Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Between August 1980 and October 1990 we treated 36 patients with home total parenteral nutrition (HTPN) with a cumulative treatment duration of 92 years. They included 14 females and 22 males ranging in age from newborn to 75 years, with a mean of 38 +/- 21. The 4 commonest indications for HTPN were short bowel syndrome (mainly due to mesenteric occlusion (50%), inflammatory bowel disease 14%), motility disorders (14%) and malabsorption (11%). All-in-one nutritional mixtures utilizing the big-bag technique were used for all patients. Broviac or Hickman catheters were implanted in 35 patients and an infusion port in 2. Infusions were administered during the night for 8-12 hours with a volumetric pump. 14 patients are still receiving HTPN (39%) while in 8 it was discontinued as they can maintain their nutritional status by the gastrointestinal route (22%). 14 patients have died (39%), 3 from HTPN-related causes (2 of sepsis and 1 of liver failure). Catheter-related sepsis was 0.42/year of HTPN. Other common complications were metabolic bone disease, deranged liver function and cholecystolithiasis. 80% were able to return to work, school, or housekeeping activities, or at least to take care of themselves and cope with HTPN unaided. Social rehabilitation was full or partial in 72% and only 29% were house-bound and needed major assistance. Patients with a poor life quality tended to be older and suffer from intestinal diseases as a manifestation of a systemic disorder, such as atherosclerosis or malignancy.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A decade of experience with home total parenteral nutrition]. 180 Feb 76

Nitric oxide contrasts with most intercellular messengers because it diffuses rapidly and isotropically through most tissues with little reaction but cannot be transported through the vasculature due to rapid destruction by oxyhemoglobin. The rapid diffusion of nitric oxide between cells allows it to locally integrate the responses of blood vessels to turbulence, modulate synaptic plasticity in neurons, and control the oscillatory behavior of neuronal networks. Nitric oxide is not necessarily short lived and is intrinsically no more reactive than oxygen. The reactivity of nitric oxide per se has been greatly overestimated in vitro because no drain is provided to remove nitric oxide. Nitric oxide persists in solution for several minutes in micromolar concentrations before it reacts with oxygen to form much stronger oxidants like nitrogen dioxide. Nitric oxide is removed within seconds in vivo by diffusion over 100 microns through tissues to enter red blood cells and react with oxyhemoglobin. The direct toxicity of nitric oxide is modest but is greatly enhanced by reacting with superoxide to form peroxynitrite (ONOO-). Nitric oxide is the only biological molecule produced in high enough concentrations to out-compete superoxide dismutase for superoxide. Peroxynitrite reacts relatively slowly with most biological molecules, making peroxynitrite a selective oxidant. Peroxynitrite modifies tyrosine in proteins to create nitrotyrosines, leaving a footprint detectable in vivo. Nitration of structural proteins, including neurofilaments and actin, can disrupt filament assembly with major pathological consequences. Antibodies to nitrotyrosine have revealed nitration in human atherosclerosis, myocardial ischemia, septic and distressed lung, inflammatory bowel disease, and amyotrophic lateral sclerosis.
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PMID:Nitric oxide, superoxide, and peroxynitrite: the good, the bad, and ugly. 894 24

Arterial occlusive disease (AOD) which is rarely described in patients with inflammatory bowel disease, is mainly associated with Crohn's disease (CD), and its etiology and natural course are unknown. We studied six patients (five women, one man) with CD and major lower extremity AOD who were treated at the Cleveland Clinic between 1985 and 1994. These were relatively young patients (age range 24-48 years) with steroid-dependent Crohn' colitis. On their presentation, five had acute onset of severe ischemic symptoms ("blue toe" syndrome in three) and one had rapid progression of claudication. All the patients had active CD and/or prior extensive bowel resections, and had no evidence of extraintestinal manifestation. Cardiovascular risk factors were smoking (n = 5), dyslipidemia (n = 3), family history of coronary artery disease (n = 3), premature menopause (n = 2), diabetes mellitus (n = 1). Arteriograms showed iliac artery involvement in all six patients and bilateral AOD in three. None of the patients had arteriographic or clinical signs of vasculitis. Five patients required arterial revascularizations, i.e., endovascular (n = 2), surgical (n = 2), and combined in one. Three patients had microscopic evidence of atherosclerosis. Lower extremity AOD in patients less than 50 yr of age and with CD may be partially related to premature atherosclerosis. Prospective screening for cardiovascular risk factors, subclinical disease, and hypercoagulability might be indicated in patients with active CD to prevent major arterial complications.
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PMID:Lower extremity arterial occlusions in young patients with Crohn's colitis and premature atherosclerosis: report of six cases. 906 77

