Functional dyspepsia and depression as an associated factor

AIM: To assess the association between depression and functional dyspepsia. PATIENTS AND METHODS: Three hundred and forty eight dyspeptic patients were included in a cross-sectional study in the gastroenterology outpatient clinic of a University Hospital in southern Brazil (Pelotas, RS) within a 1-year period (from March, 2001 to March, 2002). The assessment of depression occurred after the diagnosis of dyspepsia. The presence (or not) of depression was verified in both functional and organic dyspeptic patients. In a second moment, the results were compared, an univariate analysis was used to describe the frequencies of the interest variables and a chi-square for the comparison between proportions of the categorical variables. The logistic regression technique was used to establish the odd of functional dyspeptic patients to present depression and to control the effect of other variables in the outcome variable RESULTS: Showed greater prevalence of depression among functional dyspepsia patients (30,4%), when compared to organic dyspepsia patients (11,2%). Women showed greater risk to present functional dyspepsia (OR: 1,74, IC 95%, 1,05-2,89) and in terms of age, the group with ages between 31 to 50 years (OR: 0,28 IC 95%, 0,13-0,54) and 51 to 60 years (OR: 0,41, IC 95%, 0,17-0,96) showed protection effect (subjects within this age groups have minor risk to present functional dyspepsia). After the multivariate analysis depressed patients showed three times greater comorbidity with functional dyspepsia when compared to non-depressed patients (OR 3, 13; IC 95%; 1, 71-5, 74). DISCUSSION: The adjustment for the gender, age and marital status variables confirmed the association between functional dyspepsia and depression. Results point the need to assess the presence of depression in functional dyspepsia patients and to establish specific treatment strategies for these patients.     

A recombinant probiotic for treatment and prevention of cholera

BACKGROUND & AIMS: We have developed a therapeutic strategy based on molecular mimicry of host receptors for bacterial toxins on the surface of harmless gut bacteria. In the present study, this has been applied to the development of a recombinant probiotic for treatment and prevention of cholera, caused by Vibrio cholerae. METHODS: We expressed glycosyltransferase genes from Neisseria gonorrhoeae and Campylobacter jejuni in a harmless Escherichia coli strain, resulting in production of a chimeric lipopolysaccharide terminating in a mimic of the ganglioside GM(1). RESULTS: The recombinant bacterium was capable of binding cholera toxin, a sine qua non of virulence, with high avidity; when tested with purified cholera toxin, it was capable of adsorbing >5% of its own weight of toxin in vitro. Administration of the GM(1)-expressing probiotic also protected infant mice against challenge with virulent V cholerae, even when treatment was delayed until after establishment of infection. When treatment commenced 1 hour after challenge, 12 of 12 mice given the probiotic survived, compared with only 1 of 12 for control mice (P < .00001). CONCLUSIONS: Toxin-binding probiotics such as that described here have considerable potential for prophylaxis and treatment of cholera in humans.     

Neutrophil infiltration is implicated in the sustained thermal hyperalgesic response evoked by allergen provocation in actively sensitized rats

It has been proposed that allergen provocation induces hyperalgesia but the involvement of immunoglobulin E and leukocytes remains poorly understood. Here, we have compared the profile of allergen-evoked thermal hyperalgesic response in both passively and actively sensitized rats, and investigated the role of leukocytes in allergen-evoked nociception. Wistar rats were passively sensitized with an intraplantar injection of immunoglobulin E anti-dinitrophenylated bovine serum albumin monoclonal antibody (0.5 microg/paw), and challenged with dinitrophenylated bovine serum albumin (0.5 microg/paw) 24 h later. Alternatively, the animals were actively sensitized with a mixture of Al(OH)3 and ovalbumin and challenged intraplantarly with ovalbumin (12 microg/paw) 14 days later. We found that the thermal hyperalgesic responses set in very rapidly and with comparable intensity in both passively and actively sensitized rats. However, while in the former group the response was shorter, peaking within 1 h and reducing thereafter, a marked plateau was observed from 1 to 6 h post-challenge in the latter group. Actively sensitized rats also had higher neutrophil influx in the plantar tissue, as attested by both myeloperoxidase activity and histological analysis. Treatment of actively sensitized rats with either fucoidin (10 mg/kg, i.v) or anti-rat neutrophil antiserum (i.p.) reduced neutrophil accumulation and the late hyperalgesic response noted from 3 to 6 h post-challenge. Thus, we conclude that though immunoglobulin E-mediated mechanisms can cause thermal hyperalgesia, components of the cellular immune reaction are crucial in order to amplify and sustain the immediate hyperalgesic response triggered by allergen, in a process dependent on neutrophil recruitment.     

