Search PubMed⌕ Search

Biomedical subjects

H V Vinters

Publications and source records attributed to H V Vinters.

At least 163 records · Page 9Linked to original sources
PubMed1990

High levels of unintegrated HIV-1 DNA in brain tissue of AIDS dementia patients.

In the host cell, retroviral DNAs exist in three main forms: unintegrated linear, unintegrated circular, and integrated (the provirus). High levels of unintegrated forms of retroviral DNA often correlate with superinfection and accompanying cytopathic effects, as, for example, in the case of feline acquired immunodeficiency. In culture, HIV-1 infection also results in high levels of unintegrated viral DNA although direct correlations with cytopathicity have not been made. The low frequency of HIV-1-infected cells in patients has made it difficult to determine the structure of the viral DNA in fresh tissue samples from AIDS patients by standard methods such as Southern hybridization. The PCR technique however, which allows the detection of viral DNA at levels far below that possible by other hybridization methods is, in its conventional form, of limited use for quantitative analysis. To study the amount and form of HIV-1 DNA in primary tissue of AIDS patients we have therefore modified the PCR method. Our results indicate that each of the three species of viral DNA are detectable in blood and brain of AIDS patients, and that in autopsy samples from patients with HIV encephalitis there is a considerably higher proportion of unintegrated viral DNA.

AIDS Dementia Complex↗
PubMed1990

Specific high-affinity binding of peripheral benzodiazepine receptor ligands to brain tumors in rat and man.

Two types of benzodiazepine receptors have been identified in mammalian tissues: a central type which is localized to neuronal elements in the brain, and a peripheral type which is present on glial cells and in tissues outside the central nervous system such as kidney. The authors report an increase in specific binding of peripheral benzodiazepine receptor ligands in certain human brain tumors using computer assisted quantitative image analysis of autoradiograms. Higher densities of binding sites to a 3H-labeled selective peripheral benzodiazepine ligand, PK11195 [1-(2-chlorophenyl-N-methyl-N-(1-methylpropyl)-3-isoquinoline carboxamide] were observed in human gliomas as the malignancy of these tumors increased. Specific binding was also present in some non-glial tumors but little binding was demonstrated in necrotic tissue or normal brain. In in vitro binding studies in rats, there was a significant increase in Bmax (1089.3 +/- 232.2 fmol/mg tissue) in C6 glial tumors and LK Walker 256 metastatic tumors (924.2 +/- 183.7) compared with normal brain (62.1 +/- 12.8 fmol/mg tissue). Binding affinities were, however, similar (Kd = 2.09, 2.17, and 2.04 nmol/l, respectively). These findings suggest that the number of peripheral benzodiazepine receptors are increased in brain tumors. These receptors could be utilized in positron emission tomography to image brain tumors.

Animals↗
PubMed1990

Immunohistochemical study of cerebral amyloid angiopathy. III. Widespread Alzheimer A4 peptide in cerebral microvessel walls colocalizes with gamma trace in patients with leukoencephalopathy.

Brain tissue from 11 patients with cerebral amyloid angiopathy, changes of Alzheimer's disease, and variable degrees of subcortical leukoencephalopathy was examined by immunohistochemical methods, using primary antibodies to peptide segments representing portions of the Alzheimer A4 (beta-) peptide or gamma-trace peptide (seen most commonly in Icelandic patients with cerebral hemorrhage (hereditary cerebral hemorrhage with amyloidosis [HCHWA-I]). Variable A4 immunostaining was seen within cortical (and rarely white matter) parenchyma in the form of senile plaques (with or without central cores), and within capillary and arteriolar walls. Within individual patients, A4 deposits were often primarily parenchymal or vascular, and when they were vascular they tended to be more prominent in arteriolar than in capillary wall segments. Perivascular A4 deposits were often detected around strongly immunoreactive microvessels. Gamma-trace immunoreactivity was noted in many A4-positive microvessel walls, but staining was always less intense than with the anti-A4 antibody. We conclude that patients with severe cerebral amyloid angiopathy may show wide variation in the severity and topography of A4 deposits within brain parenchyma. A4 may colocalize with gamma-trace peptide, suggesting that A4 and gamma-trace forms of cerebral amyloid angiopathy may not be as biochemically distinctive as has been suggested. Other proteases or protease inhibitors may contribute to the pathogenesis of cerebral amyloid angiopathy or cerebral amyloid angiopathy-related stroke syndromes.

