BACKGROUND:The number of patients in need of organ transplantation in China is increased by more than 10%per year. Due to the lack of voluntary donations, China is facing a more severe donor shortage than other countries. What are the specific reasons for the shortage of donor organs in China? What is the attitude toward organ donation in Chinese citizens? What factors are affecting the implementation of organ donation in Chinese citizens?
OBJECTIVE:To investigate the influence of traditional Chinese ideas on the wil ing of Chinese citizens toward organ donation after death.
METHODS:By random cluster sampling, 900 persons selected from different social classes as research objects received questionnaire survey. Self-made questionnaire consisted of cognition, attitude and behavior of the public in face of organ donation.
RESULTS AND CONCLUSION:(1) 55.16%of persons thought that the main purpose of organ donation was to help others, 24.22%thought that the main purpose of organ donation was a manifestation of social morality, 11.94%thought that organ donation was the continuation of their lives. (2) There were 70.00%who said donations should be used for the cause of organ transplantation, in order to save more lives, and the average score was 2.53 points;while the number of persons who proposed donor organs would be applied in medical teaching was similar to that in pathological anatomy, and the average score was 1.72 and 1.75, respectively. (3) 65.01%of the public supported cardiopulmonary death standard to judge death, 24.33%supported brain death standard to judge death, and moreover, 10.66%of people did not know what to take. (4) 50.52%of people thought that the main factors affecting the organ donation was traditional Chinese culture and ideas, fol owed by the donation program and family feelings. The study found that traditional Chinese culture and ideas are the main factor affecting organ donation in the public, most people think that cardiopulmonary death standard is better to judge death and that the main purpose of organ donation is to help others that organ donation should be applied firstly to organ transplantation in order to save more lives.

Objective To evaluate the effect of bronchoscopic argon plasma coagulation thera-py on bronchial carcinoma. Methods Thirty-one bronchial carcinoma patients were diagnosed by bronchoscope and pathological tests, with or without atelectasis or obstructive pneumonia on chest X-ray or chest CT. Argon plasma coagulation therapy was performed through bronchoscope. The location of the airway lesions, the degree of obstruction, dyspnea index, and complications were evaluated. Results The patients with bronchial carcinoma were treated 1～4 times by bronchoscopic argon plas-ma coagulation therapy. Full effectiveness was achieved in 15 patients (48.4 %), partial in 12 (38.7%), and mild in the other 4 ( 12.9 % ). The overall effective rate was 100 %. Conclu-sion Bronchoscopic argon plasma coagulation therapy for bronchial carcinoma can remarkably reduce the tumor size, relieve clinical symptoms, and alleviate the obstruction caused by bronchial neoplasm. Brouchoscopic argon plasma coagulation therapy is an effective and safe method for patients with bron-chial carcinoma.

Granular cell tumor of the breast (GCTB) is a rare tumor which stems from Schwann cells.It is a largely benign tumor,but in the literature extremely infrequent cases can exhibit malignant characteristics.It tends to a particular problem as its characteristics are similar with breast carcinoma macroscopically,clinically,and radiologically.Typically,GCTB is benign and solitary lesion,yet including atypical GCTB and malignant GCTB,they can co-localize with breast malignancies multicentricity.The histopathological and immunohistochemical detection is the gold standard for diagnosis of GCTB up to now.And local expanded resection is the main treatment method at present.

This stued examined the effects of nutritional support in 56 patients suffer from COPD. The influence of nutritional support on lung function and arteny blood gases after infusion of an amino acid solution (7% Fan Ming) were observed. The results suggested theft PaO2, FEV1. FVC levels were increased significantry compared to the control group. PaOz decreased significantly in Fan Ming infusion group compared 100 control group.

BACKGROUNDTo investigate the expression of COX-2 and its relation to clinical pathophysiological features and prognosis in non-small cell lung cancer (NSCLC).

METHODSThe expression of COX-2 protein was detected in 52 NSCLC tissues by immunohistochemical (S-P) method.

