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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The morphology of the white pulp of the spleens collected from forty four patients died in widespread carcinoma of the liver and extrahepatic bile ducts was histologically evaluated by utilizing the standardized reporting system previously outlined. As a control material, the same number of age- and sex-matched patients died in myocardial infarction or cerebrovascular accident without signs of any malignancy was used. Special attention was paid to the assessment of the T- and B-lymphocyte populations responsible for the immunological reactivity. Histological characteristics suggesting an active function of both the cell-mediated and humoral immune reactions (central and peripheral lymphoid sheats, respectively) were found to be within the normal range in the control spleens, whereas in the cancer series, both these elements were profoundly deranged. The significance of the histological observations made was discussed in the light of the tumor immunology, and a conclusion was drawn that an impairment of both the humoral and cell-mediated immune responses must exist in patients dying in widespread hepato-biliary carcinoma. The applicability of the standardized reporting system used was advocated.
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PMID:Immunological reactivity in patients with widespread carcinoma of the liver and bile ducts as evaluated on the basis of spleen white pulp morphology. 625 64

Separated lymphoid cells from patients suffering from multiple sclerosis (MS) were co-cultivated with various cell lines. Over 80% of such co-cultivations showed destruction of the tissue-culture monolayers, whereas less than 5% of "normal" blood co-cultivation behaved in the same manner. Because of the possible involvement of virus in the aetiology of MS, many positive co-cultivations were 1) examined electron-microscopically, but no virus particles were seen; and 2) tested for measles and herpes viruses using immunofluorescent techniques, but these also proved negative. Leukocytes from stroke patients showed monolayer destruction in about 50% of cases. Granulocyte contamination was high in the stroke blood samples. Reduction of granulocyte numbers to "normal" levels completely abrogated the effect in the stroke samples, but had no effect on the MS co-cultivations. Monolayer destruction by MS leukocytes also appeared not to be due to lymphotoxin.
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PMID:Monolayer destruction by leukocytes from patients with multiple sclerosis. 699 97

Cytokines are important hormonal mediators, produced in tissues undergoing defence, growth and repair processes. Infection and inflammation in particular result in a cascade of cytokine induction that acts to maintain tissue homeostasis. Most cytokines act within the injured tissues, although some have an endocrine action, recruiting distant tissues in defence of the tissue producing the cytokine and many are important for regulating acquired immunity in secondary lymphoid tissues. Induction of interleukin-1 (IL-1), tumour necrosis factor (TNF) and IL-6 highlight the way in which local tissue cytokine responses are induced and act. Since most cytokines act locally, cytokine measurement presents several difficulties. Only where cytokines (such as IL-6) have a systemic action are plasma cytokine concentrations really meaningful. The presence of cytokine antagonists and soluble cytokine receptors, often released in concert with their respective cytokine agonists, presents additional complexity to interpretation. Measurement and manipulation of cytokines can contribute towards an understanding of their pathophysiological role in both experimental and clinical settings. This includes measurement of plasma IL-6, which has striking relationships to tissue inflammation. Its value is exemplified by some recent studies of stroke patients, where IL-6 reflects not only the initial response but also clinical outcome and survival.
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PMID:The pathophysiological role of cytokines. 1293 51

Atherosclerosis is a chronic inflammatory disease, and is the primary cause of heart disease and stroke in Western countries. Derivatives of cannabinoids such as delta-9-tetrahydrocannabinol (THC) modulate immune functions and therefore have potential for the treatment of inflammatory diseases. We investigated the effects of THC in a murine model of established atherosclerosis. Oral administration of THC (1 mg kg(-1) per day) resulted in significant inhibition of disease progression. This effective dose is lower than the dose usually associated with psychotropic effects of THC. Furthermore, we detected the CB2 receptor (the main cannabinoid receptor expressed on immune cells) in both human and mouse atherosclerotic plaques. Lymphoid cells isolated from THC-treated mice showed diminished proliferation capacity and decreased interferon-gamma secretion. Macrophage chemotaxis, which is a crucial step for the development of atherosclerosis, was also inhibited in vitro by THC. All these effects were completely blocked by a specific CB2 receptor antagonist. Our data demonstrate that oral treatment with a low dose of THC inhibits atherosclerosis progression in the apolipoprotein E knockout mouse model, through pleiotropic immunomodulatory effects on lymphoid and myeloid cells. Thus, THC or cannabinoids with activity at the CB2 receptor may be valuable targets for treating atherosclerosis.
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PMID:Low dose oral cannabinoid therapy reduces progression of atherosclerosis in mice. 1581 11

