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serpentine/inflammation

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The Comroe lecture on which this review is based described my research path during the past 45 years, beginning with studies of oxidant stress (hyperoxia) and eventuating in the discovery of a synthetic inhibitor of phospholipase A2 activity (called MJ33) that prevents acute lung injury in mice

Serpentine supravenous hyperpigmentation induced by the nitrosourea fotemustine.

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Two cases of serpentine supravenous hyperpigmentation developing in the area of fotemustine infusions are reported. Histological features showed an increased melanin synthesis and the presence of melanophages without focal degeneration of basal cells or dermal inflammatory infiltrate. Perls' strain
Serpentine supravenous hyperpigmentation (SSH) is a unique type of chemotherapy-associated drug eruption, characterized by hyperpigmentation along the superficial venous network. Histopathology reveals an increase in melanin production without destruction of basal cells of the epidermis or dermal

Chemokines, inflammation and the immune system.

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The chemokine superfamily comprise two families of small secreted proteins that, with the exception of RANTES, beta-TG, and PF-4, are not expressed in resting cells but are rapidly induced in response to various inflammatory and mitogenic stimuli. These proteins function as chemoattractants and

Chemokines and serpentines: the molecular biology of chemokine receptors.

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Chemokines are pro-inflammatory molecules with a diverse array of biological and biochemical functions. These molecules induce the migration of a number of leukocyte subsets including monocytes, neutrophils, and T-cells. The recent cloning of the IL-8, GRO, and MIP-1 alpha chemokine receptors
A variety of cutaneous reactions have been reported with the use of systemic 5-fluorouracil. Our patient had serpentine hyperpigmented streaks appearing 5 days after bolus infusion of 5-fluorouracil. The patient also had other skin eruptions, that is, inflammation of actinic keratoses and

Giant Serpentine Aneurysm of the Middle Cerebral Artery.

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BACKGROUND Giant serpentine aneurysms (GSAs) are a subgroup of giant intracranial aneurysms, distinct from saccular and fusiform varieties, that are defined as partially thrombosed giant aneurysms with tortuous internal vascular channel. Clinicopathologic characteristics of middle cerebral artery
Controversy exists regarding possible correlation of periodontal disease with rheumatoid arthritis (RA) and ankylosing spondylitis (AS). Confounding factors may relate to stringency of inflammatory disease diagnosis and the effect of therapeutic intervention for RA on periodontal disease. These
Calcined Serpentine (CS) is used in various formulations of alternative systems of medicine as a tonic to vital organs and as an anti-inflammatory agent. The process of calcination or incineration is believed to render non-toxic, gently absorbable, adaptable and digestible properties to the mineral
C5L2 is an enigmatic serpentine receptor that is co-expressed with the C5a receptor on many cells including polymorphonuclear neutrophils. The apparent absence of coupling of C5L2 with G proteins suggests that this receptor may modulate the biological activity of C5a, perhaps by acting as a decoy
A large number of proteins were classified into the family of G protein-coupled receptors (GPCRs). Based on their characteristic serpentine domain, they are called 7 TM receptors. Presently, their ligands and physiological functions remain unknown. In this review, we summarize what is known on these
Leukocyte functions are linked to their migratory responses, which, in turn, are largely determined by the expression profile of classical chemokine receptors. Upon binding their cognate chemokines, these G-protein-coupled receptors (GPCRs) initiate signaling cascades and downstream molecular and

[Cyclooxygenase 2 and carcinogenesis].

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The membrane glycoprotein Cox2 is regulated at transcriptional and post-transcriptional levels by pro-inflammatory agents, cytokines, growth factors, oncogenes, and tumor-promoters. Cox2 is expressed during early stages of colorectal carcinogenesis from the premalignant adenoma stage, and

[C-peptide structure, functions and molecular mechanisms of action].

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C-peptide, which is formed during the biosynthesis of insulin, has long been considered as a biologically inactive substance. However in the recent years there is convincing evidence that the deficit of C-peptide in type 1 diabetes mellitus (DM) or its excess in DM2 lead to the development of
The proteolytic cleavage product of complement component 3, (C3a), is like C4a and C5a, is a potent anaphylatoxin and induces the production of inflammatory mediators in phagocytes. Notably, mast cells respond to C3a with the release of vasoactive substances, including histamine. We have examined
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