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

The use of the recreational drug crystal methamphetamine among younger homosexual men is expanding, and with it, unsafe sex behaviors that increase the transmission of human immunodeficiency virus (HIV). This article reviews available literature on the medical and psychiatric morbidities associated with methamphetamine abuse in HIV-infected patients. Medical complications include hypertension, hyperthermia, rhabdoymyolysis, and stroke. One fatal case of ingestion of methamphetamine with HIV medication has been documented. Two fatal cases of ingestion of HIV medication with the amphetamine analogue n-methyl-3,4 methylenedioxymethamphetamine (MDMA, or "ecstasy") have also been reported. Some molecular researchers suggest that dopaminergic systems are vulnerable to the combined neurotoxicity of HIV infection and methamphetamine. Population surveys indicate high rates of HIV infection among methamphetamine abusers and high rates of unprotected anal intercourse during drug intoxication. Intoxication can sometimes produce paranoia, auditory hallucinations, and, occasionally, violent behavior. Amphetamine withdrawal commonly results in symptoms of depression. Methamphetamine is a new challenge related to treatment and prevention of HIV infection.
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PMID:Crystal methamphetamine, its analogues, and HIV infection: medical and psychiatric aspects of a new epidemic. 1499 36

chlamdAs with other organ systems, the vulnerability of the nervous system to infectious agents increases with aging. Several different infectious agents can cause neurodegenerative conditions, with prominent examples being human immunodeficiency virus (HIV-1) dementia and prion disorders. Such infections of the central nervous system (CNS) typically have a relatively long incubation period and a chronic progressive course, and are therefore increasing in frequency as more people live longer. Infectious agents may enter the central nervous system in infected migratory macrophages, by transcytosis across blood-brain barrier cells or by intraneuronal transfer from peripheral nerves. Synapses and lipid rafts are important sites at which infectious agents may enter neurons and/or exert their cytotoxic effects. Recent findings suggest the possibility that infectious agents may increase the risk of common age-related neurodegenerative disorders such as Alzheimer's disease (AD) and Parkinson's disease (PD), amyotrophic lateral sclerosis (ALS) and stroke. While scenarios can be envisioned whereby viruses such as Chlamydia pneumoniae, herpes simplex and influenza promote damage to neurons during aging, there is no conclusive evidence for a major role of these pathogens in neurodegenerative disorders. In the case of stroke, blood vessels may be adversely affected by bacteria or viruses resulting in atherosclerosis.
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PMID:Infectious agents and age-related neurodegenerative disorders. 1516 5

Neurological dysfunction as the first manifestation of AIDS has been found in 10 to 20% of symptomatic human immunodeficiency virus infections. However, stroke has rarely been reported in AIDS patients. The most common causes of cerebral infarction in AIDS are central nervous system infections: toxoplasmosis, cryptococcal meningitis and tuberculosis. Potential vascular mechanisms for cerebral infarction and transient neurological deficits among AIDS patients include deposition of antigen-antibody complexes with vasculitis and infarction, and a direct toxic effect of a viral antigen or infectious agent on vascular endothelium. The role of cryptococcal meningitis in vasculopathy is still not clear. We report a case of cerebral infarction in an HIV-infected patient, with cryptococcal meningitis as the first manifestation of AIDS.
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PMID:Cerebral infarction related to cryptococcal meningitis in an HIV-infected patient: case report and literature review. 1536 96

N-Ethyl-maleimide-sensitive factor (NSF) plays a critical role in the regulation of exocytosis. NSF regulates exocytosis by interacting with a complex containing soluble NSF attachment protein receptor (SNARE) molecules, hydrolyzing ATP, and disassembling the SNARE complex. We hypothesized that peptide inhibitors of NSF would decrease exocytosis. We now report the development of a novel set of peptides that block exocytosis by inhibiting NSF activity. These NSF inhibitors are fusion polypeptides composed of an 11 amino acid human immunodeficiency virus transactivating regulatory protein (TAT) domain fused to a 22 amino acid NSF domain. These TAT-NSF fusion polypeptides cross endothelial cell membranes, inhibit NSF hydrolysis of ATP, decrease NSF disassembly of SNARE molecules, and block exocytosis of von Willebrand factor. Control peptides have no effect on exocytosis. TAT-NSF inhibitors administered to mice prolong the bleeding time. Blood concentrations of these TAT-NSF peptides rapidly decrease within 5 min after injection and then remain constant from 10 to 60 min after injection. These TAT-NSF compounds may be useful in the treatment of a variety of diseases in which exocytosis plays a prominent role, including myocardial infarction, stroke, thrombosis, and autoimmune disorders.
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PMID:A novel class of fusion polypeptides inhibits exocytosis. 1567

Hypericin is a naturally occurring substance found in the common St. John's Wort (Hypericum species) and can also be synthesized from the anthraquinone derivative emodin. As the main component of Hypericum perforatum, it has traditionally been used throughout the history of folk medicine. In the last three decades, hypericin has also become the subject of intensive biochemical research and is proving to be a multifunctional agent in drug and medicinal applications. Recent studies report antidepressive, antineoplastic, antitumor and antiviral (human immunodeficiency and hepatitis C virus) activities of hypericin; intriguing information even if confirmation of data is incomplete and mechanisms of these activities still remain largely unexplained. In other contemporary studies, screening hypericin for inhibitory effects on various pharmaceutically important enzymes such as MAO (monoaminoxidase), PKC (protein kinase C), dopamine-beta-hydroxylase, reverse transcriptase, telomerase and CYP (cytochrome P450), has yielded results supporting therapeutic potential. Research of hypericin and its effect on GABA-activated (gamma amino butyric acid) currents and NMDA (N-methyl-D-aspartat) receptors also indicate the therapeutic potential of this substance whereby new insights in stroke research (apoplexy) are expected. Also in the relatively newly established fields of medical photochemistry and photobiology, intensive research reveals hypericin to be a promising novel therapeutic and diagnostic agent in treatment and detection of cancer (photodynamic activation of free radical production). Hypericin is not new to the research community, but it is achieving a new and promising status as an effective agent in medical diagnostic and therapeutic applications. New, although controversial data, over the recent years dictate further research, re-evaluation and discussion of this substance. Our up-to-date summary of hypericin, its activities and potentials, is aimed to contribute to this process.
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PMID:Hypericin--the facts about a controversial agent. 1563 60

