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Biomedical subjects

M Conde

Publications and source records attributed to M Conde.

At least 19 recordsLinked to original sources
PubMed2006

Nosocomial outbreak of Pseudomonas aeruginosa endophthalmitis.

We describe an outbreak of nosocomial endophthalmitis due to a common source, which was determined to be trypan blue solution prepared in the hospital's pharmacy service. We assume that viable bacteria probably gained access to the trypan blue stock solution during cooling after autoclaving. The temporal cluster of Pseudomonas aeruginosa endophthalmitis was readily perceived on the basis of clinical and microbiological findings, and an exogenous source of contamination was unequivocally identified by means of DNA fingerprinting.

Aged↗
PubMed2004

Prevalence and incidence of multiple sclerosis in Las Palmas, Canary Islands, Spain.

OBJECTIVES: To determine the prevalence and incidence of multiple sclerosis (MS) in the city of Las Palmas (Canary Islands, Spain), geographically belonging to north-western Africa, but with European ancestry. METHODS: This population-based survey was conducted for a period of 5 years (1998-2002) in a Sanitary District of Las Palmas city (28 degrees 20' N), with a population of 82,623 inhabitants. Multiple sources were periodically investigated for case ascertainment. Patients with definite and probable MS were included. RESULTS: Sixty-four patients with MS were identified on prevalence day, December 31, 2002. According to Poser's criteria the crude prevalence rate was 77.5 per 100,000 (95% CI: 59.7-98.9). This rate decreased to 73.8 (95% CI: 56.5-94.8) according to McDonald's criteria. Age-adjusted rates for the world and European standard populations were 61.6 (95% CI: 47.1-78.9) and 70.6 (95% CI: 55-89), respectively. Prevalence was higher for women aged 25-44 years. In 17 patients onset of MS occurred within the study period. Average annual incidence was 4.1 per 100,000 (95% CI: 2.4-6.6). CONCLUSIONS: The prevalence and incidence rates in Las Palmas city are close to those reported from Continental Spain and other countries of southern Europe with similar social and ethnic background. These results highlight the role of racial-ethnic factors in the genesis of MS.

Adolescent↗
PubMed2004

Micronutrient supplementation in mild Alzheimer disease patients.

OBJECTIVE: To evaluate if nutritional supplementation with or without micronutrient enhancement prevent weight loss and the progression of the disease in mild Alzheimer's Disease (AD) patients. DESIGN: Mild AD patients were recruited from an Alzheimer Day Centre. Subjects received oral liquid supplements with (Study-group: S) or without (Control-group: C) micronutrient enhancement. Intake assessment, nutritional status, biochemical parameters, cognitive function, and eating behaviour disorders were determined at baseline and at 6 months of treatment. RESULTS: At baseline both groups were not different in any variable measured. They were norm nourished, with normal biochemical parameters. Blandford scale demonstrated a mild alteration of feeding behaviour, the cognitive scale classified the patients as impaired and there was presence of memory complaints. After 6 months of nutritional supplements, a similar increase in energy consumption was observed in both groups of patients (P<0.05). In the within-group analysis, we found a trend (P=0.05) to increase body mass index; a significant increase in triceps skin fold thickness, mid-upper-arm circumference and serum magnesium, zinc and selenium, and a significant reduction in serum vitamin E (P<0.001, each). Serum cholesterol decreased substantially only in the S-group (P=0.025). No significant differences at baseline, within-group, neither between-group analysis in feeding behaviour nor in cognitive function were observed. CONCLUSIONS: According to our results no benefits in the progression of the disease was observed with micronutrient enhancement supplements. Effectiveness of nutritional supplements in preventing weight loss in mild AD patients showed a similar behaviour as observed in other populations. Due to the beneficial evolution of serum cholesterol in the S-group, this intervention deserves further investigation.

Aged↗
PubMed2003

Lifetime body mass index and risk of oral cavity and oropharyngeal cancer by smoking and drinking habits.

The influence of body mass index (BMI) on oral cancer risk was evaluated in 375 incident cases and 375 age-gender-matched hospital-based controls. Low BMIs at diagnosis and 2 years before diagnosis were associated with significantly elevated odds ratios (OR for BMI < or =22 vs >26 kg m(-2); 3.64; 95% confidence interval, CI: 2.27-5.82 and 3.31; 95% CI: 2.04-5.39, respectively). The association with low BMI, however, tended to be weaker and nonsignificant among never smokers and never drinkers.

Adult↗
PubMed2003

Gender differences in rising trends in cutaneous malignant melanoma in Spain, 1975-98.

