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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Many studies of age-related cognitive decline have failed to distinguish between usual and successful aging. Although some degree of cognitive impairment is associated with aging, when one looks at average performance, there is great variability among individuals, with many showing little or no deleterious effects of aging on intellectual abilities. Many of the risk factors for dementia and for conditions associated with cognitive impairments can be treated or controlled. Among the preventable causes of cognitive decline are the following: AIDS, Alcohol and drug abuse, Cerebrovascular disease, Exposure to organic solvents or lead, Head trauma, Overmedication, Syphilis. Other conditions that may cause cognitive decline can be controlled or treated: Atherosclerosis, Depression, Diabetes, Emphysema, High blood pressure, Obesity, Sleep disorders, Thyroid dysfunction. In addition, it may be possible to enhance the cognitive performance of even healthy elderly people through changes in diet and lifestyle. Recent data raise the possibility that improved prenatal and perinatal care and greater access to educational opportunities may result in a decreased incidence of dementia in future generations of older adults. Although they are rapidly becoming more numerous, the efficacy of cognitive training programs in preventing or slowing cognitive decline has not yet been demonstrated. Nevertheless, such programs may ameliorate cognitive impairment by reducing the psychiatric disabilities associated with anxiety and depression. The general principle underlying these strategies for limiting cognitive impairment with age is to maximize brain reserve and minimize brain damage.
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PMID:Preventing cognitive decline. 157 76

Vascular disorders comprise a wide range of diverse disease entities. Correspondingly, vessels, and even more so the endothelial which line them, show a remarkable extent of heterogeneous differentiation, e.g. between the blood vascular and lymphatic systems, along the length of the vascular trees, and in the microvascular beds of various organs. The most important morphologic criterion to discriminate between endothelia is continuity (continuous endothelial cell layer and well-formed basement membrane) versus discontinuity (intra- or intercellular gaps and/or reduced or missing basement membrane). Most blood vascular endothelia are of the continuous type, while most sinusoidal and lymphatic endothelia are discontinuous by these criteria. Antigen expression corroborates these morphologic data in that CD31, CD34, and 1F10 antigen are exclusively expressed in continuous endothelia, while MS-1 antigen is preferentially expressed in non-continuous sinusoidal endothelia. In contrast, no specific marker has as yet been described for lymphatic endothelia. Endothelial heterogeneity substantially contributes to the pathogenesis of vascular disorders. For example, in patients with acquired immunodeficiency syndrome the same infectious agent may cause either bacillary angiomatosis (a lobular capillary proliferation) or peliosis (sinusoidal dilatation, endothelial denudation, and development of blood-filled cysts) depending on whether the affected organs have predominantly continuous endothelia or noncontinuous sinusoidal endothelia. Moreover, in Kaposi's sarcoma, it is still an open question of whether the lesion is derived from blood vascular or lymphatic endothelia (Kaposi's sarcoma cells in situ do not express the von Willebrand factor+, PAL-E+, 1F10+ phenotype of mature, resting blood vascular endothelia). It is also unresolved how endothelia of either type may be differentially induced to dedifferentiate and how they are recruited into the lesion. Clearly, knowledge about endothelial heterogeneity is still too incomplete to identify the actual mechanisms and molecules that govern the pathogenesis of vascular disorders (including still others than those mentioned here such as atherosclerosis, diabetic angiopathy, and rheumatoid arthritis) affecting distinct endothelia. Further efforts in antigenic phenotyping and in cell and molecular biology of heterogeneously differentiated endothelia should be made to improve this state of affairs.
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PMID:Endothelial heterogeneity and the acquired immunodeficiency syndrome: a paradigm for the pathogenesis of vascular disorders. 160 Mar 45

