissue inhibitors of metalloproteinases (TIMPs) play a major role in extracellular matrix turnover in the lung. However, in chronic lung disorders such as idiopathic pulmonary fibrosis (IPF) and pigeon breeders' disease (PBD), TIMPs may promote an adverse non-degradative environment. We hypothesised that polymorphisms in TIMP-3 could affect susceptibility to IPF and PBD. METHODS: Two promoter variants, -915A>G and -1296T>C, were genotyped in 323 healthy subjects, 94 subjects with IPF, 115 with PBD, and 90 exposed to avian antigen but without PBD. The severity of fibrosis in lung tissue and the clinical outcome after 1 year was determined in the PBD group. RESULTS: The variants did not influence susceptibility to IPF, but the rare alleles of both variants appeared to be protective against susceptibility to PBD (odds ratio (OR) for carriage of at least one rare allele from either variant 0.48, 95% CI 0.30 to 0.76, p = 0.002). Haplotype analysis of positions -915 and -1296 estimated four haplotypes: *A*T, *G*T, *A*C and *G*C, respectively. Their frequencies differed overall between subjects with PBD and healthy subjects (p = 0.0049) and this was attributable primarily to the *G*C haplotype (OR 0.53, 95% CI 0.36 to 0.77, p = 0.001). The severity of fibrosis correlated with poorer outcome in the PBD group (r = 0.73, p<0.01) but no relationship was seen between the *G*C haplotype and outcome or fibrosis. However, PBD subjects with the *G*C haplotype did have proportionally fewer lymphocytes in their bronchoalveolar fluid than those with the common *A*T haplotype (p = 0.029). CONCLUSIONS: TIMP-3 variants appear to contribute to susceptibility to PBD. This may be through the inflammatory reaction rather than the fibrotic reaction.

Adult↗
PubMed2001

Idiopathic pulmonary fibrosis: prevailing and evolving hypotheses about its pathogenesis and implications for therapy.

Idiopathic pulmonary fibrosis is a progressive and usually fatal lung disease characterized by fibroblast proliferation and extracellular matrix remodeling, which result in irreversible distortion of the lung's architecture. Although the pathogenetic mechanisms remain to be determined, the prevailing hypothesis holds that fibrosis is preceded and provoked by a chronic inflammatory process that injures the lung and modulates lung fibrogenesis, leading to the end-stage fibrotic scar. However, there is little evidence that inflammation is prominent in early disease, and it is unclear whether inflammation is relevant to the development of the fibrotic process. Evidence suggests that inflammation does not play a pivotal role. Inflammation is not a prominent histopathologic finding, and epithelial injury in the absence of ongoing inflammation is sufficient to stimulate the development of fibrosis. In addition, the inflammatory response to a lung fibrogenic insult is not necessarily related to the fibrotic response. Clinical measurements of inflammation fail to correlate with stage or outcome, and potent anti-inflammatory therapy does not improve outcome. This review presents a growing body of evidence suggesting that idiopathic pulmonary fibrosis involves abnormal wound healing in response to multiple, microscopic sites of ongoing alveolar epithelial injury and activation associated with the formation of patchy fibroblast-myofibroblast foci, which evolve to fibrosis. Progress in understanding the fibrogenic mechanisms in the lung is likely to yield more effective therapies.

Anti-Inflammatory Agents↗
PubMed2001

Epidermoid cyst of the testis: a case report.

Epidermoid cyst of the testis is an uncommon benign tumour, with an overall incidence of 1-2% of all resected testicular masses. When imaging findings suggest that an intratesticular mass is likely to be an epidermoid cyst, conservative management (enucleation with testicular preservation) can be performed rather than orchidectomy. This case report records an epidermoid cyst in a 12-year-old boy in whom the US findings allowed testis-sparing surgery instead of orchidectomy.

Child↗
PubMed2001

Radiative lifetimes for the B1sigma(u)+ and C1pi states of the H2 molecule.