Influence of hepatitis C genotypes on lipid levels in HIV-positive patients during highly active antiretroviral therapy

BACKGROUND: The independent role of HCV genotype 3 (HCV-3) in dyslipidaemia following highly active antiretroviral therapy (HAART) is still unexplored. METHODS: Analysis of data from a cohort of 307 HIV/HCV-coinfected patients and 415 HIV-monoinfected controls was conducted. Patients with available lipid levels at baseline and minimum 3-month follow-up were ranked into three groups by HCV status (HCV-3, other HCV genotypes or HCV negative). Univariate and multivariate GEE models were performed to assess factors correlated with lipid serum levels as coefficient (Coef., defined as mean difference [mg/dl] across the follow-up). Univariate and multivariate logistic regression analyses were performed for prediction of relevant hypertriglyceridaemia (> or = 500 mg/dl) and relevant hypercholesterolaemia (> or = 240mg/dl) at 3 months of follow-up. RESULTS: HCV-3 correlated with lower triglyceridaemia (Coef.=-38.22; P=0.001), independently from the other considered variables, including age, gender and use of stavudine or lopinavir. Even though HCV infection per se appeared to be protective, HCV-3 in particular was also independently associated with lower cholesterolaemia (Coef.=-46.35; P<0.001). At logistic regression analyses, HCV-3, but not HCV-non-3, was associated with lower risk of relevant hypercholesterolaemia (odds ratio [OR] 0.06; P=0.01) and relevant hypertriglyceridaemia (OR 0.11; P=0.05), independently from other considered variables. CONCLUSIONS: Our data confirm that HCV coinfection per se is associated with lower risk of hypercholesterolaemia after HAART. This effect was particularly attributed to HCV-3, which was the only genotype associated with lower triglyceridaemia during HAART.     

Structural and phylogenetic approaches to assess the significance of human Apolipoprotein E variation

Apolipoprotein E (APOE) is an important gene whose common polymorphism, and precisely the e *4 allele, has been reportedly associated with some disorders, including Alzheimer's disease (AD) and coronary artery disease. In the course of previous surveys on AD patients and healthy individuals some rare variants were detected by means of Isoelectric focusing and denaturing high-performance liquid chromatography techniques. After a mutation in a gene is identified, the problem arises to understand its effective significance. Structure modelling and phylogenetic analysis methods are widely used to establish the possible deleterious effect of mutations. In this study their usefulness in the analysis of APOE variants was evaluated. The two combined methods provided helpful indications for distinguishing between mutations possibly involved in AD susceptibility and not deleterious mutations.     

Permeability of enamel following light-activated power bleaching

This study sought to ascertain whether in-office photocured bleaching techniques would increase permeability to enamel. A 7.1 mm2 circular area located in the middle third of the coronal portion of 90 human canines was isolated by applying an acid-resistant varnish to the remaining surfaces of the tooth. According to a randomized complete block design (n = 15), specimens were treated using a 35% hydrogen peroxide bleaching product activated by an integrated LED/diode laser (LED/laser) source or a quartz tungsten halogen (QTH) light. Bleaching was accomplished by applying the 35% hydrogen peroxide agent to the enamel surface in three 10-minute sessions, conducted at one-week intervals over a period of three weeks. For the photocured bleached groups, a bleaching agent was applied to the specimen and irradiated with the LED/laser device or the QTH light for 30 seconds. Negative control groups were exposed to artificial saliva or irradiated by the LED/laser device or the QTH light. Specimens were subjected to a histochemical coloring method that employed copper sulfate and dithio-oxamide solutions. Three 300-microm thick sections taken from the exposed area were imaged in an optical microscope. Permeability was measured in the digitized images as the percentage of copper ions penetration over the total enamel thickness. Friedman's test (alpha = 0.05) showed significant difference among groups. Least significant difference test revealed that in comparison with the group treated with 35% hydrogen peroxide only, there was no significant increase in enamel permeability when bleaching was activated by either the LED/laser or QTH light devices but all bleached groups showed higher permeability than the unbleached/nonirradiated group.