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Biomedical subjects

H V Vinters

Publications and source records attributed to H V Vinters.

At least 181 records · Page 10Linked to original sources
PubMed1989

Substance P receptor binding sites are expressed by glia in vivo after neuronal injury.

In vitro studies have demonstrated that glia can express functional receptors for a variety of neurotransmitters. To determine whether similar neurotransmitter receptors are also expressed by glia in vivo, we examined the glial scar in the transected optic nerve of the albino rabbit by quantitative receptor autoradiography. Receptor binding sites for radiolabeled calcitonin gene-related peptide, cholecystokinin, galanin, glutamate, somatostatin, substance P, and vasoactive intestinal peptide were examined. Specific receptor binding sites for each of these neurotransmitters were identified in the rabbit forebrain but were not detected in the normal optic nerve or tract. In the transected optic nerve and tract, only receptor binding sites for substance P were expressed at detectable levels. The density of substance P receptor binding sites observed in this glial scar is among the highest observed in the rabbit forebrain. Ligand displacement and saturation experiments indicate that the substance P receptor binding site expressed by the glial scar has pharmacological characteristics similar to those of substance P receptors in the rabbit striatum, rat brain, and rat and canine gut. The present study demonstrates that glial cells in vivo express high concentrations of substance P receptor binding sites after transection of retinal ganglion cell axons. Because substance P has been shown to regulate inflammatory and immune responses in peripheral tissues, substance P may also, by analogy, be involved in regulating the glial response to injury in the central nervous system.

Animals↗
PubMed1989

Cytomegalovirus in the nervous system of patients with the acquired immune deficiency syndrome.

Clinicopathological features of infection of the nervous system by cytomegalovirus (CMV) in 31 patients with the acquired immune deficiency syndrome (AIDS) are reviewed. Neuropathology was variable, ranging from rare isolated CMV inclusions in brain without associated inflammation or necrosis, to severe necrotizing ependymitis and meningoencephalitis. In 1 patient, CMV had produced a necrotizing meningoradiculitis which presented clinically as ascending paralysis. In the brains and spinal cords of 6 patients, evidence of human immunodeficiency virus (HIV) infection of neural parenchyma was seen in close proximity to CMV infection. Both viruses individually or together were associated with low grade (microglial nodule) encephalitis. In retrospect, the diagnosis of CMV had been a difficult one to make clinically in neurologically impaired patients with AIDS. The results suggest that CMV may also localize in the nervous system without significant clinical sequelae. Imaging studies and analysis of cerebrospinal fluid revealed abnormalities in many patients, but none of them (short of culture of CMV itself in two cases) appeared to be specific to this neurological complication of the immunodeficiency.

Acquired Immunodeficiency Syndrome↗
PubMed1989

Lymphadenopathic Kaposi's sarcoma in a pediatric patient with acquired immune deficiency syndrome.

A six-year-old Hispanic female with acquired immune deficiency syndrome (AIDS) and multiple opportunistic infections was found to have disseminated lymphadenopathic Kaposi's sarcoma at autopsy. She was presumed to have been infected via maternal transmission, although both HIV antibody positive parents were asymptomatic. Kaposi's sarcoma is rarely reported in pediatric AIDS, and children may not have the typical aggressive cutaneous lesions found in adults with AIDS-associated Kaposi's sarcoma.

AIDS-Related Complex↗
PubMed1988

Brain amyloid and Alzheimer disease.

Clinicopathologic features of Alzheimer disease, the commonest cause of presenile or senile dementia, are presented. Several of the microscopic brain lesions found in patients with this dementia share the staining properties of amyloid and at least two of these lesions (senile plaque cores and amyloid angiopathy) are biochemically identical. Theories pertinent to the origins of brain amyloid and its role in the pathogenesis of Alzheimer disease are discussed in relation to theories of the cause of this dementia. Possible treatments for Alzheimer disease developed from our knowledge of brain amyloid processing and biochemistry are considered.

Acetylcholine↗
PubMed1988

Abnormalities of peripheral nerve in patients with human immunodeficiency virus infection.

The purpose of this study was to assess systematically morphology of peripheral nerves from patients with human immunodeficiency virus infection (acquired immunodeficiency syndrome [AIDS] and AIDS-related complex) examined at autopsy. Sural nerve specimens were taken from 25 patients (mean age 44 years) and evaluated by routine procedures used in our laboratory. In 13 cases no detectable abnormality was seen. Twelve patients (48%) showed loss of myelinated fibers with disproportionately greater loss of large myelinated fibers. Three of these patients showed severe myelinated fiber loss; 2 had no documented symptoms and no other known predisposing factors for a peripheral neuropathy. Changes suggestive of wallerian degeneration were occasionally seen, as were epineurial and endoneurial inflammatory infiltrates. Segmental demyelination was not identified in any nerve examined. Electron microscopy revealed thickened basement membranes around small blood vessels, Schwann cells, and fibroblasts. Peripheral nerve abnormalities in patients with AIDS or ARC are frequent and their pathogenesis remains unclear.

