Objective To investigate the clinical features, therapy and prognosis of elderly patients with newly diagnosed acute promyelocytic leukemia (APL). Methods The clinical features of 21 elderly patients and 89 patients aged ＜60 with newly diagnosed APL were retrospectively analyzed. Additionally,elderly patients were divided into different groups according to the count of white blood cell (WBC). Results There were no significant differences between elderly patients and patients aged ＜60 in the aspect of sex (male/female: 11/10 vs 47/42), WBC count (high initial WBC: 23.8 % vs 16.9 %), the percentage of bone marrow blasts plus promyelocytes (0.83±0.11 vs 0.83±0.12), complete remission (CR) rate (71.4 % vs 84.3 %),the time of CR occurrence (35.7±10.1 vs 39.1±13.5), the occurrence of retinoic acid syndrome(RAS) (14.3 % vs 22.5 %), disseminated intravascular coagulation (DIC) (52.4 % vs 34.8 %) as well as 2 years overall survival rate (72.7 % vs 80.0 %) (P ＞0.05). Of the 21 elderly patients who received inductive treatment, 5 with high initial WBC and 16 without high initial WBC. The incidences of DIC, early death in high initial WBC group were 80 %, 60 % respectively, which were higher than the group without high initial WBC (43.8 %,18.8 % respectively), whereas CR rate for the group with high initial WBC (40.0 %) was lower than that for the group without high initial WBC (81.3 %). Conclusion Elderly patients with APL could have fine prognosis as well as patients aged ＜60. The results of inductive treatment of elderly patients in high initial WBC group were poor as compared with the group without high initial WBC.

Cardiovascular and cerebrovascular diseases is the most fatal diseases in the world.The prevention and treatment of cardiovascular and cerebrovascular diseases are both basic and clinical focus.Aspirin has been used as a prevention medicine in cardiovascular and cerebrovascular diseases for over a century, which is the longest one in history.Aspirin use is estimated at 100 billion tablets annually as an analgesic, antipyretic and antiplatelet drugs.However, there are still many new findings about aspirin, such as aspirin resistance and aspirin hydrolase.This paper reviews the current research advances and future directions of aspirin in cardiovascular and cerebravascwlar diseases, mainly focuses on aspirin resistance and personalized medication.

Objective: To establish a method for determination of tetrahydropalmatine in Anwei tablets. Methods: tetrahydropalmatine in Anwei Tablets was extracted by chloroform and determined by dual wavelength TLC scanning (? s=275nm,? R=340nm).Results: The average recovery was 95%.17%, RSD was 2.50% (n=5). The contents of tetrahydropalmatine in three batches were 7.45,7.17 and 7.90?g/tablet, respectively.Conclusions: The method is stable and feasible.

Objective To study the change of chromosomal centrimeric dots(Cd)aberration of patents infected by CMV after anti-virus treatment.Methods 22 cases who had spontaneous abortion early and infected by CMV(PCR detection)were studied.We analyzed their blood Cd by simultaneous silver attaining technique before and after treatment by anti-virus medicines respectively.Results The rate of Cd aberration of patients infected by CMV was higher.But after treatment by anti-virus drugs,the rate would decrease gradually(P

Objective To explore the mechanism and effects of basic fibroblast growth factor( bFGF)on skin wound healing. Methods Fibroblasts( FB)were isolated from normal skin and hypertrophic scar and cultivated by direct adherence method. FB were then treated with different concentrations of bFGF(0,0. 1,1,10,100,1 000 ng·mL-1 )and cultivated with serum-free medium for 72 hours. The proliferation and apoptosis of FB in each group were detected by cell counting and trypan blue staining. Content and gene expression of typeⅠand type Ⅲ collagen and fibronectin were determined by ELISA and RT-PCR,respectively. Results bFGF promoted the proliferation of FB at low concentrations promoted apoptosis of FB at higher concentrations. The proliferation of FB from hypertrophic scar was slower than that from the normal skin. bFGF significantly inhibited type Ⅰ collagen production from hypertrophic scar FB but not from the normal skin. Moreover,bFGF up-regulated fibronectin expression in the normal fibroblasts,but not in the hypertrophic scar. No change in type Ⅲ collagen expression and production was observed in FB from either source. Conclusion bFGF has differential effects and mechanisms on FB of the normal skin and hypertrophic scar,suggesting that bFGF may play a role in early phase of skin wound healing and scar formation.