In recent years it has become apparent that the oxidation of lipids, or lipid peroxidation, is a crucial step in the pathogenesis of several disease states in adult and infant patients. Lipid peroxidation is a process generated naturally in small amounts in the body, mainly by the effect of several reactive oxygen species (hydroxyl radical, hydrogen peroxide etc.). It can also be generated by the action of several phagocytes. These reactive oxygen species readily attack the polyunsaturated fatty acids of the fatty acid membrane, initiating a self-propagating chain reaction. The destruction of membrane lipids and the end-products of such lipid peroxidation reactions are especially dangerous for the viability of cells, even tissues. Enzymatic (catalase, superoxide dismutasse) and nonenzymatic (vitamins A and E) natural antioxidant defence mechanisms exist; however, these mechanisms may be overcome, causing lipid peroxidation to take place. Since lipid peroxidation is a self-propagating chain-reaction, the initial oxidation of only a few lipid molecules can result in significant tissue damage. Despite extensive research in the field of lipid peroxidation it has not yet been precisely determined if it is the cause or an effect of several pathological conditions. Lipid peroxidation has been implicated in disease states such as atherosclerosis, IBD, ROP, BPD, asthma, Parkinson's disease, kidney damage, preeclampsia and others.
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PMID:Lipid peroxidation and tissue damage. 1045 7

Vascular brain diseases are ranked the third as the cause of morbidity and mortality, in spite of the progress in diagnostic, therapeutic and preventive procedures. In the majority of cases of vascular brain diseases, it is ischemic brain disease, which is the final and the most severe stage of cerebral arteries atherosclerosis. Etiopathogenesis of atherosclerosis is not closer defined yet, but oxidative hypothesis is distinguished among the numerous theories. Within this theory, main place is attached to oxidative modification of LDL and Lp(a), together with numerous physiopathologic facts with the central role of reactive oxidative matters, where endothelial dysfunction is the main disorder responsible for the onset of numerous impairments, such as changes in coagulation-anticoagulation system. Considering these facts, it was established the hypothesis that in patients with IBD existed changes in hemostatic system, which were in positive correlation with the degree of cerebral atherosclerosis. The study comprised 36 patients with acute IBD and 28 patients with atherosclerotic encephalopathy. Control group was comprised of 30 patients with non-vascular diseases of similar characteristics. We investigated the correlation of the changes in hemostatic system (platelet aggregation, anti-thrombin III, D-dimer, protein C, factor VII, factor VIII, PAI-1) compared to the degree of cerebral atherosclerosis (ultrasonographically) and compared to the observed groups of patients. On the basis of all, the results of this study revealed significant increase of procoagulant factors concentration in patients with IBD, and similar changes were observed in patients with atherosclerotic encephalopathy, but less pronounced. All these changes in the total sample of patients, and particularly in patients with the pronounced cerebral atherosclerosis, are of primary and chronic character.
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PMID:The influence of the degree of cerebral atherosclerosis on the changes in hemostatic system in patients with ischemic brain disease and atherosclerotic encephalopathy. 1064 49

Chemokines are important mediators of inflammation. Animal studies suggest that inhibition of chemokine action results in a decrease in inflammation. Novel anti-inflammatory agents directed against chemokines are now available. Surgeons are uniquely positioned to treat multiple chemokine-mediated diseases. In this article, we review the biology and nomenclature of chemokines as well as their role in neutrophil migration. Further, the potential role of chemokines in various diseases related to surgical conditions, including adult respiratory distress syndrome, atherosclerosis, inflammatory bowel disease, and solid organ rejection, is reviewed. Finally, the idea that chemokines could be targets for novel therapeutic agents is discussed.
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PMID:Chemokines as mediators of diseases related to surgical conditions. 1090 85

Peroxisome proliferator-activated (PPARs) are ligand-activated transcription factors belonging to the nuclear receptor family. PPARs function as regulators of lipid and lipoprotein metabolism and glucose homeostasis and influence cellular proliferation, differentiation and apoptosis. PPARalpha is highly expressed in tissues such as liver, muscle, kidney and heart, where it stimulates the beta-oxidative degradation of fatty acids. PPARgamma is predominantly expressed in intestine and adipose tissue. PPARgamma triggers adipocyte differentiation and promotes lipid storage. The hypolipidemic fibrates and the antidiabetic glitazones are synthetic ligands for PPARalpha and PPARgamma, respectively. Furthermore, fatty acids and eicosanoids are natural PPAR ligands: PPARalpha is activated by leukotriene B4, whereas prostaglandin J2 is a PPARgamma ligand. These observations suggested a potential role for PPARs not only in metabolic but also in inflammation control. The first evidence for a role of PPARalpha in inflammation control came from the demonstration that PPARalpha deficient mice display a prolonged response to inflammatory stimuli. It was suggested that PPARalpha deficiency results in a reduced beta-oxidative degradation of these inflammatory fatty acid derivatives. More recently, PPAR activators were shown to inhibit the activation of inflammatory response genes (such as IL-2, IL-6, IL-8, TNFalpha and metalloproteases) by negatively interfering with the NF- kappaB, STAT and AP-1 signalling pathways. PPAR activators exert these anti-inflammatory activities in different immunological and vascular wall cell types such as monocyte/macrophages, endothelial, epithelial and smooth muscle cells in which PPARs are expressed. These recent findings indicate a modulatory role for PPARs in the control of the inflammatory response with potential therapeutic applications in inflammation-related diseases, such as atherosclerosis and inflammatory bowel disease.
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PMID:Peroxisome proliferator-activated receptors (PPARs): nuclear receptors at the crossroads between lipid metabolism and inflammation. 1108