AIDS-Related Complex↗
PubMed1988

The pathology of encephalic arteriovenous malformations treated by prior embolotherapy.

A pathologic study was undertaken of seven encephalic arteriovenous malformations, including five resected from one to seven days after balloon embolization, one resected 10 days after embolization with polyvinyl alcohol foam (PVA), and a large mesencephalic AVM in a patient who died eight weeks after a series of embolization procedures with PVA and silicone spheres. AVM's resected 6-7 days following balloon embolization showed focal mural and adventitial inflammatory infiltrates and parenchymal (i.e. non-vascular) necrosis of a large portion of one AVM. The AVM examined 7 days post-balloon embolization showed an intraluminal thrombus containing refractile particles surrounded by foreign body giant cells (FBGC's). The AVM removed 10 days after PVA embolotherapy showed mural and perivascular necrosis with infiltration by polymorphonuclear leukocytes. The single autopsy case showed FBGC's surrounding residual PVA, refractile particles deep within vascular walls, and marked mural thickening of AVM channel walls, changes that may represent a response to previous angionecrosis and inflammation at the time of embolization. These findings, the pathogenesis of which is discussed in detail, may help to explain some of the rare complications of iatrogenic embolotherapy with these materials, as well as providing evidence for the basis of their efficacy.

Adult↗
PubMed1988

Evidence for human immunodeficiency virus (HIV) infection of the brain in a patient with aplastic anemia.

A young female patient with a long history of intravenous drug abuse died after a fulminant course of aplastic anemia. At postmortem examination, she was found to have multinucleate giant cells and immunocytochemical evidence of human immunodeficiency virus (HIV) infection of the central nervous system. This case raises the possibility that HIV infection contributed to the patient's aplastic anemia, and suggests that HIV-associated giant cells might be found retrospectively or prospectively within the brains of patients who die of conditions other than those narrowly defined as acquired immune deficiency syndrome (AIDS) or AIDS-related complex (ARC). It furthermore emphasizes that HIV infection of the nervous system is not necessarily accompanied by clinically apparent neurological disease.

Acquired Immunodeficiency Syndrome↗
PubMed1988

Fusiform intracranial aneurysms. Clinicopathologic features.

Seven fusiform aneurysms were found at autopsy in five patients (two males and three females) over a 13-year period. The subjects were between 56 and 65 years of age. The basilar trunk was the most frequent site. Four aneurysms were of giant proportions and contained laminated thrombi. Subarachnoid hemorrhage occurred in four patients. Microscopic examination of the aneurysm walls revealed atheromatous degeneration, focal wall attenuation, mural hemorrhage, rupture, and acute and chronic inflammatory cell infiltration. These findings suggest that rupture is not rare and that atherosclerosis is but one mechanism in the pathogenesis of these lesions.

Aged↗
PubMed1988

Immunohistochemical study of cerebral amyloid angiopathy: use of an antiserum to a synthetic 28-amino-acid peptide fragment of the Alzheimer's disease amyloid precursor.

A polyclonal antibody to a synthetic peptide representing a 28-amino-acid sequence of the previously isolated and described Alzheimer's disease amyloid precursor was raised in rabbits. The antibody was used in conjunction with an avidin-biotin-peroxidase technique to stain cerebral microvessels involved by amyloid angiopathy and senile "neuritic" plaque amyloid cores. The staining method has significant advantages over standard histologic techniques used to demonstrate brain amyloid and might have important practical applications in the study of microvascular lesions associated with cerebral amyloid angiopathy, as well as in studies on the pathogenesis of Alzheimer's disease or senile dementia of Alzheimer type.

Aged↗
PubMed1988

Creutzfeldt-Jakob disease without periodic sharp wave complexes: a clinical, electroencephalographic, and pathologic study.

A comparison of clinical, EEG, and pathologic features was carried out on all cases of autopsy-proven Creutzfeldt-Jakob disease (CJD) studied over the last 10 years. Periodic sharp wave complexes (PSWCs) were present in three but absent in seven patients. Myoclonus was documented in two of the three with and in only one of the seven without PSWCs. The three with PSWCs had severe neocortical and at least mild thalamic involvement; those without PSWCs had more variable disease topography. The diagnosis of CJD should not be rejected if PSWCs are absent.

Aged↗
PubMed1988

Pathology of the pituitary gland in patients with the acquired immune deficiency syndrome (AIDS).

The pituitary gland was examined at autopsy in 88 patients who died with acquired immune deficiency syndrome (AIDS) or AIDS-related complex (ARC). Pathologic findings included focal to widespread necrosis and/or fibrosis of the anterior pituitary gland in 10 cases, evidence of cytomegalovirus infection without an apparent inflammatory component in the anterior pituitary in 3 cases, and microglial nodules in the pars nervosa in 5 cases. In one instance, a multinucleated giant cell identical to those associated with direct human immunodeficiency virus infection of brain was identified in the pars nervosa. One patient showed focal anterior pituitary infection by Cryptococcus neoformans in the context of widespread and severe cryptococcosis. These findings are discussed in relation to the possible clinical manifestations and the neuropathologic and systemic pathologic findings in AIDS patients.

