Modification of Radiation Response in Mice by Heterologous and Isologous Bone Marrow

1957 ◽  
Vol 188 (3) ◽  
pp. 555-558 ◽  
Author(s):  
L. J. Cole ◽  
J. G. Habermeyer ◽  
P. C. Nowell

A marrow transfer technique was used to study the functional state of the marrow of lethally x-irradiated mice after intravenous injection with isologous or heterologous (rat) marrow. In the former case, it was found that the marrow behaved as functionally active mouse marrow (in terms of radiation protection) at 19 days postradiation; while it was essentially inactive at 14 days although it appeared to be regenerated, as judged histologically. Irradiated mice (800 r) injected intravenously with rat marrow exhibited ‘regenerating’ marrow, but it was not active in preventing death when injected into other irradiated mice. Rat bone marrow, administered intraperitoneally to lethally x-irradiated mice failed to elicit any 15-day survivors, even with 350 mg or 700 mg doses, per mouse. This latter dose is 70 times greater than the 10 mg of isologous mouse marrow, required to evoke 50% survival.

Blood ◽  
1963 ◽  
Vol 21 (5) ◽  
pp. 594-604 ◽  
Author(s):  
TAKEO KUROYANAGI ◽  
AKIRA KURISU ◽  
HAJIME SUGIYAMA

Abstract 1. The intravenous injection of I131-labeled heterologous anti-leukocyte and anti-bone marrow antibodies into rats resulted in a high specific in vivo localization in the bone marrow, indicating the presence of localizing anti-body. 2. No in vivo localization in lungs was demonstrated, in possible contrast to the earlier concept of pulmonary emboli of clumped leukocytes sensitized with antibodies in experimental immunoleukopenia. 3. Heterologous anti-leukocyte and anti-bone marrow antibodies injected intravenously disappeared from plasma and fixed to peripheral leukocytes and bone marrow cells within 1 hour.


Blood ◽  
1965 ◽  
Vol 25 (2) ◽  
pp. 161-168 ◽  
Author(s):  
TAKEO KUROYANAGI ◽  
MASANOBU SAITO ◽  
AKIRA KURISU

Abstract The in vivo localization of heterologous anti-erythrocyte antibodies in the rat bone marrow was determined by the I131-labeled antibody technic. I131-labeled anti-erythrocyte antibodies localized specifically in the bone marrow indicating the presence of localizing antibody. Both the localizing antibody and the incomplete antibody were thermostable, whereas hemolysins and hemagglutinins were thermolabile. Following an intravenous injection of antierythrocyte antibodies in rats, hemolysins and hemagglutinins were cleared rapidly from the plasma. The incomplete antibodies became attached to circulating red cells within 6 hours and red cell sensitization persisted for 1 week. The localizing antibody localized in the bone marrow within 30 minutes, leaving no activity in plasma. The anti-erythrocyte antibodies markedly reduced the uptake of tritiated thymidine by erythroblasts in vitro, demonstrating their inhibitory effect on the proliferative capacity of erythroblasts.


1974 ◽  
Vol 75 (3) ◽  
pp. 428-434 ◽  
Author(s):  
P.-J. Czygan ◽  
M. Breckwoldt ◽  
F. Lehmann ◽  
R. Langefeld ◽  
G. Bettendorf

ABSTRACT The effect of synthetic LH-RH was studied in 100 patients with various types of ovarian insufficiency by following up the FSH- and LH-levels in plasma. LH-RH was administered in doses of 12.5, 25 and 100 μg as a rapid intravenous injection. The patients were classified according to the endocrine state of the pituitary as evidenced by the urinary gonadotrophin levels. A clear correlation between the functional state of the pituitary and its responsiveness to exogenous LH-RH was demonstrated. Most of the patients with undetectable low urinary gonadotrophin levels failed to respond. The majority of patients with gonadotrophin excretion in the normal range and those with elevated levels reacted with a dose dependent increase in circulating LH. The amount of liberated FSH however was related to the injected dose only in patients with high gonadotrophic excretion. The present study indicates that synthetic LH-RH provides a useful tool in the evaluation of the pitutiary function particularly in patients with low and with undetectable gonadotrophin excretion. The data presented in this paper also demonstrate that the functional state of the pituitary is clearly reflected by the urinary gonadotrophin levels.


