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Death
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1. Deactivation of phosphatidylinositol 3,4,5-trisphosphate/Akt signaling mediates neutrophil spontaneous death.
Match Strength: 4.734

Neutrophil spontaneous death plays essential roles in neutrophil homeostasis and resolution of inflammation, whereas the underlying molecular mechanisms are still ill-defined. Neutrophils die because of programmed cell death or apoptosis. However, treatment with inhibitor of caspases, which are responsible for the majority of apoptotic cell deaths, does not prevent the spontaneous death of neutrophils. PKB/Akt possesses prosurvival and antiapoptotic activities in a variety of cells. In this study, we show that Akt activity decreases dramatically during the course of neutrophil death. Both ... Read More »
» Published in Proc Natl Acad Sci U S A. 2006 Oct 3;103(40):14836-41. Epub 2006 Sep 20.

2. Upon intracellular processing, the C-terminal death domain-containing fragment of the p53-inducible PIDD/LRDD protein translocates to the nucleoli and interacts with nucleolin.
Match Strength: 4.348

The p53-inducible and death domain-containing PIDD/LRDD protein has been described as an adaptor protein, which forms large protein complexes with RAIDD, another death domain-containing protein, leading to recruitment, and activation of the initiator caspase-2, and p53-mediated apoptosis. Here, we describe in further detail the proteolytic processing of PIDD/LRDD that occurs in healthy cells before induction of apoptosis. We could demonstrate that the C-terminal fragment containing the PIDD death domain shuttles into the nucleoli. This translocation is mediated by or leads to the interaction ... Read More »
» Published in Biochem Biophys Res Commun. 2006 Nov 3;349(4):1329-38. Epub 2006 Sep 8.

3. Megakaryocytic dysfunction in myelodysplastic syndromes and idiopathic thrombocytopenic purpura is in part due to different forms of cell death.
Match Strength: 4.298

Platelet production requires compartmentalized caspase activation within megakaryocytes. This eventually results in platelet release in conjunction with apoptosis of the remaining megakaryocyte. Recent studies have indicated that in low-risk myelodysplastic syndromes (MDS) and idiopathic thrombocytopenic purpura (ITP), premature cell death of megakaryocytes may contribute to thrombocytopenia. Different cell death patterns have been identified in megakaryocytes in these disorders. Growing evidence suggests that, besides apoptosis, necrosis and autophagic cell death, may also be programmed. ... Read More »
» Published in Leukemia. 2006 Nov;20(11):1937-42. Epub 2006 Sep 7.

4. p27 small interfering RNA induces cell death through elevating cell cycle activity in cultured cortical neurons: a proof-of-concept study.
Match Strength: 4.196

Recent research has demonstrated that cell cycle-associated molecules are activated in multiple forms of cell death in mature neurons, and raised a hypothesis that unscheduled cell cycle activity leads to neuronal cell death. But there is little evidence that changes in endogenous level of these molecules are causally associated with neuronal cell death. Here we transfected small interfering RNA (siRNA) targeting cyclin-dependent kinase (CDK) inhibitor p27, which plays an important role in cell cycle arrest at G1-S phase, into cultured cortical neurons. Transfection of p27 siRNA reduced ... Read More »
» Published in Cell Mol Life Sci. 2006 Oct;63(19-20):2397-404. Erratum in: Cell Mol Life Sci. 2006 Dec;63(24):3090.

5. Calcium and reactive oxygen species mediated Zn2+ -induced apoptosis in PC12 cells.
Match Strength: 4.087

The release of excessive Zn(2+) from presynaptic boutons into extracellular regions contributes to neuronal apoptotic events, which result in neuronal cell death. However, the mechanisms of Zn(2+)-induced neuronal cell death are still unclear. Therefore, we investigated the dynamics of intracellular Zn(2+), calcium, and reactive oxygen species in PC12 cells. The addition of Zn(2+) produced cell death in a concentration- and time-dependent manner. (45)Ca(2+) influx occurred just after the treatment with Zn(2+), although subsequent hydroxyl radical ((*)OH) production did not begin until 3 h ... Read More »
» Published in J Pharmacol Sci. 2006 Sep;102(1):103-11.