Objective To investigate the mechanism of pulmonary fibrosis induced by paraquat (PQ),and the effect of Xuebijing injection in treatment of PQ poisoning.Methods Seventy-two male Wistar rats were randomly divided into control group,PQ poisoning group,and Xuebijing intervention group,with 24 rats in each group.Pulmonary fibrosis was induced by single garage at the dosage of 50 mg/kg of PQ,while 1 mL of distilled water was given by gavage in control group.Xuebijing injection at the dosage of 4 mL/kg were given intraperitoneally at 30 minutes after exposure to PQ in Xuebijing group,and it was repeated every 12 hours; same amount of physiological saline was given intraperitoneally in PQ group and control group.The experiment lasted for 14 days.Six rats in each group were sacrificed on 1,3,7,14 days,respectively,after insult,and 30 minutes after the last intervention.The lung tissues were harvested,the changes in pathology in lung tissue and the degree of pulmonary fibrosis were observed with optical microscope with hematoxylin-eosin (HE) staining and Masson stain.The ultrastructure changes in lung tissues were observed with transmission electron microscopic,and the content of hydroxyproline (HYP) in the lung tissue was determined by alkaline hydrolysis.The expression of mitochondrial fusion protein 2 (Mfn2) was determined by Western Blot.Results ① HE staining:in PQ group,inflammation was most marked on the 3rd day.On the 7th day,exudates in the alveoli started to be organized,and hypertrophic fibroblasts were seen to secrete slim collagen fibers,and fibrosis could be seen in alveoli.On the 14th day,intensive hyperplasia of fibroblasts could be observed,and the alveolar structure was destroyed and collapsed,with deposition of collagen deposited with formation of pulmonary fibrosis.At the same time,pathologic changes were milder in Xuebijing group than those in PQ group.② Masson staining:the degree of inflammation in alveoli and pulmonary fibrosis were less marked in Xuebijing group than those of PQ group on the 14th day.③ Under the transmission electron microscopy,it was found that the mitochondria of lung tissue cells was relatively less in number on the 14th day in PQ group,and the majority of them underwent degeneration,swelling and damage.Basement membrane became folded,alvcoli were collapsed,and fibrosis was obvious.These changes were less serious in Xuebijing group.④ Content of HYP (μg/g):contents of HYP in lung tissues on the 3rd day in PQ group and Xuebijing group were significantly higher than those in control group (743.3 ± 50.2,718.1 ± 34.0 vs.665.8± 6.6,both P＜0.05),it then increased gradually,but the contents of HYP in Xuebijing group were significantly lower on the 7th day and 14th day than those in PQ group (790.5 ± 23.8 vs.876.7 ± 42.0,812.9 ± 72.3 vs.931.3 ± 33.0,both P＜0.05).⑤ Expression of Mfn2:the expression of Mfn2 in control group was relatively lower.The expression of Mfn2 in PQ group was increased gradually under stress,but its rate was low.The expression of Mfn2 (A value) in Xuebijing group was significantly higher than that in PQ group on the 1st day (0.731 ±0.035 vs.0.618 ±0.029,P＜0.05),and it was elevated steadily,reaching the peak on the 7th day (0.732 ± 0.037 vs.0.669 ± 0.034,P＜0.05),but it was lower than that of PQ group on the 14th day (0.708 ± 0.034 vs.0.765 ± 0.041,P＜0.05).Conclusions Xuebijing reduces lung inflammatory reaction and pulmonary fibrosis as a result of PQ poisoning.The mechanism is that Xnebijing regulates and increases expression of Mfn2 in lung tissue.

Objective To explore the effects of up-and down-regulation of Cox-2 expression on the growth and radiation sensitivity of human esophageal cancer EC9706 xenograft in nude mice.Methods Cox-2 specific siRNA and Cox-2 gene eukaryotic expression vector were constructed and transfected to esophageal cancer cells EC9706, and the stable transfected cell lines were obtained by the method of G418 screening.The expressions of Cox-2 mRNA and its protein were detected by RT-PCR and Western blot, respectively.The inhibitory effects of Cox-2 regulation combined with X-ray irradiation on cancer cell growth were detected by the nude mouse xenograft assay.Results Cox-2 gene expression was significantly decreased in the Cox-2 down-regulated group and increased in the Cox-2 up-regulated group.Compared with the control group without gene transfer, the average volumes of EC9706 xenograft tumor in the Cox-2 up-and down-regulated group significantly decreased (F =34.26, P ＜ 0.05) and increased (F =26.38, P ＜ 0.05) , respectively.After 20 Gy X-ray irradiation, the average volume of xenograft was significantly reduced in the Cox-2 down-regulated group (F =16.35, P ＜ 0.05) , but it had no significantly changes in the Cox-2 up-regulated group.Conclusions Down-regulation of Cox-2 expression inhibits the growth of human esophageal cancer EC9706 xenograft in a nude mice and increases cell radiation sensitivity, but upregulation of Cox-2 expression makes tumor cells to become radioresistant.