Infections have long been recognized as a potential, if uncommon, cause of cerebrovascular disease. In recent years, with the growing recognition of the importance of inflammation in atherosclerosis, there has been renewed interest in the possibility that common infections may participate in the atherosclerotic process or lead to stroke through other mechanisms. Specific organisms that have been implicated include Chlamydia pneumoniae, herpes viruses, human immunodeficiency virus, Helicobacter pylori, and organisms associated with periodontal infections. This article outlines the epidemiological, pathological, and laboratory evidence that these infections may be associated with atherosclerosis and stroke. Although definitive proof of an association between a specific infection and stroke is generally lacking, the accumulating evidence does indicate that several types of infections may be among the modifiable risk factors that contribute to the risk of stroke.
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PMID:Do common infections cause stroke? 1647 47

Plasmodium falciparum and human immunodeficiency virus type 1 (HIV-1) infections are common in children living in sub-Saharan Africa (SSA). Both of these pathogens affect the central nervous system (CNS). Most HIV-1 infection of children in this region is acquired from infected mothers, particularly during breast-feeding and at the time of delivery. Over a third of children infected by birth will have died before their first birthday, before overt CNS manifestations have developed. The most common manifestations of primary CNS infection include neurodevelopmental delay, impaired brain growth, motor deficits, and behavioral problems. These deficits may also result from infections, neoplasm, or stroke. Cognitive impairments become more evident if the child survives for longer, but in Africa, children rarely survive past their fifth birthday. In malaria endemic areas, severe falciparum malaria usually develops after 6 months of age, and most of the CNS manifestations are more common in children over 1 year old. About 11% of children develop neurological deficits following cerebral malaria, most of which improve within 2 years of the insult. However, up to 24% of children may have neurocognitive impairments following severe malaria. The effect of milder malaria and coincidental parasitization on cognitive function is unknown. Other comorbidities that are common in SSA, such as malnutrition or micronutrient deficiencies, may influence children's neurodevelopment. The coinfection of malaria and HIV-1 may aggravate the neurodevelopmental impairments documented in these children. However, to date there are little published data, although it may have a profound effect of children living in SSA.
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PMID:Interaction between Plasmodium falciparum and human immunodeficiency virus type 1 on the central nervous system of African children. 1654 Apr 55

The introduction of highly active antiretroviral therapy (HAART) has significantly modified the course of human immunodeficiency virus (HIV) disease, with longer survival and improved quality of life of HIV-infected subjects. However, HAART regimens, especially those including protease inhibitors, have been shown to cause in a high proportion of HIV-infected patients a metabolic syndrome (lipodystrophy/lipoatrophy, dyslipidemia, type 2 diabetes mellitus, insulin resistance) that may be associated with an increased risk of cardiovascular disease (coronary artery disease and stroke). A careful stratification of the cardiovascular risk and cardiovascular monitoring of patients under HAART is needed according to the most recent clinical guidelines.
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PMID:Highly active antiretroviral therapy-associated metabolic syndrome and cardiovascular risk. 1667

Common variable immunodeficiency (CVID) is the most common symptomatic primary immunodeficiency. Patients have recurrent bacterial infections and an increased risk of developing autoimmune diseases, lung damage, and selected cancers. Since 2003, four genes have been shown to be mutated in CVID patients: ICOS, TNFRSF13B (encoding TACI), TNFRSF13C (encoding BAFF-R) and CD19. Heterozygous mutations in TNFRSF13B are also associated with CVID, whereas the other three genes are purely recessive. Recent genetic linkage studies have also identified possible loci for dominant CVID genes on chromosomes 4q, 5p and 16q. These findings markedly improved the genetic diagnosis of CVID and point towards new strategies for future genetic studies. In addition, some CVID genes might be relevant to more common diseases such as asthma and stroke.
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PMID:Deconstructing common variable immunodeficiency by genetic analysis. 1746 61

Infarction size and infections are important determinants of stroke outcome in humans. Bacterial infections are promoted by stroke-induced immunodeficiency which in experimental stroke is mainly characterized by extensive lymphocyte apoptosis and dysfunction. Pharmacological inhibition of caspases may improve stroke outcome not only by reducing apoptotic brain damage but also by attenuating stroke-induced immunodeficiency. We investigated the effects of systemic administration of the novel, non-toxic caspase-inhibitor quinolyl-valyl-O-methylaspartyl-[-2,6-difluorophenoxy]-methyl ketone (Q-VD-OPH) on stroke-induced neuronal and lymphocyte apoptosis, susceptibility to infections, and mortality in a murine model of stroke induced by middle cerebral artery occlusion (MCAO). Q-VD-OPH reduced ischemic brain damage and stroke-induced programmed cell death in thymus and spleen, decreased susceptibility to post-stroke bacteremia, and improved survival. Therefore, Q-VD-OPH may be a promising therapeutic agent in stroke.
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PMID:Protection from brain damage and bacterial infection in murine stroke by the novel caspase-inhibitor Q-VD-OPH. 1758 6


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