Corticosteroid-induced abnormality in fetal mice and H-2 haplotype: Evidence of a cytoplasmic effect

1983 ◽  
Vol 17 (2) ◽  
pp. 141-146 ◽  
Author(s):  
Michael Melnick ◽  
Mary Marazita ◽  
Tina Jaskoll

Lab Animal ◽  
2016 ◽  
Vol 45 (10) ◽  
pp. 380-384 ◽  
Author(s):  
Scott Deeney ◽  
Kyle N. Powers ◽  
Timothy M. Crombleholme
Keyword(s):  


2007 ◽  
Vol 24 (1) ◽  
pp. 35-41 ◽  
Author(s):  
Takashi Kimura ◽  
Naoko Kimura ◽  
Kiyoshi Totsukawa


1993 ◽  
Vol 192 (1) ◽  
pp. 61-68 ◽  
Author(s):  
K. Randerath ◽  
K.L. Putman ◽  
E. Randerath
Keyword(s):  


2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Fabien Aubry ◽  
Sofie Jacobs ◽  
Maïlis Darmuzey ◽  
Sebastian Lequime ◽  
Leen Delang ◽  
...  

AbstractThe global emergence of Zika virus (ZIKV) revealed the unprecedented ability for a mosquito-borne virus to cause congenital birth defects. A puzzling aspect of ZIKV emergence is that all human outbreaks and birth defects to date have been exclusively associated with the Asian ZIKV lineage, despite a growing body of laboratory evidence pointing towards higher transmissibility and pathogenicity of the African ZIKV lineage. Whether this apparent paradox reflects the use of relatively old African ZIKV strains in most laboratory studies is unclear. Here, we experimentally compare seven low-passage ZIKV strains representing the recently circulating viral genetic diversity. We find that recent African ZIKV strains display higher transmissibility in mosquitoes and higher lethality in both adult and fetal mice than their Asian counterparts. We emphasize the high epidemic potential of African ZIKV strains and suggest that they could more easily go unnoticed by public health surveillance systems than Asian strains due to their propensity to cause fetal loss rather than birth defects.



2015 ◽  
Vol 15 (3) ◽  
pp. 131-138 ◽  
Author(s):  
Takashi Kojima ◽  
Takahiro Yamada ◽  
Rina Akaishi ◽  
Itsuko Furuta ◽  
Tatsuya Saitoh ◽  
...  




Blood ◽  
1988 ◽  
Vol 71 (3) ◽  
pp. 800-803
Author(s):  
RA Fleischman

Abstract The leukemias induced by the Friend polycythemia virus and other leukemogenic retroviruses have previously not been transplantable until weeks or months after virus inoculation. Because tumor-specific immune mechanisms persist in both irradiated and nude mice, it has not been possible to determine if this result is due to rejection of cells already immortalized by retrovirus infection, or reflects an inherent limitation in the proliferative capacity and malignancy of these “preleukemic” cells. To clarify these issues, we have transplanted virus-infected bone marrow into mouse fetuses that are immunologically immature and thus incapable of graft rejection. We report here that within days of virus inoculation, transplantable cells capable of disease progression in certain fetal hosts can be detected with this technique. These results demonstrate that cells with the capacity for extensive leukemic proliferation arise very early in Friend virus- induced disease. However, successful transplantation was seen only in genetically anemic recipients (Wx/Wv), which are deficient in hematopoietic stem cells, and not in their normal littermates. Thus, in accord with recent in vitro observations, this in vivo data suggests that normal hematopoietic cells, independent of immune mechanisms, can suppress the malignant progression of transformed cells.



Reproduction ◽  
2007 ◽  
Vol 134 (2) ◽  
pp. 223-231 ◽  
Author(s):  
Wei Shen ◽  
Lan Li ◽  
Zhaodai Bai ◽  
Qingjie Pan ◽  
Mingxiao Ding ◽  
...  

Little is known about the mechanisms underlying primordial follicular formation and the acquisition of competence to resume meiosis by growing oocytes. It is therefore important to establish anin vitroexperimental model that allows one to study such mechanisms. Mouse follicular development has been studiedin vitroover the past several years; however, no evidence has been presented showing that mature oocytes can be obtained from mouse fetal germ cells prior to the formation of primordial follicles. In this study, a method has been established to obtain mature oocytes from the mouse fetal germ cells at 16.5 days postcoitum (dpc). From the initiation of primordial follicular formation to the growth of early secondary follicles, ovarian tissues from 16.5 dpc fetal mice were culturedin vitrofor 14 days. Subsequently, 678 intact secondary follicles were isolated from 182 mouse fetal ovaries and cultured for 12 days. A total of 141 oocytes inside antral follicles were maturedin vitro, and 102 oocytes underwent germinal vesicle breakdown. We found that 97 oocytes were fertilized and 15 embryos were able to form morula–blastocysts. We also analyzed various genomic imprinting markers and showed that the erasure of genomic imprinting markers in the parental generation was also imposed on the oocytes that developed from fetal germ cells. Our results demonstrate that mouse fetal germ cells are able to form primordial follicles with ovarian cells, and that oocytes within the growing follicles are able to mature normallyin vitro.



Angiology ◽  
1963 ◽  
Vol 14 (3) ◽  
pp. 110-115
Author(s):  
G.E. Christiansen ◽  
G.M. Stewart ◽  
R.L. Bacon


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