Clinical experimental stroke induces injurious local brain inflammation. However, effects on the peripheral immune system have not been well characterized. We quantified mRNA and protein levels for cytokines, chemokines, and chemokine receptors (CCR) in brain, spinal cord, peripheral lymphoid organs (spleen, lymph node, blood, and cultured mononuclear cells from these sources), and blood plasma after reversible middle cerebral artery occlusion (MCAO) or sham treatment in male C57BL/6 mice. Middle cerebral artery occlusion induced a complex, but organ specific, pattern of inflammatory factors in the periphery. At both 6 and 22 h after MCAO, activated spleen cells from stroke-injured mice secreted significantly enhanced levels of TNF-alpha, IFN-gamma, IL-6, MCP-1, and IL-2. Unstimulated splenocytes expressed increased chemokines and CCR, including MIP-2 and CCR2, CCR7 and CCR8 at 6 h; and MIP-2, IP-10, and CCR1 and CCR2 at 22 h. Also at 22 h, T cells from blood and lymph nodes secreted increased levels of inflammatory cytokines after activation. As expected, there were striking proinflammatory changes in postischemic brain. In contrast, spinal cord displayed suppression of all mediators, suggesting a compensatory response to intracranial events. These data show for the first time that focal cerebral ischemia results in dynamic and widespread activation of inflammatory cytokines, chemokines, and CCR in the peripheral immune system.
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PMID:Experimental stroke induces massive, rapid activation of the peripheral immune system. 1612 Nov 26

Sequencing of the human genome and new microarray technology make it possible to assess all genes on a single chip or array. Recent studies show different patterns of gene expression related to different tissues and diseases, and these patterns of gene expression are beginning to be used for diagnosis and treatment decisions in various types of lymphoid and solid malignancies. Because of obvious problems obtaining brain tissue, progress in genomics of neurological diseases has been slow. To address this, we demonstrated that different types of acute injury in rodent brain produced different patterns of gene expression in peripheral blood. These animal studies have now been extended to human studies. Two groups have shown that there are specific genomic profiles in the blood of patients after ischemic stroke that are highly sensitive and specific for predicting stroke. Other recent studies demonstrate specific genomic profiles in the blood of patients with Down syndrome, neurofibromatosis, tuberous sclerosis, Huntington disease, multiple sclerosis, Tourette syndrome, and others. In addition, data demonstrate specific profiles of gene expression in the blood related to different drugs, toxins, and infections. Although all of these studies are still preliminary basic scientific endeavors, they suggest that this approach will have clinical applications to neurological diseases in humans.
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PMID:The future of genomic profiling of neurological diseases using blood. 1710 21

Chemokines and chemokine receptors, primarily found to play a role in leukocyte migration to the inflammatory sites or to second lymphoid organs, have recently been found expressed on the resident cells of the central nervous system (CNS). These proteins are important for the development of the CNS and are involved in normal brain functions such as synaptic transmission. Increasing lines of evidence have implicated an involvement for chemokines and their receptors in several neurodegenerative disorders, including Alzheimer's disease (AD), Parkinson's disease (PD), human immunodeficiency virus-associated dementia (HAD), multiple sclerosis (MS), and stroke. Specific inhibition of the biological activities of chemokine receptors could gain therapeutic benefit for these neurodegenerative disorders. In recent years, non-peptide antagonists of chemokine receptors have been disclosed and tested in relevant pharmacological models and some of these inhibitors have entered clinical trials. The aim of this review is to outline the recent progress regarding the role of chemokines and their receptors in neurodegenerative diseases and the advancements in the development of chemokine receptor inhibitors as potential therapeutic approaches for these neurodegenerative diseases.
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PMID:The many roles of chemokine receptors in neurodegenerative disorders: emerging new therapeutical strategies. 1797 99