BACKGROUND: Cutaneous malignant melanoma (CMM) morbidity and mortality rates have increased over the past several decades all around the world, but some developed countries have experienced recent declines in mortality from CMM among the young and middle-aged and even a reversal in the long-term increase in deaths attributable to CMM. OBJECTIVES: To describe CMM mortality trends, by age and gender, in Spain between 1975 and 1998. METHODS: Crude, age-adjusted, truncated, cumulative, age-specific and potential years of life lost rates of CMM mortality were calculated by gender. Age and period Poisson regression models were fitted to gender- and age-specific CMM mortality rates. RESULTS: In males there were marked increases in all CMM mortality rates between 1975 and 1994, followed by their decrease during 1995-98. In contrast, rates rose in females between 1975 and 1998. There were annual increases of 13% in the risk of dying among males and 33% among females. Relative risks of CMM mortality increased with age in both genders: (i) 21.75 (95% confidence interval, CI 17.32-27.30) in males, and (ii) 28.27 (95% CI 24.99-31.97) in females in the > or = 70-year-old group, when compared with those < 35 years. CONCLUSIONS: CMM mortality rates continue to rise in females while males have experienced a recent reversal of this trend in Spain. Emphasizing the danger of overexposure to ultraviolet radiation may be especially important in females.

Adolescent↗
PubMed2002

Macrophage inducible nitric oxide synthase gene expression is blocked by a benzothiophene derivative with anti-HIV properties.

Nitric oxide (NO) has been shown to mediate multiple physiological and toxicological functions. The inducible nitric oxide synthase (iNOS) is responsible for the high output generation of NO by macrophages following their stimulation by cytokines or bacterial antigens. The inhibition of TNF alpha-stimulated HIV expression and the anti-inflammatory property of PD144795, a new benzothiophene derivative, have been recently described. We have now analyzed whether some of these properties could be mediated by an effect of PD144795 on NO-dependent inflammatory events. We show that PD144795 suppresses the lipopolysaccharide-elicited production of nitrite (NO(-)(2)) by primary peritoneal mouse macrophages and by a macrophage-derived cell line, RAW 264.7. This effect was dependent on the dose and timing of addition of PD144795 to the cells. Suppression of NO(-)(2) production was associated with a decrease in the amount of iNOS protein, iNOS enzyme activity and mRNA expression. The effect of PD144795 was partially abolished by coincubation of the cells with LPS and IFN gamma. However, the inhibitory effect of PD144795 was not abrogated by the simultaneous addition of LPS and TNF alpha, which indirectly suggests that the effect of PD144795 was not due to the inhibition of TNF alpha synthesis. Additionally, PD144795 did not block NF-kappa B nuclear translocation induced by LPS. Inhibition of iNOS gene expression represents a novel mechanism of PD144795 action that underlines the anti-inflammatory effects of this immunosuppressive drug.

Animals↗
PubMed2001

Cyclic nucleotides modulate store-mediated calcium entry through the activation of protein-tyrosine phosphatases and altered actin polymerization in human platelets.

Agonists elevate the cytosolic calcium concentration in human platelets via a receptor-operated mechanism, involving both Ca(2+) release from intracellular stores and subsequent Ca(2+) entry, which can be inhibited by platelet inhibitors, such as prostaglandin E(1) and nitroprusside which elevate cAMP and cGMP, respectively. In the present study we investigated the mechanisms by which cAMP and cGMP modulate store-mediated Ca(2+) entry. Both prostaglandin E(1) and sodium nitroprusside inhibited thapsigargin-evoked store-mediated Ca(2+) entry and actin polymerization. However, addition of these agents after induction of store-mediated Ca(2+) entry did not affect either Ca(2+) entry or actin polymerization. Furthermore, prostaglandin E(1) and sodium nitroprusside dramatically inhibited the tyrosine phosphorylation induced by depletion of the internal Ca(2+) stores or agonist stimulation without affecting the activation of Ras or the Ras-activated phosphatidylinositol 3-kinase or extracellular signal-related kinase (ERK) pathways. Inhibition of cyclic nucleotide-dependent protein kinases prevented inhibition of agonist-evoked Ca(2+) release but it did not have any effect on the inhibition of Ca(2+) entry or actin polymerization. Phenylarsine oxide and vanadate, inhibitors of protein-tyrosine phosphatases prevented the inhibitory effects of the cGMP and cAMP elevating agents on Ca(2+) entry and actin polymerization. These results suggest that Ca(2+) entry in human platelets is directly down-regulated by cGMP and cAMP by a mechanism involving the inhibition of cytoskeletal reorganization via the activation of protein tyrosine phosphatases.