6. Anesthesiologists are living longer: mortality experience 1992 to 2001.
Match Strength: 4.039

STUDY OBJECTIVE: To determine whether there has been any recent change in the mortality experience of American anesthesiologists. DESIGN: Retrospective analysis of obituary reports to the Physician Master File (PMF) of the American Medical Association. MEASUREMENTS: Data were collected from the PMF of anesthesiologists and obstetricians. All data were identified from the PMF. A total of 1525 obituaries of anesthesiologists and 2773 obituaries of obstetricians during the study period, 1992 to 2001, were reviewed. Mean age of living or mean age at death of anesthesiologists and obstetricians, as ... Read More »
» Published in J Clin Anesth. 2006 Sep;18(6):405-8. Comment in: J Clin Anesth. 2006 Sep;18(6):403-4.

7. Determinants of sudden cardiac death in patients with persistent atrial fibrillation in the rate control versus electrical cardioversion (RACE) study.
Match Strength: 3.966

This report evaluated the correlates of sudden cardiac and nonsudden cardiac death in patients with persistent atrial fibrillation randomized to rate or rhythm control in the RAte Control vs Electrical cardioversion (RACE) study. Sudden cardiac death was observed in 16 patients, 8 patients in each group. Previous myocardial infarction resulted in a 4.9-fold increased risk of sudden death (95% confidence interval 1.8 to 13.2). The use of beta blockers showed their protective nature (hazard ratio 0.2, 95% confidence interval 0.05 to 0.9). The randomized treatment strategy, heart rhythm during ... Read More »
» Published in Am J Cardiol. 2006 Oct 1;98(7):929-32. Epub 2006 Aug 11.

8. RTP801 is elevated in Parkinson brain substantia nigral neurons and mediates death in cellular models of Parkinson's disease by a mechanism involving mammalian target of rapamycin inactivation.
Match Strength: 3.800

The molecules underlying neuron loss in Parkinson's disease (PD) are essentially unknown, and current therapies focus on diminishing symptoms rather than preventing neuron death. We identified RTP801 as a gene whose transcripts were highly induced in a cellular model of PD in which death of neuronal catecholaminergic PC12 cells was triggered by the PD mimetic 6-OHDA. Here, we find that RTP801 protein is also induced in this and additional cellular and animal PD models. To assess the relevance of these observations to PD, we used immunohistochemistry to compare RTP801 expression in postmortem ... Read More »
» Published in J Neurosci. 2006 Sep 27;26(39):9996-10005.

9. Edelfosine and perifosine induce selective apoptosis in multiple myeloma by recruitment of death receptors and downstream signaling molecules into lipid rafts.
Match Strength: 3.768

Multiple myeloma (MM) is an incurable B-cell malignancy, requiring new therapeutic strategies. We have found that synthetic alkyl-lysophospholipids (ALPs) edelfosine and perifosine induced apoptosis in MM cell lines and patient MM cells, whereas normal B and T lymphocytes were spared. ALPs induced recruitment of Fas/CD95 death receptor, Fas-associated death domain-containing protein, and procaspase-8 into lipid rafts, leading to the formation of the death-inducing signaling complex (DISC) and apoptosis. TNF-related apoptosis-inducing ligand receptor-1/death receptor 4 (TRAIL-R1/DR4) and TRAIL ... Read More »
» Published in Blood. 2007 Jan 15;109(2):711-9. Epub 2006 Sep 26.

10. Urothelial cells malignantly transformed by exposure to cadmium (Cd(+2)) and arsenite (As(+3)) have increased resistance to Cd(+2) and As(+3)-induced cell death.
Match Strength: 3.752

This laboratory has shown that both Cd(+2) and As(+3) can malignantly transform human urothelial cells. The present study examined metal resistance and the mechanism of cell death when the parental and malignantly transformed UROtsa cells were exposed to Cd(+2) and As(+3). It was shown that the malignantly transformed UROtsa cells were more resistant to the toxic effects of both metals. The assessment of the mode of cell death demonstrated that the parental UROtsa cells died by both apoptosis and necrosis when exposed to either metal. It was shown that apoptosis was the more prominent ... Read More »
» Published in Toxicol Sci. 2006 Dec;94(2):293-301. Epub 2006 Sep 15.

