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Journals Progress in Clinical and Biolo...

Progress in Clinical and Biological Research

https://read.qxmd.com/read/9669924/endotoxin-and-sepsis-molecular-mechanisms-of-pathogenesis-host-resistance-and-therapy-proceedings-of-the-4th-conference-of-the-international-endotoxin-society-nagoya-japan-october-23-27-1996
#1
(no author information available yet)
No abstract text is available yet for this article.
1998: Progress in Clinical and Biological Research
https://read.qxmd.com/read/9575578/the-pathogenic-role-of-lbp-in-gram-negative-sepsis-and-septic-shock
#2
REVIEW
D Heumann, S Lengacher, D Le Roy, C V Jongeneel, M P Glauser
No abstract text is available yet for this article.
1998: Progress in Clinical and Biological Research
https://read.qxmd.com/read/9575577/the-role-of-interleukin-6-in-endotoxin-induced-inflammatory-responses
#3
REVIEW
T van der Poll, S J van Deventer
No abstract text is available yet for this article.
1998: Progress in Clinical and Biological Research
https://read.qxmd.com/read/9575576/role-of-nitric-oxide-and-reactive-oxygen-species-in-endotoxin-shock
#4
JOURNAL ARTICLE
T Yoshikawa, H Takano, M Kondo
No abstract text is available yet for this article.
1998: Progress in Clinical and Biological Research
https://read.qxmd.com/read/9575575/interaction-of-lipopolysaccharide-with-a-mammalian-lyso-phosphatidate-acyltransferase-lpaat-transfected-into-e-coli-and-effect-of-lisofylline-on-lpaat-transfected-into-mammalian-cells
#5
JOURNAL ARTICLE
S L Bursten
1. Lipid A and LPS stimulate LPAAT activity (and hence unsaturated PA formation) in RMC membranes and whole cells. 2. This correlates with cell phenotypic and membrane changes associated with small G proteins. 3. Unsaturated PA and Lipid A have similar effects on cells when given exogenously. 4. Human LPAAT-alpha and -beta isoforms were cloned and transfected into E. coli, demonstrating the ability to restore PA synthesis and reduce lyso-PA accumulation in plsC strains (LPAAT deficient mutants), as well as restoring growth at high temperatures...
1998: Progress in Clinical and Biological Research
https://read.qxmd.com/read/9575574/suppression-of-tnf-and-other-proinflammatory-cytokines-by-the-tetravalent-guanylhydrazone-cni-1493
#6
REVIEW
K J Tracey
No abstract text is available yet for this article.
1998: Progress in Clinical and Biological Research
https://read.qxmd.com/read/9575573/prevention-of-endotoxin-shock-through-targeting-leukocyte-adhesion-molecules
#7
JOURNAL ARTICLE
H Higashi, N Mukaida, A Harada, S Watanabe, N Ikeda, Y Suzuki, K Matsushima
No abstract text is available yet for this article.
1998: Progress in Clinical and Biological Research
https://read.qxmd.com/read/9575572/natural-and-synthetic-polypeptides-that-recognize-the-conserved-lipid-a-binding-site-of-lipopolysaccharides
#8
JOURNAL ARTICLE
M Porro, A Rustici, M Velucchi, D Agnello, P Villa, P Ghezzi
No abstract text is available yet for this article.
1998: Progress in Clinical and Biological Research
https://read.qxmd.com/read/9575571/the-molecular-basis-for-therapeutic-concepts-utilizing-cd14
#9
JOURNAL ARTICLE
F Stelter, M Bernheiden, R Menzel, S Witt, R S Jack, U Grunwald, X Fan, C Schütt
The CD14 molecule is a key receptor on myeloid lineage cells involved in the recognition of lipopolysaccharide (LPS) and Gram-negative bacteria. The application of its soluble form, sCD14, has been shown to protect mice from lethality in LPS-induced shock. Therefore the protein or its derivatives may be considered as a possible therapeutic alternative for the treatment of patients suffering from Gram-negative septic shock. In this study we performed an alanine scan of amino acids 1 to 152 of human CD14. Twenty-three substitution mutants were generated and stably transfected into CHO-cells...
1998: Progress in Clinical and Biological Research
https://read.qxmd.com/read/9575570/natural-and-synthetic-lps-and-lipid-a-analogs-or-partial-structures-that-antagonize-or-induce-tolerance-to-lps
#10
JOURNAL ARTICLE
N Qureshi, B Jarvis, K Takayama, N Sattar, J Hofman, P Stütz
No abstract text is available yet for this article.
