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1.
Journal of Clinical Otorhinolaryngology Head and Neck Surgery ; (24): 1213-1216, 2015.
Article in Chinese | WPRIM | ID: wpr-747900

ABSTRACT

OBJECTIVE@#To study the radition injury of tracheal mucous membrane tissue after interstitial implanted radioactive 125I in normal rabbit,improve the safety of clinical application.@*METHOD@#Sixty New Zealand rabbits, weighing 2.15-2.30 kg, were randomly divided into 1 w, 1 m, 2 m, 4 m and the control group, the control group was further divided into four subgroups. The 0.8mCi 125I seeds were implanted into the tissue by the first tracheal ring in the treatment groups and nonradioactive seeds were implanted in the control group. Taking the tracheal mucous membrane tissue for pathological examination by HE staining to observe the mucosal injury and VEGF, Pan-Cadherin immunohistochemical staining to observe the expression in differernt time.@*RESULT@#Immunohistochemical staining: VEGF and Pan-Cadherin have statistically significant differences in the expression on different time, the expression is dynamic.@*CONCLUSION@#The expression of VEGF and Pan-Cadherin reflect the radioactive 125I seed has little influence on normal trachea tissue and the damage can be repaired by the regeneration of the basal cell.


Subject(s)
Animals , Rabbits , Brachytherapy , Iodine Radioisotopes , Radiation Injuries , Pathology , Trachea , Pathology , Radiation Effects
2.
Journal of Experimental Hematology ; (6): 43-47, 2000.
Article in Chinese | WPRIM | ID: wpr-354910

ABSTRACT

Acute myeloid leukemia (AML) is considered to be a malignancy that is intrinsically resistant to methotrexate (MTX). As compared to acute lymphoblastic leukemia (ALL) blasts, AML blasts, except those of acute monocytic leukemia (AML-M(5)), form fewer amounts of long chain polyglutamate of MTX (MTXPG), when incubated with MTX, thus providing an explanation for their lack of responsiveness to MTX. To explore the novel approach of treatment in patients with AML-M(5), the U937 cell line, which has the monocytic characters, was used. Cell growth inhibition was mearsured by XTT assay after 24 and 48 hours in the continuous presence of various concentrations of MTX ranging from 1 nmol/L to 100 micro mol/L. After 24 hours MTX treatment, the IC(50) value for U937 cells was 0.04 micro mol/L. After 48 hours treatment, the IC(50) was 0.037 micro mol/L and IC(90) was 0.39 micro mol/L. To understand the mechanism of MTX cytotoxicity, the process of cell death was analyzed. A variety of assays, including trypan blue exclusion, flow cytometry, light microscopy (Wright's staining) and DNA fragment electrophoresis, were performed. There were no significant apoptotie changes after shorter exposure of MTX (4 and 6 hours). After 8 hours at various concentrations of MTX treatment ranging from 5 nmol/L to 10 micro mol/L, the percentage of the cells in the pre-G(1) (apoptotic) was 3.2% at 0.1 micro mol/L and it reached a peak of 18.2% at 5.0 micro mol/L. The DNA synthesis in S-phase was inhibited from 41.2% (0.01 micro mol/L) to 19.1% (10 micro mol/L). DNA ladder band, a feature of apoptosis, was observed. The arrest of cell growth and apoptotic properties induced by MTX have lead to its evaluation as a potentially therapeutic agent in the treatment of AML-M(5).

3.
Acta Nutrimenta Sinica ; (6)1956.
Article in Chinese | WPRIM | ID: wpr-553433

ABSTRACT

Objective: To observe the effects of zinc deficiency on peripheral blood lymphocyte phenotypic distribution and the balance between Th1 and Th2 cells in growing rats. Methods: Two-color cytofluorometric analysis was used. Results: Compared with zinc adequate (ZA) and paired-fed (PF) groups, peripheral blood lymphocytes in zinc deficient (ZD) rats had higher percentage of CD8+ cells (cytolytic T cells), lower percentage of CD4+ cells (T helper cells) and lower percentage of CD45RA+ cells (pure B lymphocytes).In addition, zinc deficiency selectively caused reduction of Th1-like CD45RC+CD4+ cells , but Th2-like CD45RC-CD4+cells had no significant changes in weanling rats. Zinc supplementation could reverse these changes. Conclusion: Dietary zinc deficiency leads to changes of lymphocyte phenotypic distribution and the imbalance of Th1 and Th2 subsets. These changes are reversible.

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