Actins↗
PubMed2001

Analysis of IgG response to experimental infection with RH Toxoplasma gondii in goats.

The IgG response of goats experimentally infected with RH Toxoplasma gondii has been analysed using an indirect ELISA and Western-blot analysis. Specific IgG antibodies were first detected at 14 days post-inoculation (p.i.), reaching a peak by day 35 p.i. and showing slight fluctuations until the end of the experiment (91 p.i.). Specific IgG showed a reactivity over a whole range of peptides (125-24 kDa approximately), but the highest reactivity was observed against a group of antigens with a molecular weight between 34 and 28 kDa, in particular against a 30 kDa fraction which is considered to represent the major surface protein of T. gondii named p30 or SAG-1.

Animals↗
PubMed2001

Methane and hydrogen exhalation in normal children and in lactose malabsorption.

UNLABELLED: Methane (CH4) and hydrogen (H2) are gases produced in the colon by the breakdown of carbohydrates, due to the action of anaerobic methanogenic bacteria. No papers have been published in pediatrics concerning these gases production and exhalation. Understanding of the pattern of H2, CH4, carbon dioxide (CO2), butyrates, indolellipsis,etc., production and exhalation, which may differ in gastrointestinal diseases, may be helpful as far as the diagnosis and treatment of some gastrointestinal conditions is concerned. Exhalation of H2, CH4 and CO2 by breath air was studied in basal conditions in 338 normal infants and in 27 lactose malabsorbers. Moreover, stools collected and stored for 10-12 h in anaerobic and aerobic conditions were incubated in anaerobiosis at 38 degrees C. After a 4-h incubation period, H2, CH4 and CO2 were determined. RESULTS: Methane production is independent of hydrogen production; the number of children producing CH4 increases from 0% at 12 months of age to 44% at the age of 9 years. In lactose malabsorption, we found 26 children producing increased quantities of H2 and no methane, and only one producing methane but no hydrogen, which proves that methanogenic bacteria are independent of H2-producing bacteria, and that CH4 determination is compulsory in the study of lactose malabsorption. The incubation of stools in an anaerobic milieu at 38 degrees C for 4 h, in an attempt to imitate the human colon, showed a great production of methane and less of H2 in the stools collected and stored in anaerobic conditions. The same incubation method was applied to the stools collected and stored in aerobic conditions: production of H2 and CH4 was much lower than in the collected and stored anaerobic group. The appearance of CH4 in the stools of the aerobic group proves that methanogenic bacteria are, to a small degree, resistant to oxygen. CONCLUSIONS: The study of gas exhalation in pediatrics merits more study by researchers, with a view to defining a special pattern of gas production in pathological conditions. The anaerobic stool incubation method is a good model for studying gas production under the effect of different diets and the gas production pattern in gastrointestinal diseases.

Aerobiosis↗
PubMed1999

Oxidative stress triggers STAT3 tyrosine phosphorylation and nuclear translocation in human lymphocytes.

Oxidizing agents are powerful activators of factors responsible for the transcriptional activation of cytokine-encoding genes involved in tissue injury. In this study we show evidence that STAT3 is a transcription factor whose activity is modulated by H2O2 in human lymphocytes, in which endogenous catalase had previously been inhibited. H2O2-induced nuclear translocation of STAT3 to form sequence-specific DNA-bound complexes was evidenced by immunoblotting of nuclear fractions and electrophoretic mobility shift assays, and vanadate was found to strongly synergize with H2O2. Moreover, anti-STAT3 antibodies specifically precipitated a protein of 92 kDa that becomes phosphorylated on tyrosine upon lymphocyte treatment with H2O2. Phenylarsine oxide, a tyrosine phosphatase inhibitor, and genistein, a tyrosine kinase inhibitor, cooperated and cancelled, respectively, the H2O2-promoted STAT3 nuclear translocation. Evidence is also presented, using Fe2+/Cu2+ ions, that.OH generated from H2O2 through Fenton reactions could be a candidate oxygen reactive species to directly activate STAT3. Present data suggest that H2O2 and vanadate are likely to inhibit the activity of intracellular tyrosine phosphatase(s), leading to enhanced STAT3 tyrosine phosphorylation and hence its translocation to the nucleus. These results demonstrate that the DNA binding activity of STAT3 can be modulated by oxidizing agents and provide a framework to understand the effects of oxidative stress on the JAK-STAT signaling pathway.