1998: Progress in Clinical and Biological Research
https://read.qxmd.com/read/9575569/the-protective-effect-of-prostaglandin-e1-on-endotoxin-induced-hepatocyte-injury
#11
JOURNAL ARTICLE
H Shimada, A Nakano, H Kurosawa, S Natori, Y Fujii
No abstract text is available yet for this article.
1998: Progress in Clinical and Biological Research
https://read.qxmd.com/read/9575568/production-of-nontoxic-lipid-a-by-chemical-modification-and-its-antagonistic-effect-on-lps-activity
#12
JOURNAL ARTICLE
K Tanamoto
No abstract text is available yet for this article.
1998: Progress in Clinical and Biological Research
https://read.qxmd.com/read/9575567/reconciling-the-concepts-of-endotoxin-sensitization-and-tolerance
#13
REVIEW
M A Freudenberg, R Salômao, A Sing, I Mitov, C Galanos
No abstract text is available yet for this article.
1998: Progress in Clinical and Biological Research
https://read.qxmd.com/read/9575566/role-of-cd14-in-infection-studies-in-cd14-deficient-mice
#14
JOURNAL ARTICLE
A Haziot, N Hijiya, S M Goyert
No abstract text is available yet for this article.
1998: Progress in Clinical and Biological Research
https://read.qxmd.com/read/9575565/stimulation-of-human-t-lymphocytes-by-lipopolysaccaride-lps-in-the-presence-of-autologous-and-heterologous-monocytes
#15
JOURNAL ARTICLE
T Mattern, H D Flad, A J Ulmer
No abstract text is available yet for this article.
1998: Progress in Clinical and Biological Research
https://read.qxmd.com/read/9575564/apoptotic-cell-death-in-response-to-lps
#16
REVIEW
T Yokochi, A Morikawa, Y Kato, T Sugiyama, N Koide
No abstract text is available yet for this article.
1998: Progress in Clinical and Biological Research
https://read.qxmd.com/read/9575563/lipopolysaccharide-lps-antibodies-regulate-cellular-uptake-of-lps-and-lps-induced-proinflammatory-responses
#17
REVIEW
C A Ohl, M Pollack
No abstract text is available yet for this article.
1998: Progress in Clinical and Biological Research
https://read.qxmd.com/read/9575562/endotoxin-tolerance-alters-macrophage-membrane-regulatory-g-proteins
#18
JOURNAL ARTICLE
M Makhlouf, B Zingarelli, P V Halushka, J A Cook
Administration of sublethal doses of endotoxin (LPS) or tumor necrosis factor-alpha (TNF alpha) renders rats tolerant to supralethal doses of LPS. Peritoneal macrophages from tolerant rats are refractory to LPS induced arachidonic acid (AA) metabolism and cytokine production in vivo, and exhibit reduced membrane GTPase activity and GTP gamma S binding. Since LPS stimulated AA metabolism is mediated by Gi alpha proteins, we sought to determine whether Gi alpha and/or other G proteins are reduced in LPS tolerance...
1998: Progress in Clinical and Biological Research
https://read.qxmd.com/read/9575561/molecular-mechanisms-responsible-for-endotoxin-tolerance
#19
JOURNAL ARTICLE
B Yoza, K LaRue, C McCall
Bacterial lipopolysaccharide endotoxin (LPS) is a potent activator of a number of inflammatory genes, including interleukin-1 (IL-1). IL-1 and other cytokines such as tumor necrosis factor alpha (TNF alpha) are essential mediators in inducing severe sepsis syndromes (SS). Major cellular targets of LPS are blood or tissue leukocytes, such as macrophages and neutrophils. These cells can respond and adapt to LPS, the latter phenomenon is known as LPS tolerance. In animals, LPS tolerance is a highly effective mechanism of protection against the lethal syndrome of severe sepsis...
1998: Progress in Clinical and Biological Research
https://read.qxmd.com/read/9575560/antibiotic-mediated-release-of-endotoxin-and-the-pathogenesis-of-gram-negative-sepsis
#20
REVIEW
D C Morrison
Since the earliest days of antibiotic chemotherapy to treat infection with Gram-negative microbes, investigators have recognized that such treatments may result in the release of microbial constituents that might, in turn, exacerbate the pathophysiological manifestations of disease. Both in vitro studies and in vivo animal experiments have over the years provided evidence in support of this concept; however, the actual clinical importance of this phenomenon to patients with Gram-negative sepsis is unclear. Recently published reports from a number of laboratories have shown that cell wall-active antibiotics that differ in their fundamental mechanisms of action in disrupting microbial growth (via selective interactions with various penicillin binding proteins) also differ in their relative ability to induce the release of biologically active endotoxin both in vitro and in vivo...
1998: Progress in Clinical and Biological Research
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