Objective To quantitatively analyze and evaluate the content of rehabilitation policy for people with disabilities in China. Methods This study focused on ten national policies of disability rehabilitation issued from 2021 to 2023.It employed text mining techniques to process policy texts and constructed a policy modeling consistency index model for dis-ability rehabilitation policies in China.The relevant policies were evaluated and analyzed quantitatively. Results The disability rehabilitation policies in China were relatively comprehensive in terms of policy transparency,op-erational mechanisms and policy nature.However,there was still a need for optimization in terms of policy per-spectives,target groups,incentive mechanisms,and other aspects. Conclusion The overall quality of disability rehabilitation policy texts at the national level in China is relatively good.There is a need to further enhance the predictability of policy objectives,clarify the responsibilities and division of labor among various departments,and improve policy incentive mechanisms in future policy formulation,which will further refine China's disability rehabilitation policy system and contribute to high-quality develop-ment of the disability cause.

Zinc oxide nanoparticles(ZnO NPs)have been gradually introduced into people's lives due to their excellent properties.In daily contact,ZnO NPs can enter the human body in a variety of ways and accumulate in tissues and organs.Inhalation is an important means by which ZnO NPs enter the human body and deposit in lungs.Studies have shown that exposure of lungs to ZnO NPs will cause a range of negative effects.The mechanism of pulmonary toxicity induced by ZnO NPs is related to Zn2+release,oxidative stress,DNA damage,autophagy,inflammation and pulmonary surfactant dysfunction.This paper reviews the pulmonary toxicity and mechanisms of ZnO NPs,and summarizes the prevention and treatment strategies,which provides scientific basis for safer use of nanomaterials,and potential intervention strategies for the prevention and treatment of nanotoxicity.

An 18-year-old female presented with painful erythema and nodules on both legs for more than 2 years.Dermatological examination showed irregularly sized,mildly indurated,tender,deep subcutaneous nodules arising in diffused infiltrated dark erythematous patches in the inner and posterior region of the left leg.Histopathology showed no significant changes in the epidermis.There were perivascular lymphoid cell infiltrates in the dermis and subcutis.Multiple sites of necrosis of blood vessel walls with vascular occlusions were noted.The lumens of some blood vessels were filled with lymphocytes,among which were many atypical cells with hyperchromatic nuclei and pathologic mitotic figures.Immunohistochemistry showed that lymphocytes in the cavities of blood vessels were positive for CD3(+++),CD3ε(+++),CD2(+),CD56(+++),granzyme B(+++),perforin(+++),CD30(+),Ki67 (+++,100％ ),but negative for CD20,CD5,CD7,CD4,CD8,TdT,anaplastic lymphoma kinase,early membrane antigen (EMA) or pan cytokeratin (pCK).The endothelial cells lining the blood vessels stained positively for CD34.The intravascular lymphocytes were also positive for EBER1/2 by in situ hybridization.A diagnosis of cutaneous intravascular NK/T cell lymphoma was made.

The effect of Smac gene on the TRAIL-induced apoptosis of the prostate cancer cell line PC-3 and the molecular mechanism were investigated.The Smac gene was transfected into PC-3 cells under the induction of liposome.The intrinsic Smac gene expression was detected by Western blotting.After treatment with TRAIL as an apoptosis inducer,in vitro cell growth activity was assayed by MTT colorimetry.The apoptosis rate of PC-3 cells was determined by annexin V -FITC and propidium iodide staining flow cytometry.The expression of cellular XIAP and caspase-3 genes was examined by Western blotting.Smac-transfected cells (PC-3/Smac group) had significantly increased Smac protein level as compared with PC-3 controls (P＜0.01).After induction with 100-200 ng/mL TRAIL for 12-36 h,cellular proliferation rate in PC-3/Smac group was significantly lower than in PC-3 controls (P＜0.05).After induction with 100 ng/mL TRAIL for 24 h,the apoptosis rate in PC-3/Smac group was significantly enhanced as compared with that of PC-3 controls (P＜0.05).Accordingly,the XIAP expression level was down-regulated significantly (P＜0.05) and caspase-3 subunit P20 was up-regulated significantly (P＜0.05).It is suggested that the over-expression of cellular Smac can inhibit inhibitor of apoptosis proteins (IAPs),enhance caspases activity and the apoptosis rate of PC-3 cells induced by TRAIL,which may provide a useful experimental basis for prostate cancer therapy.