Arsenicals↗
PubMed1999

Characterization of calcineurin in human neutrophils. Inhibitory effect of hydrogen peroxide on its enzyme activity and on NF-kappaB DNA binding.

We describe here a specific calcineurin activity in neutrophil lysates, which is dependent on Ca2+, inhibited by trifluoroperazine, and insensitive to okadaic acid. Immunoblotting experiments using a specific antiserum recognized both the A and B chains of calcineurin. Neutrophils treated with cyclosporin A or FK 506 showed a dose-dependent inhibition of calcineurin activity. The effect of oxidant compounds on calcineurin activity was also investigated. Neutrophils treated with hydrogen peroxide (H2O2), where catalase was inhibited with aminotriazole, exhibited a specific inhibition of calcineurin activity. However, the addition of reducing agents to neutrophil extracts partially reversed the inhibition caused by H2O2. A similar inhibitory effect of H2O2 on calcineurin activity was observed to occur in isolated lymphocytes. This is the first demonstration that redox agents modulate calcineurin activity in a cellular system. In addition, electrophoretic mobility shift assays revealed that lipopolysaccharide-induced activation of NF-kappaB in human neutrophils is inhibited by cell pretreatment with H2O2 in a dose-dependent manner. These data indicate that calcineurin activity regulates the functional activity of lipopolysaccharide-induced NF-kappaB/Rel proteins in human neutrophils. These data indicate a role of peroxides in the modulation of calcineurin activity and that the H2O2-dependent NF-kappaB inactivation in neutrophils occurs in concert with inhibition of calcineurin.

Calcineurin↗
PubMed1999

Phenylarsine oxide increases intracellular calcium mobility and inhibits Ca(2+)-dependent ATPase activity in thymocytes.

A rise in intracellular Ca(2+) levels has been implicated as a regulatory signal for the initiation of lymphocyte proliferation. In the present study the mechanism underlying the elevation of [Ca(2+)] induced by phenylarsine oxide [PAO] was investigated in thymocytes. This agent inhibits HIV-1 replication and also NF-kappaB-mediated activation. It has been reported that the PAO-induced Ca(2+) elevation results from an enhanced plasma membrane calcium permeability in T cells. Here, we present biochemical evidence that the PAO-induced Ca(2+) increase was independent of external Ca(2+). Consistent with these facts, when [Ca(2+)](i) was depleted by prolonged incubation of the cells in Ca(2+)-free medium, PAO addition did not lead to [Ca(2+)](i) increase. These data indicate the involvement of intracellular organelles of thymocytes as the source of Ca(2+). Moreover, evidence is presented that PAO inhibited Ca(2+)-dependent ATPase activity from thymocytes and sarcoplasmic reticulum from skeletal muscle. This inhibition was dose-dependent, with a IC(50) of about 30 microM for both preparations of enzyme. The ability of PAO to inhibit Ca(2+)-dependent ATPase represents a novel mechanism of action for this drug. Present data suggest that the PAO-dependent [Ca(2+)](i) increase could be mainly the result of inhibition of Ca(2+)-dependent ATPase. In addition, we describe also a Ca(2+)-dependence for PAO effect on tyrosine phosphorylation.

Animals↗
PubMed1998

[Hepatocellular carcinoma associated to porphyria cutanea tarda and hepatitis C virus infection without cirrhosis].

The molecular basis of porphyria cutanea tarda is defective activity of hepatic uroporphyrinogen decarboxylase. A common characteristic is liver dysfunction than goes from cirrhosis to hepatocellular carcinoma. A high prevalence of hepatitis C virus markers has been demonstrated. We study a patient with PCT and hepatitis C virus markers that finally develops to hepatocellular carcinoma without previous cirrhosis. Previous studies with association of PCT and hepatitis C virus markers, have found liver diseases ranging from cirrhosis to hepatocellular carcinoma. The importance of this study is the absence of cirrhosis.

Carcinoma, Hepatocellular↗
PubMed1998

[The sensorineural component of hearing loss associated with cholesteatoma].

Patients with cholesteatoma often suffer neurosensorial hearing loss with variable bone conduction thresholds. Its origin is debated and has been attributed to the ototoxicity of topical drugs, immune reactions, effects of ototoxic antibiotics applied to the ear, etc. A selected series of 50 patients who underwent surgery for chronic ear disease due to cholesteatoma in our ENT department were studied to evaluate the possible origin of the bone conduction component of hearing loss. Different clinical, audiological, and surgical aspects were analyzed, including cholesteatoma site and extension, age, sex, evolution of the symptoms, pure tone audiometry data, middle ear involvement, the operation performed, and the occurrence of complications. Bone conduction thresholds were reported as pure tone differential thresholds (affected vs non-affected ear). A specific cholesteatoma-related neurosensorial hearing loss was observed that might lead to irreversible hearing loss. Neurosensorial involvement seems to be related mainly to the duration of symptoms, type of surgery, certain specific clinical aspects, and complications.

