ETS-1 gene in human leukemia cells.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to K Toyama.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Nineteen patients with inv(16)(p13q22) or del(16) in myeloid leukemia are described. Eight showed inv(16)(p13q22), including one with de novo acute myeloid leukemia (AML-M2) and seven with de novo acute myelomonocytic leukemia (AMML-M4). Additional chromosome changes were detected in five of the cases; the most common change was trisomy 22. All but one of the de novo M2 and M4 leukemia patients with inv(16)(p13q22) showed initial bone marrow eosinophilia (greater than 5%) with basophilic granules. The remaining 11 showed deletion of the long arm of a chromosome no. 16 [del(16)(q22 or q23)]. Eight of the 11 were diagnosed as having chronic myelomonocytic leukemia, three transformed into an acute phase with M4 morphology; none of them gained complete remission. Two of the remaining three patients with del(16) were diagnosed as having M4 leukemia without marrow eosinophilia. The remaining one was a case of M4 leukemia following a myelodysplastic syndrome. The findings indicate that del(16) might be related to chronic myelomonocytic leukemia or leukemia with a prior history of myelodysplastic syndrome without evidence of marrow eosinophilia. On the other hand, inv(16)(p13q22) is highly associated with de novo AML especially AMML-M4 with bone marrow eosinophilia and a favorable prognosis.
The lateral geniculate nucleus (LGN) of a fetal rat was transplanted to the visual cortex (VC) of a neonatal rat. A current source-density analysis of field potentials and an intracellular study of neuronal responses were conducted in slice preparations by electrical stimulation of transplanted LGN and host VC. The results indicated that synaptic connections were established reciprocally between the transplanted LGN and the host VC.
The visual cortex of the cat is characterized by marked modifiability of neuronal responsiveness by visual experience in infancy, and stereotyped pattern of functional architectures in adulthood. The question of how the plasticity of the infant visual cortex is compatible with the regular patterns of the adult visual cortex has been a central problem of the brain neuroscience. This question was answered by quantifying the plasticity in the visual cortical circuitry of the infant kittens as changes in synaptic transmission produced after conditioning stimulation of the visual pathway. The results indicate that the solution of this question is the heterogeneous distribution of the synaptic plasticity in the infant visual cortex: the plasticity is not uniformly present in the visual cortical circuitry, but is limited only to a part of the circuitry (the cortico-cortical synapses in the supragranular layers). Therefore, the visual function (photic responsiveness) may be learned during the postnatal life of the kittens by the supragranular cells with plastic synapses, while the other cortical cells with fewer plastic synapses put prenatally designed constraints on the learning, so that the learning yields the adult cortical circuitry with regular patterns of organization.
As congenital malformations may be caused by perturbations of glycolytic flux on early embryogenesis [16], effects of hypoglycaemia were investigated by using rat embryo organ culture. Nine and one-half day old rat embryos were grown in vitro for 48 h (day 9 1/2 to 11 1/2) in the presence of hypoglycaemic serum for different hours during the culture period. Hypoglycaemic serum was obtained from rats given insulin intraperitoneally. On exposure to hypoglycaemic serum during the first 24 h of culture (day 9 1/2 to 10 1/2), embryos showed marked growth retardation and had increased frequencies of neural lesions (42.7% versus 0%, p less than 0.01), in contrast to hypoglycaemic exposure during the second 24 h of culture (day 10 1/2 to 11 1/2), where only minor growth retardation and low frequencies of neural lesions (2.4% versus 0%, NS) were seen. Even exposure to hypoglycaemic serum for a relatively short period (8 h) during the first 24 h of culture resulted in neural lesions at the frequency of 9.3-13.3%. The embryos exposed to hypoglycaemia demonstrated decreased glucose uptake and lactic acid formation, indicating decreased energy production via glycolysis that constitutes the principal energy pathway at this stage of embryonic development. These results suggest that hypoglycaemia during critical periods of embryogenesis has adverse effects on the development of the embryo and these effects might be mediated through metabolic interruption of embryogenesis.
Explore the source record for details and available documents.
The lateral geniculate nucleus (LGN) of fetal Wistar rats was transplanted to the visual cortex (VC) of 33 neonatal Wistar rats. Histological examination showed transplanted cells in all the host brains. Intensively labeled cells were demonstrated in the transplant by labeling with true blue. Electrophysiological studies with brain slice preparations demonstrated that the transplanted LGN sent axons and made excitatory monosynaptic connections mainly in layer IV of the VC area 17. Corticogeniculate projections were also demonstrated in the transplanted LGN.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.