Over the last 10 years, our knowledge of immunologically mediated processes involving the myocardium appears to have made quantum leaps. New and important disease entities such as AIDS have appeared and the cardiologist now becomes an important member of the "AIDS team." Our understanding of "older diseases" such as sarcoidosis, Lyme disease, systemic lupus and other connective tissue syndromes has significantly increased. The concept of high-dose steroid therapy for these processes may, in fact, turn out to be futile and more selective, as less dangerous immunosuppression is being introduced. This concept has significantly advanced in the field of cardiac transplantation where immunosuppression has now been usurped by specific immunotherapy aimed at selective aspects of the immune sequence. New and exciting concepts will emerge from the molecular biology laboratory that will have direct bearing on the management of patients with cardiovascular disorders. This information explosion will force the cardiovascular physician to become more in tune with the world of immunology and molecular biology. Many obvious, significant problems remain, such as accelerated atherosclerosis in the transplant patient and the role of myocarditis in the patient with heart failure. However, it will truly be an exciting decade in which to work and watch the unraveling of these mysteries and hopefully, the study of today's problems will give way to solutions and a clearer understanding of the heart as a target of immune injury.
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PMID:The heart as a target organ of immune injury. 191 12

Much of the research related to cardiopulmonary bypass in recent years has been directed toward defining the changes in plasma and blood cells during bypass. In this review, recent information is reexamined for six areas of current interest. These areas are complement activation, immune response, anaphylactic reactions, coagulation, and cerebral dysfunction. Complement may be activated by either the classical or alternate pathway during cardiopulmonary bypass and protamine administration. Membrane oxygenators appear to diminish the degree of complement activation. Complement is a major factor in the whole body inflammatory response; which often accompanies cardiopulmonary bypass. A product of complement activation, C5a- desArg, causes activation and aggregation of granulocytes. Other products of complement activation lead to lysis of blood cells including granulocytes and red cells. Bubble oxygenators appear to have a distinct disadvantage compared to membrane oxygenators regarding infection. Airborne microorganisms are more likely to be entrained into circulating blood with bubble oxygenators than with membrane oxygenators. Bubble oxygenators cause a greater decrease in leukocyte number and function than membrane oxygenators. Anaphylactic reactions have been associated with use of antibiotics, blood products, protamine, and volume expanders during cardiopulmonary bypass. Protamine reactions may be on an immunological basis or due to direct toxicity of the drug. Free radicals including superoxide, hydrogen peroxide, and the hydroxyl radical may be generated during cardiopulmonary bypass and reperfusion. Free radical scavengers including; vitamin E, coenzyme Q, vitamin C, mannitol, and glutathione have been studied. The avoidance of blood transfusion because of risk of transmitted infection including AIDS has become a major goal in cardiac surgery. Factors that correlate with increased transfusion requirement include low hematocrit, female gender, increased age, small body size, low ejection fraction, reoperation, and emergency operation. Heparin resistance due to antithrombin III deficiency is being recognized more commonly. Antithrombin III deficiency may be corrected with fresh frozen plasma. Patients with heparin induced thrombocytopenia may be difficult to manage. Several management protocols are suggested. The most straightforward appears to be the use of aspirin preoperatively and platelet transfusions postoperatively. The incidence of cerebral dysfunction after cardiopulmonary bypass depends on the sensitivity of the test or indicator used. Perioperative stroke is associated with intrinsic cerebrovascular disease and atherosclerosis of the ascending aorta. Retinal angiograms during cardiopulmonary bypass show that microemboli are very common. Cerebroplegia has been shown to extend the period of safe circulatory arrest in animals. Much of the new knowledge concerning cardiopulmonary bypass is the result of close collaboration between cardiac surgeons and nonsurgical scientists.
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PMID:Pathophysiology of cardiopulmonary bypass: current issues. 213 41