Pneumonia constitutes a serious medical complication and major cause of death in patients after cerebral stroke. In a mouse model of cerebral ischemia (MCAO), we have recently demonstrated that stroke animals spontaneously develop severe bacterial pneumonia which is preceded by a stress-mediated suppression of cellular immune responses in primary and secondary lymphoid organs. However, little is known about the mechanisms leading to impaired pulmonary antimicrobial immune response after cerebral ischemia. In this study, we demonstrate a rapid up-regulation of the immunomodulatory neuropeptide alpha-melanocyte-stimulating hormone (MSH) in the lung within 24 h after cerebral ischemia. Systemic administration of the naturally occurring alpha-MSH receptor-1 (MC-1R) antagonist agouti immediately after MCAO significantly reduced pulmonary bacterial burden at 72 h. In contrast, administration of recombinant alpha-MSH further increased bacterial load in lungs of MCAO animals. In addition, cerebral ischemia resulted in a strong modulation of local pulmonary immunity with increased production of IL-10 by lung macrophages, reduced pulmonary lymphocyte counts, as well as decreased lymphocytic IFN-gamma but increased IL-4 production. However, alpha-MSH blockade by administration of agouti did not prevent changes in lung immune cell numbers or cytokine production suggesting that suppression of cellular immune responses is not the primary mechanism of alpha-MSH mediated inhibition of pulmonary antibacterial defenses. This study indicates an important role of alpha-MSH for the increased infectious susceptibility after cerebral ischemia and may provide new therapeutic strategies to prevent post-stroke infectious complications.
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PMID:Alpha-MSH promotes spontaneous post-ischemic pneumonia in mice via melanocortin-receptor-1. 1830 33

Experimental studies were made of rat immunoreactivity in experimental modeling of acute hemorrhagic stroke in staphylococcal infection. Bactericidal activity and reserve bactericidal activity of neutrophils in NBT-test enhance while mid-molecular CIC level decreases because of phagocyte activation. ABA high titers in blood reflect activation of autoimmune processes. Splenic mass increased suggesting activation of proliferation of splenic lymphoid cells or enhanced migration of immature lymphoid cells from bone marrow to the spleen. Experimental animals had suppressed functional activity of main lymphoid cells populations in blast-transformation reaction which may affect the course of early recovery, promote activation of infectious bacterial process, autoaggression. The results of the studies can serve the basis for further investigations of immune mechanisms involved in development of hemorrhagic stroke in the presence of infectious process.
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PMID:[Rat immunoreactivity in experimental modeling of acute autohemorrhagic bihemispheric stroke in the presence of staphylococcal infection]. 1894 71

Stroke induces a strong inflammatory reaction in the brain and depresses the immune system. We sought to assess longitudinal changes in T-cell numbers in the lymphoid organs of living mice after brain ischemia. Middle cerebral artery occlusion was carried out in transgenic mice expressing green fluorescent protein (GFP+) in the T-cell population under the control of the hCD2 locus control region. Imaging was performed by three-dimensional fluorescence molecular tomography (FMT) before and at several time points after ischemia or sham operation and in controls. At day 7, GFP+ cell content in lymphoid organs was measured postmortem by flow cytometry. GFP+ cell numbers and in vivo FMT signal intensity were reduced at day 7 after ischemia and, to a lesser extent, after sham operation. Linear regression analysis demonstrated that postmortem GFP+ cell numbers and corresponding in vivo FMT data were significantly correlated in the thymus (r2 = .65, p < .0001) and lymph nodes (r2 = .67, p < .0001). These relationships allowed inferring the number of GFP+ T cells from in vivo FMT data. The results show the time course reduction of T-cell content in the lymphoid organs of living mice, providing in vivo evidence of lymphoid organ atrophy after stroke and, to a lesser extent, after head surgery with craniectomy and dura mater opening in sham-operated mice.
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PMID:Imaging changes in lymphoid organs in vivo after brain ischemia with three-dimensional fluorescence molecular tomography in transgenic mice expressing green fluorescent protein in T lymphocytes. 1912 86


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