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Biomedical subjects

J H Morris

Publications and source records attributed to J H Morris.

At least 37 records · Page 2Linked to original sources
PubMed1992

Disseminating tumor cells and their interactions with leukocytes visualized in the brain.

Brain tumors are increasingly prevalent. Recent advances focus attention on individual, disseminated tumor cells that cannot be imaged or eliminated. Cells of the immune system may be ideally suited to attack individual tumor cells, but more basic understanding is needed. We describe a rat model, using the lacZ reporter gene, that allows identification of individual tumor cells, and tumor-leukocyte interactions in vivo. The model demonstrates how widely tumor can disseminate, without secondary tumorigenesis or recruitment of nonneoplastic cells. It demonstrates that leukocytes have access to disseminating tumor. Among its many applications, this work lays a foundation for developing cell-mediated immunotherapy against individual brain tumor cells.

Animals↗
PubMed1992

Magnetic resonance imaging of the acute effects of interstitial neodymium:YAG laser irradiation on tissues.

RATIONALE AND OBJECTIVES: Laser irradiation therapy in deep tissues requires a monitoring method other than visual guidance. Magnetic resonance imaging (MRI) can be used for this purpose because it visualizes soft tissue structures and heat distribution. METHODS: The authors performed interstitial laser irradiations in rat livers with various laser outputs and measured the sizes of laser-induced lesions. MRI of these lesions was done ex vivo and compared with the histologic findings. Laser-induced lesions also were studied in rabbit brain, liver, and skeletal muscle to show the influences of tissue optical and thermal properties. Imaging of interstitial laser irradiation also was performed in vivo in rabbit brains. RESULTS: MRI depicted the laser-induced lesions produced with different laser outputs and tissue types. MRIs of rabbit brain in vivo effectively demonstrated the signal decrease during heating and acute tissue changes. CONCLUSION: MRI has potential for monitoring interstitial laser surgery or hyperthermia.

Animals↗
PubMed1990

The effects of irradiation on major histocompatibility complex expression and lymphocytic infiltration in the normal rat brain and the 9L gliosarcoma brain tumor model.

The effects of irradiation on major histocompatibility complex (MHC) expression and lymphocytic infiltration in the normal rat brain and the 9L gliosarcoma brain tumor model were examined. Doses of irradiation administered were biologically equivalent to that used in the treatment of patients with malignant gliomas. No significant change in immune parameters was observed following irradiation in the normal rat brain. In the 9L gliosarcoma model irradiation did not suppress MHC expression or lymphocytic infiltration. These findings suggest that prior exposure to therapeutic irradiation need not adversely affect subsequent immunotherapies, and provide a foundation for future studies of immunomodulation in the irradiated brain.

Animals↗
PubMed1990

Clinical patterns of failure following stereotactic interstitial irradiation for malignant gliomas.

The vast majority of patients treated for malignant gliomas with surgery, conventional radiation therapy, and systemic chemotherapy recur within 2 cm of their original disease site as documented by CT scanning. We have analyzed the clinical patterns of failure in patients treated with stereotactic interstitial irradiation (brachytherapy) for malignant gliomas in order to determine if this modality has altered the recurrence pattern in this disease. Between December 1985 and December 1989, 53 patients with malignant glioma were treated with stereotactic interstitial irradiation using temporary high activity iodine-125. Thirty-three patients were treated as part of a primary treatment protocol that included 5940 cGy external beam prior to implantation. Twenty patients were treated at time of recurrence. The median dose of radiation given at implantation was 5040 cGy for the primary lesions and 5450 cGy for the recurrent lesions. Twenty-two patients have suffered relapse as documented by clinical and radiographic studies. The predominant patterns of failure in these 22 patients were in the margins of the implant volume (8) and distant sites (10) within the CNS (distant ipsilateral or contralateral hemisphere, spinal axis) or extraneural. Thus, marginal and distant recurrences accounted for 82% of the relapses in our patients. We conclude stereotactic interstitial irradiation has changed the recurrence pattern in patients with malignant glioma with true local recurrence no longer being the predominant pattern of failure as is seen with conventional therapy.

