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arabinoside/atrofia

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[Atrophy of the granular layer of the cerebellar cortex in patients with nonlymphoblastic leukemia treated with cytosine arabinoside].

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The reported analysis comprised 81 patients dying of acute non-lymphoblastic leukaemia type M1, M2, M4 and blastic crises in chronic myelocytic leukaemia. It was observed that the number of cases of cerebellar granular layer atrophy rose markedly in the years 1984-1990 as compared with 1976-1983

Cerebellar degeneration caused by high-dose cytosine arabinoside: a clinicopathological study.

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Twenty-four patients with leukemia or lymphoma refractory to conventional chemotherapy were given a course of systemic, high-dose cytosine arabinoside (3 gm/m2 every 12 hours for twelve doses). Four patients developed cerebellar degeneration during treatment. Ataxia of gait and limb movements,

The role of apoptosis in atrophy of the small gut mucosa produced by repeated administration of cytosine arabinoside.

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Progressive atrophy of ileal crypts and villi following daily administration of cytosine arabinoside to mice was found to be the result of suppression of mitosis and marked enhancement of apoptosis in the crypt epithelium. The amount of apoptosis produced by each dose decreased as the atrophy

Filamentous degeneration of neurons. A possible feature of cytosine arabinoside neurotoxicity.

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BACKGROUND The use of high-dose cytosine arabinoside (Ara-C) may be complicated by a characteristic form of cerebellar neurotoxicity. Other reported manifestations of neurologic dysfunction include signs of possible cranial neuropathies, for which a neuropathologic substrate has not been previously

Cerebellar atrophy caused by high-dose cytosine arabinoside: CT and MR findings.

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Fatal peripheral neuropathy associated with axonal degeneration after high-dose cytosine arabinoside in acute leukaemia.

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BACKGROUND Active hexose correlated compound (AHCC) (a mixture of polysaccharides, amino acids, lipids and minerals derived from cultured mycelia of a Basidiomycete mushroom, Lentinula edodes) was used to assess amelioration of alopecia (hair loss) caused by cytosine arabinoside (Ara-C) and

Astrocytes protect cultured neurons from degeneration induced by anoxia.

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Neurons grown in cultures of dissociated brain cells degenerate when exposed to anoxia and deprived of glucose. We have developed culture systems in which neurons can be grown in the presence or absence of astrocytes and have used them to study the influence of astrocytes on the neuronal

Experimental necrosis and arrest of proliferation of Schwann cells by cytosine arabinoside.

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In developing rat cervical sympathetic trunks, Schwann cells proliferate intensely during the first week after birth but axonal populations do not increase. Thus, experimental inhibition of DNA synthesis should affect Schwann cells and spare axons whose cell bodies are not dividing. The present

Encephalopathy, myelopathy, optic neuropathy, and anosmia associated with intravenous cytosine arabinoside.

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Coma, hemiparesis, unilateral optic neuropathy, and anosmia manifested in a patient with leukemia after he received only three courses of intravenous high-dose cytosine arabinoside (ARA-C). The patient's mental status returned to normal after several days, and his hemiparesis resolved. However, the

Experimental retinal dysplasia due to cytosine arabinoside.

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Retinal dysplasia was produced in newborn rats treated postnatally with the antimitotic substance, cytosine arabinoside (ara-C). In rats examined from 6 to 60 days, there were numerous retinal rosettes surrounded by photoreceptor cells and bipolar cells containing photoreceptor cell processes,

Simultaneous administration of granulocyte-macrophage colony-stimulating factor and cytosine arabinoside for the treatment of relapsed acute myeloid leukemia.

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The treatment of patients with relapsed or refractory acute myeloid leukemia (AML) with high dose cytosine arabinoside (ara-C) results in short-lived complete response rates of 30-50%. We have previously shown that entry of myeloid leukemic cells into S phase can be accelerated in vitro through the

Prevention of 1,2-dibromo-3-chloropropane (DBCP)-induced kidney necrosis and testicular atrophy by 3-aminobenzamide.

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The poly(ADP-ribosyl)transferase inhibitor, 3-aminobenzamide (3-ABA), reduced morphological evidence of 1,2-dibromo-3-chloropropane (DBCP)-induced DNA damage determined by alkaline elution. The DBCP plasma, kidney, and testis tissue doses determined between 1 and 8 hr after a single intraperitoneal

Astroglia-induced detachment of central neurons but astroglia-dependent growth of peripheral neurons in rat embryonic spinal cord primary cultures.

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In mixed primary cultures, intrinsic neurons from embryonic mammalian brains degenerate secondary to their detachment from the substratum and this is caused by the under-growing co-cultured astroglia. In the present study we sought to find out whether or not peripheral neurons, sensory and motor
OBJECTIVE While MR findings in progressive multifocal leukoencephalopathy (PML) have been described previously, usually in retrospective studies with limited sample size, what has not been well addressed is whether any are predictive of longer survival. Our participation in a large prospective
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