During infection the vascular endothelial cell (EC) undergoes important immunologic alterations leading to increased leukocyte-EC adherence and initiation of a host inflammatory response. ECs express class 2 immune response genes and the interleukin 1 gene to a greater degree during infection and thus may be capable of amplifying the lymphocytic proliferative process. Lymphokines generated from stimulated lymphocytes, notably interferon-gamma, may in turn further enhance EC-leukocyte adherence and class 2 antigenic presentation by ECs. The ECs of different organ systems appear variable in terms of their immunologic capabilities. Infection of the endothelium has been demonstrated for an array of human pathogens, and even subclinical infection of ECs may ultimately assume importance in disease processes such as atherosclerosis. A potential role of the EC in the pathogenesis of newer infectious diseases, such as AIDS, is becoming evident and warrants further attention.
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PMID:Vascular endothelium in immunology and infectious disease. 249 65

Nonhuman primates are excellent animal models for human diseases because of their close relationship to humans. Indeed, comparisons of the chromosomes and DNA homologies between primates and humans testify to the commonality of the genetic material between these phylogenetically related species. Not surprisingly, this close relationship at the genotypic level extends to the phenotypic level. Thus, the patho-physiological responses of humans and nonhuman primates to internal and external insults are remarkably similar. Two types of human diseases for which nonhuman primates are paramount animal models are discussed. One type includes diseases with defined, single agent etiologies and to which all members of the species are genetically susceptible. Examples of these are leprosy, AIDS, hepatitis and Parkinson's disease. A second type represents diseases that have a substantial genetic component, but are multifactorial and are greatly influenced by the environment. Examples of these are diabetes, lymphoma, atherosclerosis, alcoholic cirrhosis and anxiety disorders. Nonhuman primates are also ideally suited to the role of animal models in the new area of human gene therapy. In the future, biomedical research will focus increasingly on genetic manipulations such as the transfer of genes from one individual to another to correct genetic diseases, particularly those diseases caused by single recessive gene defects. Before gene transfers are attempted in humans, they should be done in nonhuman primates. In a real sense, nonhuman primates, as animal models, represent the "step to man."
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PMID:Genetic significance of some common primate models in biomedical research. 360 96

Human cytomegalovirus (HCMV) can establish lifelong persistence after primary infection with reactivation occurring as a result of immunosuppression. There is much evidence that molecular interactions between the immune system and the HCMV are responsible for immune escape. HCMV in many cells especially in mononuclear blood cells during latency are frequently the source of transmission and spreading and results in a variety of disorders. In this review some data about acute infection in immunocompetent host (mononucleosis, hepatitis), about intrauterine HCMV infection, about infection and endogenous reinfection in bone marrow and solid organ transplant recipients (pneumonitis) and about HCMV disease in AIDS patients (encephalitis, neuropathy, retinitis, colitis) are investigated. Moreover, HCMV associated vasculitis is described in patients with myocarditis, rheumatoid arthritis or polyradiculopathy. HCMV could play an important role in atherosclerosis. Several types of human malignancy have been linked to HCMV and it has been shown that HCMV ie genes upregulate expression of cellular oncogenes. The diagnosis of HCMV infection is carried out by viremia in cell culture using immediate early antigen staining, by antigenaemia which appears to be an early quantitative and predictive tool, by HCMV DNA detection using hybridization and PCR, and by IgM and IgG antibody evaluation. Two antiviral drugs are used for treatment: ganciclovir and phosphonoformic acid; few resistant clinical isolates have been reported. Specific gammaglobulin activity is discussed. HCMV vaccine is not available.
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PMID:[Current status of human cytomegalovirus disease]. 759 23

