Arteriosclerosis

Cerebral arteriosclerosi Cerebral metabolism Cerebrocuprein Cerebrospinal fluid... 

Yohimbine (104), also from the bark of C.johimbe K Schum. and from the roots of R. serpentina (1. ) Benth. has a folk history (unsubstantiated) of use as an aphrodisiac. Its use has been confirmed experimentally as a local anesthetic, with occasional employment for rehef ia angiaa pectoris and arteriosclerosis, but is frequently contraindicated by its undesired renal effects. Yohimbine and some of its derivatives have been reported as hahuciaogenic (70). In addition, its pattern of pharmacological activities ia a variety of animal models is so broad that its general use is avoided. All ten carbon atoms of secologanin (102) as well as the entire skeleton of tryptamine (98, R = H) are clearly seen as iatact portions of this alkaloid. 

Among the examples of monoindole bases being discussed, vincamine (109) is the principal alkaloid of Vinca minorC. and has received some notoriety because it apparently causes some improvement in the abiUties of sufferers of cerebral arteriosclerosis (78). It is beheved that this is the result of increasing cerebral blood flow with the accompanying increase in oxygenation of tissue as a result of its action as a vasodilator. 

Aggravation of cardiovascular disease (i.e., decreased exercise capacity in patients with angina pectoris, intermittent claudication, or peripheral arteriosclerosis)... 

In the vasculature, ANG H not only increases contraction of smooth muscle cells, but is also able to induce vascular injury. This can be prevented by blocking NFkB activation [3] suggesting a link between ANG II and inflammation processes involved in the pathogenesis of arteriosclerosis (see below). Thus, ACE inhibitors not only decrease vascular tone but probably also exert vasoprotective effects. 

ACE inhibitors inhibit the degradation of bradykinin and potentiate the effects of bradykinin by about 50-100-fold. The prevention of bradykinin degradation by ACE inhibitors is particularly protective for the heart. Increased bradykinin levels prevent postischemic reperfusion arrhythmia, delays manifestations of cardiac ischemia, prevents platelet aggregation, and probably also reduces the degree of arteriosclerosis and the development of cardiac hypertrophy. The role of bradykinin and bradykinin-induced NO release for the improvement of cardiac functions by converting enzyme inhibitors has been demonstrated convincingly with use of a specific bradykinin receptor antagonist and inhibitors of NO-synthase. 

In summary, the lysophospholipids are local mediators that regulate development, tissue regeneration and homoeostasis, but also play a role in inflammation, arteriosclerosis and cancer. 

Arrhythmogenic Right Ventricular Dysplasia/ Cardiomyopathy Aiteriogenesis Arteriosclerosis Arylhydrocarbon Receptor L-Ascorbic Acid ASF Family of Transporters Asn-linked Glycosylation ASON... 

Peripheral vasodilating drugs are chiefly used in the treatment of peripheral vascular diseases, such as arteriosclerosis obliterans, Raynaud s phenomenon, and spastic peripheral vascular disorders. Short-term use is rarely beneficial or permanent. Improvement, if it occurs, takes place gradually during weeks of therapy. 

Xu, Q. et al. (1992). Induction of arteriosclerosis in normocholesterolemic rabbits by immunization with heat shock protein 65. Arterioscler. Thromb. 12, 789-799. 

Concerning adherent cells there are few studies in the literature. Some of them deal with the influence of stirrer speed on microcarrier cultures. Most studies using defined forces are from medical research. These studies, as well as those with production cells, use different types of exposure systems based on the parallel plate theory. They investigate the influence of stress on cell morphology and viability which is most important for arteriosclerosis research. 

Cardin AD, Weintraub HJR (1989) Molecular modeling of protein- glycosammoglycan interactions. Arteriosclerosis 9 21-32... 

Proliferation of vascular smooth muscle cells is one of the most important features of arteriosclerosis. Vascular smooth muscle cells display a unique... 