11. Effects of statin therapy on arrhythmic events and survival in patients with nonischemic dilated cardiomyopathy.
Match Strength: 3.705

OBJECTIVES: We sought to evaluate whether statins were associated with a survival benefit and significant attenuation in life-threatening arrhythmias in patients with nonischemic dilated cardiomyopathy. BACKGROUND: Statins are associated with a reduction in appropriate implantable cardioverter-defibrillator (ICD) therapy in patients with coronary artery disease and improved clinical status in nonischemic dilated cardiomyopathy. METHODS: The effect of statin use on time to death or resuscitated cardiac arrest and time to arrhythmic sudden death was evaluated in 458 patients enrolled in the ... Read More »
» Published in J Am Coll Cardiol. 2006 Sep 19;48(6):1228-33. Epub 2006 Aug 28.

12. Maternal morbidity and mortality associated with delivery after intrauterine fetal death.
Match Strength: 3.675

Objective: To determine the maternal morbidity and mortality associated with delivery after intrauterine fetal death (IUFD) and to find out the place of fetal destructive procedures and cesarean section. Design: Cross-sectional study. Place and Duration of Study : Labour Room, Nishtar Hospital, Multan from January to December 2003. Patients and Methods: All women were included in the present study who presented before the onset of labour pains, after intrauterine fetal death at 26 weeks or onward with singleton pregnancy. Assessment of maternal demographic characteristics, gestational age at ... Read More »
» Published in J Coll Physicians Surg Pak. 2006 Oct;16(10):648-51.

13. Differential efflux of mitochondrial endonuclease G by hNoxa and tBid.
Match Strength: 3.593

The Bcl-2 family of proteins regulates mitochondrial functions during cell death by modulating the efflux of death-promoting proteins such as cytochrome c and endonuclease G. Upon the binding of death ligands to their receptors, caspase-8 cleaves Bid, a BH3-only protein, into tBid that causes the mitochondrial damages resulting in the release of cytochrome c and endonuclease G. Also, another BH3-only protein, hNoxa, has been shown to induce the efflux of cytochrome c from the mitochondria. Whether the efflux proteins from the mitochondria in response to tBid or hNoxa are the same or different, ... Read More »
» Published in J Biochem Mol Biol. 2006 Sep 30;39(5):556-9.

14. Comparison of mortality rates in statin users versus nonstatin users in a United States veteran population.
Match Strength: 3.591

Statins have been shown to be effective in reducing cardiovascular events and overall mortality in primary and secondary prevention trials. This study was designed to examine the effect of statin use on overall death. Cross-sectional data were obtained from the Department of Veterans Affairs Veterans Integrated Service Network 16 database for approximately 1.5 million veterans followed up in 10 hospitals in the southern United States. Statins were prescribed more often to elderly subjects with a history of coronary artery disease, hypertension, diabetes mellitus, current smoking, and using ... Read More »
» Published in Am J Cardiol. 2006 Oct 1;98(7):923-8. Epub 2006 Aug 7.

15. Death receptor ligation triggers membrane scrambling between Golgi and mitochondria.
Match Strength: 3.503

Subcellular organelles such as mitochondria, endoplasmic reticulum (ER) and the Golgi complex are involved in the progression of the cell death programme. We report here that soon after ligation of Fas (CD95/Apo1) in type II cells, elements of the Golgi complex intermix with mitochondria. This mixing follows centrifugal dispersal of secretory membranes and reflects a global alteration of membrane traffic. Activation of apical caspases is instrumental for promoting the dispersal of secretory organelles, since caspase inhibition blocks the outward movement of Golgi-related endomembranes and ... Read More »
» Published in Cell Death Differ. 2006 Sep 29;