Amyloid↗
PubMed1990

Use of a new mixture for embolization of intracranial vascular malformations. Preliminary experimental experience.

The internal carotid artery system in swine has a special anatomic configuration similar to a brain "arterial-arterial malformation." The internal carotid artery breaks up into a multitude of fine channels (rete mirabile) situated at the base of the skull on the side of the hypophysis. This anatomic arterial model was used to analyze acute and chronic angiographic and histological changes after occlusion of the rete mirabile with I) avitene, II) avitene, and 50% ethanol, III) avitene, 30% ethanol and Polyvinyl alcohol, IV) avitene 50% ethanol and Polyvinyl alcohol, V) IBCA and VI) silk. Histopathological changes observed in the rete mirabile six weeks following occlusion demonstrated that a mixture of avitene, 30% ethanol and Polyvinyl alcohol and IBCA produced the best anatomic results. Embolization with avitene, PVA and ethanol induced a more bland histological reaction than the one observed with IBCA. Preliminary clinical experience with this mixture is reassuring in those cases in which the AVM was surgically resected. The partially thrombosed AVM was easily depressed and compressed by the neurosurgeon allowing for satisfactory hemostasis in and around the nidus of the AVM.

Animals↗
PubMed1990

Plasma cell granuloma of the brain.

We describe a 29-year-old woman with a plasma cell granuloma arising in the right superior temporal gyrus. The mass appeared on computed tomography as a well-circumscribed area of increased density that markedly enhanced with administration of contrast. Microscopic examination showed a mixed cell population with a predominance of plasma cells, including plasma cells showing cytologic atypia, as well as necrosis with polymorphonuclear leukocytes, and the tumor was characterized immunohistochemically by polyclonal plasma cell proliferation.

Adult↗
PubMed1990

Cerebral amyloid angiopathy and granulomatous angiitis: immunohistochemical study using antibodies to the Alzheimer A4 peptide.

Neuropathologic study of an 82-year-old male who died from massive cerebral hemorrhage showed extensive amyloid angiopathy, with morphologic and immunohistochemical characteristics similar to those observed in Alzheimer's disease, associated with granulomatous angiitis, including the presence of numerous giant cells. Some of the giant cells contained, in their cytoplasm, congophilic material immunoreactive for the Alzheimer A4 peptide, supporting the hypothesis that the granulomatous angiitis may, in part, represent a foreign body reaction to A4 amyloid deposition.

Aged↗
PubMed1990

Neuropathologic findings after bone marrow transplantation: an autopsy study.

Clinicopathologic records and neuropathologic tissues of 109 patients who underwent necropsy after treatment with bone marrow transplantation (BMT) were examined. Underlying disorders included leukemia (70), aplastic anemia (25), solid tumors (7), lymphoma (5), Hodgkin's disease (1) and Wiskott-Aldrich syndrome (1). There were 34 females and 75 males, ranging in age from 2 to 56 years. Survival after transplantation averaged 3.6 months. The most common findings were cerebrovascular lesions (29), including hematomas, hemorrhagic necrosis, and infarcts. Central nervous system infections comprised the next most common finding, including 10 fungal and four bacterial infections. A recurrence of underlying malignancy for which transplant had been performed occurred in five patients. Leukoencephalopathy of varying severity was found in eight patients, half of whom had received intrathecal chemotherapy and/or cranial radiation. Patients with systemic graft-versus-host disease had a variety of nonspecific neuropathologic findings in the nervous system; however, nearly half (44%) showed no detectable changes. Other nonspecific alterations included hypoxic/ischemic changes, vascular siderocalcinosis, and neuroaxonal spheroids (associated with hemorrhage or necrosis). These findings provide a guide as to likely causes of a neurologic syndrome in a patient who has undergone BMT, and can be compared with neuropathologic findings in other forms of immunosuppression.

Adolescent↗
PubMed1990

Traumatic neuroma of the eyelid associated with ptosis.

A 17-year-old boy presented with persistent swelling and ptosis of the eyelid after blunt injury. Histologic examination revealed a clinically unsuspected traumatic neuroma. Ptosis and the traumatic neuroma persisted despite two eyelid operations. Traumatic neuroma is rare after blunt trauma; it has not been previously reported in the eyelid. It is important to identify this lesion because complete excision may help to prevent recurrence.

