Bicalutamide dose-dependently inhibits proliferation in human prostatic carcinoma cell lines and primary cultures

OBJECTIVE: Androgen antagonists inhibit prostatic cell proliferation in normal and pathological conditions and are useful antitumor agents in prostatic carcinoma (PCa). Bicalutamide (BCLT) is a well-known non-steroidal antiandrogenic agent able to interfere with androgen receptor (AR). We tested the efficacy of BCLT in inhibiting proliferation of human PCa cell lines and of primary cultures from biopsies of PCa patients. MATERIALS AND METHODS: Human prostatic carcinoma cell lines (PC3, DU145, LNCaP ALVA 31 and ND1) and short-term primary tissue cultures from PCa patients were treated with BCLT. Cell proliferation and orange acridine and ethidium bromide fluorescence staining studies were performed. RESULTS: BCLT was able to inhibit, significantly and dose-dependently, cell proliferation in AR-positive human PCa cell lines and in 10 cases of primary cultures with Gleason grades 4 to 8. Its action appears to be mainly apoptotic in AR-positive cells and cytotoxic in AR-negative cells. CONCLUSION: BCLT, which inhibits growth in both human PCa cell lines and PCa primary cultures from patients with medium and low-grade tumors, deserves attention as a potential widely effective antiandrogenic monotherapy in prostatic carcinoma. However, its efficacy in AR-negative cells requires further research.     

特异性IgY对烧伤鼠继发感染白念珠菌预防作用的实验研究

目的：探讨白念珠菌特异性ＩｇＹ对烧伤鼠继发感染白念珠菌的预防作用。方法：自烧伤继发感染白念珠菌病人创面分离出的白念珠菌免疫蛋鸡,并将人住房鸡产的蛋中分离出提取的特异性ＩｇＹ用行烧伤感染白念珠菌大鼠。结果：特异性ＩｇＹ能明显抑制烧伤鼠创面（痂下组织）继发感染白念珠菌,与对照组比有显著差异。结论：白念珠菌特异性ＩｇＹ有助于烧伤鼠预防白念珠菌的继发感染。     

吸入性损伤气管切开问题的临床讨论

目的：为了进一步探讨吸入性损伤病人的气管切开时机与指征。方法：回顾性总结分析了１９８１～１９９８年１７３例吸入性损伤的处理方法。他们中轻、中、重度吸入性损伤分别为９４．５３和２７例,行气管切开５７例。结果：全组死亡５６例,病死率与烧伤情有一定关系,但主要死罪仍为吸入性损伤程度,２４小时之内行气管切开病死率偏低。结论：中、重度吸入性损伤宜尽早衽气管切开治疗,并有预防意义。     

Efficient retrovirus-mediated gene transduction into murine hematopoietic stem cells and long-lasting expression using a Transwell coculture system

The neomycin phosphotransferase (neo) gene was transduced into murine hematopoietic stem cells by culturing a recombinant retrovirus- producing cell line in a Transwell (Costar, Cambridge, MA) (bottomed with a porous membrane) hung into a Dexter-type long-term bone marrow (BM) culture. Gene transduction into stem cells retaining long-term reconstitution ability was successfully performed by using protocols of total 15 to 18 days of culture including establishment of the Dexter culture, transduction, and G418 selection. In the irradiated recipients of these cells, a large majority of the BM, thymus, and spleen cells as well as peripheral blood (PB) leukocytes were of donor origin and the neo gene was present in these organs up to 21 weeks after cell transfer. One third to two thirds of the in vitro colony-forming cells in the BM of the recipient mice were resistant to cultivation with G418. It was further found that the hematopoietic system of secondary recipients given BM cells from a primary recipient mouse was predominated by original donor-type cells. The transduced neo gene was detected in the PB, BM, thymus, and spleen cells of these secondary recipients. These results indicate that our procedure of retroviral vector-mediated gene transfer is highly effective in safely introducing a gene into pluripotent hematopoietic stem cells.     

SRC family kinase (SFK) inhibition reduces rhabdomyosarcoma cell growth in vitro and in vivo and triggers p38 MAP kinase-mediated differentiation

Recent data suggest that SRC family kinases (SFKs) could represent potential therapeutic targets for rhabdomyosarcoma (RMS), the most common soft-tissue sarcoma in children. Here, we assessed the effect of a recently developed selective SFK inhibitor (a pyrazolo[3,4-d]pyrimidine derivative, called SI221) on RMS cell lines. SI221, which showed to be mainly effective against the SFK member YES, significantly reduced cell viability and induced apoptosis, without affecting non-tumor cells, such as primary human skin fibroblasts and differentiated C2C12 cells. Moreover, SI221 decreased in vitro cell migration and invasion and reduced tumor growth in a RMS xenograft model. SFK inhibition also induced muscle differentiation in RMS cells by affecting the NOTCH3 receptor-p38 mitogen-activated protein kinase (MAPK) axis, which regulates the balance between proliferation and differentiation. Overall, our findings suggest that SFK inhibition, besides reducing RMS cell growth and invasive potential, could also represent a differentiation therapeutic strategy for RMS.