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Query: UMLS:C0019693 (HIV)
 170,526 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Mounting evidence suggests that cognitive dysfunction developing as a result of HIV-1 infection is mediated at least in part by generation of excitotoxins and free radicals in the brain. This syndrome is currently designated HIV-1-associated cognitive/motor complex, was originally termed the AIDS Dementia Complex, and for simplicity, is called AIDS dementia in this review. Recently, brains of patients with AIDS have been shown to manifest neuronal injury and apoptotic-like cell death. How can HIV-1 result in neuronal damage if neurons themselves are only rarely, if ever, infected by the virus? Experiments from several different laboratories have lent support to the existence of HIV- and immune-related toxins in a variety of in vitro and in vivo paradigms. In one recently defined pathway to neuronal injury, HIV-infected macrophages and microglia, or immune-activated macrophages and astrocytes (activated by the shed HIV-1 envelope protein, gp120, or other viral proteins and cytokines), appear to secrete excitants and neurotoxins. These substances may include arachidonic acid, platelet-activating factor, free radicals (NO. and O2.-), glutamate, quinolinate, cysteine, amines, and as yet unidentified factors emanating from stimulated macrophages and reactive astrocytes. A final common pathway for neuronal susceptibility is operative, similar to that observed in stroke and several neurodegenerative diseases. This mechanism involves excessive activation of N-methyl-D-aspartate (NMDA) receptor-operated channels, with resultant excessive influx of Ca2+ and the generation of free radicals, leading to neuronal damage. With the very recent development of clinically tolerated NMDA antagonists, there is hope for future pharmacological intervention.
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PMID:Neuronal injury associated with HIV-1: approaches to treatment. 959 52

This study was undertaken to attempt to identify correlations between microsporidial seroprevalence data in man, clinical diseases and groups of people at the risk of HIV/AIDS infection. Groups of patients were selected according to the predilection of members of the genus Encephalitozoon for nervous and kidney tissue. Female prostitutes and alcohol and intravenous drug abusers were selected as groups at risk of HIV/AIDS infections. A total of 401 samples of human sera were examined for the presence of antimicrosporidial IgG antibodies by ELISA test with a titre of 600 considered borderline positivity. The highest occurrence of antimicrosporidial antibodies was found in the groups of alcohol abusers (16% from 43 patients), intravenous drug abusers (11% from 9 patients) and prostitutes (10% from 80 women) for E. cuniculi antigen and in the groups of psychiatric patients (14% from 44 patients), malaria patients (11% from 38 patients) and alcohol abusers (7% from 43 patients) for E. hellem antigen. The occurrence of specific antibodies of the six examined diagnostic units (glomerulonephritis chronica, pyelonephritis chronica, schizophrenia, dementia, multiple sclerosis and cerebral stroke) was statistically significant only in patients with pyelonephritis chronica and dementia (p < 0.05). No cases of microsporidial infection were found among the female prostitutes by parasitological examination, although one case of giardiasis was identified. Sera of patients with high anti-E. cuniculi and anti-E. hellem antibodies (titres in ELISA of 600 and above) were confirmed by Western blot using E. cuniculi and E. hellem polypeptides, respectively. These results suggest that the examined patients could show residual antibodies from past or latent infections.
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PMID:The serological surveillance of several groups of patients using antigens of Encephalitozoon hellem and E. cuniculi antibodies to microsporidia in patients. 968 20

We evaluated 81 thalassaemia major and 4 thalassaemia intermedia patients (48 M, 37 F), median age 17 years; 62/85 patients were HCV-positive, 3/85 HIV-positive, 19/85 were splenectomized. Forty normal healthy children were recruited as the control group. The number of thrombotic events was studied retrospectively. Platelet poor plasma was filtered and quick-frozen at -70 degrees C until time of assay. APC resistance was measured in an activated thromboplastin time and results were expressed as normalized ratio. All tests were done with diluted 1 in 5 (v/v) factor V deficient plasma and with undiluted plasma. Molecular genetic investigation of factor V gene was performed with polymerase chain reaction, followed by digestion of amplified products with restriction enzyme Mnl I. Data obtained with molecular investigation revealed the presence of 4 heterozygous subjects for factor V Leiden (4.7%). Functional tests were able to detect all heterozygotes for factor V Leiden both with undiluted and with diluted plasma, and there were no false negative subjects. However, undiluted plasma revealed a greater number of false positive subjects (n=15) than did diluted plasma. Therefore, tests done with undiluted and diluted plasma revealed a 100% sensitivity, while specificity was 81% for undiluted plasma and 97% for diluted plasma. Only one thrombotic event was observed in one of the 85 studied patients, as a case of stroke in a thalassaemia intermedia patient with APC resistance. In the same patient an additional thrombogenic risk factor was represented by a pronounced haematocrit increase at the beginning of her transfusion regimen.
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PMID:Resistance to activated protein C in thalassaemic patients: an underlying cause of thrombosis. 971 25

