Research for fault recovery based on MPLS is not only one of important research fields but also the base of development of the next generation network.The thesis presents an New method of MPLS-based recovery to solve the packet loss problem of Makam and delay and packet disorder problems of Haskin,making use of retracing mechanism and the search of Local Repair Path.The result of simulation experiment shows that new method of MPLS-based recovery has less packet disorder and much lower delay and packet losses.

Objective To develop a quantitative,highly sensitive,low detection limit and fast endotoxin(ET) biosensing detection system by utilizing the piezoelectric crystal's damping effect(non-mass effect) in the liquid phase environment.Methods The sensor probe of better performance (eliminating the quality load effects and improving the liquid solid coupling effect) was obtained by using the smoothing processing and hydrophilic processing of a quartz crystal sensor probe surface,thus the stability and repeatability of measurement were increased and the low detection limit of measurement was decreased.The whole measurement system was made into a miniature and automated endotoxin detection system by using CPLD device and LabView software to realize the automatic collection,and analysis and results display of measurement data.Results The good linear relationship existed between different concentrations of endotoxin and the stable value of frequency shift.Conclusion By the established data of frequency shift,the endotoxin concentration can be obtained accurately and conveniently.

The human immune system has the regulatory functions of eradicating pathogens and limiting excessive inflammation, which protect the surrounding tissue from being damaged. The immune bal-ance of self-limiting is mainly controlled by complex interactions between antigen-presenting cells ( APCs ) and T cells. However, the immune balance is destroyed in cancer, which results in immune evasion and tumor metastasis or promotes the development of drug resistance. Immune checkpoints play critical roles in the immune system. Therefore, blocking tumor immune evasion by targeting the immune checkpoints has be-come a research focus in the treatment of relapsed or refractory malignant tumors. Currently, in the studies of malignant lymphomas, some phaseⅠ/Ⅱclinical studies of immune checkpoint inhibitors have achieved sur-prising results. This review will discuss the regulation and immunotherapy of immune checkpoints in malig-nant lymphomas.

Castleman disease (CD) is a rare polyclonal lymphoproliferative disorder characterized by enlarged hyperplastic lymph node(s). Unicentric Castleman disease (UCD) is an indolent condition often treated by local approaches. On the contrary, pa-tients with multicentric Castleman disease (MCD) have less favorable prognoses and require systemic treatments. Cytotoxic chemother-apy has been widely used to treat MCD with varying degrees of response because of the toxicity risk of the treatment. The pathogenesis remains unknown;however, most pieces of evidence to date point toward human herpes virus 8 (HHV-8) and deregulated overproduc-tion of interleukin (IL-6). Discovery of putative etiologic factors and targets in MCD, particularly HHV-8, CD20, and IL-6, has translat-ed to the use of rituximab, anti-IL-6-based, and antiviral therapy. Good results have been realized through targeting HHV-8 replication, CD20, and IL-6 pathways. In this article, we reviewed the classification, pathogenesis, and current treatments of CD and provided in-sights into future treatment strategies based on disease biology.

Objective To compare the efficacy and adverse reaction of teniposide (VM-26) plus carboplatin (TC regimen) and etoposide (VP-16) plus carboplatin (EC regimen) in treatment of newly diagnosed small cell lung cancer (SCLC), and the possible role of VM-26 on prevention of brain metastasis of SCLC. Methods A total of 102 previously untreated SCLC patients without brain metastasis were divided into VP-16 group received EC regimen (n=64) and VM-26 group received TC regimen(n=38). The carboplatin dosages in two groups were calculated by blood concentration-area under the curve(AUC)=5, and intravenous infusion of 1 h for the first day. In VM-26 group, VM-26 70 mg/m2+normal saline 500 mL was intravenously infused of 2 h for 1-3 days. VP-16 100 mg/m2+normal saline 500 mL was given to VP-16 group, 1 h for 1-3 days. Twenty-one day was for 1 treatment cycle. The curative effect, prognosis and adverse reaction were compared between two groups. Results The overall response rates (ORR) and disease control rates (DCR) were 78.9%(30/38) and 97.4%(37/38) in VM-26 group, respectively, and 76.6%(49/64) and 95.3%(61/64) in VP-16 group, respectively, with no significant differences between the two groups (χ2=0.078 and 0.283, P<0.05). The median progression-free survival (PFS) was 10 months (95%CI 7.4-12.6) in VM-26 group and 9 months (95%CI 6.4-11.6) in VP-16 group (χ2=0.029,P=0.866). The median overall survival (OS) was 18 months (95%CI 16.5-19.5) and 16 months (95%CI 9.9-22.1) in VM-26 group and VP-16 group (χ2=0.217,P=0.642), respectively. The survival rates for 1,2 and 3 years were 73.7%, 36.8%and 18.4%in VM-26 group, and 71.9%, 37.5%and 18.8%in VP-16 group, respectively, with no significant differences between the two groups (P>0.05). The brain metastasis rate was significantly higher in VP-16 group [43.8%(28/64)] than that of VP-26 group [21.1%(8/38),χ2=5.379,P=0.02). The adverse reactions were mainly grade 1/2 bone marrow suppression in two groups. Conclusion TC is a highly active regimen for treatment of SCLC. There is no difference in the ef?fectiveness and adverse reactions versus EC. Application of VM-26 can reduce the incidence of brain metastasis in SCLC patients.

