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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We observed a lot of immune system disorders significantly influencing the development and clinical course of stroke. Depression of cell-mediated immune reactivity was observed in the early stage of stroke. It was manifested by the decrease of the number of T lymphocytes, depression in lymphocyte blastogenesis, diminished production of the migration inhibition factor and reduced delayed-type skin reactivity. Observed depression was probably caused by severe metabolic and endocrinological disorders often seen in the acute phase of the disease and related with increased patients' susceptibility to infections. Simultaneously we observed that the elevated total WBC was an independent stroke risk factor and predictor of 30-days stroke fatality. The activation of the adhesion molecules expression on granulocytes (CD18) and the increased cytokine production by leukocytes could favour leukocytes influence to the ischemic area and potentiate brain injury. The chronic inflammation could be also responsible for the development of vascular injuries leading to the ischemia. In our studies we demonstrated the high levels of antibodies to cardiolipins and heat shock proteins and the increased blood levels of immune complexes (i.c.). We observed the presence of Chlamydia pneumoniae and CMV antigens in isolated i.c. It suggests that different markers of chronic inflammation observed at very early stage of the disease are probably related with the chronic infection potentially leading to the development of atherosclerotic lesions and destabilization of atherosclerotic plaque.
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PMID:[The relationship between immunological parameters with etiopathogenesis and clinical course of stroke]. 1098 97

Chlamydia pneumoniae, a respiratory pathogen, has been suggested as a risk factor for cardiovascular disease. Epidemiologic data are very controversial. Histopathologic and microbiologic studies have established an association between atherosclerosis and presence of C. pneumoniae, consistently finding C. pneumoniae DNA and antigens in atherosclerotic arteries. C. pneumoniae has been cultured from atherosclerotic arteries in several centers. An etiologic role for C. pneumoniae in initiation, acceleration of atherosclerosis, and/or acute ischemia remains debatable. In vitro studies have shown that C. pneumoniae can induce foam cell formation, low-density lipoprotein oxidation, and proinflammatory and procoagulant cytokine expression. Animal models of de novo initiation or enhancement of atherosclerosis have been developed. Preliminary trials of secondary prevention of coronary artery disease complications by antimicrobial agents show modest results. Better diagnostic tools, more diverse animal models, and clinical trials of primary prevention are needed. Meanwhile, results of ongoing large clinical trials on secondary prevention are eagerly awaited, but may not be definitive.
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PMID:Chlamydia pneumoniae and Cardiovascular Disease. 1185 55

Atherogenesis is a disease of middle-sized and large-caliber blood vessels that can be divided into three major phases. The initial lesions of early atherosclerosis are characterized by the adhesion and subendothelial emigration of blood-borne monocytes, which differentiate into macrophages and provide the morphologic basis for the formation of foam cells and fatty streak lesions. These lesions are found in most children and teenagers in industrialized nations. The next key event in atherogenesis is the proliferation of smooth muscle cells within the intima and media, resulting in the gradual compromise of the vessel lumen. Myofibroblastic cells also contribute to lesion growth through the production of excessive amounts of extracellular matrix. Such lesions are clinically silent unless progression to the next phase continues: the lesions degenerate, forming a mostly necrotic "lipid core" consisting of extracellular lipid, cholesterol crystals, inflammatory cells and necrotic debris. A fibrous cap is formed which prevents the interaction of blood cells, particularly of platelets with the highly proaggregatory material found in the lipid core. However, continuous inflammatory activity and/or heightened mechanical stress (i.e., in hypertension) tends to weaken the fibrous caps. Eventually, plaque rupture ensues, platelets aggregate, and the lesions become clinically manifest in such dramatic events as myocardial infarction, stroke, or mesenteric ischemia. Research into lesion formation and progression is limited by the fact that lesions develop in silence over many decades and that animal models only incompletely model the situation in humans. Most currently debated concepts accept the "response to injury" hypothesis formulated by the late Russell Ross and the multi-factorial nature of atherogenesis. The discussion today circles around the relative contributions of low density lipoproteins (oxidized or enzymatically modified LDL?), the immune response (adaptive or innate?), infectious agents (CMV, Chlamydia pneumoniae?), and/or hereditary factors, to name only a few of the most widely debated concepts. Irrespective of the outcome of this pathomechanistic discussion, the knowledge of established risk factors (hypercholesterolemia, hypertension, diabetes, smoking, etc.) and protective interventions (lifestyle changes, physical exercise, "healthy" diets, effective dietary and pharmacologic control of hyperglycemia, blood pressure or hyperlipidemia) has helped to define atherosclerosis as a "new entity" that has little to do with the archaic concept of a "degenerative" vessel disease. The new concept takes us into the responsibility--puts us in charge of our own and our patients' cardiovascular risk--whether we like it or not. The smoking obese doctor no longer fits into the modern medical landscape.
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PMID:[Atherosclerosis--progression by nonspecific activation of the immune system]. 1197 79