Antiphospholipid antibodies associated with the antiphospholipid syndrome (APS) have been shown to bind plasma proteins, particularly beta 2-glycoprotein I (beta2-GPI). In this study the incidence of antibodies to solid-phase prothrombin was examined in patients with antiphospholipid syndrome and a variety of other inflammatory disorders. Significantly elevated levels of IgG anti-prothrombin (anti-PT) antibodies were detected in 63% of patients with APS (n = 27, median 22 arbitrary units: AU), 33% with SLE (n = 92, median 14 AU). 45% with rheumatoid factor (n = 22, median 16 AU), 21% with carotid artery stenosis (n = 21, median 15 AU), 32% with stroke (n = 38, median 13 AU). 67% of patients with a false positive serology for syphilis (n = 21, median 24 AU), 37% with HIV (n = 30, median 14 AU), 29% with syphilis (n = 14, median 19 AU) and 3% with infectious mononucleosis (n= 30, median 9 AU). In addition, a group of lupus anticoagulant (LA) positive patients (n = 48) was examined for antibodies to prothrombin, beta2-GPI and cardiolipin. 10 (21%) patients had raised levels of IgG anti-PT antibodies, 30 (62%) had significantly elevated levels of anti-beta2-GPI antibodies and 15 (31%) had elevated levels of anticardiolipin antibodies (ACA). Of the LA-positive patients, 15 (43%) were identified with definite APS, eight (23%) with probable APS, two (6%) with possible APS and 10 (28%) patients had no clinical evidence of APS. In conclusion, antibodies to prothrombin were found in a variety of inflammatory disorders and were therefore not specific for the APS. However, identification of the plasma proteins recognized by antibodies from patients with APS may provide insight into the pathogenic mechanisms involved in the heterogenous clinical manifestations of the APS.
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PMID:Antibodies to prothrombin in antiphospholipid syndrome and inflammatory disorders. 973 36

Nitric oxide (NO) is a unique biological messenger molecule which mediates diverse physiologic roles. NO mediates blood vessel relaxation by endothelium, immune activity of macrophages and neurotransmission of central and peripheral neurons. NO is produced from three NO Synthase (NOS) isoforms: Neuronal NOS (nNOS), endothelial NOS, and inducible NOS (iNOS). In the central nervous system, NO may play important roles in neurotransmitter release, neurotransmitter reuptake, neurodevelopment, synaptic plasticity, and regulation of gene expression. However, excessive production of NO following a pathologic insult can lead to neurotoxicity. NO plays a role in mediating neurotoxicity associated with a variety of neurologic disorders, including stroke, Parkinson's Disease, and HIV dementia.
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PMID:Nitric oxide in neurodegeneration. 993 44

African Americans suffer disproportionately from several major health problems associated with high morbidity and mortality. The 1985 DHHS Secretary's Task Force Report on Blacks and Other Minorities identified six major disease categories of excess deaths for African Americans compared with whites by applying the lower death rate for whites to the American population. The report provided a stimulus for public and private action to begin to address the health disparities between minority and nonminority populations. This article examines three of the leading causes of death for African Americans and assesses the extent to which the health disparity between African Americans and whites has been reduced. The three leading causes of death for African American males are diseases of the heart, cancer, and HIV infection/AIDS. The conditions are the same for African American females except stroke replaces HIV infection. Three health outcomes measures are discussed: life expectancy, excess death rates, and years of potential life lost. A widening of the gap between the races was found for diseases of the heart and HIV infection for males and for cancer for females. An extensive list of barriers to reducing the disparity are presented from the scientific literature and strategies for reducing the three health problems are recommended.
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PMID:The three leading causes of death in African Americans: barriers to reducing excess disparity and to improving health behaviors. 998 6

The authors report two pediatric patients with definite human immunodeficiency virus infection whose initial presentation was stroke and seizure. The first patient was a 3-year-old female who developed acute hemiparesis as the first manifestation. The other, a 2-month-old infant, had focal seizures secondary to cerebral infarction. Investigations revealed ischemic infarction of the thalamus, hypothalamus, and internal capsule in the first patient and cerebral cortex in the second. Further investigations failed to demonstrate any other causes of these cerebral infarctions. Opportunistic infection of the central nervous system was not documented. The authors emphasize that cerebrovascular accident may be the initial presentation in human immunodeficiency virus infection in children. Human immunodeficiency virus infection must be included in the differential diagnosis, and testing for the disease is mandatory in the investigation of stroke in any child who is at risk of having this infection.
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PMID:Stroke and seizures as the presenting signs of pediatric HIV infection. 1046 51