The effect of Smac gene on the TRAIL-induced apoptosis of the prostate cancer cell line PC-3 and the molecular mechanism were investigated. The Smac gene was transfected into PC-3 cells under the induction of liposome. The intrinsic Smac gene expression was detected by Western blotting. After treatment with TRAIL as an apoptosis inducer, in vitro cell growth activity was assayed by MTT colorimetry. The apoptosis rate of PC-3 cells was determined by annexin V-FITC and propidium iodide staining flow cytometry. The expression of cellular XIAP and caspase-3 genes was examined by Western blotting. Smac-transfected cells (PC-3/Smac group) had significantly increased Smac protein level as compared with PC-3 controls (P<0.01). After induction with 100-200 ng/mL TRAIL for 12-36 h, cellular proliferation rate in PC-3/Smac group was significantly lower than in PC-3 controls (P<0.05). After induction with 100 ng/mL TRAIL for 24 h, the apoptosis rate in PC-3/Smac group was significantly enhanced as compared with that of PC-3 controls (P<0.05). Accordingly, the XIAP expression level was down-regulated significantly (P<0.05) and caspase-3 subunit P20 was up-regulated significantly (P<0.05). It is suggested that the over-expression of cellular Smac can inhibit inhibitor of apoptosis proteins (IAPs), enhance caspases activity and the apoptosis rate of PC-3 cells induced by TRAIL, which may provide a useful experimental basis for prostate cancer therapy.

In our previous study,we identified a novel testis-specific expressed gene 2(TSEG-2)from mouse testis.To further investigate its functions,35 male Balb/c mice(8 weeks old)were divided into cryptorchidism group(n=20),sham group(n=10),and control group(n=5).In cryptorchidism group,the right testes were anchored to the inner lateral abdominal wall.In situ hybridization(ISH)was applied to measure the localization of TSEG-2 in mouse testis.Real-time quantitative PCR was performed to detect the expression of TSEG-2 gene.Meanwhile,under the mediation of polyethylenimine(PEI),the recombinant vector pEGFP-TSEG-2(n=5)or empty vector(mock,n=5)was transfected into the testis of male mice.The transfection efficiencies were measured under a fluorescence microscope.The apoptosis of spermatogenic cells was detected by terminal deoxynuleotidyl-mediated nick end labeling(TUNEL).The results showed that TSEG-2 was expressed in convoluted seminiferous tubules,more precisely,in spermatogonia and spermatocytes.As compared with sham and control groups,the TSEG-2 transcription was significantly enhanced(P<0.05)and was correlated with apoptosis of spermatogenic cells in cryptorchid testes(P<0.05).PEI was efficient in mediating transfection of TSEG-2 into seminiferous tubules of testis.One week post-transfection,intratesticular injection of TSEG-2 resulted in increased apoptosis of spermatogenic cells in vivo (P<0.05).These results indicate that TSEG-2 may participate in the apoptosis of spermatogenic cells and the pathogenesis of cryptorchidism.