Curcumin, contained in the rhizome of the plant Curcuma longa Linn, is a naturally occurring phytochemical that has been used widely in India and Indonesia for the treatment of inflammation. The pleiotropic cytokine tumor necrosis factor-alpha (TNF) induces the production of interleukin-1 beta (IL-1), and, together, they play significant roles in many acute and chronic inflammatory diseases. They have been implicated in the pathogenesis of intracellular parasitic infections, atherosclerosis, AIDS and autoimmune disorders. This report shows that, in vitro, curcumin, at 5 microM, inhibited lipopolysaccharide (LPS)-induced production of TNF and IL-1 by a human monocytic macrophage cell line, Mono Mac 6. In addition, it demonstrates that curcumin, at the corresponding concentration, inhibited LPS-induced activation of nuclear factor kappa B and reduced the biological activity of TNF in L929 fibroblast lytic assay.
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PMID:Inhibition of tumor necrosis factor by curcumin, a phytochemical. 778 95

We describe the cardiovascular abnormalities found at autopsy in patients with AIDS and a description of the opportunistic infections in these cases studied between January 1988 and August 1993. There were 51 cases with such diagnosis. Pericardial effusion appeared in 9, pleural effusion in 7, myocarditis in 5, 7 with pericarditis, endocarditis in 6, left ventricular hypertrophy in 20, right ventricular hypertrophy in 21 and evidence of atherosclerosis in 15. Thus, data of cardiovascular damage was present in 42.7% of our patients. The cardiovascular abnormalities in this group are common, in contrast to the paucity of clinical findings. Diagnosis of cardiac pathology was made in only 12% of them. So in every case with diagnosis of AIDS, a careful clinical examination and cardiac diagnostic oriented tests must be done for detection of these abnormalities.
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PMID:[The autopsy findings in 51 cases of AIDS with cardiovascular damage]. 784 Jul 32

There is a need to change the policy of unselective iron supplementation during periods of life with physiologically increased cell proliferation. Levels of iron stores to be regarded as adequate during infancy and pregnancy are still not well established. Recent data support the view that it is not justified to interfere with physiological adaptations developed through millions of years by sophisticated and precisely coordinated regulation of iron absorption, utilization and storage. Recent data suggest that the chelatable intracellular iron pool regulates the expression of proteins with central importance in cellular iron metabolism (TfR, ferritin, and erythroid 5-aminolevulinic synthetase) in a coordinately controlled way through an iron dependent cytosolic mRNA binding protein, the iron regulating factor (IRF). This factor is simultaneously a sensor and a regulator of iron levels. The reduction of ferritin levels during highly increased cell proliferation is a mirror of the increased density of TfRs. An abundance of data support the vigorous competition for growth-essential iron between microbial pathogens and their vertebrate hosts. The highly coordinated regulation of iron metabolism is probably crucial in achieving a balance between the blockade of readily accessible iron to invading organisms and yet providing sufficient iron for the immune system of the host. The most evident adverse clinical effects of excess iron have been observed in immunodeficient patients in tropical countries and in AIDS patients. Excess iron also increases the risk of initiation and promotion of malignant processes by iron binding to DNA and by the iron-catalysed release of free radicals. Oxygen radicals were shown to damage critical biomolecules leading, apart from cancer, to a variety of human disease states, including inflammation and atherosclerosis. They are also involved in processes of aging and thrombosis. Recent clinical trials have suggested that the use of iron-chelators, natural and synthetic antioxidants, and anti-TfR monoclonal antibodies can contribute in retarding malignant cell proliferation. Hypoferraemia during pregnancy is--like haemodilution--an adaptation to the risks involved in the natural hypercoagulable state of pregnancy. It may also serve to prevent the risk of infections and mutagenicity in the highly proliferating tissues of the foetus. Blunted erythropoiesis has been revealed during the first 30 weeks of pregnancy by the use of the newly developed method of determining the soluble serum transferrin receptor. The lack of increase in erythropoietin levels proves that there is no hypoxia. Decreases in Hb and iron levels are parts of a physiological adaptation. As a consequence they should neither be treated nor prevented. It is stressed that whenever a widespread and ingrained routine medical intervention has to be changed it is essential to first monitor the potential health effects of the recommended change in a national policy.
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PMID:Adequate iron stores and the 'Nil nocere' principle. 824 2


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