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William E. Hunt, Bertha A. Bouroncle and John N. Meagher

complications in 9 of these. At necropsy in 11 of the 12 cases (91 per cent) there was microscopic evidence of invasion of the central nervous system. Critchley and Greenfield 3 in 1930 reported a series of patients with chloroma and leukemia who exhibited spinal symptoms. Another 14 cases of leukemia with cerebral involvement were added by Diamond. 4 Five of these were myelogenous, 4 lymphatic, 2 myeloblastic, 2 stem cell, and one monocytic in type. In all cases he described infiltration of the pia mater and perivascular spaces. He stated that the infiltration about the

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Victor E. Albites

containing fibers of reticulin. The labeling of this tumor as either a reticulum-cell sarcoma, 1 primary mesenchymal tumor of the brain, 25 perithelial sarcoma, 14 microglioma, 6 or stem-cell sarcoma indicates, as Losli 18 pointed out, a lack of “unanimity of thought to taxonomy.” The matter is complicated further by the various attempts of classification made by those who have studied these tumors. 1 , 3, 15, 17, 19, 24, 25 In a recent comprehensive study, Kernohan and Uihlein 16 reviewed a series of 40 patients with neoplasms that had similar histologic

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Cushing's Syndrome and the Hypophysis

A Re-evaluation of Pituitary Tumors and Hyperadrenalism

Richard L. Rovit and Richard Berry

secretion has been assigned to two groups of cells: the beta-1 group, formerly called basophils, and the gamma group, 24 sometimes referred to as amphophils, 59, 74 mucoid cells 68 or beta-3 cells, 23 which are the large non-granular chromophobe cells ( Fig. 8 ). Both the beta-1 and gamma cells arise from the same primordial stem cell, the small chromophobe. Under certain conditions of extreme pituitary hyperactivity, 23, 24, 42 the beta-1 cells become “degranulated” and are converted into gamma cells ( Fig. 8 ). This new schema allows us to understand how Cushing

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Bernard Peison and David Voris

unclassified for the time being. Most of the confusion as to the proper nomenclature of this group of tumors, stems from the various definitions of a reticulum cell. This cell has been defined as either a primitive undifferentiated stem cell or the histiocyte that derives from it. The primitive reticulum or stem cell is neither phagocytic nor metallophilic and is not a part of the reticuloendothelial system. It is a primitive multipotent cell that can give rise to the fixed tissue histiocyte or macrophage. 11 Microglial histiocytes are phagocytic; they become impregnated

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Gerard M. Lehrer and Howard S. Maker

metabolism closely resembles that of immature brain. There is no evidence to suggest that a tumor-specific metabolism exists which is related to the neoplastic process. The metabolism of glial tumors growing under optimal conditions so closely resembles that of the stem cell that the tumor may serve as a chemical model of some glial functions. References 1. Lehrer GM : The quantitative histochemistry of human glial tumors , in Fields WS , Sharkey PC (eds) : The Biology and Treatment of Intracranial Tumors . Springfield, Ill

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John Mealey Jr., Tsu T. Chen and Robert Shupe

schedule used clinically in the treatment of brain tumors. The range of doses used experimentally ranged from 1 to 8 times the doses used for human treatments in terms of body weight. The higher doses used in vitro , however, were of the same order of magnitude found effective in vivo against several experimental murine gliomas. 33, 38 Rapidly proliferating normal hematopoietic stem cells, in contrast, were 3 to 12 times more sensitive to BCNU in vivo than were the murine gliomas and a transplantable lymphoma, respectively. 43, 44 The overall response of tumor

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Takao Hoshino and Charles B. Wilson

nonproliferating cells into the proliferating pool or through some mechanism blocking the movement of cells into nondividing compartments, causes the population of neoplastic cells to expand. A shorter cell cycle time relative to that of normal tissue of origin characterizes the growth kinetics of some experimental tumors. 22 On the other hand, cell cycle time of certain other tumors is much longer than that of the tissues from which they originate, although present methods do not allow comparison of neoplastic with normal-tissue stem cells. 18 If a simple alteration in cell

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Darell D. Bigner and Charles B. Wilson

antigens are valuable for distinguishing neural from non-neural cells, but are of little use in distinguishing “glial” from “neuronal” cells. Herschman examined his cell lines for cortisolinducible glycerol phosphate dehydrogenase and found that eight lines were positive, but the ion-flux assays showed that among those eight were three that had evidence of neuronal nature. These dual biochemical criteria made Herschman suspect that some of his cells had both neuronal and glial properties, a possibility that is consistent with transformation of “stemcells during

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Andrew G. Shetter and William H. Sweet

for brain-stem cells responsive to upper or lower dental-pulp activation. 15, 17, 21, 30 This contrasts sharply with the findings in our experimental model in which the location and the extent of metabolic activity produced by pulp stimulation in the two divisions were separate and distinct. Shigenaga, et al., 25 have identified single neurons in the dorsomedial portion of the rat nucleus caudalis that are evoked by mandibular incisor pulp stimulation, and their work correlates quite closely with our data. We are unaware of any single-unit recording studies in

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Experimental delayed radiation necrosis of the brain

Part 1: Effect of early dexamethasone treatment

Albert N. Martins, Ralph E. Severance, James M. Henry and Thomas F. Doyle

most, if not all, of the lesions develop as the consequence of injury to blood vessels. 2, 9, 12, 23, 24, 28, 36 According to this hypothesis, ionizing radiation damages stem cells that supply mature endothelial cells to replace those lost through natural attrition. 29, 40 This sets the stage for progressive failure of the microcirculation of the brain that leads to a break in the blood-brain barrier, chronic vasogenic edema and demyelination, petechial hemorrhages, and thrombosis. The parenchyma may also show a broad spectrum of secondary ischemic changes from