In our previous study, we identified a novel testis-specific expressed gene 2 (TSEG-2) from mouse testis. To further investigate its functions, 35 male Balb/c mice (8 weeks old) were divided into cryptorchidism group (n=20), sham group (n=10), and control group (n=5). In cryptorchidism group, the right testes were anchored to the inner lateral abdominal wall. In situ hybridization (ISH) was applied to measure the localization of TSEG-2 in mouse testis. Real-time quantitative PCR was performed to detect the expression of TSEG-2 gene. Meanwhile, under the mediation of polyethylenimine (PEI), the recombinant vector pEGFP-TSEG-2 (n=5) or empty vector (mock, n=5) was transfected into the testis of male mice. The transfection efficiencies were measured under a fluorescence microscope. The apoptosis of spermatogenic cells was detected by terminal deoxynuleotidyl-mediated nick end labeling (TUNEL). The results showed that TSEG-2 was expressed in convoluted seminiferous tubules, more precisely, in spermatogonia and spermatocytes. As compared with sham and control groups, the TSEG-2 transcription was significantly enhanced (P<0.05) and was correlated with apoptosis of spermatogenic cells in cryptorchid testes (P<0.05). PEI was efficient in mediating transfection of TSEG-2 into seminiferous tubules of testis. One week post-transfection, intratesticular injection of TSEG-2 resulted in increased apoptosis of spermatogenic cells in vivo (P<0.05). These results indicate that TSEG-2 may participate in the apoptosis of spermatogenic cells and the pathogenesis of cryptorchidism.

ysis, which had important reference values for further studying biological functions of UP Ⅱ gene and targeted therapeutic strategy for TCC of bladder.

The expression of X-linked inhibitor of apoptosis protein (XIAP) gene and its effect on chemotherapeutic sensitivity in bladder carcinoma was explored. By using immunohistochemistry,the expression of XIAP was detected in 47 bladder carcinomas and 5 normal bladder tissues. The XIAP gene was transfected into bladder cancer cell line T24 by liposome and the positive clone was screened by G418. Cellular XIAP mRNA level was detected by RT-PCR. Low-dose mitocycin C was administered to induce the apoptosis of T24 cells. The in vitro growth of bladder carcinoma cells was analyzed by MTT colorimetry, and the apoptosis rate was assayed by TUNEL methods. It was found XIAP was moderately expressed in bladder carcinomas with the the positive rate being 78.73% (37/47), but the positive rate was not correlated with carcinoma stages and grades (P＜0.05). XIAP mRNA level in transfected T24 cells was significantly increased by 3.8 times as compared with that in the cells not transfected with XIAP. After treatment with low-dose mitomycin C (0.005 and 0.05 mg/mL), the growth rate in XIAP no-transfected control group was increased by (11.60±0.25)% and (16.51±0.87)% (P＜0.05), and the apoptosis rate was decreased by (10.1±0.2)% and (11.9±0.2%) (P＜0.05) respectively as compared with XIAP transfected group. It was concluded that XIAP was expressed in most of bladder carcimoma samples. Overexpression of XIAP in T24 could significantly reduce the MMC-induced apoptosis of bladder carcinoma, suggesting its effect on the chemotherapeutic sensitivity of T24 cells.

The expression of X-linked inhibitor of apoptosis protein (XIAP) gene and its effect on chemotherapeutic sensitivity in bladder carcinoma was explored. By using immunohistochemistry, the expression of XIAP was detected in 47 bladder carcinomas and 5 normal bladder tissues. The XIAP gene was transfected into bladder cancer cell line T24 by liposome and the positive clone was screened by G418. Cellular XIAP mRNA level was detected by RT-PCR. Low-dose mitomycin C was administered to induce the apoptosis of T24 cells. The in vitro growth of bladder carcinoma cells was analyzed by MTT colorimetry, and the apoptosis rate was assayed by TUNEL methods. It was found XIAP was moderately expressed in bladder carcinomas with the the positive rate being 78.73% (37/47), but the positive rate was not correlated with carcinoma stages and grades (P<0.05). XIAP mRNA level in transfected T24 cells was significantly increased by 3.8 times as compared with that in the cells not transfected with XIAP. After treatment with low-dose mitomycin C (0.005 and 0.05 mg/mL), the growth rate in XIAP no-transfected control group was increased by (11.60+/-0.25)% and (16.51+/-0.87)% (P<0.05), and the apoptosis rate was decreased by (10.1+/-0.2)% and (11.9+/-0.2%) (P<0.05) respectively as compared with XIAP transfected group. It was concluded that XIAP was expressed in most of bladder carcinoma samples. Overexpression of XIAP in T24 could significantly reduce the MMC-induced apoptosis of bladder carcinoma, suggesting its effect on the chemotherapeutic sensitivity of T24 cells.