Adolescent↗
PubMed1989

Breast carcinoma metastatic to a meningioma. Case report and review of the literature.

We describe a patient who developed an intracranial mass that consisted of a meningioma and metastatic breast cancer. A literature review revealed 12 similar cases. In epidemiologic studies, the incidence of meningioma in patients with breast cancer is higher than expected. Both tumors are more common in women, have been reported to flare during pregnancy, and express hormone receptors. In a patient with breast cancer, an intracranial mass with radiographic features suggestive, but atypical, of a meningioma should be evaluated surgically. The lesion may represent a metastasis, a meningioma, or both.

Bone Neoplasms↗
PubMed1989

Diffuse senile plaques occur commonly in the cerebellum in Alzheimer's disease.

Diffuse senile plaques are characterized by the presence of beta protein (beta P), also called A4 protein, in a dispersed form and the apparent lack of associated dystrophic neurites or reactive glial cells. They are the most common type of senile plaque found in the cerebral cortex in Alzheimer's disease (AD), Down's syndrome (DS), and normal aging. Here is reported the frequent presence of diffuse senile plaques in the molecular layer of cerebellar cortex in AD. Typical neuritic plaques were never detected in this location, making the cerebellar molecular cortex a useful site for the study of diffuse plaques because diffuse plaques in the cerebral cortex are intermingled with neuritic plaques. Diffuse cerebellar plaques were detected by modified Bielschowsky silver stain in 47 of 100 cases of clinically and pathologically diagnosed AD and in none of 40 aged demented and nondemented controls. They were immunolabeled by antibodies to purified AD meningeal or cortical beta P, and to a synthetic beta P but not by two antibodies to the carboxyl- and amino-termini of the beta protein precursor (beta PP), which label a subgroup of cerebral cortical plaques. This latter result suggests that the beta P deposited in the cerebellar molecular layer may be derived from a form of the beta PP from which the carboxyl and amino terminal regions of the precursor have already been cleaved. Diffuse cerebellar plaques were not recognized by antibodies to neurofilaments, tau, and PHF, all of which detect dystrophic neurites in cerebral cortical neuritic plaques. Also, no association of reactive astrocytes or microglial cells with diffuse cerebellar plaques was observed. Thus, diffuse cerebellar plaques represent multifocal deposits of noncompacted beta P that cause little or no morphologic reaction in their microenvironment.

Aged↗
PubMed1988

Protein chemical and immunocytochemical studies of meningovascular beta-amyloid protein in Alzheimer's disease and normal aging.

As a comparison to previous analyses of purified amyloid plaque cores from Alzheimer's disease (AD) brain, we performed protein chemical and immunocytochemical studies on amyloid filaments extracted from meningeal blood vessels of patients with Alzheimer's disease. Results were compared with those obtained from identically prepared fractions of aged normals without cerebral amyloid angiopathy or other microscopic findings of AD. The amyloid isolation method of Glenner and Wong was modified, including an extraction with sodium dodecyl sulfate (SDS). Gel electrophoresis of purified amyloid from AD meninges yielded bands centered at 4.2 kDa. Sequencing of the HPLC-purified amyloid protein from AD meninges confirmed the published beta-protein sequence for residues 1-30 and 35-40, with the exception of glutamic acid rather than glutamine at position 11. N-terminal heterogeneity was not prominent. No sequence beyond residue 40 was obtained. Proteins of similar but not identical mol. wt. were present in HPLC-purified fractions of normal meninges; neither the beta-protein sequence nor any other interpretable sequence was detected in such fractions. Two antisera raised against the purified AD meningovascular amyloid protein identified the 4.2 kDa band on Western blots of AD preparations; no protein band in this region was labeled in control preparations. The 4.2 kDa band in AD meningeal preparations was also lableled by an antiserum to synthetic beta-peptide but not by an antiserum to the carboxyl terminus of the beta-protein precursor. Both the AD meningovascular amyloid antisera selectively labeled amyloid in cortical and meningeal vessels and plaque cores; tangles, plaque neurites, and cells of normal CNS and numerous non-neural tissues were unstained. The antisera also labeled the occasional deposits of vascular amyloid and less frequent plaque core amyloid found in some aged individuals without AD. We conclude that (1) the meningovascular amyloid beta-protein of AD, whose sequence has been confirmed and extended to residue 40, was not immunocytochemically detectable in neurofibrillary tangles; (2) beta-protein could not be detected in meningeal preparations from aged controls who lack light microscopically visible meningovascular amyloid; and (3) the vascular and plaque core amyloid present in aged normals is antigenically cross-reactive with AD meningovascular amyloid.