RESULTSThe positive COX-2 expression was observed in 25 (48.1%) cases of NSCLC tissues. The positive rate of COX-2 expression was 76.5% and 34.3% in adenocarcinoma and squamous cell carcinoma respectively (P < 0.01). The positive rate of COX-2 expression in T3+T4 disease (92.3%) was remarkably higher than that in stage T1+T2 (33.3%) (P < 0.01). There was a remarkable difference in COX-2 expression rate between clinical stage I+II (28.1%) and clinical stage III+IV (80.0%) groups (P < 0.01). The positive rate of COX-2 expression was 83.3% in those with lymph node metastasis, but only 17.9% in those without lymph node metastasis (P < 0.01). In addition, there were significant differences in positive rate of COX-2 expression among patients with ≤2, > 2 but < 5, ≥5 years of survival span respectively (P < 0.01).

CONCLUSIONSOverexpression of COX-2 in NSCLC, especially in adenocarcinoma, is closely related to invasion, lymph node metastasis and clinical stage of lung cancer. It may play a role in development of NSCLC, and also may be a prognostic marker.

BACKGROUNDTo investigate the expression and its clinical significance of MMP-2 and MMP-9 in non-small cell lung cancer (NSCLC), so as to provide reference in diagnosis, treatment and determining prognosis of NSCLC.

METHODSMMP-2 and MMP-9 expression was detected in 32 lung cancer tissues, 32 paracancerous lung tissues and 10 benign pulmonary lesion tissues by immunohistochemical method with anti-MMP-2 and anti-MMP-9 antibody.

RESULTS(1)Expression of MMP-2 (90%, 36/40) and MMP-9 (83%, 33/40) in cancer tissues was significantly higher than that in paracancerous tissues (22% and 13%) and benign pulmonary disease tissues (0) (P < 0.01). (2)Expression level of MMP-2 and MMP-9 was significantly related to lymph node metastasis and TNM staging, and histologic classification and differentiation (P < 0.05).

CONCLUSIONSMMP-2 and MMP-9 expression in NSCLC tissue is remarkably higher than that in paracancerous tissues and benign pulmonary tissues. Detaction of MMP-2 and MMP-9 expression in lung cancer tissue might be helpful to determine metastasis, staging of the cancer, and predict the prognosis of patients with NSCLC.

Objective To investigate the antitumor activity of the procaspase-3 activator SM-1 in BGC-823 cells in vivo and in vitro and the mechanisms.Methods The inhibitory effects of SM-1 on proliferation of BGC-823 cells were evaluated using MTT method, the cell apoptosis rate was detected by flow cytometry, and the expression of caspase-3 protein and procaspase-3 mRNA was detected by Western blotting and RT-PCR, respectively.SM-1 Antitumor activity was evaluated using the xenograft of BGC-823 cells in nude mice.Results SM-1 effectively inhibited the proliferation in vitro and in-duced apoptosis of BGC-823 cells in a dose-dependent manner.After treatment with SM-1 for 48 h, the protein expression levels of caspase-3 and mRNA expression levels of procaspase-3 were increased.SM-1 significantly inhibited growth of BGC-823 xenograft tumor at the 300 mg/kg dose and the inhibition rate was 56.3%(P<0.05).Conclusion SM-1 can significantly inhibit the tumor growth of BGC-823 cells in vivo and in vitro.The mechanism is possibly related to the activation of procaspase-3 and induced apoptosis of tumor cells.

Aim To explore the effect of chemical hypoxia-mimetic agent,cobalt chloride(CoCl2)on inflammatory reaction in human keratinocytes(HaCat cells).Methods After HaCat cells were treated with CoCl2 at different concentrations to set up a chemical hypoxia-induced cell model of skin injury,cell viability,intracellular reactive oxygen species(ROS),mitochondrial membrane potential(MMP),the levels of both interleukin 6(IL-6)and interleukin 8(IL-8)as well as the expression of heme oxygenase-1(HO-1)were detected.Results The viability of HaCat cells was reduced by CoCl2 at the concentrations from 500 to 3 000 ?mol?L-1,and the higher CoCl2 doses,the lower cell viability was.CoCl2 induced oxidative stress reaction(increasing ROS production and decreasing MMP).CoCl2 induced inflammatory reaction,enhancing the release of IL-6 and IL-8.CoCl2 at concentrations from 1 000 to 3 000 ?mol?L-1 upregulated HO-1 expression in HaCat cells.Conclusion CoCl2 induces not only oxidative stress,but also inflammatory reaction,increasing the release of both IL-6 and IL-8,as well as HO-1 expression.