Noninvasive nuclear magnetic resonance was used to measure the relaxation decay curves of naturally occurring 23Na ions in several biological systems. Experimental results showed an increase of membrane bound population for pathologic samples as compared with control. The bound sodium population was put in evidence using singular value decomposition method. Thus, the singular values that are obtained without any a priori from the fitting the relaxation decay curves are a new parameter in characterizing the cellular state. In the presence of artificial biological membranes, 23Na bound strongly to membranes containing phosphatidylcholine (PC) and phosphatidylserine (PS), but not to membranes consisting of only PC. A large bound population also appeared in the presence of apoptotic epithelial cells, which are known to translocate PS to the cell surface. A role for PS was confirmed by showing that sodium binds to the surface of epithelial cells infected with Chlamydia psittaci, and the amplitude of the bound population increases with a time-course similar to the appearance of PS on the surface of dying cells. Finally, this approach could distinguish between normal perfused liver and liver undergoing ischemia, due most likely to the exposure of surface PS on apoptotic and necrotic cells in the damaged tissue. Taken together, these studies demonstrate that the analysis of 23Na relaxation decay curves could reveal the presence of cells undergoing apoptosis and/or necrosis in living tissues. Noninvasive 23Na NMR measurements could thus be envisioned for controlling the quality of organs before transplantation, for the detection of asymptomatic infections that result in death of the host cell or inflammation of the tissue, and for characterizing the efficiency of novel apoptosis-inducing drugs to treat cancer.
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PMID:Evidences on sodium ions compartmentalization in biological systems due to pathological states. A noninvasive NMR study. 1465 74

In the group of patients (n = 19), with advanced atheromatous ischemia of the legs the presence and titres of rum IgG, IgA, and IgM antibodies for Chlamydia pneumoniae (Cp) were measured. Those were compared with controls (n = 12). Additionally in the patients undergoing surgery (revascularisation or amputation), specimens of atheromatous arteries were examined for the presence of Cp. In the general population among the people at the age over 60 years the presence of antibodies was common (IgG 100%, IgA 92%). In the patients with the atheromatous ischemia of the legs the antibodies to Cp were found only in: IgG 79%, IgA 79% of them. In 21% of patients (n = 4) we were able to confirm the presence of Cp in an artery wall. However we found that three of them had undetectable titres of serum IgG, IgA, IgM. In case of an individual patient seropositivity to Cp seems not to be a good marker of active chlamydial infection.
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PMID:[Chlamydia pneumoniae in patients with atherosclerotic ischemia of the lower limbs]. 1467 94

Traditional risk factors only in part explain the risk differential between the general population and the population of patients with chronic nephropathies. Uncontrolled hyperphosphatemia and high calcium phosphate product constitute risk factors for cardiovascular calcifications, cardiac ischemia, and adverse cardiovascular outcomes, yet inflammation may be an even more important trigger of vascular calcification than these metabolic derangements. Homocysteine predicts cardiovascular events in ESRD, but evidence that this sulfur amino acid is directly implicated in the high cardiovascular mortality of uremic patients is still lacking. It seems unlikely that Chlamydia pneumoniae is a major risk factor in dialysis patients because the association between anti-Chlamydia antibodies and incident cardiovascular events seems to depend largely on the confounding effect of some traditional risk factors. Oxidative stress and raised plasma concentration of asymmetric dimethylarginine (ADMA) are pervasive in ESRD, and high ADMA in these patients may be at least in part the expression of the high rate of generation of oxidants. ADMA per se seems responsible for a 52% increase in the risk of death and for a 34% increase in the risk of cardiovascular events in dialysis patients.
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PMID:Novel cardiovascular risk factors in end-stage renal disease. 1468 78

Recent findings indicate that immunological factors are involved not only in the pathogenesis of age-related macular degeneration (AMD), but also in its treatment. Earlier data showing the presence of inflammatory cells in affected areas of AMD retinas support this statement. Although a possible role for autoimmunity was initially suggested, it has never reached general acceptance. Microorganisms have also been implied in the pathogenesis of AMD. Both serum antibacterial antibody levels and positive DNA tests from neovascular membranes have pointed to a possible role for Chlamydia pneumoniae in the pathogenesis of AMD. New data is providing evidence for the hypothesis that deposits between Bruch's membrane and the retinal pigment epithelium (RPE) cell layer may act as a stimulus for the local activation of the complement system. This may lead to a further growth of the deposits due to the strong chemotactic activity of certain complement activation products (such as C5a) with an influx of inflammatory cells. The buildup of cells and extracellular deposits may lead to local ischemia resulting in the activation of RPE cells. These activated RPE cells are thought to release angiogenic stimuli leading to choroidal neovascularization, which is the most serious complication of AMD. The fact that immunosuppressive drugs such as triamcinolone acetonide and anecortave acetate are capable of inhibiting choroidal neovascularization is consistent with an inflammatory component in the pathogenesis of AMD. Specific immunotherapy directed at certain cytokines or growth factors is now being investigated at both the animal and patient levels. Various clinical trials involving engineered antibodies are now being applied to block angiogenic factors such as the vascular endothelial growth factor (VEGF). An approach using gene therapy to influence angiogenesis by inducing the production of the pigment epithelium-derived factor (PEDF) was able to block neovascularization in an experimental murine model. Besides trying to block ongoing processes in AMD, retinal transplantation is now also being investigated as a treatment option. The fact that the retina is possibly an immunoprivileged tissue in combination with experimental data showing that the subretinal space is an immunoprivileged site is an indication that transplantation would not suffer from the rejection process. A larger obstacle is the question whether transplanted retinal tissue will regain its functional properties.
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PMID:Immunological factors in the pathogenesis and treatment of age-related macular degeneration. 1580 63