Cocaine abuse has been associated with vasculitis and stroke, and is suspected to influence the progression of AIDS dementia. Cocaine may enhance HIV-1 neuroinvasion by actions directed at the blood-brain barrier. HIV-1 appears to penetrate the human brain microvascular endothelial cell barrier by a paracellular route breached by tumor necrosis factor-alpha (TNF-alpha). Cocaine's effects on the blood-brain barrier were investigated using human brain microvascular endothelial cells and peripheral blood monocytes. Cocaine (10(-5) M and 10(-6) M) increased molecular permeability of the barrier and viral invasion by the macrophage-tropic HIV-1(JR-FL) into the brain chamber. Cocaine also augmented apoptosis of brain endothelial cells and monocytes, increased secretion of four chemokines (interleukin-8, interferon-inducible protein-10, macrophage inflammatory protein-1alpha, and monocyte chemoattractant protein-1) and the cytokine, TNF-alpha, by human monocytes. TNF-alpha enhanced invasion of the brain compartment by macrophage-tropic, lymphotropic, and bitropic HIV-1 strains. These data indicate that HIV-1 neuroinvasion can be increased by (a) cocaine's direct effects on brain microvascular endothelial cells and (b) paracrine effects of cocaine-induced pro-inflammatory cytokines and chemokines on the blood-brain barrier.
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PMID:Cocaine opens the blood-brain barrier to HIV-1 invasion. 1006 3

Laboratory services of the early 21st century will be heavily influenced by significant demographic redistributions and shifts in the incidence and prevalence of disease. A persistent influx of immigrants literally will change the face of the U.S. population. Persons born between 1946 and 1964 will reach middle and old age and will require testing for arthritis, diabetes, cardiac dysfunction, Alzheimer's disease, and stroke. Efforts to combat infertility will expand. Tuberculosis, wrongly assumed to be under control, will continue to proliferate. Testing will be needed for the millions of people living with AIDS and for the millions more infected or suspected to be infected with HIV. Cancer screening and information from genetic markers will widen. Public screenings will be routinely offered in assorted sites. As the national focus shifts from curing illness to promoting health, laboratory tests will assess healthy persons to a greater degree than ever.
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PMID:Changing disease patterns, shifting demographics: effects on laboratory services. 1017 18

We present SPET brain perfusion findings in 32 patients who suffered mild traumatic brain injury without loss of consciousness and normal computed tomography. None of the patients had previous traumatic brain injury, CVA, HIV, psychiatric disorders or a history of alcohol or drug abuse. Their ages ranged from 11 to 61 years (mean = 42). The study was performed in 20 patients (62%) within 3 months of the date of injury and in 12 (38%) patients more than 3 months post-injury. Nineteen patients (60%) were involved in a motor vehicle accident, 10 patients (31%) sustained a fall and three patients (9%) received a blow to the head. The most common complaints were headaches in 26 patients (81%), memory deficits in 15 (47%), dizziness in 13 (41%) and sleep disorders in eight (25%). The studies were acquired approximately 2 h after an intravenous injection of 740 MBq (20.0 mCi) of 99Tcm-HMPAO. All images were acquired on a triple-headed gamma camera. The data were displayed on a 10-grade colour scale, with 2-pixel thickness (7.4 mm), and were reviewed blind to the patient's history of symptoms. The cerebellum was used as the reference site (100% maximum value). Any decrease in cerebral perfusion in the cortex or basal ganglia less than 70%, or less than 50% in the medial temporal lobe, compared to the cerebellar reference was considered abnormal. The results show that 13 (41%) had normal studies and 19 (59%) were abnormal (13 studies performed within 3 months of the date of injury and six studies performed more than 3 months post-injury). Analysis of the abnormal studies revealed that 17 showed 48 focal lesions and two showed diffuse supratentorial hypoperfusion (one from each of the early and delayed imaging groups). The 12 abnormal studies performed early had 37 focal lesions and averaged 3.1 lesions per patient, whereas there was a reduction to--an average of 2.2 lesions per patient in the five studies (total 11 lesions) performed more than 3 months post-injury. In the 17 abnormal studies with focal lesions, the following regions were involved in descending frequency: frontal lobes 58%, basal ganglia and thalami 47%, temporal lobes 26% and parietal lobes 16%. We conclude that: (1) SPET brain perfusion imaging is valuable and sensitive for the evaluation of cerebral perfusion changes following mild traumatic brain injury; (2) these changes can occur without loss of consciousness; (3) SPET brain perfusion imaging is more sensitive than computed tomography in detecting brain lesions; and (4) the changes may explain a neurological component of the patient's symptoms in the absence of morphological abnormalities using other imaging modalities.
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PMID:SPET brain perfusion imaging in mild traumatic brain injury without loss of consciousness and normal computed tomography. 1045 61


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