Autoradiographic study of chick limb cartilage in vivo and in vitro and its response to mitomycin C (MMC)

1975 ◽  
Vol 93 (3) ◽  
pp. 440-446 ◽  
Author(s):  
Shamer Singh ◽  
D.N. Sinha ◽  
G.C. Prasad
2001 ◽  
Vol 183 (7) ◽  
pp. 2259-2264 ◽  
Author(s):  
Yan Wei ◽  
Amy C. Vollmer ◽  
Robert A. LaRossa

ABSTRACT Mitomycin C (MMC), a DNA-damaging agent, is a potent inducer of the bacterial SOS response; surprisingly, it has not been used to select resistant mutants from wild-type Escherichia coli. MMC resistance is caused by the presence of any of four distinctE. coli genes (mdfA, gyrl, rob, andsdiA) on high-copy-number vectors. mdfAencodes a membrane efflux pump whose overexpression results in broad-spectrum chemical resistance. The gyrI (also called sbmC) gene product inhibits DNA gyrase activity in vitro, while the rob protein appears to function in transcriptional activation of efflux pumps. SdiA is a transcriptional activator of ftsQAZ genes involved in cell division.


Blood ◽  
2004 ◽  
Vol 104 (11) ◽  
pp. 3171-3171
Author(s):  
Yue Si ◽  
Cordula Leurs ◽  
Edward Srour ◽  
Samantha Ciccone ◽  
Helmut Hanenberg ◽  
...  

Abstract Fanconi anemia (FA) is a complex autosomal recessive genetic disorder characterized within the hematological system by progressive bone marrow aplasia, a high propensity to develop acute myeloid leukemia, and hypersensitivity to alkylating agents including mitomycin c. The identification of individual FA genes raises the potential of using gene transfer technology to express/introduce the functional cDNA in/into deficient autologous stem cells. We have previously shown that in the absence of genetic correction with a retroviral mediated Fancc transgene, ex vivo culture of Fancc−/− stem/progenitor cells (HSPC) predisposes uncorrected Fancc−/− HSPC cells to clonal hematopoiesis (Haneline, Blood 2003). Therefore we examined the potential of a helper-free human foamy virus (HFV) derived construct that encodes both the human FANCC and EGFP transgenes to transduce murine Fancc−/− HSC in the absence of prestimulation. In initial experiments, we determined that 40–80% of progenitors were transduced following a single overnight HFV infection using a 20:1 moiety of infection. Subsequent studies demonstrated that HFV efficiently transduced primitive hematopoietic progenitors in G0 and G1 phases of the cell cycle as evidenced both by using multicolor fluorescence activated cell sorting and subsequent culture of sorted cell populations in high proliferating potential (HPP-CFC) and low proliferating potential colony forming assays. Aliquots of HFV transduced cells that were transduced with the construct encoding both Fancc and EGFP, or the reporter transgene only were transplanted into irradiated recipient mice. Four months following transplantation, bone marrow cells were isolated from the reconstituted recipients and clonogenic assays were established in a range of mitomycin c (MMC) concentrations. In these experiments, the MMC hypersensitivity of Fancc−/− progenitors was corrected to wild-type levels. To assess quantitatively the potential of HFV expressed FANCC to correct stem cell repopulating ability, we next utilized the competitive repopulating assay. In two replicate experiments, we determined that the repopulating activity of HFV-transduced Fancc−/− stem cells was comparable to wildtype controls six months following transplantation in primary and secondary recipients. Collectively, these data provide in vivo evidence that the HFV vector is an efficient vehicle for introducing a functional hFANCC transgene into quiescent Fancc−/− HSC in the absence of prestimulation and for complementing the cellular FA defect in vitro and in vivo.


2013 ◽  
Vol 15 (1) ◽  
Author(s):  
Lee MacKenzie Fischer ◽  
Juan Luis Vásquez ◽  
Julie Gehl ◽  
Gregers G Hermann ◽  
Niels B Larsen
Keyword(s):  

1995 ◽  
Vol 5 (3) ◽  
pp. 168-171 ◽  
Author(s):  
L. E. Pablo ◽  
T. Ramírez ◽  
R. Álvarez ◽  
I. González ◽  
J. M. Larrosa ◽  
...  

Background Failure of filtering surgery may be related to excessive wound healing in the surgical area. This effect diminishes with the use of antimetabolic agents. Mitomycin-C (MMC) has proved to be the most effective drug to reduce myofibroblastic proliferation in experimental in vivo and in vitro models. To our knowledge, the objective changes induced by mitomycin-C in the size of wound healing areas have not been investigated. Methods: Filtering surgery was performed on both eyes of 40 pigmented rabbits. Preoperatively one of the eyes received MMC (0.5 mg/ml), and the fellow eye received balance salt solution as placebo. Animals were killed on days 6, 15, 30 and 58. Microscopic healing areas were measured by digital procedures. The areas of target and fellow control eyes were compared by the Wilcoxon test. Results This study showed significant differences (p<0.05) between treated and untreated groups, the healing are a gradually becoming smaller. Conclusions Objective methods to quantify the microscopic effects of MMC can be useful to improve our knowledge about the action on this antimetabolite and to enable us to adjust more accurately the timing and dosage when applying the drug in glaucoma filtering surgery.


2011 ◽  
Vol 32 (11) ◽  
pp. 1402-1410 ◽  
Author(s):  
Qian-mei Zhou ◽  
Xiu-feng Wang ◽  
Xin-jun Liu ◽  
Hui Zhang ◽  
Yi-yu Lu ◽  
...  

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