Vascular cell adhesion molecule-1 (VCAM-1) regulates leukocyte migration from the blood into tissues. VCAM-1 expression is induced on endothelial cells during inflammatory bowel disease, atherosclerosis, allograft rejection, infection, and asthmatic responses. During these responses, VCAM-1 forms a scaffold for leukocyte migration. VCAM-1 also activates signals within endothelial cells resulting in the opening of an "endothelial cell gate" through which leukocytes migrate. Immediately following this migration, the endothelial cell-endothelial cell contact is re-established. VCAM-1 outside-in signals are mediated by NADPH oxidase production of reactive oxygen species and subsequently activation of matrix metalloproteinases. These signals are required for endothelial cell shape changes and leukocyte migration. In addition, VCAM-1-activated signals in endothelial cells are regulated by cytokines indicating that it is important to consider both endothelial cell adhesion molecule expression and function during inflammatory processes.
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PMID:VCAM-1 signals during lymphocyte migration: role of reactive oxygen species. 1243 82

Inflammation is overall a protective response, whose main goal is to liberate the human being of cellular lesions caused by micro-organisms, toxins, allergens, etc., as well as its consequences, and of death cells and necrotic tissues. Chronic inflammation, which is detrimental to tissues, is the basic pathogenic mechanism of hypersensitivity reactions against xenobiotics. Other frequent pathologies, for instance atherosclerosis, chronic hepatitis, inflammatory bowel disease (IBD), liver cirrhosis, lung fibrosis, psoriasis, and rheumatoid arthritis are also chronic inflammatory diseases. Chemical mediators of inflammation are derived from blood plasma or different cell-type activity. Biogenic amines, eicosanoids and cytokines are within the most important mediators of inflammatory processes. The different activities of eicosanoids derived from arachidonic acid (20:4 n-6) versus those derived from eicosapentaenoic acid (20:5 n-3) are one of the most important mechanisms to explain why n-3, or omega-3, polyunsaturated fatty acids (PUFA) exhibit anti-inflammatory properties in many inflammatory diseases. Dietary supplements ranging 1-8 g per day of n-3 PUFA have been reportedly beneficial in the treatment of IBD, eczema, psoriasis and rheumatoid arthritis. In addition, recent experimental studies in rats with experimental ulcerative colitis, induced by intrarectal injection of trinitrobenzene sulphonic acid, have documented that treatment with n-3 long-chain PUFA reduces mucosal damage as assessed by biochemical and histological markers of inflammation. Moreover, the defence antioxidant system in this model is enhanced in treated animals, provided that the n-3 PUFA supply is adequately preserved from oxidation.
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PMID:Polyunsaturated fatty acids and inflammatory diseases. 1244 11

Conjugated linoleic acid (CLA) is a mixture of positional (e.g. 7,9; 9,11; 10,12; 11,13) and geometric (cis or trans) isomers of octadecadienoic acid. This compound was first shown to prevent mammary carcinogenesis in murine models. Later investigations uncovered a number of additional health benefits, including decreasing atherosclerosis and inflammation while enhancing immune function. The mechanisms of action underlying these biological properties are not clearly understood. The aim of this review is to highlight recent advances in CLA research related to experimental inflammatory bowel disease. In addition, two possible mechanisms of action (i.e. endoplasmic and nuclear) were discussed in detail in the context of enteric inflammatory disorders. Conjugated linoleic acid was first implicated in down-regulating the generation of inducible eicosanoids (i.e. PGE(2) and LTB(4)) involved in early micro-inflammatory events (endoplasmic). More recently, CLA has been shown to modulate the expression of genes regulated by peroxisome proliferator-activated receptors (PPARs; nuclear). In pigs, prolonged dietary CLA treatment stimulated the expression of PPAR-gamma in the muscle. Thus, evidence supporting both mechanistic theories of CLA acting through eicosanoid synthesis and PPAR activity is available. The further understanding of the anti-inflammatory mechanisms of action of CLA may yield novel nutritional therapies for enteric inflammation.
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PMID:Colonic anti-inflammatory mechanisms of conjugated linoleic acid. 1246 64


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