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W Hickey

Publications and source records attributed to W Hickey.

8 recordsLinked to original sources

Braincutting for psychiatrists: the time is ripe.

In the past two decades, neuroscientific investigations such as postmortem and neuroimaging studies have revealed a variety of regional brain disturbances in major mental illnesses. These emerging findings are difficult to appreciate fully without a sufficient grasp of the neuroanatomy of the regions identified in these studies. The authors have developed, for psychiatrists-in-training, a braincutting exercise designed to highlight the neuroanatomical features of specific regions; namely, regions with behavioral affiliations relevant to contemporary hypotheses about the brain bases of major mental disorders. The focus of the braincutting is markedly different from the traditional braincuttings that have been available to trainees in neurology, neurosurgery, and neuropathology. This article describes the authors' approach to braincutting and the behavioral neuroanatomy seminar of which it is a part.

Brain↗

An interferon-inducible molecule on brain endothelium which controls lymphocyte adhesion mediated by integrins.

We undertook a search for cytokine-inducible molecules present on brain endothelium and which are involved in the control of lymphocyte adhesion. We screened 39 monoclonal antibodies (mAb) against rat brain endothelium in vitro, and identified five recognizing cytokine-inducible molecules. None of the 39 antibodies blocked lymphocyte adhesion, but one antibody (4A2), produced a 400% enhancement of lymphocyte binding. The 4A2 antigen is induced on brain endothelium by interferon-gamma (INF-gamma) but not tumour necrosis factor-alpha (TNF-alpha), at 6-48 hr. It is preferentially expressed near inter-endothelial cell junctions, but it also expressed on all lymphocytes and weakly on aortic endothelium in vitro. In vivo, it is not detectable on cells in the normal central nervous system (CNS), however it appears in the CNS during T-cell mediated immune reactions. Triggering of cells via this molecule enhances integrin-mediated adhesion of lymphocytes to brain endothelium, primarily via LFA-1. Unlike ICAM-1, 4A2 antigen is induced on endothelium of both Lewis and PVG strains. Although, it has some functional properties of human CD31, the 4A2 antigen is not rat CD31. The cellular localization of this molecule, its actions on integrin-mediated adhesion and its induction by IFN-gamma, all indicate that the 4A2 antibody recognizes a molecule involved in the control of lymphocyte migration into the brain.

Animals↗

BCL2 protein is topographically restricted in tissues characterized by apoptotic cell death.

The BCL2 protooncogene encodes an inner mitochondrial membrane protein that blocks programmed cell death. BCL2 was isolated from the chromosomal breakpoint of follicular B-cell lymphoma. Transgenic mice that overexpress BCL2 display extended survival of resting B cells. In this study we use a monospecific anti-human BCL2 antibody to define the distribution of BCL2 protein within organized tissues. BCL2 is restricted within germinal centers to the follicular mantle and to portions of the light zone implicated in the selection and maintenance of plasma cells and memory B cells. BCL2 is present in the surviving T cells in the thymic medulla. All hematopoietic lineages that derive from a renewing stem cell also display BCL2. A limited number of nonlymphoid tissues demonstrate BCL2 and can be grouped as (i) glandular epithelium in which hormones or growth factors regulate hyperplasia and involution, (ii) complex differentiating epithelium such as skin and intestine characterized by long-lived stem cells, and (iii) long-lived postmitotic cells such as neurons. Within these tissues that demonstrate apoptotic cell turnover, BCL2 is often topographically restricted to long-lived or proliferating cell zones. BCL2's function as an antidote to apoptosis may confer longevity to progenitor and effector cells in these tissues.

Adult↗

Positron emission tomography in patients with glioma. A predictor of prognosis.

Positron emission tomography (PET) studies have been performed using 18-F-fluorodeoxyglucose in 29 adult subjects with primary brain tumors. Seventy-two percent of the patients were treated previously. The glucose metabolic state in the lesions was increased in 16 patients, and was normal or decreased in 13 patients. The hypermetabolic tumors tended to behave in a more malignant fashion. Patients with hypermetabolic tumors had a median survival of 7 months after PET scan, compared to 33 months for those with hypometabolic lesions. Among the high-grade glioma patients, the PET results separated them into a good prognosis group (hypometabolic, with 78% 1-year survival) and a poor prognosis group (hypermetabolic, with a 29% 1-year survival after PET). These results suggest that glucose metabolic studies may provide an independent measure of the aggressiveness of a brain tumor, and may supplement pathologic grading.

Adult↗

Sequential computerized tomography and positron emission tomography studies in a patient with malignant glioma.

Computerized tomography (CT) and positron emission tomography (PET) using fluorine-18-deoxyglucose were performed in a patient with malignant glioma over a one-year period. Postoperatively and during radiation therapy, there was slight improvement in metabolic activity in the hemisphere ipsilateral to the tumor. After radiation therapy and during chemotherapy, there was a rapid and then gradual decline in whole brain metabolic rate by 39%. This might have been explained by radiation effect on brain. The tumor area was metabolically similar to the adjacent brain until one year after diagnosis, when an area of abnormal increased activity was noted. Even though CT scans showed minimal evidence of tumour growth, a large glioblastoma multiforme was found at autopsy at the site of the increased activity. Radiation leukoencephalopathy was also observed at autopsy. It is concluded that PET studies may offer new information regarding the metabolic effects of anti-tumor therapy, and may demonstrate regrowth of tumor prior to CT.

Brain↗

Chemical-shift MR imaging of the femoral head: an in vitro study of normal hips and hips with avascular necrosis.

To study the conventional and chemical-shift MR images of fatty, hemopoietic, and ischemic bone marrow, four normal femurs from autopsies and six femoral heads from total hip replacement done for avascular necrosis (AVN) were imaged with a small-bore 1.4-T MR unit. T1- and T2-weighted spin-echo images, fat- and water-selective spin-echo images, and out-of-phase images were obtained. The specimens were then sectioned, radiographed, and studied histologically. The capital epiphysis and greater trochanter in normal femurs had the highest signal on T1-weighted, fat-selective, and out-of-phase images owing to their high fat content. Fat-selective and water-selective images accurately depicted regions of fat and water, whereas T1-weighted, T2-weighted, and out-of-phase images were misleading in some cases. On T2-weighted images, a double line consisting of a rim of low signal with a high-signal inner border was noted surrounding AVN lesions. Histologic correlation showed that the low-signal outer rim was due to sclerotic bone, while the high-intensity inner border was due to granulation tissue and/or chondroid metaplasia. Fractures within the six AVN lesions were best seen on T2-weighted images, but these could not be distinguished from granulation tissue. On T2-weighted images, the weight-bearing cartilage had lower signal in five of six femoral heads with AVN. We conclude that the MR appearance of AVN reflects its complex histopathology. Direct spin-echo chemical-shift imaging can help correlate MR images with histology by providing information not available from conventional or out-of-phase images.

Adult↗