Aged↗
PubMed1988

Clinically diagnosed Alzheimer's disease: autopsy results in 150 cases.

One hundred fifty autopsy brains from patients with clinically diagnosed Alzheimer's disease (AD) were examined pathologically. The brains were received consecutively over a 3-year period from numerous sources as part of a research program in which one brain half was frozen for biochemical studies and the other half was fixed in formalin. One hundred thirty-one (87%) of the 150 cases fulfilled histological criteria for AD, with or without additional findings, such as Parkinson's disease or stroke. At least a minimal degree of amyloid angiopathy was found in every brain showing histopathological abnormalities of AD. Twenty-three (18%) of the 131 AD brains had Lewy bodies in neurons of the substantia nigra. Thirteen of the 19 non-AD cases were diagnosed as other neurodegenerative disorders. In only 2 cases was no histological correlate for the patient's dementia found. We conclude that (1) the many physicians who diagnosed these cases did so highly accurately; (2) degenerative changes in the substantia nigra were more common in patients with AD than has been reported for the general aged population; (3) amyloid angiopathy was a constant accompaniment of AD, although its severity varied widely; (4) vascular dementia was rarely clinically misdiagnosed as AD; (5) neuropathological findings were insufficient to account for the clinical syndrome of dementia in less than 2% of cases; (6) the histological criteria established by the National Institutes of Health/American Association of Retired Persons Workshop on the Diagnosis of Alzheimer's Disease worked well in assessing this large series.

Aged↗
PubMed1988

Cavernous hemangioma of the thoracic spinal cord.

A 25-year-old woman presented with a four-year history of progressive right-lower-extremity weakness and atrophy and a left hemisensory deficit was found. Metrizamide-enhanced spinal CT scan showed an intramedullary lesion at the level of T1-T2; this had expanded the cord in fusiform fashion but showed no evidence of a cystic component. Surgical resection was performed and the pathological diagnosis was cavernous hemangioma. Two and one-half years later, her left hemisensory deficit was worsening and a spinal MRI showed high signal intensity mass in the region of the previous surgery consistent with chronic hematoma which was re-evacuated with some improvement in the patient's neurological condition.

Adult↗
PubMed1988

Decreased iodine-123 IMP caudate nucleus uptake in patients with Huntington's disease.

To determine whether I-123 isopropyl iodoamphetamine (IMP) uptake is reduced in the basal ganglia of patients with Huntington's disease compared with that in aged-matched normal and abnormal control subjects, a caudate ratio was defined that compared the average separation (in pixel units) between the midline and the left and right caudate heads to the width of the brain as measured on transaxial cross-sections of I-123 IMP SPECT brain images. For six patients with Huntington's disease, the average caudate ratio was 29.0% (SD +/- 2.7%), significantly higher than that for 12 normal volunteer subjects (average caudate ratio, 19.1% +/- 3.5%; p less than 0.001) and 13 patients with a variety of other neurologic disorders (average caudate ratio, 19.3 +/- 2.2%; p less than 0.001).

Amphetamines↗
PubMed1987

Transient cysts of the fetal choroid plexus: morphology and histogenesis.