Adolescent↗
PubMed1990

Central nervous system involvement in nephropathic cystinosis.

Nephropathic cystinosis, an autosomal recessive lysosomal storage disorder due to impaired cystine transport, causes damage to multiple organs that results in end-stage renal disease, hypothyroidism, and retinopathy, usually in childhood. Dialysis and renal transplantation now frequently enable patients with cystinosis to live into adulthood. Examinations at autopsy of a 28-year-old man who died of complications of this disease showed deposits of cystine crystals in multiple organs. There was severe cerebral involvement with multifocal cystic necrosis, dystrophic calcification, spongy change, and vacuolization that had produced profound neurologic deficits. Electron microscopy of the brain documented cytoplasmic deposition of cystine crystals in membrane bound vacuoles within the cytoplasm of pericytes and within parenchymal cells of the white matter. While affected patients who have received renal transplants may no longer die from renal failure, serious, potentially life-threatening, neurologic complications of this disorder may supervene.

Adult↗
PubMed1990

Transtentorial herniation caused by an intracranial mass lesion following high-dose methotrexate.

A patient with intracranial osteosarcoma that arose 16 years after radiation therapy for hereditary retinoblastoma developed fatal cerebral edema and brainstem herniation after she received a single dose of intravenous methotrexate. Autopsy demonstrated extensive necrosis of the tumor mass, as well as necrotizing vascular damage within the neoplasm. Although high-dose methotrexate has been shown to be useful in the treatment of primary osteogenic sarcoma, the tumoricidal effects of therapy appear to have caused a fatal rise in intracranial pressure.

Adolescent↗
PubMed1990

CD4-independent, productive infection of a neuronal cell line by human immunodeficiency virus type 1.

One neuronal cell line (SK-N-MC) was found to be susceptible to productive infection by multiple isolates of the human immunodeficiency virus type 1 (HIV-1). Characterization of SK-N-MC cells showed that these cells are neuroectodermal in origin in that they express dopamine hydroxylase, catecholamines, neuron-specific enolase, and neurofilaments. Despite their susceptibility to HIV-1 infection, SK-N-MC cells had no detectable CD4 and this infection was not blocked by anti-CD4 monoclonal antibodies (OKT4A, Leu3A) or recombinant soluble CD4. These experiments demonstrated that certain cells of neuroectodermal origin are susceptible to infection in vitro by HIV-1 via a CD4-independent mechanism.

Animals↗
PubMed1990

Immunoreactive A4 and gamma-trace peptide colocalization in amyloidotic arteriolar lesions in brains of patients with Alzheimer's disease.

Cerebral amyloid angiopathy (CAA) defines a biochemically heterogeneous entity that manifests as effacement of cerebral microvessel walls by a fibrillar material with characteristic tinctorial properties. In biochemical terms, the amyloid that infiltrates blood vessels in CAA is composed of the A4 or beta peptide of Alzheimer's disease (AD), a molecule related to gamma trace or cystatin C (seen in patients with hereditary cerebral hemorrhage with amyloidosis in Iceland, HCHWA-I), or the PrP characteristic of spongiform encephalopathy and scrapie. Using antibodies to synthetic peptides representing portions of the 4.2-kd Alzheimer A4 peptide and the gamma-trace peptide, we immunostained sections of brain from patients with AD, senile dementia of Alzheimer's type, and CAA with associated leukoencephalopathy. Immunohistochemical studies demonstrated colocalization of the A4 and gamma-trace peptides within arteriolar walls, but only rarely in A4 amyloidotic capillaries or senile plaque cores of amyloid. When gamma-tracelike reactivity was noted in capillary walls, it was sometimes noted within the cytoplasm of pericytes. Immunostaining was always more intense when the anti-A4 antibody was used as the primary antibody. Gamma-trace immunostaining was more prominent on the adventitial component of arteriolar walls, whereas A4 staining was usually seen more diffusely throughout the blood vessel wall, especially in the media. Rarely individual pericytelike cells showed prominent gamma-trace immunoreactivity. These findings suggest that A4 and gamma-tracelike molecules may colocalize within arteriolar walls within the brains of patients with AD, and highlight the fact that CAA identified with AD and HCHWA-I are not as biochemically distinct as was assumed previously. Furthermore these findings suggest that other peptidases or protease inhibitors may be found within amyloidotic microvessel walls and may contribute to senile brain change and CAA-related strokes, including hemorrhage and encephalomalacia.

