While biological identification technology has brought positive impacts to society,it has also raised ethical issues,such as privacy protection and fair application.Taking the technical dimension as the main line is the foundation of efficient and agile governance of ethical issues in biological identification technology.Based on the technology track theory,a framework for ethical governance of biological identification technology was constructed,and the track and ethical governance technology of biological identification technology were sorted out.The key to efficient governance lies in the application of ethical governance technologies such as privacy and security protection and fairness detection at the three levels of the entire lifecycle of biological identification technology,including data,algorithms,and systems.Taking Hikvision's facial recognition technology as an example,this paper elaborated that increasing the application of ethical governance technology is of great significance to ensure the trustworthy and sustainable development of biological identification technology.

Objective:To establish and verify a dynamic web-based nomogram for predicting futile recanalization after thrombectomy in acute ischemic stroke.Methods:Three hundred and four acute ischemic stroke patients admitted to the Second Affiliated Hospital of Soochow University from May 2017 to April 2021 were retrospectively enrolled. All these patients underwent mechanical thrombectomy and obtained successful recanalization. The eligible patients were randomly divided into training group ( n=216) and test group ( n=88) by 7∶3. The nomogram was established and internally validated with the data of the training group, and externally validated with the data of the test group. For the training group, multivariate Logistic regression analysis was performed by including all variables with P<0.05 in univariate analysis, and the independent predictors of futile recanalization were screened out to construct a nomogram. In the training group and the test group, the performance of the nomogram was verified by C-index, calibration chart and decision curve analysis respectively. Results:No significant difference was detected between the training group and the test group in futile recanalization [134/216 (62.0%) vs 56/88 (63.6%), χ 2=0.07, P=0.794]. Multivariate Logistic regression analysis showed that age ( OR=1.04,95% CI 1.00-1.08, P=0.033), National Institutes of Health Stroke Scale (NIHSS) score on admission ( OR=1.11,95% CI 1.04-1.19, P=0.001), neutrophil to lymphocyte ratio ( OR=1.19,95% CI 1.07-1.32, P=0.001), glycated hemoglobins ( OR=2.02,95% CI 1.34-3.05, P<0.001), poor collateral status ( OR=10.87,95% CI 4.08-29.01, P<0.001), postoperative high density ( OR=11.38,95% CI 4.56-28.40, P<0.001) were independent risk factors for futile recanalization. The C-index of this nomogram in the training group and the test group was 0.92 (95% CI 0.877-0.954, P<0.001) and 0.93 (95% CI 0.87-0.98, P<0.001), respectively. Conclusion:This web-based nomogram, including age, NIHSS score on admission, neutrophil to lymphocyte ratio, glycated hemoglobin, poor collateral status and postoperative high density, predicted individual probability of futile recanalization after mechanical thrombectomy with good discrimination and clinical utility.

According to the clinical features of "pharyngeal itch and cough",wind evil is the main pathogenic factor.This paper systematically summarizes the relevant clinical literature on the treatment of laryngeal cough from the perspective of external wind,internal wind and both internal and external wind.The treatment method and curative effect can provide evidence from the wind treatment.

Objective To investigate the effect of cystatin C (CysC) concentration on outcome of intravenous thrombolysis in patients with acute ischemic stroke.Methods The consecutive patients with acute ischemic stroke who underwent intravenous thrombolysis were enrolled retrospectively.They were divided into a good outcome group (≤2) and a poor outcome group (＞2) according to the Rankin scale.They were also divided into a hemorrhagic transformation (HT) group and a non-HT group according to whether they had HT or not.Their demographic data and clinical data were compared.Results A total of 103 patients with acute ischemic stroke treated with intravenous thrombolysis were enrolled,44 in the good outcome group,59 in the poor outcome group; 23 in the TH group,and 80 in the non-HT group.The age (62.34 ± 13.41 years vs.68.09 ± 9.74 years; t-2.521,P =0.013),baseline CysC concentration (1.008±0.28 mg/L vs.1.27±0.86 mg/L; t=2.237,P=0.027),incidence of HT (14％ vs.34.9％; x2 =6.016,P =0.014) and National Institutes of Health Stroke Scale (NIHSS) score (10.39 ± 3.11 vs.18 ±2.65; t =13.35,P ＜0.001) in the good outcome group were significantly lower than those in the poor outcome group.Multivariate logistic regression analysis showed that there was no significant independent correlation between CysC and clinical outcome (odds ratio 1.783,95％ confidence interval 0.443-7.185 ; P =0.416).The baseline CysC concentration (1.41 ± 0.54 mg/L vs.0.96± 0.18 mg/L; t =3.941,P=0.001) and the NIHSS score (15.96 ± 3.7 vs.13.05 ±4.87; t =3.017,P =0.004) in the non-HT group were significantly lower than those in the HT group.Multivariate logistic regression analysis showed that the plasma CysC concentration ＞ 1.03 mg/L (odds ratio 9.050,95％ confidence interval 2.384-34.359; P =0.001) was an independent risk factor for HT.Conclusions The increased baseline plasma CysC concentration was associated with the occurrence of HT in patients with acute ischemic stroke after intravenous thrombolysis therapy,but it was not associated with the outcomes.

