Interleukin (IL) 1,IL 6,plasminogen activator inhibitors 1(PAI 1),tumor necrosis factor(TNF),endothelin, silectin E, tissue factor(TF) and platelet activating factor(PAF)etc. participated in pathological processes of disseminated intravascular coagulation(DIC).Diagnosis of DIC should possess:①procoagulant system activation,②fibrinolytic system activation,③inhibitor consumption,④cytokine release,⑤cellular activation, and ⑥resultant end organ damage. For an objective diagnosis of DIC,①,②,③,⑥must be present and documented by appropriate laboratory parameters. To remove the triggering process or the underlying disease during the treatment of DIC was fundamental. Anticoagulation therapy and component therapy were the foundation stone. The inhibitor of proteinase, thrombin, factor ?a,and drugs of enhancing anticoagulation or (and) fibrinolytic, ie, platelet activating factor (PAF),activating protein C (APC),recombinant thrombomodulin (rTM) etc. are effective drugs in studying and developing.

The spectrum of renal lesions that was seen in patients with myeloma include myeloma kidney, or cast nephropathy; light chain (AL) amyloidosis; monoclonal Ig deposition disease(MIDD); and less frequently, cryoglobulinemic glomerulonephritis and proliferative glomerulonephritis.ln native renal biopsy studies of patients with myeloma and renal disease, 40 % to 63 % had east nephropathy, 19 % to 26 % had light-chain deposition disease, 7 % to 30 % had amyioidosis, and 1% had eryoglobulinemie renal disease. The renal pathology of cast nephropathy, MIDD, and amyloidosis was diverse.Extrarenal manifestations of MIDD, as with amyloidosis, were frequent, the incidence of renal insufficiency and ESRD was high.The morbidity and mortality were a significant increase.Patient and renal survival were significantly worse in patients with coexisting nephropathy.Therapy of renal lesions with myeloma was similar to that for multiple myeloma and consisted of chemotherapy alone,and treated renal insufficiency with hemodialysis and peritoneal dialysis, and used of high-dosage chemotherapy followed by ASCT to reduced the level of light-chain production.

Refractory central nervous system (CNS) lymphoma in patients with non-Hodgkin lymphoma (NHL) carries a poor prognosis, with a median survival of 2-6 months. CNS involvement in NHL is associated with young age, advanced stage, number of extranodal sites, elevated lactate dehydrogenase, and international prognostic index (IPI) score. The most promising treatment of autologous stem cell transplant can extend median survival from 10 to 26 months. CNS prophylaxis is required during the initial treatment of NHL subtypes that carry a high risk of CNS relapse, such as Burkitt lymphoma (BL), and lymphoblastic lymphoma.The use of CNS prophylaxis in the treatment of diffuse large B-cell lymphoma is controversial because of the low risk of CNS relapse (≈5 %) in this population. The risk models that aim to identify predictors of CNS relapse in NHL.

Since its discovery as the first human tumor associated virus, Epstein-Barr virus (EBV) has been implicated in the development of a wide range of B-cell lymphoproliferative disorders, including Burkitt' slymphoma, classic Hodgkin' s lymphoma and lymphomas arising in immunocompromised individuals (posttransplant and HIV-associated lymphoproliferative disorders). T-cell lymphoproliferative disorders that have been reported to be EBV associated include a subset of peripheral T-cell lymphomas, angioimmunoblastic T-cell lymphoma, extranodal nasal type natural killer/T-cell lymphoma, and other rare histotypes. EBV encodes a series of products interacting with or exhibiting homology to wide variety of antiapoptotic molecules,cytokines, and signal transducers, hence promoting EBV infection, immortalization and transformation.However, the exact mechanism by which EBV promotes oncogenesis is still an area of active debate. This review is focused on the pathology, diagnosis, classification, and pathogenesis of EBV-associated lymphomas.Recent advances in EBV cell-based immunotherapy, which is beginning to show promise in the treatment of EBV-related disorders, are discussed.