Aged↗
PubMed1989

The acquired immunodeficiency syndrome (AIDS) dementia complex.

The acquired immunodeficiency syndrome (AIDS) dementia complex is a frequent and devastating complication of infection with human immunodeficiency virus-type 1 (HIV-1). Features of the AIDS dementia complex include decreased memory, the inability to concentrate, apathy, and psychomotor retardation. Typical neuropathologic findings include gliosis, focal necrosis of neurons, perivascular inflammation, formation of microglial nodules, multinucleated giant cells, and demyelination. That HIV-1 is the direct cause of this neurologic syndrome is strongly supported by the available evidence. In addition, several studies have identified the monocyte-macrophage as the predominant cell type in the brain infected with HIV-1. However, the mechanisms by which the infected monocytes-macrophages mediate neurologic dysfunction and destruction have not been elucidated.

Acquired Immunodeficiency Syndrome↗
PubMed1989

Severe neuropathy in a patient with acquired immune deficiency syndrome (AIDS). Evidence for widespread cytomegalovirus infection of peripheral nerve and human immunodeficiency virus-like immunoreactivity of anterior horn cells.

A patient with acquired immune deficiency syndrome (AIDS) developed a progressive neuromuscular disorder which included a sensory component, severe weakness and muscle wasting, and fasciculations. At autopsy, there was evidence of severe peripheral neuropathy, as well as widespread cytomegalovirus (CMV) infection within the central and peripheral nervous system. Although the anterior horn cell complement within the spinal cord appeared normal, there was also evidence of human immunodeficiency virus (HIV)-like immunoreactivity of rare anterior horn cells, as judged by immunohistochemical staining. This patient illustrates the complexity of pathogenetic mechanisms operative in AIDS patients with neuromuscular disease, and suggests that at least some examples of neuromuscular disease in patients with this syndrome may be related to widespread CMV infection of the peripheral nerve (including microvascular endothelial cells) and, more rarely, direct HIV infection of some anterior horn cells.

Acquired Immunodeficiency Syndrome↗
PubMed1989

Stroke related to cerebral amyloid angiopathy: the significance of systemic vascular disease.

A retrospective postmortem analysis of 25 cases of cerebral amyloid angiopathy (CAA) in the setting of Alzheimer's disease or senile dementia of the Alzheimer type (AD/SDAT) is reported. Seven patients experienced clinically significant cerebral infarcts or hemorrhages or both. There was no statistically significant difference in the incidence of infarcts or hemorrhages in hypertensive and nonhypertensive patients. Hypertension does not appear to be an additional risk factor in the causation of cerebral infarct or hemorrhage associated with CAA in the setting of AD/SDAT. Just over half of patients with CAA and significant ischemic and/or hemorrhagic brain lesions showed atherosclerosis of the circle of Willis, sometimes in the context of severe disseminated atheromatous disease.

Aged↗
PubMed1989

Lymphomatoid granulomatosis and malignant lymphoma of the central nervous system in the acquired immunodeficiency syndrome.

While primary and secondary malignant lymphomas have been well-documented in the CNS of patients with the acquired immunodeficiency syndrome (AIDS), only one case of lymphomatoid granulomatosis (LG) involving the CNS has been reported. We present three AIDS patients with multiple grossly evident foci of necrosis in the cerebral hemispheres which, on histologic evaluation, were seen to contain angiocentric mixed chronic inflammatory infiltrates with atypical mononuclear cells, luminal thrombosis, and infarction, which is typical of LG. LG was also identified in sections of the lung in one case. Lymphoma was found in other regions of the brain in two cases, suggesting the evolution of LG into cerebral lymphoma. In addition, widespread perivascular multinucleate syncytial giant cells, associated with human immunodeficiency virus (HIV) infection of the CNS, were identified in all patients. The features of LG, its relationship to lymphoma, and the possible etiologic role of an immunodeficiency state or the HIV virus in the pathogenesis of LG are discussed.

Acquired Immunodeficiency Syndrome↗