ObjectiveTo evaluate the primary effect of granulocyte-monocyte colony stimulating factor (GM-CSF) as an immunotherapy option for treatment of residual disease after alloHSCT.Methods Immunotherapy was performed on two patients with blood malignancy to treat residual disease after allo-HSCT. The patient one,who was diagnosed as having MDS-RAEB Ⅱ,showed bone marrow displasis and incomplete chimerism 6 months after unrelated donor HSCT.Immunosuppressive drug was withdrawn without induction of graft-versus-host disease (GVHD).The patient two B-ALL demonstrated a residual disease at molecular level 30 days post-transplantation.Both of them were given GMCSF (300 μg) subcutaneously once every two days for totally three weeks.During the whole period,skin itch and rash,liver function,subgroups of lymphocytes,and MDSCs and DCs in peripheral blood were investigated.Results In case one,grade Ⅰskin acute GVHD (aGVHD) appeared as early as one week after GM-CSF administration,as well as grade Ⅱ (skin and liver) by the end of the third weeks,and GM-CSF injection was withdrawn.One month later since the start of GM-CSF,the patient showed normal bone marrow morphology and full donor type chimerism. Cyclosporine A (CsA), mycophenolate mofetil and methylprednisolone were administered for two weeks to control GVHD.In the other case,grade Ⅰ aGVHD occurred 9 days after GMCSF administration,and whole blood CsA maintained at 0.134-0.472 μmol/L.Prednisone (30mg per day for 5 days) was used to control grade Ⅱ GVHD from the 11th day after GM-CSF,and grade Ⅰ GVHD continued without any intervention.On the 30th day after GM-CSF treatment,bone marrow aspiration showed complete molecular remission.In both of the two cases,no differences in lymphocytic subtypes were revealed before and after GM-CSF administration,while there were trends of increased DC number and decreased MDSCs in peripheral blood.ConclusionThe administration of GM-CSF as an immunotherapy option for blood malignancy may contribute to the clearance of residual disease after Allo-HSCT.

Objective To analyze the outcome of idarubicin-intensified myeloablastive conditioning regimen in allogeneic peripheral blood stem cell transplantation (allo-PBSCT) in patients with myelodysplastic syndromes (MDS). Methods From August 2004 to July 2009, 12 patients with MDS were treated with alIo-PBSCT following the idarubicin-intensified conditioning regimen. The conditioning regimen was idarubicin (15 mg/m~2), continuous intravenous infusion for 20 h, days-12 to-10; busulfan (0.8 mg/kg), intravenous infusion every 6 h, days-6 to-4; cyclophosphamide (1.8 g/m~2), intravenous infusion every 6 h, days-3 to-2; cyclosporine A combined with short-term methotrexate was used for the prophylaxes of acute graft versus host disease (aGVHD). Results All twelve patients achieved Trilineage engraftment, and were well tolerated to this regimen. Eight patients survived, and the overall survival was 66.7%, disease-free survival (DFS) 58.3%. Two patients relapsed. OS for neither WHO subgroups nor IPSS subgroups had statistically significant difference. Conclusion Allo-PBSCT with idarubicin-inteusified conditioning regimen is an effective treatment with reduction of the relapse rate for MDS patients.