Involvement of the central nervous system(CNS)in multiple myeloma(MM)is very uncommon.and it has been observed in approximately 1% of the MM patients.This review summarizes the clinical and laboratory characteristics and treatment modalities of 109 patients with CNS myelomatosis(CNS MM)reported in the literatures.CNS MM has a wide spectrum of neurological symptoms and signs.No guidelines for therapy of CNS MM are available,which has resulted in a large variation in the treatment schedules.Treatment options include intrathecal chemotherapy(IT),systemic chemotherapy(SC),cranial irradiation(CI)or a combination.The prognosis of CNS MM remains poor,with an overall median survival from the time of diagnosis to death of 2.0 months(range 0.1-25 months).Patients who were treated with CI had a significantly(P=0.004)longer survival time when compared with patients without CI.

Mantle cell lymphoma is included in the World Health Organization classification as distinct lymphoma subtype characterized by the t(11;14)(q13;q32) translocation,which results in overexpression of Cyclin D1.The clinical presentation often includes extranodal involvement,particularly of the bone marrow and gut.The prognosis of patients with mantle cell lymphoma (median overall survival,3-5 years) is poorest among B-cell lymphoma patients,even though a prospectively difficult to identify subgroup can survive for vears with little or no treatment. Conventional chemotherapy is not curative but obtains frequent remissions (60%-90%) which are usually shorter (1-2 years) compared with other lymphoma entities.Very intensive regimens,including autologous and allogeneic stem cell transplantation,seem required to improve the outcome,but with the median age of diagnosis being 60 years or more,such approaches are feasible only in a limited proportion of patients.The possibility of treating patients based on prognostic factors needs to be investigated prospectively.

Objective:To explore the mode,methods,and attentive problems of bilingual teaching of Burn Surgery for Seven-year medical program students.Methods:The bilingual teaching project of Burn Surgery was considered comprehensively from various angles,such as the teaching mode,methodology,teacher training,teaching material selection and teaching management in specialized course.Conclusion:It is very necessary to develop bilingual education for Seven-year program students.The course of bilingual teaching should be student-oriented to improve their integrated ability of English and to assure mastery of professional theory and knowledge.

Recenly,the incidence of posttransplatation lymphoproliferative disorder(PTLD) is rising,Immunodeficiency and EBV-infection are risk factors of pathogenesis related. The majority of PTLD originates from malignant proliferation of B-cell.Typical pathologic findings of PTLD are large number of plasmacytoid B cells in lymphotic tissue and often with necrosis in regional areas. Molecular biology findings are ras or p53 gene mutation and c-myc?bcl-6 gene rearrangement. Highly immunosuppressed patients may present with diffuse infiltration and functional failure of multiple organs,the prognosis is poor. Except for the decrease or discontinuation of the immunosuppressive therapy,antiviral agents and interferon- ?,anti B-cell monoclonal antibodies,autologous EBV-specific cytotoxic T cell and combination chemotherapy may achieve better responses.

In the 46th annual meeting of the American Society of Hematology, the advance in the treatment of maligmant hematological disease concentrats on targeted therapies, including oblimersen,combination therapy rituximab with the chemotherapeutic agent, proteasome inhibitor bortezomid, flavorpiridol and radioimmunotherapy. Hematopoietic cell transplantation (HCT) is an effective therapy of maligmant hematological disease. The foremost advantage of the nonmyeloablative or reduced-intensity HCT is the reduction of treatment-related mortality .

Acetylation of lysine residues of core histone N-terminal domains has been found correlatively associated with transcriptional activation in eukaryotes. Recent studies showed that some transcriptional regulators with histone acetyltransferase(HAT) and deacetylase(HDAC) activities may play a causative role in regulating gene expression. The link between tumorigenic processes and misregulated or mistargeted HAT and HDAC activities has been reported.