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Biomedical subjects

J Booss

Publications and source records attributed to J Booss.

49 records · Page 3Linked to original sources
PubMed1977

Role of viremia in the suppression of T-cell function during murine cytomegalovirus infection.

The suppression of T-cell deoxyribonucleic acid (DNA) synthesis by serum from mice acutely with murine cytomegalovirus (MCMV) was investigated. Spleen cells from uninfected mice were exposed to concanavalin A in the presence of serum taken from mice at various times after infection with MCMV. The capacity of the serum to suppress DNA synthesis first appeared at day 3 postinfection and was associated with free infectious virus. Addition of MCMV to serum from uninfected mice also suppressed DNA synthesis. Ultracentrifugation of serum from mice acutely infected with MCMV removed most of the virus and aborgated the inhibition of DNA synthesis. However, in two of four experiments, serum from mice in weeks 4 and 5 postinfection did not contain infectious MCMB but did suppress. Therefore, it appears that MCMV itself can suppress DNA synthesis of T cells; however, this may not be the exclusive mechanism of suppression exerted by serum from MCMB-infected mice.

Animals↗
PubMed1976

Cerebrospinal fluid IgG level in herpes simplex encephalitis.

Elevated levels of immunoglobulin G (IgG) in the cerebrospinal fluid (CSF) were associated with elevated herpes antibody in the CSF in a case of herpes simplex encephalitis. The case was also characterized by a prolonged course and a difficult virus isolation.

Antibodies, Viral↗
PubMed1975

Correlation of survival from murine cytomegalovirus infection with spleen cell responsiveness to Concanavallin A.

Spleen cells from nonlethally MCMV-infected weanling and adult DBA/2 mice had diminished responses to Con A stimulation. In contrast, only lethal MCMV infections were associated with a complete suppression of the Con A response. The immune response to SRBC was depressed even in asymptomatic infections of weanling and adult mice. A marked maturation of resistance to the lethal effects of MCMV infection was found to occur during the fourth week of life.

Age Factors↗
PubMedDate not supplied

Prevention of a first stroke: a review of guidelines and a multidisciplinary consensus statement from the National Stroke Association.

OBJECTIVE: To establish, in a single resource, up-to-date recommendations for primary care physicians regarding prevention strategies for a first stroke. PARTICIPANTS: Members of the National Stroke Association's (NSA's) Stroke Prevention Advisory Board and Cedars-Sinai Health System Department of Health Services Research convened on April 9, 1998, in an open meeting. The conference attendees, selected to participate by the NSA, were recognized experts in neurology (9), cardiology (2), family practice (1), nursing (1), physician assistant practices (1), and health services research (2). EVIDENCE: A literature review was carried out by the Department of Health Services Research, Cedars-Sinai Health System, Los Angeles, Calif, using the MEDLINE database search for 1990 through April 1998 and updated in November 1998. English-language guidelines, statements, meta-analyses, and overviews on prevention of a first stroke were reviewed. CONSENSUS PROCESS: At the meeting, members of the advisory board identified 6 important stroke risk factors (hypertension, myocardial infarction [MI], atrial fibrillation, diabetes mellitus, blood lipids, asymptomatic carotid artery stenosis), and 4 lifestyle factors (cigarette smoking, alcohol use, physical activity, diet). CONCLUSIONS: Several interventions that modify well-documented and treatable cardiovascular and cerebrovascular risk factors can reduce the risk of a first stroke. Good evidence for direct stroke reduction exists for hypertension treatment; using warfarin for patients after MI who have atrial fibrillation, decreased left ventricular ejection fraction, or left ventricular thrombus; using 3-hydroxy-3 methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors for patients after MI; using warfarin for patients with atrial fibrillation and specific risk factors; and performing carotid endarterectomy for patients with stenosis of at least 60%. Observational studies support the role of modifying lifestyle-related risk factors (eg, smoking, alcohol use, physical activity, diet) in stroke prevention. Measures to help patients improve adherence are an important component of a stroke prevention plan.

Alcohol Drinking↗
PubMedDate not supplied

Mechanisms of injury to the central nervous system following experimental cytomegalovirus infection.

A guinea pig model was used to determine the mechanisms of injury to the central nervous system by cytomegalovirus. Focal, well-contained, histopathologic responses included the microglial nodule without residua, and the ependymitis with focal residual glial scarring. Higher virus dose infection in the brain resulted in inflammatory necrosis with an astrocytic response to injury. However, monocytes and microglia were the predominant responding cells of host defense. A vasogenic pathogenesis was suggested by the involvement of the vascular endothelium, and separately by central nervous system vasculitis, demonstrated here for the first time in this model. Hence, our studies suggest four potential mechanisms of injury to the central nervous system by cytomegalovirus: viral cytopathology, inflammatory mediators from cells of the monocyte series, two separate types of vascular impairment, and astroglial scarring.

Animals↗
PubMedDate not supplied

Progressive multifocal leukoencephalopathy in AIDS: are there any MR findings useful to patient management and predictive of patient survival? AIDS Clinical Trials Group, 243 Team.