With RKR electronic potentials for the B1sigma(u)+, C1pi(u) and X1sigma(u)+ states in conjunction with Huffaker's correction and appropriate asymptotic functions, the unperturbed radiative lifetimes of rovibrational levels of the B1sigma(u)+ and C1pi(u) states of H2 are calculated. Comparison with previous calculations is presented. Better lifetimes for B1sigma(u)+ are obtained in present work.

Half-Life↗
PubMed2001

Idiopathic pylephlebitis and idiopathic sclerosing peritonitis in a man with protein S deficiency.

Idiopathic pylephlebitis and primary sclerosing peritonitis are two highly unusual entities. To our knowledge, the association of the two diseases has not been described previously. We report a 42-year-old patient with a protein S deficiency who presented with fever and chills, in whom idiopathic pylephlebitis was diagnosed. A year later, the patient was readmitted because of recurrent vomiting and weight loss. An exploratory laparotomy yielded diagnosis of sclerosing peritonitis, which resolved after surgery. The short time interval between the processes suggests that they were related to each other, and also to the protein S deficiency.

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

Surfactant protein gene A, B, and D marker alleles in chronic obstructive pulmonary disease of a Mexican population.

Chronic obstructive pulmonary disease (COPD) is characterized by chronic inflammation. It is most likely the result of complex interactions of environmental and genetic factors. Because pulmonary surfactant components play important roles in normal lung function, innate host defence, and inflammation in the lung, this study investigated the hypothesis that the surfactant protein genes are involved in certain cases of COPD. Genotype analysis of surfactant protein (SP)-A, SP-B, SP-B-linked microsatellite, and SP-D marker alleles was performed in patients with COPD (n=97) and smoker (n=82) or nonsmoker (n=99) controls. Univariate and multiple logistic regression analyses were performed. The regression analysis results between COPD and smokers revealed several COPD susceptibility alleles (AA62_A, B1580_C, D2S388_5), based on an odds ratio (OR >2.5). The predictive ability of this model for developing COPD is good (c=0.926). Allele-allele (B1580_C and D2S388_5) and allele-environment (i.e. smoking) interactions were detected. When smoker controls were compared to nonsmoker controls, marker D2S388 5 appeared to be smoking-independent (p=0.874), whereas marker alleles AA62_A (p=0.045) and B1580_5 (p=0.007) were smoking-dependent. Males were at higher risk (OR=6.05, p=0.001), and smoking (>50 packs x yr(-1)) increased risk (OR=5.38, p=0.007). Males and alleles of loci flanking SP-B were associated with more severe cases (forced expiratory volume in one second/forced vital capacity < or = 40%). The present results indicate that the surfactant protein alleles may be useful in chronic obstructive pulmonary disease by either predicting the disease in a subgroup and/or by identifying disease subgroups that may be used for therapeutic intervention. These observations should now be confirmed in a larger study, designed according to strict epidemiological criteria.

Aged↗
PubMed2001

Study of antiphospholipid antibodies in patients treated with antiepileptic drugs.

BACKGROUND: Antiphospholipid antibodies (lupus anticoagulant and anticardiolipin antibodies) are associated with a variety of clinical situations, including drug-intake, but their relationships with antiepileptic drugs have been scarcely investigated. OBJECTIVE: To determine the prevalence of antiphospholipid antibodies in patients treated with antiepileptic drugs and the associated risk of thrombotic events. PATIENTS AND METHODS: We performed the serologic study of thirty-six consecutively prospectively recruited epileptic patients treated with diverse antiepileptic drugs during 44.38 +/- 8.08 months (mean +/- SD) in which antiphospholipid antibodies were determined using cardiolipin and a mixture of phospholipid from rabbit brain as antigen for detection of cardiolipin and lupus anticoagulant by ELISA and in addition lupus anticoagulant was carried out also using coagulometric assays. A clinical evaluation was done in order to determine the presence of thrombotic events in the following five years. RESULTS: Antiphospholipid antibodies were detected in 43% of these patients, in most of them as anticardiolipin antibodies (IgM subtype). The patients did not present thrombotic events during the time of the study. CONCLUSION: Antiphospholipid antibodies are positive in a high proportion of these patients but thrombosis were not found during the study duration. This may be explained by the fact that the profile of aCL positivity not associated to positive LA observed in these patients does not confer a risk for thrombotic events.