Histone deacetylase inhibitors (HDACI) can improve the acetylation status of histone N-terminal, which will exert the effect on treatment. The N-terminal of histone modifications belongs to the category of epigenetics. Epigenetics mainly refers to the study of the heritable variation without change in DNA sequence. HDACI had been paid much attention as a new non-cytotoxic an-ti-cancer targeted drug. Thus, the application of this drug in clinical research is widespread. After the U.S. Food and Drug Administra-tion approved two HDACIs for the treatment of cutaneous T-cell lymphoma, the clinical applications of HDACI in other subtypes of T-cell lymphoma have obtained increasing attention. Studies on the mechanism of HDACI provide the theoretical basis for the applica-tion of HDACIs in other subtypes of T-cell lymphoma. In this article, we reviewed the mechanism and clinical trials of HDACIs on the treatment of T-cell lymphoma.

Clinical data of 13 patients with primary pulmonary lymphoma(PPL),treated in Tianjin Medical University Cancer Hospital from January 1999 to December 2009,were retrospectively reviewed.There were 8 patients with mucosa-associated lymphoid tissue(MALT)marginal zone lymphoma,2 patients with diffuse large B cell lymphoma,1 patient with NK/T cell lymphoma,1 patient with nodular sclerosis Hodgkin's lymphoma,and 1 patients with lymphocytic predominance Hodgkin's lymphoma.The main clinical symptoms were cough,fever,night sweat and weight loss.Two patients did not have any symptoms.Pulmonary consolidation shadows and multiple nodules were the main findings of CT scan.An air bronchogram was often seen in the consolidation imaging.The overall 5-year survival rate was 9/13 for all patients;while that was 7/8 for MALT marginal gone lymphoma.

Double-hit lymphoma (DHL) is a kind of disease with features intermediated between diffuse large B-cell lymphoma (DLBCL) and Burkitt lymphoma (BL),usually accompanied by myc gene breakpoint with other recurrent chromosomal breakpoint and mainly involving myc and bcl-2 translocation.The presentation of this disease is characterized by elevated serum lactate dehydrogenase levels,B symptoms,bone marrow involvement,advanced stage disease,extranodal involvement,and central nervous system involvement.Because its features are similar with DLBCL and BL,it's difficult to distinguish them by pathological diagnosis.At present,the differential diagnosis is mainly by chromosomal analysis (G-banding),FISH and immunohistochemistry.This subtype received a poor response to conventional chemotherapy for DLBCL,and has a poor prognosis.The median survival time is only 0.2-1.5 years.Currently,the main regimens include RCHOP,RICE,RCVD,methotrexate prophylaxis for central nervous system involvement,high-dose chemotherapy and bone marrow transplantation.

The incidence rate is high in Asia country, accounting for 15 %-20 % of Non-Hodgkin lymphoma. Every phynotype has different heterogeneity, therapeutic effect and prognosis are also different. There is no standard rigemen for T cell lymphoma at present. CHOP like regimen is commonly used. But therapeutic effect is not as good as we expected. Clinical research shows that dose and intensity regimen, such as m-BACOD,ProMACE-CytaBOM, MACOP-B, do not exhibit survival advantage compared with CHOP regimen. New treatment includes cytotoxic drug, such as gemcitabine. As first line therapy for T cell lymphoma or as salvage therapy for refractory or relapsed T cell lymphoma, the therapeutic effect is good. Gemcitabine based regimen is new for PTCL. Alemtuzumab is a humanized CD52 mono-clonal antibody and is expected as good effect on PTCL therapy. Zanolimumab is a humanized mono-clonal antibody which targets CD4 antigen on T cell. Phase Ⅱclinical research has also got good effect. Denileukin difiitox and Pralatrexate also have good effect on PTCL therapy in clinical researches. Autologous stem cell transplantation(ASCT) is also used in PTCL therapy.

Objective:This study aimed to investigate the inhibitory effect of zoledronic acid (ZOL) alone or the combined treat-ment of ZOL and paclitaxel (PTX) on the cell growth of lung cancer cell line in vitro. Methods:The effects of different concentrations of ZOL alone, 2 nM PTX, and combined treatment of ZOL and PTX on the growth of A-549 cell line were determined using methyl thi-azolyl tetrazolium (MTT) method. The mechanism of the curative effect was analyzed by flow cytometry on the basis of apoptotic rate. AKT, phospho-AKT, ERK, phospho-ERK, and Bcl-2 expressions were determined by western blot analysis. AKT and ERK gene ex-pressions were determined by RT-PCR. Results:MTT results showed that ZOL alone could inhibit the growth of lung cancer cell line A-549 in a dose-dependent manner. The combined therapy of ZOL and PTX could inhibit cell growth. This combined treatment is more effective than the single treatment with either ZOL or PTX alone. The synergistic inhibition rate is dependent on drug sequencing. Fur-thermore, maximum inhibition was induced by sequence order, i.e., initial treatment with PTX and then with ZOL. RT-PCR results dem-onstrated that the mRNA of ERK and AKT of the group treated with PTX and then ZOL were lower than that in other treatment groups. Western blot analysis results demonstrated that the ERK and AKT levels of the treated groups were parallel in the cell line. However, the lowest phospho-ERK, phospho-AKT, and Bcl-2 levels were observed in the PTX then ZOL group. The cell lines treated with PTX alone and ZOL alone ranked second and third among the lowest results, respectively. The highest level was observed in the control group. Conclusion: The combined ZOL and PTX treatment induced the downregulation of phospho-ERK, phospho-AKT, and Bcl-2 protein expressions in RAF/MEK/ERK and PI3K/AKT signaling pathway. This pathway could be one of the synergistic antitumor mechanisms of the two drugs.