Intensive Care Society's Acute Physiology and Chronic Health Evaluation (APACHE II) study in Britain and Ireland: a prospective, multicenter, cohort study comparing two methods for predicting outcome for adult intensive care patients.

Objective: To compare the ability of two methods--Acute Physiology and Chronic Health Evaluation (APACHE II) and Mortality Prediction Model (MPM)--to predict hospital outcome for a large group of intensive care patients from Britain and Ireland.

Design: Prospective, multicenter, cohort study.

Setting: Twenty-six general intensive care units in Britain and Ireland.

[The role of modern imaging methods in the determination of childhood obesity].

Authors compare on the basis of their examinations carried out with modern imaging methods the ultrasound and computer tomography techniques in order to determine the fatty layer of the body surface and the visceral fatty quantities. Ultrasound is well usable and documentable to determine the fatty layer of the body surface, because it is not invasive. Computer tomography is more precise but it is a methodology involving x-ray burden.

Progressive multifocal leukoencephalopathy complicating Wiskott-Aldrich syndrome. Report of a case and review of the literature of progressive multifocal leukoencephalopathy with other inherited immunodeficiency states.

Objective: To describe the occurrence of progressive multifocal leukoencephalopathy (PML) in association with Wiskott-Aldrich syndrome, an X-linked recessive disorder with impairment of both cellular and humoral immunity.

Design: A detailed analysis of this patient's clinical illness, immunologic factors, neuroradiographic findings, and brain histopathologic conditions was undertaken. The medical literature on PML complicating congenital immunodeficient states was also reviewed.

HIV-1 infection of subcortical astrocytes in the pediatric central nervous system.

Early reports of pediatric HIV-1-associated neuropathology described the presence of viral particles in some astrocytes, implicating direct infection of the immature nervous system as a contributing factor to the observed neuropathology. Several recent reports suggest that in those astrocytes infected with HIV-1, the level of antigenic expression of the proviral genome is below the sensitivity limits of conventional histochemical techniques. Identification of these astrocytes would instead require the use of a highly sensitive radiolabeled DNA or RNA probe for in situ hybridization to detect the persistent viral nucleic acids.

Overexpression and reactivation of binding activity of the recombinant CTF/NF-1 transcription factor.

The transcription factor CTF/NF-1 is a multifunctional cellular protein which participates in the expression of host and viral genes and in the replication of viral DNA. A procedure was developed to obtain recombinant CTF/NF-1 protein in order to help identify the binding sites of CTF/NF-1 protein in the regulatory region of viral sequences. Cloning and expression of the CTF/NF-1 gene downstream from a T7 RNA polymerase promoter resulted in an insoluble protein produced in Escherichia coli.

Temporal patterns of human immunodeficiency virus type 1 transcripts in human fetal astrocytes.

Human immunodeficiency virus type 1 (HIV-1) infection of the developing central nervous system results in a dementing process in children, termed HIV-1-associated encephalopathy. Infection of astroglial elements of the pediatric nervous system has been demonstrated and suggests that direct infection of some astrocytes may contribute to the neurologic deficit. In this model, HIV-1 establishes a persistent state of infection in astrocytes, which can be reactivated by the cytokines tumor necrosis factor alpha (TNF-alpha) and interleukin 1 beta (IL-1 beta).

A mechanism of quinolinic acid formation by brain in inflammatory neurological disease. Attenuation of synthesis from L-tryptophan by 6-chlorotryptophan and 4-chloro-3-hydroxyanthranilate.

Quinolinic acid (QUIN), kynurenic acid (KYNA) and L-kynurenine (L-KYN) are neuroactive kynurenine pathway metabolites that accumulate in inflammatory neurological diseases. These increases were attributed to the induction of indoleamine-2,3-dioxygenase (IDO), the enzyme that converts L-tryptophan into L-KYN. Direct conversion of L-tryptophan into QUIN by brain tissue occurs in conditions of CNS inflammation, but not by normal brain tissue.

Intensive Care Society's APACHE II study in Britain and Ireland--II: Outcome comparisons of intensive care units after adjustment for case mix by the American APACHE II method.

Objectives: To compare outcome between intensive care units in Britain and Ireland both before and after adjustment for case mix with the American APACHE II method and to validate the American APACHE II method in Britain and Ireland.

Design: Prospective, cohort study of consecutive admissions to intensive care units.

Setting: 26 general intensive care units in Britain and Ireland.

Intensive Care Society's APACHE II study in Britain and Ireland--I: Variations in case mix of adult admissions to general intensive care units and impact on outcome.

Objectives: To describe the extent of variation in the case mix of adult admissions to general intensive care units in Britain and Ireland and investigate the impact of such variation on outcome.

Design: Prospective, cohort study of consecutive admissions to intensive care units.

Setting: 26 general intensive care units in Britain and Ireland.

Human immunodeficiency virus type 1 infection of the brain.

Direct infection of the central nervous system by human immunodeficiency virus type 1 (HIV-1), the causative agent of AIDS, was not appreciated in the early years of the AIDS epidemic. Neurological complications associated with AIDS were largely attributed to opportunistic infections that arose as a result of the immunocompromised state of the patient and to depression. In 1985, several groups succeeded in isolating HIV-1 directly from brain tissue.

Lack of JC viral genomic sequences in multiple sclerosis brain tissue by polymerase chain reaction.