Objective To explore whether the phosphorylation of NF-κB P65 subunit is involved in the cytotoxicity to and inflammation in an immortal human keratinocyte cell line HaCaT during cobalt chloride (CoCl2-induced chemical hypoxia. Methods HaCaT cells were treated with CoCl2 of 2 mmol/L to set up a chemical hypoxia-induced cell model of injury. Then, RNA interference was used to down-regulate the expression of P65 in CoCl2-induced HaCaT cells. After additional culture, cell viability was tested by cell counting kit8 (CCK-8), the levels of interleukin 6 (IL-6) and interleukin 8 (IL-8) were detected by ELISA kits, phosphorylated and total P65 protein was measured by Western blot. Results The exposure of HaCaT cells to 2 mmol/L CoCl2 for 0 to 4 hours enhanced the phosphorylation of P65, which began at 0.5 hour, peaked at 1.5 hours, and restored to the normal level at 4 hours, and the level of P65 phosphorylation was about 6.6 times that in the untreated control group. The CoCl2 of 2 mmol/L decreased the cell viability of HaCaT cells in a time dependent manner, and a significant difference was observed in the viability of HaCaT cells between CoCl2-treated and untreated HaCaT cells at 2, 4, and 6 hours (P ＜ 0.05, 0.01, 0.01 ). The release of IL-6 and IL-8 from HaCaT cells was also promoted by CoCl2 treatment. The knockdown of P65 expression with siRNA markedly suppressed the CoCl2-induced cytotoxicity to and increase in the release of IL-6 and IL-8 from HaCaT cells,despite of an increment in cell viability by about 11%. Conclusion The phosphorylated P65 subunit mediates CoCl2-induced cytotoxicity and inflammatory injury to HaCaT cells.

BACKGROUNDLung cancer is one of the leading causes of cancer-related death in mankind. To exploit antitumor drug from plant has been a highlight at home and abroad. The aim of this study is to investigate the apoptosis of human lung adenocarcinoma cell line A549/DDP induced by ginsenoside Rh₂ (G-Rh₂) and to explore its possible molecular mechanism.

METHODSThe growth inhibition effect of G-Rh₂ on A549/DDP cells was evaluated by MTT assay. Cell cycle analysis, apoptosis index and tumor related gene expression were detected by flow cytometry. The changes of sApo-1/Fas level in the cell culture supernatant were determined by ELISA method.

RESULTS(1) G-Rh₂ significantly inhibited the growth of A549/DDP cells in a dose-time-de-pendent manner. (2) After 24 hours' treatment with G-Rh₂, apoptosis index of trial group was significantly higher than that of control group (P < 0.001). The proportion of cells in G0/G1 phase in trial group was much higher than that in control group (P < 0.01), while proportion in S phase in trial group was markedly lower than that in control group (P < 0.01). There was no significant difference in proportion in G2/M phase between trial group and control group (P > 0.05). (3) The positive expression rate of p53 and Fas in trial group was significantly higher than that in control group (P < 0.01, P < 0.001), while the positive expression rate of Bcl-2 in trial group was significantly lower than that in control group (P < 0.001). (4) The level of sApo-1/Fas in A549/DDP cell culture supernatant in trial group was remarkably lower than that in control group (P < 0.05).

CONCLUSIONSG-Rh₂ can induce the apoptosis of A549/DDP cells. Its molecular mechanism may be up-regulating expression of p53 and Fas and down-regulating expression of Bcl-2.