Dietary consumption of polyphenols is associated with a lower risk of degenerative diseases. In particular, protection of serum lipids from oxidation, which is a major step in the development of arteriosclerosis, has been demonstrated. More recently, new avenues have been explored in the capacity of polyphenols to interact with the expression of the human genetic potential. The understanding of the interaction between this heterogeneous class of compounds and cellular responses, due either to their ability to interplay in the cellular antioxidant network or directly to affect gene expression, has increased. 

One main line of future research could be in the inhibitory/activating effect on key enzymes involved in the pathogenesis of arteriosclerosis. In particular, enzymes regulating signal transduction involved in phosphorylation of proteins, such as PKC and tyrosine protein kinase, seems to be somehow modulated by different polyphenols and may represent a possible target for polyphenol activity. 

RAJAVASHISTH T B, YAMADA H and MiSHRA N K (1995) Transcriptional activation of macrophage stimulating factor gene by minimally modified LDL Arteriosclerosis, Thrombosis and Vascular Biology 15, 1591-8. 

FRUEBis J, GONZALEZ v, siLVESTRE M and PALiNSKi w (1997) Effect of probucol treatment on gene expression of VCAM-1, MCP-1, and M-CSF in the aortic wall of LDL receptor-deficient rabbits during early sihsro genss.is, Arteriosclerosis, Thrombosis and Vascular Biology 17, 1289-302. 

BHAKDi s (1998) Atherogenic properties of enzymatically degraded LDL selective induction of MCP-1 and cytotoxic effects on human macrophages Arteriosclerosis, Thrombosis and Vascular Biology 18, 1376-85. 

Selective inhibition of tumor necrosis factor-induced vascular cell adhesion molecule-1 gene expression by a novel flavonoid. Lack of effect on trascriptional factor NF-kB Arteriosclerosis, Thrombosis and Vascular Biology 16, 1501-8. 

HAYEK T, FURHMAN B, VAYA J, ROSENBLAT M, BELINRY P, COLEMAN R, ELIS A, AVIRAM M (1997) Reduced progression of atherosclerosis in apolipoprotein E-deficient mice following consiunption of red wine, or its polyphenols quercetin or catechin, is associated with reduced susceptibility of LDL to oxidation aggregation, Arteriosclerosis, Thrombosis and Vascular Biology, 17, 2744-52. 

PRINCEN H M, VAN DUYVENVOORDE W, BUYTENHEK R, BLONK C, TIJBURG L B, LANGIUS J A, MEINDERS A E, PUL H (1998) No effect of consiunption of green and black tea on plasma lipid antioxidant level and on LDL oxidation in smokers, Arteriosclerosis, Thrombosis and Vascular Biology, 18, 833-41. 

Mammals lack the ability to synthesize astaxanthin or convert dietary astaxanthin into vitamin A. Unlike p-carotene, astaxanthin has no pro-vitamin activity in these animals. Astaxanthin has been shown in both in vitro and in a study with human subjects to be effective for the prevention of the oxidation of low-density protein, suggesting that it can be used to prevent arteriosclerosis, coronary artery disease, and ischemic brain development. A number of astaxanthin health products are under study. 

Balia, G., Jacobs, H.S., Eaton, J.W., Belcher, J.D. and Vercel-totti, G.M. (1991). Hemin a physiological mediator of low-density lipxjprotein oxidation and endothelial injury. Arteriosclerosis 11, 1700-1711. 

Morel, D.W., DiCorleto, P.E. and Chisholm, G.M. (1984). Endothelial and smooth muscle cells alter low density lipoprotein in vitro by fi ee radical oxidation. Arteriosclerosis 4, 357-364. 

Parthasarathy, S., Printz, D.J., Boyd, D., Joy, L. and Steinberg, D. (1986). Macrophage oxidation of LDL generates a modified form recognised by the scavenger receptor. Arteriosclerosis 6, 505-510. 

Henriksen, T., Mahoney, E.M. and Steinberg, D. (1983). Enhanced macrophage degradation of biologically modified low density lipoprotein. Arteriosclerosis 3, 149-159. 

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