Adolescent↗
PubMed2001

Climatic effects on Salmonella survival in plant and soil irrigated with artificially inoculated wastewater: preliminary results.

The use of wastewater to replace other water resources for irrigation is highly dependent on whether the health risk and environmental impacts entailed are acceptable or not. Total count and species of microorganisms found in wastewater vary widely because of climatic conditions, season, population sanitary habits and disease incidence. Salmonella, one of the genera associated with waterborne diseases, lives in the intestine. Thus, it is widely accepted that they have a limited survival period under environmental conditions. Wastewater management practices and the ability of Salmonella to survival under field conditions would determine the health risk associated with its presence in wastewater. Although chlorination is widely used, there are situations in which Salmonella is able to survive the sudden stress imposed by this technique. The aim of this experiment was to contribute to the study of the climatic and soil effects on pathogen survival under agricultural field conditions in order to assess which were the best wastewater management practices from both health and economic points of view. Five pots filled with soil seeded with Medicago sativa and an automatic weather station were used. A secondary effluent was artificially inoculated with Salmonella. In addition, open plates (filled with sterilised soil) and ultraviolet radiation isolated plates (filled with non-sterilised soil) were used. As soil heat emission contributes to the environmental conditions around the bacteria, standardised meteorological temperature data had to be carefully used in the bacterial survival studies under agricultural conditions. Radiation was the main cause of Salmonella mortality as its effect was more important than natural soil bacteria competence. Higher reduction of Salmonella counts could have been associated with longer spring days. Soil was able to effectively remove Salmonella. Subsurface drip irrigation methods could provide an effective tool to prevent health risk associated with wastewater irrigation.

Agriculture↗
PubMed2001

CCL18/DC-CK-1/PARC up-regulation in hypersensitivity pneumonitis.

Hypersensitivity pneumonitis (HP) is a lung inflammatory disorder characterized by accumulation of T lymphocytes. However, the mechanisms implicated in this process remain undefined. We examined the expression of dendritic cell (DC)-derived CC chemokine 1 (CK1)/CCL18, a chemokine putatively involved in naive T cell recruitment, in lungs from 10 patients with HP, 9 patients with idiopathic pulmonary fibrosis (IPF), and 20 healthy lungs. CCL18 was measured by real-time quantitative PCR and localized in lungs by in situ hybridization and immunohistochemistry. CCL18 expression was significantly increased in lungs affected by HP in comparison with lungs affected by IPF (2,085+/-393 vs. 1,023+/-110; P<0.05) and controls (2,085+/-393 vs. 467+/-94; P<0.01). Macrophages, DCs, and alveolar epithelial cells were the main sources of CCL18. There was a direct correlation between the levels of tissue CCL18 and the number of lymphocytes in the bronchoalveolar lavage fluids. High levels of CCL18 were detected in the subacute rather than the chronic phase of HP. These findings suggest a role for CCL18 in the pathogenesis of HP.

Alveolitis, Extrinsic Allergic↗
PubMed2000

Radiative lifetimes for the B1piu state of the Na2 molecule.

A study of the radiative lifetimes calculation of the Na2 B1piu state is presented. RKR electronic potentials are considered. The studied vibrational levels are for v' = 0-33 (B1piu) and v" = 0-65 (chi1sigmag+). The rotation is considered for values of J' = 1-225 (B1piu). The Einstein emission coefficients are calculated for the specified B1piu rovibrational levels (for Q line and R, P lines, for all ground state vibrational levels). With the inverse of Einstein emission coefficients sum, the radiative lifetimes are calculated. These calculated lifetimes are in good agreement with the experimental and previously calculated (with RKR potentials) lifetimes, but now great extension of considered rovibrational levels is considered. The bound-free contribution is irrelevant for Na2 lifetimes of the B1piu state. The perturbation between Na2 B1piu and alpha1sigmau+ states is considered.

Sodium↗