BACKGROUND AND PURPOSE: While MR findings in progressive multifocal leukoencephalopathy (PML) have been described previously, usually in retrospective studies with limited sample size, what has not been well addressed is whether any are predictive of longer survival. Our participation in a large prospective clinical trial of AIDS patients with biopsy-proved PML and MR correlation allowed us to test our hypothesis that certain MR features could be found favorable to patient survival. METHODS: The patient cohort derived from a randomized multicenter clinical trial of cytosine arabinoside for PML. Pretreatment T1- and T2-weighted noncontrast images (n = 48) and T1-weighted contrast-enhanced images (n = 45) of 48 HIV-positive patients with a PML tissue diagnosis as well as the follow-up images in 15 patients were reviewed to determine signal abnormalities, lesion location and size, and the presence or absence of mass effect, contrast enhancement, and atrophy, and to ascertain the frequency of these findings. A statistical analysis was performed to determine if any MR abnormalities, either at baseline or at follow-up, were predictive of patient survival. RESULTS: No MR abnormalities either on univariate or multivariate analysis significantly correlated with patient survival, with the exception of mass effect, which was significantly associated with shorter survival. The mass effect, however, always minimal, was infrequent (five of 48). More severe degrees of cortical atrophy and ventricular dilatation, lesion location and size, and other MR variables were not predictive of outcome. CONCLUSION: Except for mass effect, we found no MR findings predictive of the risk of death in patients with PML. The mass effect, however, was so infrequent and minimal that it was not a useful MR prognostic sign.

AIDS Dementia Complex↗
PubMedDate not supplied

Cytomegalovirus encephalitis: neuropathological comparison of the guinea pig model with the opportunistic infection in AIDS.

The AIDS epidemic has transformed the importance of cytomegalovirus (CMV) as a pathogen for the adult human central nervous system (CNS). At autopsy, about 25 percent of AIDS cases have cytopathologic evidence of CNS infection by CMV. Since almost nothing is known of the host CNS-viral interactions, we have developed a laboratory model of CMV infection of the brain in the guinea pig. In the present paper, we review the syndromes of CMV infection of the human CNS and compare the neuropathological findings of the opportunistic CMV brain infection in AIDS with the model. Destructive meningoencephalitis, perivascular infiltrates, and subependymal inflammation are found in both, but the glial nodule is the most characteristic feature of each. Thus, we demonstrate that the model faithfully reflects the histopathology of the human disease. Furthermore, since we have found that CNS infection is achieved following systemic infection in the guinea pig, the model recapitulates the sequence of infection in humans.

Acquired Immunodeficiency Syndrome↗
PubMedDate not supplied

Neurology of AIDS virus infection: a clinical classification.

Infection with the AIDS virus itself (HIV, HTLV-III, LAV, ARV) is associated with a full spectrum of neurological disorders. The application of diagnostic studies for HTLV-III infection has demonstrated that these neurologic disorders can be the first manifestation of AIDS or occur in the absence of AIDS. The most common conditions associated with HTLV-III infection alone are a subacute encephalopathy (AIDS dementia) and peripheral neuropathy; however, vacuolar myelopathy and both acute and chronic aseptic meningitis are also common. Congenital (or neonatal) transmission of the virus can result in a mental retardation syndrome of delayed onset. The AIDS virus is neurotropic as well as targeting T-helper lymphocytes. The virus has been readily identified in neural tissues and cerebrospinal fluid, including instances in which other central nervous system infections, such as toxoplasmosis, coexist. Hence, recognition of an appropriate syndrome, neurodiagnostic studies, and exclusion (or treatment) of other infections, as well as evidence for HTLV-III infection are required for diagnosis. The development of successful therapy will require agents which cross the blood-brain barrier.

Acquired Immunodeficiency Syndrome↗
PubMedDate not supplied

Biopsy histopathology in herpes simplex encephalitis and in encephalitis of undefined etiology.

The histopathology of herpes simplex encephalitis (HSE) has been described principally from postmortem studies which reveal end-stage disease. Biopsy material, which selects an earlier stage in disease development, has been used principally to isolate virus, identify viral particles, and locate viral antigens. Further, little attention has been paid to the histopathology of biopsies of encephalitis of undefined etiology. In the present study, sections from biopsies which yielded virus and those which were negative for virus were evaluated in a systematic and controlled manner. Biopsies yielding virus were characterized by meningeal inflammation, perivascular infiltrates, and glial nodules. Biopsies which did not yield virus and which failed to reveal another diagnosis were characterized by nonspecific gliosis. Thus the early histiopathology of HSE is characterized by early signs of inflammation in the absence of necrosis and generally differs from biopsies in which virus is not isolated.

Biopsy↗
PubMedDate not supplied

Types of immunological failure in the "slow-virus" encephalopathies and multiple sclerosis.

The pathogenesis of the slow virus encephalopathies and multiple sclerosis is reviewed within the framework of the immune response. The diseases are analyzed for the component of the immune response that appears to be crucial to the host's failure to control the disease. Thus, the absence of an immune response in the spongiform encephalopathies appears to reflect a failure of antigen recognition. Progressive multifocal leukoencephalopathy (PML), subacute sclerosing panencephalitis (SSPE), and progressive rubella panencephalitis (PRP) may result principally from a failure of effector mechanisms. In PML the failure usually occurs within the setting of an immunosuppressive illness. Conversely, in SSPE and PRP the effector failure seems to result from the nature of the host-virus interaction itself. Finally, evidence is accumulating that a defect of immunoregulation plays a significant role in multiple sclerosis.

Antigens, Viral↗