Human endotoxin tolerance is associated with enrichment of the CD14+ CD16+ monocyte subset.

Prior exposure to lipopolysaccharides (LPS) induces a state of cell resistance to subsequent LPS restimulation, known as endotoxin tolerance, mainly by repressing the expression of pro-inflammatory cytokines. We established an endotoxin tolerance model in human monocytes Endotoxin-tolerant cells showed a decrease in IκBα degradation and diminished expression of Tumor necrosis factor (TNF) (both messenger RNA [mRNA] and protein content). The myeloid differentiation factor 88 (MyD88)/MyD88 splice variant (MyD88s) ratio, an indirect way to test the Toll-like receptor 4 (TLR4) MyD88-dependent signaling cascade, did not change in endotoxin-tolerant cells when compared to LPS-stimulated or -unstimulated ones.

Nitric oxide metabolite production during exercise in chronic fatigue syndrome: a case-control study.

Background: Chronic fatigue syndrome (CFS) is a disabling illness of unknown etiology that is characterized by fatigue associated with a reduced ability to work, lasting for more than 6 months, and accompanied by a specific set of symptoms. The diagnosis remains difficult because of the absence of laboratory tests and is, therefore, made largely on the basis of the symptoms reported by the patient. The aim of this study was to analyze differences in blood nitrate levels in CFS patients and a matched control group after a physical exercise test.

Glycosylated VCAM-1 isoforms revealed in 2D western blots of HUVECs treated with tumoral soluble factors of breast cancer cells.

Background: Several common aspects of endothelial phenotype, such as the expression of cell adhesion molecules, are shared between metastasis and inflammation. Here, we analyzed VCAM-1 variants as biological markers of these two types of endothelial cell activation. With the combination of 2-DE and western blot techniques and the aid of tunicamycin, we analyzed N-glycosylation variants of VCAM-1 in primary human endothelial cells stimulated with either TNF or tumoral soluble factors (TSF's) derived from the human breast cancer cell line ZR75.

First CT findings and improvement in GOS and GOSE scores 6 and 12 months after severe traumatic brain injury.

Primary Objective: To analyse the association between individual initial computerized tomography (CT) scan characteristics and Glasgow Outcome Scale (GOS) and Extended Glasgow Outcome Scale (GOSE) improvement between 6 months and 1 year.

Methods And Procedures: Two hundred and twenty-four adult patients with severe traumatic brain injury and Glasgow Coma Scale (GCS) score of 8 or less who were admitted to an intensive care unit were studied. GOS and GOSE scores were obtained 6 and 12 months after injury in 203 subjects.

Improvement in GOS and GOSE scores 6 and 12 months after severe traumatic brain injury.

Primary Objective: To assess improvements in Glasgow Outcome Scale (GOS) and GOS extended (GOSE) scores between 6 months and 1 year following severe traumatic brain injury (TBI).

Methods And Procedures: One studied 214 adult patients with severe TBI with Glasgow Coma Scale (GCS) <9 admitted to Intensive Care Unit (ICU). GOS scores were obtained 6 and 12 months after injury in 195 subjects.

Allelochemical stress causes inhibition of growth and oxidative damage in Lycopersicon esculentum Mill.

The aim of this study was to analyse the effect of allelochemical stress on Lycopersicon esculentum growth. Our results showed that allelochemical stress caused by Sicyos deppei aqueous leachate inhibited root growth but not germination, and produced an imbalance in the oxidative status of cells in both ungerminated seeds and in primary roots. We observed changes in activity of catalase (CAT), ascorbate peroxidase (APX), superoxide dismutase (SOD), glutathione reductase (GR) and the plasma membrane NADPH oxidase, as well as in the levels of H(2)O(2) and O(2) (*-) in seeds at 12 and 24 h, and in primary roots at 48 and 72 h of treatment, which could account for the oxidative imbalance.

Bcl-2 protects against oxidative stress while inducing premature senescence.

Replicative senescence is a cellular response to stress that has been postulated to serve as a tumor suppression mechanism and a contributor to aging. Numerous experimental studies have demonstrated that an apparently identical senescent state can also be prematurely induced in vitro in different cell types following sublethal oxidative stress stimuli. The former suggests a molecular link between cell cycle regulation and cell survival that could involve regulatory proteins such as Bcl-2.

Organ- and tissue-specific alterations in the anti-apoptotic protein Bcl-2 in CD1 female mice of different ages.

The anti-apoptotic protein Bcl-2, which also has cytoprotective and antioxidant functions might be one of the crucial factors that altogether, establish how a cell may deal with stress and damage, contributing to longevity. Among the controversial issues to understand Bcl-2 functions in vivo, is to establish its content and variation in tissues during an organismal lifespan. In this work we analyzed the changes of Bcl-2 levels in lung, liver, heart, kidney, spleen and brain homogenates obtained from CD1 mice throughout their lifespan (newborn to 24 months).

Dehydroepiandrosterone inhibits the proliferation of human umbilical vein endothelial cells by enhancing the expression of p53 and p21, restricting the phosphorylation of retinoblastoma protein, and is androgen- and estrogen-receptor independent.

Dehydroepiandrosterone (DHEA), a steroid hormone, modified the proliferation of human umbilical vein endothelial cells in a dose-dependent manner. Its inactive sulfate ester (DHEA-S) and two of its metabolites -- estradiol and testosterone -- had no inhibitory effect at physiological concentrations. Antiproliferation was associated with arrest in the G1 phase of the cell cycle, but not with cell death, as evaluated by cleavage of poly(ADP-ribose) polymerase and exposure of phosphatidylserine.

Senescent phenotype achieved in vitro is indistinguishable, with the exception of Bcl-2 content, from that attained during the in vivo aging process.

Senescent phenotype can be attained by diverse agents, thus suggesting that there might be molecular differences between the senescence achieved in vivo and the senescence-like state attained in vitro under culture conditions. In this study we compare the senescent phenotype reached by cells derived from young animals when cultured in vitro with the one associated with the in vivo aging process. Several in vitro senescence parameters, including MTT reduction, proliferation rate, DNA synthesis, SA-beta-gal staining, and both in vivo and in vitro Bcl-2 content, were determined.

CD4+ and CD19+ splenocytes undergo apoptosis during an experimental murine infection with Taenia crassiceps.

The Taenia crassiceps cysticercus is a cestode that naturally and experimentally infects rodents in which it reproduces by budding. In the laboratory, a persistent cellular immunosuppression with a concomitant increasing load of parasites has been observed in experimentally infected BALB/cAnN mice. In this study, enhanced apoptosis was found in spleen cells from 30-day infected mice with a typical "ladder-patterned" DNA fragmentation and an increase in phosphatidylserine expression.

Ceramide promotes the death of human cervical tumor cells in the absence of biochemical and morphological markers of apoptosis.

C8-ceramide, a synthetic cell-permeable analog of endogenous ceramides, interfered with cell proliferation, and was cytotoxic to papilloma virus-containing human cervix carcinoma cells, CALO, INBL, and HeLa, that match two clinical stages of tumor progression. C8-ceramide (3 microM) markedly reduced the tumor cell number after 48 h of treatment, an effect that endured even after the removal of C8-ceramide. The carcinoma cells showed morphologic changes, characteristic of necrosis and released lactate dehydrogenase (LDH).