2018 ◽  
Vol 18 ◽  
Author(s):  
Chaitra Venugopal ◽  
Christopher Shamir ◽  
Sivapriya Senthilkumar ◽  
Janitri Venkatachala Babu ◽  
Peedikayil Kurien Sonu ◽  
...  

2019 ◽  
Vol 19 (14) ◽  
pp. 1695-1702 ◽  
Author(s):  
Mohsen Cheki ◽  
Salman Jafari ◽  
Masoud Najafi ◽  
Aziz Mahmoudzadeh

Background and Objective: Glucosamine is a widely prescribed dietary supplement used in the treatment of osteoarthritis. In the present study, the chemoprotectant ability of glucosamine was evaluated against cisplatin-induced genotoxicity and cytotoxicity in rat bone marrow cells. Methods: Glucosamine was orally administrated to rats at doses of 75 and 150 mg/kg body weight for seven consecutive days. On the seventh day, the rats were treated with a single injection of cisplatin (5 mg/kg, i.p.) at 1h after the last oral administration. The cisplatin antagonistic potential of glucosamine was assessed by micronucleus assay, Reactive Oxygen Species (ROS) level analysis, hematological analysis, and flow cytometry. Results: Glucosamine administration to cisplatin-treated rats significantly decreased the frequencies of Micronucleated Polychromatic Erythrocytes (MnPCEs) and Micronucleated Normchromatic Erythrocytes (MnNCEs), and also increased PCE/(PCE+NCE) ratio in bone marrow cells. Furthermore, treatment of rats with glucosamine before cisplatin significantly inhibited apoptosis, necrosis and ROS generation in bone marrow cells, and also increased red blood cells count in peripheral blood. Conclusion: This study shows glucosamine to be a new effective chemoprotector against cisplatin-induced DNA damage and apoptosis in rat bone marrow cells. The results of this study may be helpful in reducing the harmful effects of cisplatin-based chemotherapy in the future.


1979 ◽  
Vol 29 ◽  
pp. 85
Author(s):  
Nobuyoshi Yoshida ◽  
Kohtaro Taniyama ◽  
Chikako Tanaka

2019 ◽  
Vol 10 (1) ◽  
Author(s):  
Haiyan Shi ◽  
Xiaoli Li ◽  
Junling Yang ◽  
Yahong Zhao ◽  
Chengbin Xue ◽  
...  

Abstract Background Emerging evidence suggests that neural crest-derived cells (NCCs) present important functions in peripheral nerve regeneration to correct the insufficiency of autogenous Schwann cells. Postmigratory NCCs have been successfully isolated from adult rat bone marrow in our previous work. In this study, we aim to provide neural crest-derived Schwann cell precursors (SCPs) for repair of nerve defects in adult rats, and partially reveal the mechanisms involved in neuroregeneration of cell therapy. Methods A clonal cell line of neural crest precursors of rat bone marrow origin (rBM-NCPs) with SCP identity was expanded in adherent monolayer culture to ensure the stable cell viability of NCPs and potentiate the repair of nerve defects after rBM-NCPs implantation based on tissue engineering nerve grafts (TENG). Here the behavioral, morphological, and electrophysiological detection was performed to evaluate the therapy efficacy. We further investigated the treatment with NCP-conditioned medium (NCP-CM) to sensory neurons after exposure to oxygen-glucose-deprivation (OGD) and partially compared the expression of trophic factor genes in rBM-NCPs with that in mesenchymal stem cells of bone marrow origin (rBM-MSCs). Results It was showed that the constructed TENG with rBM-NCPs loaded into silk fibroin fiber scaffolds/chitosan conduits repaired 10-mm long sciatic nerve defects more efficiently than conduits alone. The axonal regrowth, remyelination promoted the reinnervation of the denervated hind limb muscle and skin and thereby alleviated muscle atrophy and facilitated the rehabilitation of motor and sensory function. Moreover, it was demonstrated that treatment with NCP-CM could restore the cultured primary sensory neurons after OGD through trophic factors including epidermal growth factor (EGF), platelet-derived growth factor alpha (PDGFα), ciliary neurotrophic factor (CNTF), and vascular endothelial growth factor alpha (VEGFα). Conclusions In summary, our findings indicated that monolayer-cultured rBM-NCPs cell-based therapy might effectively repair peripheral nerve defects partially through secreted trophic factors, which represented the secretome of rBM-NCPs differing from that of rBM-MSCs.


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