16. Acute morphological sequelae of photodynamic therapy with 5-aminolevulinic acid in the C6 spheroid model.
Match Strength: 3.441

OBJECTIVE: Aminolevulinic acid (ALA)-mediated photodynamic therapy (PDT) may represent a treatment option for malignant brain tumors. We used a three-dimensional cell culture system, the C6 glioma spheroid model, to study acute effects of PDT and how they might be influenced by treatment conditions. METHODS: Spheroids were incubated for 4 h in 100 mug/ml ALA in 5% CO(2) in room air or 95% O(2) with subsequent irradiation using a diode laser (lambda = 635 nm, 40 mW/cm(2), total fluence 25 J/cm(2)). Control groups were "laser only", "ALA only", and "no drug no light". Annexin V-FITC, a marker ... Read More »
» Published in J Neurooncol. 2006 Sep 27;

17. High energy compound stability during experimental brain death.
Match Strength: 3.422

The aim of this study was to examine the effect of sudden brain death (BD) on myocardial function and high energy phosphate (HEP) stores. BD was induced by cerebral vessel ligation in six swine (BD group) that were compared to six control swine. At the end of the BD period (3 hours), harvested hearts were stored at 4 degrees C. Myocardial tissue HEP were assessed by: (i) (31)P-NMR spectroscopy of left ventricle for phosphocreatine (PCr), adenosine triphosphate (ATP), inorganic phosphate (Pi) and intracellular pH (pHi), and by (ii) HPLC for ATP, ADP, and AMP levels in left ventricle biopsies. ... Read More »
» Published in Transplant Proc. 2006 Sep;38(7):2285-6.

18. Withdrawing implantable defibrillator shock therapy in terminally ill patients.
Match Strength: 3.392

PURPOSE: The purpose of this study is to review a multidisciplinary strategy used to identify patients with terminal illnesses and initiate withdrawal of implantable cardioverter defibrillator (ICD) shock therapy as part of a comprehensive comfort care approach. With indications for ICDs increasing, more patients are receiving devices. Once protected from an arrhythmic death, these patients may develop other terminal diseases such as cancer or congestive heart failure. It is appropriate to withdraw defibrillator shock therapy when such patients desire only comfort care. METHODS: The charts of ... Read More »
» Published in Am J Med. 2006 Oct;119(10):892-6.

19. Differential mechanisms of conjunctival cell death induction by ultraviolet irradiation and benzalkonium chloride.
Match Strength: 3.388

PURPOSE: To determine the molecular mechanisms of conjunctival cell death on exposure to the quaternary ammonium preservative benzalkonium chloride (BAC) and ultraviolet (UV) irradiation. METHODS: Chang conjunctival cells, either wild-type or stably transfected with various constructs encoding antiapoptotic molecules or transiently transfected with siRNA targeting the beclin-1 gene, were exposed to BAC or UV radiation Cell death was analyzed morphologically with fluorescence and electron microscopy, and molecular mechanisms of death were studied by using immunofluorescence, cell fractionation, ... Read More »
» Published in Invest Ophthalmol Vis Sci. 2006 Oct;47(10):4221-30.

20. Cholinergic receptor-independent dysfunction of mitochondrial respiratory chain enzymes, reduced mitochondrial transmembrane potential and ATP depletion underlie necrotic cell death induced by the organophosphate poison mevinphos.
Match Strength: 3.290

Our current understanding of the nature of cell death that is associated with fatal organophosphate poisoning and the underlying cellular mechanisms is surprisingly limited. Taking advantage of the absence in an in vitro system of acetylcholinesterase, the pharmacological target of organophosphate compounds, the present study evaluated the hypothesis that the repertoire of cholinergic receptor-independent cellular events that underlie fatal organophosphate poisoning entails induction of mitochondrial dysfunction, followed by bioenergetic failure that leads to necrotic cell death because of ATP ... Read More »
» Published in Neuropharmacology. 2006 Dec;51(7-8):1109-19. Epub 2006 Sep 18.

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