Objective To illustrate the clinical relevance of distinct PML-RARα fusion gene isoforms in acute promyelocytic leukemia (APL). Methods The nested reverse transcriptase polymerase chain reaction (RT-PCR) was used to detect the long (L) or short (S) PML-RARα fusion gene isoforms in 92 newly diagnosed APL so as to evaluate the clinical feature, therapeutic reaction and prognosis of the two fusion gene isoforms. Results PML-RARα fusion gene was positive in all 92 APL patients, of which 52(56.5 %) was L type and 40 (43.5 %) was S type. There were no significant differences between L type and S type in the aspect of sex, age, white blood cell count,the percentage of bone marrow blasts plus promyeloeytes and chromosome before treatment. And there were no significant differences between the two isoforms in complete remission (CR) rate, the time of getting CR as well as the occurrence of retinoic acid syndrome (RAS), disseminated intravascular coagulation (DIC), intraeranial hemorrhage. Also, there were no significant differences in overall survival rate (OS) and relapse-free survival rate (RFS) between the two isoforms. Conclusion PML-RARα fusion gene isoforms in APL were not correlated with clinical therapeutic effect or prognosis.

Objective:To produce and identify antiCK20 monoclonal antibody.Methods:Lymphocytes from the spleen of mice being immunonized by CK20 antigen were fused with the myeloma cell line(SP2/0) using PEG4000.Hybridodma cells were established by selective growth of the fusion cells in the HT medium,and the presence of antiCK20 antibody was screened by inderect ELISA,and the clonality was achieved by limiting dilution.We have incubated cloning cells into mouse abdominal cavity to produce ascitic fluid contained monoclonal antibody.Chromatography with SPA-Sepharose CL-4B affinity column were emploied to isolate the monoclonal antibody from ascitic fluid.Finally,the antibody were tested the activities and sentivities,isoforms and titer through Western blot,two directions immuning diffusion of agar and ELISA.Results:Only one hybridoma cell line,secreating McAb against CK20,had been established.The modal number of chromosome is 101(99-103).The results of identifications showed that the antibodies kept high activitis and sensitivitis in detecting sample.The titer of ascitic fluid and the McAb purified are 1∶10~6 equally.The immunoglobulin of the McAb is classified as IgG1.Conclusion:AntiCK20 monoclonal antibody have been produced succesfully with high sensitive and active and was named L20031030.

Background Corneal neovascularization (CNV) is one of the causes of corneal blindness.Studies showed that ADP-ribosylation factor (ARF) can regulate the growth of tumor cells,and inhibiting ARF will decrease angiogenesis.However,whether ARF antagonist plays an action on CNV is unclear.Objective The aim of this study was to explore the effect and mechanism of ARF inhibitor on alkali-burn induced CNV.Methods Sixty clean male BABL/c mice aged 7-8 weeks were divided into PBS group and ARF antagonist group according to randomized number table.CNV models were induced by NaOH burn method in all the mice.ARF at the concentration of 0.5 g/L(0.5 ml) was intraperitoneally injected 3 times per week for 1 week followed the induction of CNV in the ARF antagonist group,and 0.5 ml PBS was used in the PBS group.CNV was examined 2,4,7,14 days after injection by the slit lamp microscope and the CNV related area in the cornea was calculated.Betore modeling(0 day) and 4,7,14 days after modeling,real-time PCR and Western blot were used to analyze the expressions of ARF mRNA and protein in the corneas.Forteen days after modeling,the expression of the CD31 in the CNV was detected using immnofluorescence of corneal whole mount;the expression of vascular endothelial growth factor(VEGF) in the cornea was assayed by Western blot.Cellular wound scratch test was employed to evaluate the effects of ARF antagonist on proliferation and migration of human retinal vascular endothelial cells (RECs).All animal experiments were done in accordance with the ARVO Statement for the Use of Animals in Ophthalmic and Vision Research and Guideline for the Care and Use of Laboratory Animals on the the Soochow University Animal Care Committee.Results ARF mRNA and protein were expressed in the mice corneas in both the PBS group and the ARF antagonist group at various time points.The expression of ARF mRNA in mice corneas was enhanced with the lapse of the time (Ftime =65.17,P =0.00),but no significant difference was found among the groups (Fsroup =1.98,P=0.18).There was also significant difference in the expression of ARF protein in mice corneas at different time points in the ARF antagonist group (F =10.77,P =0.00).The related CNV area was 0.45±0.05 in the ARF antagonist group,and that in the PBS group was 0.72±0.11,with significant difference between them (t =-3.87,P ＜ 0.05).The green fluorescence area of C D31 expression in the cornea was smaller in the ARF antagonist group than that of the PBS group.Expression level of VEGF in the ARF antagonist group was 1.20±0.21,and that in the PBS group was 2.47±0.33,showing a significant difference (t =-5.62,P ＜ 0.05).As the increase of ARF antagonist concentration,the inhibiting rate of cell proliferation was reinforced among 10,100 and 1 000 μg/L ARF antagonist groups (F=8.47,P =0.02).Twenty-four hours after scratch test,the migrating distance of human RECs was (5.46±1.32) μm and (5.04±1.68) μm in the 100 μg/L and 1 000 μg/L ARF antagonist groups,respectively,which were shorter than (8.49± 1.18) μm of the PBS group (t=-2.94,-2.91,both at P＜0.05).Conclusions ARF inhibitor can reduce CNV by down-regulating the expression of VEGF in alkaline burn cornea and inhibiting the proliferation and migration of vascular endothelial cells.