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1.
Clin Infect Dis ; 61(2): 211-8, 2015 Jul 15.
Article in English | MEDLINE | ID: mdl-25838286

ABSTRACT

BACKGROUND: Helicobacter pylori, the main cause of peptic ulcer disease and gastric cancer in adult populations, is generally acquired during the first years of life. Infection can be persistent or transient and bacterial and host factors determining persistence are largely unknown and may prove relevant for future disease. METHODS: Two cohorts of healthy Chilean infants (313 total) were evaluated every 3 months for 18-57 months to determine pathogen- and host-factors associated with persistent and transient infection. RESULTS: One-third had at least one positive stool ELISA by age 3, with 20% overall persistence. Persistent infections were acquired at an earlier age, associated with more household members, decreased duration of breastfeeding, and nonsecretor status compared to transient infections. The cagA positive strains were more common in persistent stools, and nearly 60% of fully characterized persistent stool samples amplified cagA/vacAs1m1. Persistent children were more likely to elicit a serologic immune response, and both infection groups had differential gene expression profiles, including genes associated with cancer suppression when compared to healthy controls. CONCLUSIONS: These results indicate that persistent H. pylori infections acquired early in life are associated with specific host and/or strain profiles possibly associated with future disease occurrence.


Subject(s)
Feces/microbiology , Helicobacter Infections/epidemiology , Helicobacter pylori/isolation & purification , Antibodies, Bacterial/blood , Antigens, Bacterial/genetics , Asymptomatic Diseases , Bacterial Proteins/genetics , Child, Preschool , Chile/epidemiology , Cohort Studies , Enzyme-Linked Immunosorbent Assay , Gene Expression Profiling , Helicobacter Infections/immunology , Helicobacter Infections/microbiology , Helicobacter pylori/genetics , Helicobacter pylori/pathogenicity , Host-Pathogen Interactions , Humans , Infant , Polymerase Chain Reaction , Prospective Studies , Time Factors
2.
Rev. chil. endocrinol. diabetes ; 5(1): 6-12, ene. 2012. graf, ilus
Article in Spanish | LILACS | ID: lil-640646

ABSTRACT

Background: Circadian cortisol production results from the interaction of the circadian production of ACTH, the autonomic nervous system and intrinsic factors within the gland. An additional regulator is the neuro-hormone melatonin. In human adrenal gland cultures, melatonin inhibited ACTH stimulated cortisol production and Per1 mRNA expression. ACTH actions on the adrenal involve early and late responses. Aim: To investigate the effects of melatonin on the time course of ACTH stimulated cortisol production and of Per1 expression in the lamb adrenal gland. Material and Methods: Adrenal glands and plasma of five newborn lambs were obtained. Adrenal glands were cut in 15 mg explants. Three of these explants were stored for RNA extraction. The rest of explants were using in different culture protocols with ACTH and melatonin. Results: Lambs had an in vivo a circadian variation in plasma cortisol and in adrenal Per1 expression. In vitro, ACTH stimulated an early and late increase in cortisol production and an early increase in Per1 expression reaching a maximum at 3 hours of treatment. Melatonin inhibited the early Per1 response to ACTH without affecting the early ACTH stimulated cortisol production. However, melatonin inhibited the late response of cortisol production to ACTH. Conclusions: The inhibitory actions of melatonin on Per1 response to ACTH may contribute to the inhibitory effects of melatonin on adrenal steroidogenic response to ACTH.


Subject(s)
Animals , Adrenal Glands/metabolism , Hydrocortisone/metabolism , Adrenocorticotropic Hormone/metabolism , Melatonin/metabolism , Period Circadian Proteins , RNA, Messenger/metabolism , Circadian Rhythm , Culture Techniques , Sheep , Time Factors
3.
Mol Cell Endocrinol ; 349(1): 68-75, 2012 Feb 05.
Article in English | MEDLINE | ID: mdl-21840372

ABSTRACT

Throughout gestation, the close relationship between mothers and their progeny ensures adequate development and a successful transition to postnatal life. By living inside the maternal compartment, the fetus is inevitably exposed to rhythms of the maternal internal milieu such as temperature; rhythms originated by maternal food intake and maternal melatonin, one of the few maternal hormones that cross the placenta unaltered. The fetus, immature by adult standards, is however perfectly fit to accomplish the dual functions of living in the uterine environment and developing the necessary tools to "mature" for the next step, i.e. to be a competent newborn. In the fetal physiological context, organ function differs from the same organ's function in the newborn and adult. This may also extend to the developing circadian system. The information reviewed here suggests that the fetal circadian system is organized differently from that of the adult. Moreover, the fetal circadian rhythm is not just present simply as the initial immature expression of a mechanism that has function in the postnatal animal only. We propose that the fetal suprachiasmatic nucleus (SCN) of the hypothalamus and fetal organs are peripheral maternal circadian oscillators, entrained by different maternal signals. Conceptually, the arrangement produces internal temporal order during fetal life, inside the maternal compartment. Following birth, it will allow for postnatal integration of the scattered fetal circadian clocks into an adult-like circadian system commanded by the SCN.


Subject(s)
Circadian Rhythm , Fetus/physiology , Adrenal Glands/embryology , Adrenal Glands/metabolism , Animals , Female , Fetus/metabolism , Humans , Maternal-Fetal Exchange , Melatonin/metabolism , Melatonin/physiology , Pregnancy , Suprachiasmatic Nucleus/embryology , Suprachiasmatic Nucleus/metabolism
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