摘要:

ABSTRACTDevelopmental changes of hematological features of anemic CFO mice (hea/hea) were studied in comparison with those of normal mice (+/+ orhea/+). Anemia of newbornhea/heamice was not severe, but was easily distinguishable from normal littermates by their yellow body color and also by their blood smear pictures which showed abundant erythroblasts. This disease proceeded rather progressively though many died around 10 days after birth and none survived after aged 25 days. Erythrocyte count, hematocrit percentage and hemoglobin content ofhea/heamice became to be nearly 50% of those of normals during development. On the other hand, leukocyte number ofhea/heamice was 3 to 8 times as many as that of normals. Although hepatomegaly was not evident, splenomegaly was remarkable inhea/heamice after aged 15 days: Platelet number ofhea/heawas about 3 times as many as that of normals. On the contrary, megakaryocytes in the bone marrow ofhea/heamice were much fewer than those of normals. Nucleated cells, mainly orthochromatophilic erythroblasts, in the circulation ofhea/heamice were strikingly 80 to 100 times as many as those of normals. This progressively developed anemia caused byheaseemingly affected the differentiation of erythroid cells, but also that of myeloid cells and that of megakaryocytes.

ISSN:0914-3505    

DOI:10.1111/j.1741-4520.1985.tb01001.x

出版商:Blackwell Publishing Ltd    

年代:1985

数据来源: WILEY

摘要:

ABSTRACTMaternal administration of a single dose (20 mg/kg) of cyclophosphamide on day 12 of gestation in CF rats (Sperm += day zero) resulted in the reduction deformities of the limbs of the fetuses and increase in the volume of amniotic fluid at term. Chronological observations of 535 fetuses at 24 hour intervals from day 13 through day 20 revealed variations in the volume of amniotic fluid. On day 13 and 14 it was markedly reduced as compared to corresponding controls (P<0.001). Though there was a gradual rise on day 15 and 16 it was again decreased during day 17 to 19. However, on day 20 it was found to be markedly increased. The associated oligohydramnios observed during the organo‐genetic period probably has a role in the causation of reduction deformities of the fetal limb

ISSN:0914-3505    

DOI:10.1111/j.1741-4520.1985.tb01002.x

出版商:Blackwell Publishing Ltd    

年代:1985

数据来源: WILEY

摘要:

ABSTRACTAzosemide produced bent long bones such as wavy ribs in rat fetuses, but these abnormalities could not be found in the adult offspring. In the present study, the morphological sequence from appearance to disappearance of wavy ribs was examined in cartilage‐bone double stained specimens of fetuses and pups from mothers treated with azosemide on day 16 of gestation. The first detected change of the skeletal abnormalities was inhibition of bone deposition in the ossification centers of fetuses on day 17 of gestation. A bend first appeared on day 18 of gestation, and consisted of cartilage and portion stained neither alcian blue nor alizarin red S. Ossification began at this stage. From day 19 of gestation onward, ossification progressed toward the ends of the cartilage model including the bent region. The bend disappeared in most pups as bone in the bent region grew on days 10–14 postpartum. The present findings imply that the bend may be caused by difference in growth between cartilaginous and unstained portions, and a surface remodeling of bones may straighten the bend in the subsequent bone gro

ISSN:0914-3505    

DOI:10.1111/j.1741-4520.1985.tb01003.x

出版商:Blackwell Publishing Ltd    

年代:1985

数据来源: WILEY

摘要:

ABSTRACTSupraependymal cell clusters in the retina induced by treatment with ethylnitrosourea in fetal and. neonatal rats are described. Following the early cytotoxic effects of this drug on the matrix layer, the supraependymal cell clusters began to form a protrusion from the matrix layer into the intraretinal space through the defective portion of the outer limiting membrane. The supraependymal cell clusters consisted of matrix cells and neurons, or matrix cells, neurons, photoreceptor‐like cells, and glial cells depending on the time of treatment. The clusters became smaller in size, but they remained at least for 7 days after treatment. Our findings indicate that defect of the outer limiting membrane induced by the cytotoxic effect of ethylnitrosourea may be an essential factor for the formation of supraependymal cell clusters, and that the clusters can be regarded as a type of tissue malformation or dysontogenetic anomal

ISSN:0914-3505    

DOI:10.1111/j.1741-4520.1985.tb01004.x

出版商:Blackwell Publishing Ltd    

年代:1985

数据来源: WILEY

摘要:

ABSTRACTAtaxic Shambling mouse was investigated biochemically as well as morphologically to find any specific changes which would be compatible with their ataxic behaviors. Biochemical studies revealed that calcium uptake by the brain synaptosomes of ataxic mouse was decreased to about 30% at 30 mM potassium medium of the control and that the neuron specific enolase activity was lowered a half the value of control synaptosomes, while morphological investigations by Baker's staining for phospholipids disclosed little evidences of phospholipidosis in the nervous tissues and in other organs of the ataxic Shambling mouse. NAD dehydrogenase as well as myosin ATPase staining on the hindlimb muscles of the ataxic Shambling mouse showed a local atrophy and a certain derangement of muscle fibers.These results were discussed in relation to our previous finding of lowered phosphatidylserine synthesis by the brain microsomes which participated at the neuronal transport and transmission in the synaptosomes. Consequently, the ataxic behaviors of Shambling mouse would be ascribed to defective metabolism of phspholipids and decreased brain specific enolase in the synaptosomal fractions which may possibly result in reduced calcium uptake by the synaptosomes regulating neural transmission processes.

ISSN:0914-3505    

DOI:10.1111/j.1741-4520.1985.tb01005.x

出版商:Blackwell Publishing Ltd    

年代:1985

数据来源: WILEY

摘要:

ABSTRACTA woman resulted in premature ovarian failure following gonadotrophin treatment for secondary sterility is described. The state of ovarian failure was confirmed by increased serum gonadotrophin titers, decreased serum estrogen levels, and lack of ovarian follicles on histological examination. The cause of premature ovarian failure was investigated and 47,XXX karyotype was found in chromosomal analysis. The role of sex chromosome abnormalities in the pathogenesis of this entity is discussed. Key words: premature ovarian failure, 47,XXX, gonadotrophin treatment

ISSN:0914-3505    

DOI:10.1111/j.1741-4520.1985.tb01006.x

出版商:Blackwell Publishing Ltd    

年代:1985

数据来源: WILEY

ISSN:0914-3505    

DOI:10.1111/j.1741-4520.1985.tb01007.x

出版商:Blackwell Publishing Ltd    

年代:1985

数据来源: WILEY