Humans ; Myelodysplastic Syndromes ; diagnosis ; Prognosis

Humans ; Lymphoma, Large-Cell, Anaplastic ; diagnosis ; enzymology ; therapy ; Receptor Protein-Tyrosine Kinases

Adolescent ; Adult ; Child ; Child, Preschool ; Female ; Graft vs Host Disease ; prevention & control ; Hematopoietic Stem Cell Transplantation ; methods ; Humans ; Male ; Middle Aged ; Nutritional Status ; Nutritional Support ; Young Adult

Humans ; Lymphoma, Large B-Cell, Diffuse ; Societies, Medical ; United States

Adolescent ; Adult ; Aged ; Antineoplastic Combined Chemotherapy Protocols ; therapeutic use ; Child ; Cyclophosphamide ; therapeutic use ; Dexamethasone ; therapeutic use ; Disease-Free Survival ; Doxorubicin ; therapeutic use ; Female ; Follow-Up Studies ; Hematopoietic Stem Cell Transplantation ; Humans ; L-Lactate Dehydrogenase ; blood ; Lymphoma, T-Cell ; blood ; drug therapy ; therapy ; Male ; Middle Aged ; Neoplasm Recurrence, Local ; Remission Induction ; Retrospective Studies ; Survival Rate ; Transplantation, Autologous ; Vincristine ; therapeutic use ; Young Adult

Aclarubicin ; Adolescent ; Adult ; Antineoplastic Combined Chemotherapy Protocols ; Child ; Cytarabine ; Female ; Granulocyte Colony-Stimulating Factor ; Humans ; Male ; Middle Aged ; Precursor Cell Lymphoblastic Leukemia-Lymphoma ; therapy ; Young Adult

Graft vs Host Disease ; metabolism ; surgery ; Graft vs Tumor Effect ; HLA Antigens ; genetics ; Hematopoietic Stem Cell Transplantation ; Humans ; Receptors, KIR ; genetics ; metabolism

Adult ; Female ; Hematopoietic Stem Cell Transplantation ; Humans ; Lymphoma, Extranodal NK-T-Cell ; surgery ; Male ; Middle Aged ; Retrospective Studies ; Young Adult

Objective To summarize the diagnostic and therapeutic experience of a patient with chronic graft versus host disease (cGVHD) related polymyositis (PM) after allogeneic hematopoietic stem cell transplantation (allo-HSCT).Methods A patient with acute lymphocytic leukemia in com- plete remission received sibling allo-HSCT,and cyclosporine and methotrexate were adopted to pre- vent GVHD.Results Eleven days after HSCT,WBC＞0.5?10~9/L,13 days after HSCT,PLT＞20?10~9/L;27 days after HSCT,chromosome analysis of bone marrow cells showed 99% donor type. Seventeen days after HSCT,Ⅰ~0 acute GVHD of skin occurred,and it was cured by intravenous injec- tion of dexamethasone and methotrexate.Eight months after HSCT,cGVHD of liver happened.Al- though treated by tacrolimus and azathioprine,enzymes of liver were still elevated.At last,tacrolimus combined with sirolimus were used,and enzymes of liver subsided gradually.However,the serum creatine phosphokinase (CK) began to rise from 9 U/L to 3010 U/L,and fatigue all over the patient occurred.Finally,the symptom relapsed,and disability involved with the origin of limbs appeared. The electromyogram and magnetic resonance imaging of concerned muscles confirmed the PM diagno- sis.Although treated with methylprednisolone and plasma exchange,the patient died due to asphyxia, while the CK as high as 21 010 U/L.Conclusion PM is a rare kind of manifestations of cGVHD. When the key muscle tissue was involved,the prognosis is poor.

Objective:To investigate the molecular interaction between non-structural protein 3 serine protease of hepatitis C virus(HCV)and wild type P53,and to lay the basis for elucidating the mechanism of oncogenesis of hepatocellular carcinoma(HCC)after infection of HCV.Methods:The recombinant plasmids,pGAD424-NS3,pGAD424-NS315aa- and pGAD424-NS330aa-,were constructed and the interaction between NS3 serine protease and its cofactor NS4A,the interaction between wild type P53 and NS3 serine protease and its N-truncated mutants were dectected qualitatively and quantitatively in yeast two-hybrid system.Results:The results indicated that interaction existed not only between full-length NS3 serine protease and P53,but also between N-truncated mutants of NS3 serine protease and P53.Furthermore,the difference between enzyme activity unit(IU)of β-gal induced by these interactions was not significant(P>0.05).Conclusions:NS3 serine protease of hepatitis C virus and its N-truncated mutants can interact with wild type P53,and the region of NS3 serine protease involved in the interaction may be located in its C-terminal,but not in its N-terminal.