The main adaptable response to increased temperature is heat shock response resulting in induction of proteins called heat shock proteins (HSP). They are present in all cells under proper growth conditions and they create 5-10% of the whole protein contents. HSP were divided into five basic groups according to their approximate molecular mass, expressed in kDa and called respectively: HSP 100, HSP 90, HSP 70, HSP 60 and small HSP. Heat shock proteins can act like antigens in many infectious diseases. Immunological response against proteins from HSP 60, HSP 70 and HSP 90 families was observed in diseases caused by bacterial and protozoan pathogens. It is known that ischemia and reperfusion activate HSP genes transcription in heart cells of various experimental animals. Human and Chlamydia pneumoniae HSP 60 were found in patients with stable coronary disease. Hence many researchers connect the increase of ischaemia with the passed infection caused by Chlamydia pneumoniae, which can influence the origin or development of atheromatous plaque in the vascular wall. HSPs play an important role in hyperthermic therapy commonly used together with irradiation. Moreover, works on the possibility of HSP application to delay of disease process in neurodegenerative diseases, such as Parkinson or Alzheimer diseases are conducted. The paper presents characteristics of heat shock proteins, role in the state of health and disease and possibilities of their usage in monitoring and/or treatment of diseases, e.g. cancers.
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PMID:[Heat shock proteins and their characteristics]. 1624 38

The activation of the immunologic system plays an immportant role in the initiation of atherogenesis, as shown in numerous studies. However the role of infectious agents in this process still remains controversial. The aim of this study was to investigate the involvement of heat shock protein as a link between infection and peripheral arterial disease. 31 patients suffering from lower limb ischemia were enrolled in the study. Patients were divided into 2 groups. Group I - patients with peripheral arterial disease, group II patients with diabetic macroangiopathy. The control group consisted of 11 healthy volunteers. Blood samples were taken from each participant in order to determine serum concentrations of anti Chlamydia pneumoniae, CMV and HSP 60/65 antibodies. Statistic analysis showed anti-C. pneumoniae IgG (p< 0.025) and anti-CMV IgG (p<0.0157) antibodies were significantly more frequent in both study groups in comparison with healthy controls. Antibodie levels were also found significantly higher than in controls. Mean concentration of anti-C. pneumoniae IgG in the study group was 69.67574 vs. 18.59722 [AU/ml] in the control group (p<0.01). Analogical anti CMV IgG levels in the study group were 337.6516 vs 121.3778 [AU/ml] in controls (p<0.025). Similar changes in antibody concentration were noticed for the C. pneumoniae IgA index. 0.835258 vs. 0.176333 (p< 0.005). Antibodies against HSP 60/65 were present in significantly higher titre (p<0.005). No significant differences in antibody levels were detected beteween groups I and II. The positive correlation between anti-C. pneumoniae Ig A (r=0.3910; p<0.03) and anti HSP 60/65 antibodies titre, as well as anti-C. pneumoniae Ig G (r= 0.7151; p<0.00009) and anti HSP 60/65 speaks for the heat shock protein involvement in atherosclerotic plaque development.
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PMID:[Role of chronic infection and heat shock proteins in peripheral arterial disease]. 1815 51

Stroke is among the most common causes of death and persisting disability and therefore represents a great social and economic burden worldwide. In order to lower this burden it is essential to identify risk factors and respective preventive strategies. Besides the established stroke risk factors (e.g. hypertension, diabetes, hypercholesterolemia, atrial fibrillation) both acute and chronic infectious diseases have emerged as risk factors for stroke. Mainly acute respiratory tract infection but also urinary tract infections independently increase the risk of ischemic stroke. Such additional risk was shown to be highest for infection within 3 days before ischemia and the risk steadily declines with increasing time intervals between infection and stroke. Associations between stroke incidence and mortality and influenza epidemics have been demonstrated. Observational studies showed an inverse association between influenza vaccination and stroke risk; however, interventional studies in this field have not been performed so far. Chronic infections, presently discussed as stroke risk factors mainly include periodontitis and infections with Helicobacter pylori (Hp) and Chlamydia pneumoniae (Cp). Although most respective studies identified these infectious diseases as independent stroke risk factors interventional trials have not been performed so far and causality is not proven, yet. There is preliminary evidence that the number of pathogens to which a subject had been exposed to rather than single pathogens are associated with the risk of stroke or other cardiovascular diseases. Chronic infectious diseases are treatable conditions and their identification as causal contributors to stroke risk could offer new avenues in stroke prevention.
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PMID:Infection, its treatment and the risk for stroke. 1935 97


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