Adolescent↗
PubMed1997

A newly synthesized molecule derived from ruthenium cation, with antitumour activity, activates NADPH oxidase in human neutrophils.

To determine the nature of the mechanism by which certain derived ruthenium (Ru) complexes induce regression in tumour growth, we have investigated the possibility that this mechanism was associated with an increase of superoxide anion (O2-. production by phagocytic cells, which are usually found in tumour nodes. Here we present evidence that a newly synthesized complex, Ru3+-propylene-1, 2-diaminotetra-acetic acid (Ru-PDTA), derived from Ru and the sequestering ligand (PDTA), specifically stimulates O2-. production. This increase was associated with the translocation of cytosolic factors p47(phox) and p67(phox) of NADPH oxidase to the plasma membrane. The Ru-PDTA-complex-dependent O2-. production was abrogated by staurosporine, partially inhibited by diphenylene iodonium, and it was insensitive to pertussis toxin or dibutyryl cyclic AMP pretreatment. An increase of cytosolic Ca2+ levels were also detected in neutrophils treated with the Ru-PDTA complex. Also, Ru-PDTA complex induced the phosphorylation of tyrosine residues of several proteins as assessed by Western blotting. Present data are consistent with the possibility that Ru-PDTA-dependent antitumour effects are due in part to the complex's ability to stimulate the release of toxic oxygen metabolites from phagocytic cells infiltrating tumour masses.

Antineoplastic Agents↗
PubMed1997

The Bamako Initiative in Benin and Guinea: improving the effectiveness of primary health care.

The objective of the health system revitalization undergone in Benin and Guinea since 1986 is to improve the effectiveness of primary health care at the periphery. Second in a series of five, this article presents the results of an analysis of data from the health centres involved in the Bamako Initiative in Benin and Guinea since 1988. Data for the expanded programme of immunization, antenatal care and curative care, form the core of the analysis which confirms the improved effectiveness of primary health care at the peripheral level over a period of six years. The last available national data show a DPT3 immunization coverage of 80% in 1996 in Benin and 73% in 1995 in Guinea. In the Bamako Initiative health centres included in our analysis, the average immunization coverage, as measured by the adequate coverage indicator, increased from 19% to 58% in Benin and from less than 5% to 63% in Guinea between 1989 to 1993. Average antenatal care coverage has increased from 5% in Benin and 3% in Guinea to 43% in Benin and 51% Guinea. Utilization of coverage with curative care has increased from less than 0.05 visit per capita per year to 0.34 in Guinea and from 0.09 visit per capita per year to 0.24 in Benin. Further analysis attempts to uncover the reasons which underlie the different levels of effectiveness obtained in individual health centres. Monitoring and microplanning through a problem-solving approach permit a dynamic process of adaptation of strategies leading to a step by step increase of coverage over time. However, the geographical location of centres represents a constraint in that certain districts in both countries face accessibility problems. Outreach activities are shown to play an especially positive role in Guinea, in improving both immunization and antenatal care coverage.

Benin↗
PubMed1997

Implementation of the Bamako Initiative: strategies in Benin and Guinea.

Two West African countries, Benin and Guinea, have been reorganizing their peripheral health systems since 1986, with the goal of improving access to primary health care (PHC). A comprehensive approach evolve, based on improving effectiveness, optimizing efficiency, ensuring financial variability and promoting equity. These strategies were launched as the Bamako Initiative by the World Health Organization's Regional Assembly in 1987. This is the first in a series of five articles on the Bamako Initiative in Benin and Guinea. The strategies implemented in these two countries are discussed. Subsequent articles discuss the improved health indicators, impact on service costs efficiency, and community empowerment through local cost recovery and equity implications. The health center is the basis for a revitalized primary care system. From here, an integrated minimum health care package is readily accessible to meet basic community health needs. Through the Bamako Initiative program, drugs and other essential resources are always available, regular contract between the community health service providers and communities has increased, and the quality of care has improved while also becoming more efficient. Community health resources are managed locally through joint microplanning and monitoring, involving health personnel and village committees. Community ownership, fostered by local budgeting and decision making, is an essential pillar for the success of the system.

Benin↗