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Similar Activation (similar + activation)

Distribution by Scientific Domains

Medical Sciences	75%

Selected Abstracts

Do stress reactions cause abdominal obesity and comorbidities?

OBESITY REVIEWS, Issue 2 2001
P. Björntorp
Summary ,Stress' embraces the reaction to a multitude of poorly defined factors that disturb homeostasis or allostasis. In this overview, the activation of the hypothalamic-pituitary-adrenal (HPA) axis and the sympathetic nervous system have been utilized as objective measurements of stress reactions. Although long-term activation of the sympathetic nervous system is followed by primary hypertension, consequences of similar activation of the HPA axis have not been clearly defined. The focus of this overview is to examine whether or not repeated activation of these two stress centres may be involved in the pathogenesis of abdominal obesity and its comorbidities. In population studies adrenal hormones show strong statistical associations to centralization of body fat as well as to obesity. There is considerable evidence from clinical to cellular and molecular studies that elevated cortisol, particularly when combined with secondary inhibition of sex steroids and growth hormone secretions, is causing accumulation of fat in visceral adipose tissues as well as metabolic abnormalities (The Metabolic Syndrome). Hypertension is probably due to a parallel activation of the central sympathetic nervous system. Depression and ,the small baby syndrome' as well as stress exposure in men and non-human primates are followed with time by similar central and peripheral abnormalities. Glucocorticoid exposure is also followed by increased food intake and ,leptin resistant' obesity, perhaps disrupting the balance between leptin and neuropeptide Y to the advantage of the latter. The consequence might be ,stress-eating', which, however, is a poorly defined entity. Factors activating the stress centres in humans include psychosocial and socioeconomic handicaps, depressive and anxiety traits, alcohol and smoking, with some differences in profile between personalities and genders. Polymorphisms have been defined in several genes associated with the cascade of events along the stress axes. Based on this evidence it is suggested that environmental, perinatal and genetic factors induce neuroendocrine perturbations followed by abdominal obesity with its associated comorbidities. [source]

ORIGINAL ARTICLE: Pregnancy Does not Deter the Development of a Potent Maternal Protective CD8+ T-Cell Acquired Immune Response Against Listeria Monocytogenes Despite Preferential Placental Colonization

AMERICAN JOURNAL OF REPRODUCTIVE IMMUNOLOGY, Issue 1 2010
Lakshmi Krishnan
Problem Listeria monocytogenes (LM) preferentially colonizes the placenta and causes fetal loss and systemic disease during pregnancy. As systemic CD8+ T-cell memory is critical in controlling LM infection, we addressed the issue as to whether it is modulated during pregnancy. Method of study Pregnant mice were infected with LM and their immune response was quantified relative to the non-pregnant cohort using advanced immunological techniques. Results Pregnant mice exhibited progressive and massive placental LM infection leading to fetal resorptions. In contrast, they harbored significantly lower bacteria in spleen and liver relative to non-pregnant controls, and rapidly cleared systemic infection. Both pregnant and non-pregnant mice exhibited similar activation of systemic innate immunity. Moreover, LM infection in pregnant and non-pregnant hosts evoked strong antigen-specific cytolytic CD8+ T cells that produced IFN-,. Consequently, LM infection initiated during pregnancy afforded long-term protective memory to secondary infection. Conclusion Maternal hosts generate a normal Listeria -specific adaptive immunity in particular CD8+ T-cell memory response suggesting that systemic listeriosis during pregnancy may be an immunopathology associated with placental infection. [source]

Up-regulation of pro-inflammatory genes as adaptation to hypoxia in MCF-7 cells and in human mammary invasive carcinoma microenvironment

CANCER SCIENCE, Issue 4 2010
Marco Tafani
The role of tumor cells in synthesizing pro-inflammatory molecules is still controversial. Here we report that hypoxic treatment of the MCF-7 human mammary adenocarcinoma cell line induced activation of hypoxia-inducible factor 1, (HIF-1,) and nuclear factor-kappa B (NF-,B). Importantly, hypoxia regulated expression of alarmin receptors such as the receptor for advanced glycation end products (RAGE) and the purinoreceptor (P2X7R), and up-regulated inflammatory response (IR) genes such as the inducible enzymes nitric oxide synthase (NOS2), cycloxygenase (COX2), and the acute-phase protein pentraxin-3 (PTX3). Hypoxia also stimulated chemokine (C-X-C motif) receptor 4 (CXCR4) mRNA synthesis. In fact, the CXCR4 ligand stromal-derived factor-1, (SDF-1,) increased invasion and migration of hypoxic MCF-7 cells. Inhibition of HIF-1, by chetomin and NF-,B by parthenolide reduced mRNA and protein expression of the studied molecules and prevented invasion of hypoxic MCF-7 cells. Moreover, solid invasive mammary tumor microenvironment was analyzed after laser-capture microdissection (LCMD) comparing tumor versus host normal tissue. Nuclear translocation of HIF-1, and NF-,B and up-regulation of IR, CXCR4, estrogen receptor , (ER,), and epithelial growth factor receptor (EGFR) was observed in tumor but not in host normal tissue in the absence of a local inflammatory leukocyte infiltrate. We conclude that under hypoxic conditions MCF-7 cells acquire a pro-inflammatory phenotype, and that solid human mammary carcinoma evidenced a similar activation of HIF-1,, NF-,B, and IR genes in malignant tumor cells as compared to the normal host tissues. We suggest a role for IR activation in the malignant progression of transformed cells. (Cancer Sci 2010; 101: 1014,1023) [source]

A comparison of brain activation patterns during covert and overt paced auditory serial addition test tasks

HUMAN BRAIN MAPPING, Issue 6 2008
Cristina Forn
Abstract The Paced Auditory Serial Addition test (PASAT) is a sensitive task for evaluating cognitive impairment in patients with diffuse brain disorders, such as multiple sclerosis patients. Brain areas involved in this task have been investigated in diverse fMRI studies using different methodologies to control the subjects' responses during scanning. Here, we examined the possible differences between overt and covert responses during the PASAT task in 13 volunteers. Results showed similar activations in parietal and frontal brain areas during both versions of the task. The contrast between the two conditions (overt and covert) indicated that differences in these two methodologies were minimal. Unlike the covert condition, the overt version of the task obtained significant activations in the left superior and inferior frontal gyrus, bilateral occipital cortex, caudate nucleus and cerebellum. As expected, no significant overactivations were observed in the covert when compared with the overt condition. Discussion focuses on the lower cost of using verbal responses to monitor performance during the PASAT task, which might be generalisable to other frontal lobe tasks requiring discrete responses. Hum Brain Mapp, 2008. © 2007 Wiley-Liss, Inc. [source]