Summary: The inhibitory effects ofparthenolide (PTL) on angiogenesis induced by multiple myeloma (MM) cells in vitro, and the mechanism were investigated. Human MM line RPMI8226 cells were cultured in vitro. The effects of MM culture supernatant on the migration and tubule formation ability of human umbilical vein endothelial cells (HUVECs) treated with PTL were observed. By using Western blot, the expression of p65 and IκB-α in MM cells was detected. RT-PCR was used to assay the expression of VEGF, IL-6, MMP2 and MMP9 mRNA in MM cells. ELISA was used to measure the levels of VEGF and IL-6 in MM cell culture supernatant. The expression of MMP2 and MMP9 in MM cells was examined by immunohistochemistry. (1) In 3.5, 5.0, 7.5 and 10 μmol/L PTL groups the number of migrated cells was 310±56, 207±28, 127±21 and 49±10 respectively, which was significantly different from that in positive control group (598±47) (P<0.01). In 3.5 and 5.0 μmol/L PTL groups the areas of capillary-like structures were 0.092±0.003 and 0.063±0.002 mm2, significantly less than in positive control group (0.262±0.012 mm2) (P<0.01), but in 7.5 and 10 μmol/L PTL groups no capillary-like structures were found;(2) After treatment with different concentrations of PTL for 48 h, the expression of p65 protein was gradually decreased, while that of IκB-α was gradually enhanced with the increased concentration of PTL;(3) After treatment with 3.5,5.0, 7.5 and 10 μmol/L PTL for 48 h, the VEGF levels in the supematant were 2373.4±392.2,1982.3±293.3, 1247.0±338.4 and 936.5±168.5 pg/mL respectively, significantly different from those in positive control group (2729±440.0 pg/mL) (P<0.05). After treatment with 7.5 and 10 μmol/L PTL, the IL-6 levels in the culture supernatant were 59.6±2.8 and 41.4±9.8 pg/mL respectively, significantly lower than in positive control group (1287.3±43.5 pg/mL) (P<0.05);(4) RT-PCR revealed that PTL could significantly inhibit the expression of VEGF and IL-6 mRNA in MM cells, but not influence the expression of MMP2 and MMP9 mRNA.;(5) Immunohisto chemistry indicated that PTL had no significant effects on the expression of MMP2 and MMP9 protein in MM cells. It was concluded that the abilities of the culture supematant of MM cells treated with PTL to induce endothelial cells migration and tubule formation were significantly reduced, suggesting PTL could obviously inhibit the angiogenesis induced by MM cells. PTL could decrease NF-kappaB activity and significantly suppress the expression of VEGF and IL-6 mRNA and protein, which might contribute to the mechanism by which PTL inhibited the angiogenesis induced by MM cells.

BACKGROUNDPeroxisome proliferator-activated receptor-gamma (PPAR-γ) is a kind of nuclear hormone receptor, which plays important roles in regulating metabolisms. Recently, PPAR-γ was found to express in tumor tissues and cells (including lung cancer), which could be activated by its ligands and affect the differentiation, proliferation and apoptosis of tumor cells. The aim of this study is to investigate the relationship between PPAR-γ expression and clinicopathological characteristics of lung cancer, and to discuss the effect of PPAR-γ activators on lung cancer growth and the mechanisms of apoptosis induction for lung cancer.

METHODSExpression of PPAR-γ was detected in 15 non-cancerous pulmonary tissues and 64 lung cancer tissues by immunohistochemistry, and the average OD values were investigated by image analysis. Expression of PPAR-γ was detected in lung cancer cell lines by RT-PCR and Western blot. After treated with PPAR-γ activators, apoptosis of cells was detected by TUNEL, and caspase-3 activity was detected by using caspase-3 activity detection kit.

RESULTSExpression of PPAR-γ in lung cancer tissues was significantly higher than that in non-cancerous pulmonary tissues. Expression of PPAR-γ was closely related to histological classification, cell differentiation and TNM stages of lung cancer. PPAR-γ could express in two lung cancer cell lines, in which caspase-3 activity was significantly increased and obvious apoptosis was induced after treated with PPAR-γ activators.

CONCLUSIONSPPAR-γ is closely associated with clinicopathological characteristics of lung cancer. Activated PPAR-γ can increase caspase-3 activity to induce apoptosis of cells. PPAR-γ may be a new target for diagnosis and treatment of lung cancer in the future.

To study the mechanisms involved in the inhibition of chronic myeloid leukemic cells (K562) proliferation induced by arsenic trioxide (As2O3) and to explore the potential role of Survivin, an inhibitor of apoptosis protein, in the regulation of As2O3 induced cell apoptosis, K562 cells were cultured with As2O3 of different concentrations. Cells were collected for proliferation analysis by MTT assay. Cell cycle distribution and cell apoptosis were analyzed by flow cytometry. Expression of Survivin protein and mRNA were detected by flow cytometry and RT-PCR, respectively. Our results showed that As2O3(2-10 micromol/L) inhibited K562 cells growth effectively, but it did not induce cells apoptosis significantly. The percentage of K562 cells at G2/M phase increased in proportion to As2O3 concentrations, and the expression of Survivin mRNA and content of Survivin protein was up-regulated accordingly. It is concluded that As2O3 inhibited K562 cells growth by inducing cell cycle arrest mainly at G2/M phase. Over-expression of Survivin gene and protein might be one of the possible mechanisms contributing to K562 cells' resistance to As2O3-induced apoptosis.
Antigens, Neoplasm ; biosynthesis ; genetics ; Antineoplastic Agents ; pharmacology ; Apoptosis ; drug effects ; Arsenicals ; pharmacology ; Cell Cycle ; drug effects ; Cell Division ; drug effects ; Humans ; Inhibitor of Apoptosis Proteins ; K562 Cells ; Microtubule-Associated Proteins ; biosynthesis ; genetics ; Neoplasm Proteins ; Oxides ; pharmacology ; RNA, Messenger ; biosynthesis ; genetics