In this report, we correlate the clinical and morphologic features of bilateral choroid plexus cysts in three fetuses. These cysts were detected as incidental findings during sonography at 18 to 20 weeks gestation before elective abortion. Two fetuses were normal; the third had trisomy 18. All cysts were present bilaterally in the posterior horns of the lateral ventricles and ranged from 0.5 cm to 1.0 cm in diameter. The walls were translucent, and the cavities were filled with clear serous fluid, except for the left cyst in the third fetus, which was hemorrhagic. The cysts were surrounded by the loose stroma of the choroid plexus. We believe that the formation of these cysts is related to the histogenesis of the choroid plexus. Although such cysts have now been described by sonographers in several fetuses with chromosomal anomalies, this association may reflect ascertainment bias. At this time, we therefore advise caution in interpreting sonographic evidence of isolated choroid plexus cysts as anomalous.

Brain Diseases↗
PubMed1987

Tau antisera recognize neurofibrillary tangles in a range of neurodegenerative disorders.

Neurofibrillary tangles occur in a number of apparently distinct neurodegenerative diseases and in normal aging of the human brain. Antibodies raised against Alzheimer's disease paired helical filaments immunolabel the tangles seen in all other tangle-associated disorders examined to date. The neuronal microtubule-associated protein, tau, has recently been identified as an antigenic component of neurofibrillary tangles and senile plaque neurites in Alzheimer's disease. Three different polyclonal antibodies with strong tau immunoreactivity are examined in this study. These antibodies were found to immunostain tangles in normal aged brain and in brains affected by a range of neurodegenerative disorders, including Down's syndrome, Alzheimer's disease plus Parkinson's disease, progressive supranuclear palsy, and the parkinsonism-dementia complex of Guam, as well as Pick bodies in Pick's disease. The findings further illustrate the relative nonspecificity of neurofibrillary lesions in neurodegenerative disorders.

Aged↗
PubMed1987

Tau epitopes are incorporated into a range of lesions in Alzheimer's disease.

The neuronal microtubule-associated phosphoprotein, tau, has been identified as a major antigenic component of paired helical filaments in Alzheimer's disease (AD). The extent and distribution of altered tau antigens in AD brain, other than those found in neurofibrillary tangles (NFT) and senile plaque (SP) neurites, has not been widely discussed. We have examined tau immunoreactivity in AD using the monoclonal antibody (MAb), 5E2, raised against human fetal tau. Four types of abnormalities were recognized by MAb 5E2, each having some counterpart in Bielschowsky silver impregnations: 1) NFT; 2) thickened neurites in SP; 3) diffuse perikaryal staining seen in some neurons apparently lacking NFT; and 4) a dispersed network of randomly oriented thickened neurites not clustered into discrete plaques but found in NFT- and SP-rich cerebral cortex. These four alterations could also be recognized using three different polyclonal antibodies which had strong tau immunoreactivity but were optimally shown by MAb 5E2. Our findings demonstrate the complexity of altered tau-immunoreactive neuronal elements and emphasize the widespread abnormality of microtubule-associated proteins in AD cortex.

Alzheimer Disease↗
PubMed1987

Thallium-201 brain tumor imaging: a comparative study with pathologic correlation.

In patients with gliomas who were stable or improving, we noted a disparity between clinical status and computed tomography (CT) brain scan results. To elucidate this finding, 29 patients were sequentially scanned with 2.0 mCi of 201Tl (5-30 min), 20 mCi [99mTc]gluceptate (GH) (3-4 hr) and 7-10 mCi 67Ga (48-72 hr). A total of 198 images were obtained. A set of three scans at a midpoint in follow up was selected for analysis. Seven patients who died had neuropathologic data available; brain sections were reconstructed to match radionuclide views without knowledge of image results. In the seven patients with autopsy data, 201Tl offered the most accurate correlation with viable tumor. Gallium-67 gave similar results in patients not receiving steroids. Technetium-99m GH scans could not allow differentiation between tumor, necrosis, and edema. Similarly, the CT scan could not routinely differentiate between fibrotic, nonfibrotic, necrotic, and neoplastic tissue. In the 22 patients without autopsy data, 201Tl scans commonly showed smaller and more focal abnormal uptake when compared with [99mTc]GH and 67Ga scans. Thallium-201 scans more accurately reflect viable tumor burden than other radionuclide studies of primary brain tumors, are minimally affected by concomitant steroid administration, can be performed immediately following tracer administration, and complement the anatomic data obtained from CT scans.

Adolescent↗