With DNA extracted from brain specimens from 19 multiple sclerosis, 5 progressive multifocal leukoencephalopathy, 1 Alzheimer's disease, and 8 nonneurological control subjects, polymerase chain reaction was performed using nested sets of primer pairs amplifying segments of the large T and VP1 antigen-encoding sequences of JC virus. Both sequences were detected in each of the 5 brain specimens of progressive multifocal leukoencephalopathy but in none of the 19 multiple sclerosis, 1 Alzheimer's disease, or the 8 control brain specimens.

Interaction of the human polyomavirus, JCV, with human B-lymphocytes.

The human polyomavirus, JCV, is the causative agent of the central nervous system demyelinating disease progressive multifocal leukoencephalopathy (PML). The principal target of JCV infection in the central nervous system (CNS) is the myelinating oligodendrocyte. However, the site of JCV multiplication outside of the CNS and the mechanism by which virus gains access to the brain are not known.

Progressive multifocal leukoencephalopathy in HIV-1-infected children.

Objective: To describe the clinical and pathologic features of two HIV-1-infected children with progressive multifocal leukoencephalopathy (PML).

Design: Case report.

Setting: University-affiliated, public-health trust hospital.

Adjacent nuclear factor-1 and activator protein binding sites in the enhancer of the neurotropic JC virus. A common characteristic of many brain-specific genes.

JC virus is a neurotropic virus that causes the demyelinating disease progressive multifocal leukoencephalopathy in humans. In order to understand the neurotropic nature of this virus, we examined the binding of nuclear proteins to the viral regulatory region. A close association of nuclear factor-1 (NF-1) and Jun protein binding sites was found.

Improved electrochemiluminescent label for DNA probe assays: rapid quantitative assays of HIV-1 polymerase chain reaction products.

We describe the characterization and utility of a new electrochemiluminescent (ECL) label for oligonucleotides, utilizing phosphoramidite chemistry. This phosphoramidite of the tris(2,2-bipyridine)ruthenium(II) complex, bis(2,2-bipyridine)(4-[4-(2-cyanoethoxy-N,N-diisopropyl-amino) phosphinoxybutyl]4'-methyl)2,2-bipyridine ruthenium(II) dihexafluorophosphate or Origen phosphoramidite, enables the direct incorporation of the label during automated DNA synthesis. Efficiency of this automated synthesis allows the direct utilization of probes without further purification.

Detection of JC virus DNA in peripheral lymphocytes from patients with and without progressive multifocal leukoencephalopathy.

Progressive multifocal leukoencephalopathy (PML) results from lytic infection of oligodendrocytes by JC virus (JCV). Although JCV has been identified in mononuclear cells in bone marrow and hematogenous dissemination of the virus to the central nervous system has been suspected, JCV has never been clearly demonstrated in the peripheral circulation. Using polymerase chain reaction technology, we examined peripheral lymphocytes of 19 patients with brain biopsy-proven PML for the JCV genome.

Relapsing and remitting human immunodeficiency virus-associated leukoencephalomyelopathy.

We describe a 33-year-old homosexual man with a steroid-responsive, remitting and relapsing leukoencephalopathy associated with recent human immunodeficiency virus type 1 (HIV-1) seroconversion. Biopsy of a parieto-occipital lesion revealed demyelination and astrogliosis with focal necrosis. Detailed investigations demonstrated no pathogens in the brain other than HIV-1.

Pathogenesis and molecular biology of progressive multifocal leukoencephalopathy, the JC virus-induced demyelinating disease of the human brain.

Studies of the pathogenesis and molecular biology of JC virus infection over the last two decades have significantly changed our understanding of progressive multifocal leukoencephalopathy, which can be described as a subacute viral infection of neuroglial cells that probably follows reactivation of latent infection rather than being the consequence of prolonged JC virus replication in the brain. There is now sufficient evidence to suggest that JC virus latency occurs in kidney and B cells. However, JC virus isolates from brain or kidney differ in the regulatory regions of their viral genomes which are controlled by host cell factors for viral gene expression and replication.

Persistent human immunodeficiency virus type 1 infection in human fetal glial cells reactivated by T-cell factor(s) or by the cytokines tumor necrosis factor alpha and interleukin-1 beta.

Human immunodeficiency virus type 1 (HIV-1) infection of the brain has been associated with a severe dementing illness in children and adults. However, HIV-1 antigens are most frequently found in macrophages and microglial cells. To determine the extent of susceptibility of neuroglial cells to infection, the HIV-1 genome was introduced into cells cultured from human fetal brain tissue.

Human astrocytes stimulate HIV-1 expression in a chronically infected promonocyte clone via interleukin-6.

Human promonocyte cells chronically infected with human immunodeficiency virus type (HIV-1) (clone U1.1.5) were grown in the presence of media conditioned by human astrocytes and glioma cell lines U251 and 253.

Human fetal Schwann cells support JC virus multiplication.

The human papovavirus JC virus (JCV), the etiologic agent of progressive multifocal leukoencephalopathy, displays a narrow host range for growth, preferentially infecting oligodendrocytes, the myelin-producing cells of the central nervous system. In tissue culture, human fetal brain cells have been used for JCV propagation because of their ability to support JCV virion production. In this study, we evidence that a human fetal cell type derived from the peripheral nervous system can be productively infected with JCV.