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N Sánchez

Publications and source records attributed to N Sánchez.

At least 19 recordsLinked to original sources
PubMed2005

Does Helicobacter pylori have a pathogenic role in bronchiectasis?

AIM: To investigate the presence of Helicobacter pylori (H. pylori) in bronchial biopsies of patients with bronchiectasis, by histochemical and immunochemical staining. SETTING: 800-bed tertiary university hospital. METHODS: Observational study. PATIENTS: forty-six patients with bronchiectasis in a stable clinical condition and 8 control patients. INTERVENTIONS: Serum samples determination of IgG levels for H. pylori by ELISA. Immunostaining with an anti-H. pylori antibody (NCL-HPp, Novocastra) of bronchial mucosa obtained by fiberoptic bronchoscopy from both patients with bronchiectasis and controls. RESULTS: Twenty-one out of 46 patients with bronchiectasis (46%) had positive serology for H. pylori. We obtained 40 bronchial biopsies in patients with bronchiectasis and 8 bronchial biopsies in control patients. No evidence of H. pylori was obtained in the bronchial samples of both patients and controls. CONCLUSIONS: The results of our study could not demonstrate the presence of H. pylori in bronchial specimens from patients with bronchiectasis.

Adult↗
PubMed1999

[Mycobacterial infections in HIV-infected patients in Cali, Colombia].

The prevalence of mycobacterial infections was determined in a sample of 155 individuals infected with human immunodeficiency virus (HIV) who were treated in the Social Security Institute (SSI) of Cali, Colombia. A tuberculin test (2 TU PPD RT23) was used, and the presence of mycobacteria was checked through direct microscopy and culturing blood, urine, feces, and gastric aspirate. When clinically indicated, samples of cerebrospinal fluid, bone marrow, and sputum were also examined and cultivated. The absence of reactivity to tuberculin was significantly more frequent in the patients than in the controls (91.3%, compared to 57.4%; chi 2 = 33, P = 0). The prevalence of tuberculosis was 6.5%, in comparison with 0.04% among a group of HIV-negative ISS members (exact binomial 95% confidence interval: 0.0313% to 0.1154%). Nontuberculous mycobacteria (NTM), present in 43 patients, were significantly more frequent than Mycobacterium tuberculosis (27.7%, versus 6.5%; chi 2 = 24.78, P = 0.000,001), but they caused illness only in some cases. The most common species were those of the M. avium-intracellulare complex. M. avium-intracellulare and M. fortuitum had a total prevalence of 7.1% and were the most-prevalent NTM that caused disease in these patients (4.5%); they were also responsible for three cases of disseminated infection. Clinical disease caused by M. tuberculosis or NTM and complete tuberculin anergy were associated with stage-IV HIV infection and with CD4 lymphocyte counts < or = 400/microL. However, the lack of immunocellular response, shown by limited tuberculin reactivity, was found beginning with the asymptomatic HIV carrier stage. The progressive deterioration of the immune system of HIV-positive patients is the determining factor in the high morbidity and mortality with mycobacteria infections and requires prompt chemoprophylaxis or treatment.

AIDS-Related Opportunistic Infections↗
PubMed1998

Ring A reductions of progestins are not essential for estrous behavior facilitation in estrogen-primed rats.

In Experiment 1 six dose levels (range 0.66-2000 microg) of progesterone (P) and two synthetic progestins with a double bond at C6: megestrol acetate (MA) and chlormadinone acetate (CA), which cannot be reduced at C5, were injected to estrogen-primed (2 microg estradiol benzoate 42 h earlier) ovariectomized (ovx) rats. The three progestins elicited significant lordosis and proceptive behaviors. Potency analysis showed that MA was the most potent progestin for stimulating estrous behavior, followed by P and CA. These results suggest that ring A reduction of progestins to 5alpha/5beta metabolites is not essential for the facilitation of estrous behavior in ovx estrogen-primed rats. Progestins with the 3-ketone group and a double bond at C4 can also be reduced at C3 to yield 3alpha-hydroxysteroid metabolites potentially capable of stimulating estrous behavior. In Experiment 2, the relevance of the formation of 3alpha-hydroxysteroid metabolites for estrous behavior facilitation was tested by concurrently injecting indomethacin (1.5 mg), a blocker of 3alpha-hydroxysteroid oxidoreductase, with 400 microg of P, MA, or CA to ovx estrogen-primed rats. Indomethacin failed to block the stimulatory effect of these progestins on estrous behavior. These results suggest that 3-ketosteroid reduction is also not essential for estrous behavior facilitation by progestins.

3-Hydroxysteroid Dehydrogenases↗
PubMed1997

The aberrant cell walls of boron-deficient bean root nodules have no covalently bound hydroxyproline-/proline-rich proteins.

B-deficient bean (Phaseolus vulgaris L.) nodules examined by light microscopy showed dramatic anatomical changes, mainly in the parenchyma region. Western analysis of total nodule extracts examined by sodium dodecyl sulfate-polyacrylamide gel electrophoresis showed that one 116-kD polypeptide was recognized by antibodies raised against hydroxyproline-rich glycoproteins (HRGPs) from the soybean (Glycine max) seed coat. A protein with a comparable molecular mass of 116 kD was purified from the cell walls of soybean root nodules. The amino acid composition of this protein is similar to the early nodulin (ENOD2) gene. Immunoprecipitation of the soybean ENOD2 in vitro translation product showed that the soybean seed coat anti-HRGP antibodies recognized this early nodulin. Furthermore, we used these antibodies to localize the ENOD2 homolog in bean nodules. Immunocytochemistry revealed that in B-deficient nodules ENOD2 was absent in the walls of the nodule parenchyma. The absence of ENOD2 in B-deficient nodules was corroborated by performing hydroxyproline assays. Northern analysis showed that ENOD2 mRNA is present in B-deficient nodules; therefore, the accumulation of ENOD2 is not affected by B deficiency, but its assembly into the cell wall is. B-deficient nodules fix much less N2 than control nodules, probably because the nodule parenchyma is no longer an effective O2 barrier.

Boron↗