AIDS-Related Complex↗
PubMed1988

Immunohistochemical study of cerebral amyloid angiopathy. II. Enhancement of immunostaining using formic acid pretreatment of tissue sections.

Cerebral amyloid angiopathy (CAA) is a biochemically heterogeneous entity most commonly associated with stroke syndromes, Alzheimer's disease (AD), Down's syndrome, and miscellaneous neurologic conditions. The authors have applied and extended (using formic acid pretreatment of histologic sections) an immunocytochemical technique that used antibody to a synthetic 28-amino acid peptide representing a segment of the AD amyloid precursor, to study CAA and related parenchymal amyloid deposits in brain tissues originally derived from: 1) patients with CAA with or without typical clinicopathologic features of AD, cerebral hemorrhage, and infarcts; 2) a young boy with angiocentric brain amyloid; 3) patients with familial (Icelandic, Dutch) forms of cerebral hemorrhage caused by CAA; and 4) Japanese patients with nonfamilial CAA-related brain hemorrhage, sometimes associated with histopathology characteristic of AD. Formic acid pretreatment of sections resulted in markedly enhanced staining of senile plaque core and microvascular, especially capillary, amyloid, and some apparent staining of the neuritic component of senile plaques. Perivascular halos of immunoreactive material were observed frequently. Neurofibrillary tangles were not immunolabeled, nor were blood vessels or any parenchymal components within cerebral white matter. CAA in Japanese patients with nonfamilial encephalic hemorrhages appeared immunocytochemically identical to AD-related CAA. Arterioles in brains that had severe CAA frequently showed significant stenosis of their lumina by nonamyloid hyaline or cellular material.

Adolescent↗
PubMed1987

High molecular weight Alzheimer's disease amyloid peptide immunoreactivity in human serum and CSF is an immunoglobulin G.

A radioimmunoassay (RIA) was developed to detect the 4200 Dalton amyloid (A4) peptide or it's precursor (A4P) in human serum or cerebrospinal fluid (CSF). A synthetic peptide containing the first 28 amino acids of the 43 amino acid A4 peptide was covalently coupled to bovine thyroglobulin and a polyclonal antiserum in rabbits was prepared. This antiserum was specific for vascular amyloid and neuritic plaques in Alzheimer's disease brain as detected by immunoperoxidase. The synthetic peptide, which has a tyrosine at residue 10, was iodinated with chloramine T and [125I]iodine and was purified to homogeneity by C4 reverse phase high performance liquid chromatography (HPLC). Extraction of human serum over a C18 Sep Pak cartridge indicated immunoreactive A4 peptide was not detectable in human serum. Conversely, high molecular weight A4 peptide immunoreactivity was detectable in human serum, at a concentration of 8.9 +/- 1.2 pmol-eq./ml, and in human CSF, at a concentration of 0.25 +/- 0.01 pmol-eq./ml, giving a CSF/serum ratio of 3.2%. The immunoreactivity in human serum was nearly completely removed by affinity deletion of serum immunoglobulin G (IgG), but not by affinity removal of IgA or IgM. Serum immunoreactivity was decreased 90% in hypogammaglobulinemia, and was increased 83% in human cord serum. There was no statistical difference in serum A4 immunoreactivity in Alzheimer's serum or CSF. Serum immunoreactivity in Down's syndrome was increased 50%. These studies indicate the high molecular weight A4P immunoreactivity in human serum or CSF is an IgG. Whether the A4 precursor in Alzheimer's disease is, in fact, an IgG, or whether there is an antibody in human serum and CSF that cross reacts with the A4 precursor cannot be determined until the serum immunoreactivity is purified and structurally characterized.

Alzheimer Disease↗
PubMed1987

Dual infection of the central nervous system by AIDS viruses with distinct cellular tropisms.

Human immunodeficiency virus (HIV) is the causative agent of the acquired immune deficiency syndrome (AIDS). A large number of AIDS patients show evidence of neurologic involvement, known as AIDS-related subacute encephalopathy, which has been correlated with the presence of HIV in the brain. In this study, two genetically distinct but related viruses were isolated from one patient from two different sources in the central nervous system: brain tissue and cerebrospinal fluid. Both viruses were found to replicate in peripheral blood lymphocytes, but only virus from brain tissue will efficiently infect macrophage/monocytes. The viruses also differ in their ability to infect a brain glioma explant culture. This infection of the brain-derived cells in vitro is generally nonproductive, and appears to be some form of persistent or latent infection. These results indicate that genetic variation of HIV in vivo may result in altered cell tropisms and possibly implicate strains of HIV with glial cell tropism in the pathogenesis of some neurologic disorders of AIDS.

Acquired Immunodeficiency Syndrome↗