Inflammatory bowel disease (IBD) includes two similar yet distinct conditions called ulcerative colitis (UC) and Crohn's disease (CD). These diseases affect the digestive system and cause the inflammation of in...Inflammatory bowel disease (IBD) includes two similar yet distinct conditions called ulcerative colitis (UC) and Crohn's disease (CD). These diseases affect the digestive system and cause the inflammation of intestinal tissue, form sores and bleed easily. Most children with IBD are diagnosed in late childhood and adolescence. However, both UC and CD have been reported as early as in infancy. Most information pertaining to the epidemiology of IBD is based upon adult studies. Symptoms include abdominal pain, cramping, fatigue and diarrhea. Genetic factors play a significant role in determining IBD susceptibility. Epidemiological data support a genetic contribution to the pathogenesis of IBD. Recently, numerous new genes have been identified as being involved in the genetic susceptibility to IBD: TNF- 308A, CARD15 (NOD2), MIF-173, N-acetyltransferase 2 (NAT2), NKG2D (natural killer cell 2D), STAT6 (signal transducer and activator of transcription 6), CTLA-4 (cytotoxic T lymphocyte antigen-4), MICA-MICB (major histocompatibility complex A and B), HLA-DRB1, HLA class-Ⅱ, IL-18, IL-4, MICA-A5, CD14, TI R4, Fas-670, p53 and NF-kB. The characterization of these novel genes has the potential to identify therapeutic agents and aid clinical assessment of phenotype and prognosis in patients with IBD (UC and CD).展开更多
Objective: The aim of our study was to analyze the long-term results of rituximab combined with temozolomide in treatment of elderly patients (> 60 years) with relapsed primary central nervous system lymphoma (PCNS...Objective: The aim of our study was to analyze the long-term results of rituximab combined with temozolomide in treatment of elderly patients (> 60 years) with relapsed primary central nervous system lymphoma (PCNSL). Methods: Twelve postoperative elderly patients (> 60 years) were treated between August 2004 and October 2009. Temozolomide 100 mg/m2 to 200 mg/m2 days 1 to 7 and 15 to 21 and rituximab 375 mg/m2 days 1, 5, 8, 22. The maximum number of rituximab cycles was two. After one or two cycles of this combination, patients with an objective response and an acceptable level of toxicity continued treatment with single agent temozolomide (days 1 to 5, every 28 days). The overall survival was analyzed by using Kaplan-Meier. Results: The overall survival was 9 months. Toxicity was very mild with no grade 3-4 neurotoxicity toxic events. Conclusion: Rituximab combined with temozolomide seems to yields substantial long-term survival with moderate toxicity for the treatment of elderly relapsed PCNSL.展开更多
Objective: Detecting the expression and mutation of human telomeric repeat binding factor (hTRF1) in 10 malignant hematopoietic cell line cells on the base of determining its genomic structure and its four pseudoge...Objective: Detecting the expression and mutation of human telomeric repeat binding factor (hTRF1) in 10 malignant hematopoietic cell line cells on the base of determining its genomic structure and its four pseudogenes to clarify ifhTRF1 mutation is one of the factors of the activation of telomerase. Methods: hTRFlcDNA sequences were obtained from GenBank, its genome structure and pseudogenes were forecasted by BLAST and other biology information programs and then testified by sequencing. Real-time RT-PCR was used to detect the expression of h TRFlmRNA in 10 cell line cells, including myelogenous leukemia cell lines K562, HL-60, U-937, NB4, THP-I, HEL and Dami; lymphoblastic leukemia cell lines 6T-CEM, Jurkat and Raji. Telomerase activities of cells were detected by using telomeric repeat amplification (TRAP)-ELISA protocol. PCR and sequencing were used to detect mutation of each exon ofhTRF1 in 10 cell line cells. Results: hTRF1 gene, mapped to 8q13, was divided into 10 exons and spans 38.6 kb. Four processed pseudogenes ofhTRF1 located on chromosome 13, 18, 21 and X respectively, was named as ψhTRFI-13, ψhTRFI-18, ψhTRF1-21 and ψhTRFI-X respectively. All cell line cells showed positive telomerase activity. The expression of hTRF1 was significantly lower in malignant hematopoietic cell lines cells (0.0338, 0.0108-0.0749) than in normal mononuclear cells (0.0493, 0.0369-0.128) (P=0.004). But no significant mutation was found in all exons of hTRF1 in 10 cell line cells. Four variants were found in part ofintron 1, 2 and 8 ofhTRF1. Their infection on gene function is unknown and needs further studies. Conclusion: hTRF1 mutation is probably not one of the main factors for telomerase activation in malignant hematopoietic disease.展开更多
Nano-ZrO2 particles were modified by poly(ethylene terephalate) prepolymer(pre-PET) via polycondensation.FT-IR,TEM,and TGA results showed that pre-PET was successfully grafted on the surface of nano-ZrO2particles.Comp...Nano-ZrO2 particles were modified by poly(ethylene terephalate) prepolymer(pre-PET) via polycondensation.FT-IR,TEM,and TGA results showed that pre-PET was successfully grafted on the surface of nano-ZrO2particles.Compared to the original nano-ZrO2,the grafted nano-ZrO2 had better compatibility with the polycarbonate(PC) matrix and could be dispersed more homogeneously in PC.Hence,interfacial adhesion between ZrO2 and PC was enhanced.The mechanical properties of the resultant PC/nano-ZrO2 composite like tensile strength and notched impact strength were greatly improved.Calculated respectively from tensile yield stress PC/nano-ZrO2 composites,the interfacial interaction parameter B was employed to quantitatively characterize the effective interfacial interaction between the nano-ZrO2 and PC matrix.展开更多
基金Supported by The Science Foundation of Health Bureau of Shaanxi Province,China,No.04D26
文摘Inflammatory bowel disease (IBD) includes two similar yet distinct conditions called ulcerative colitis (UC) and Crohn's disease (CD). These diseases affect the digestive system and cause the inflammation of intestinal tissue, form sores and bleed easily. Most children with IBD are diagnosed in late childhood and adolescence. However, both UC and CD have been reported as early as in infancy. Most information pertaining to the epidemiology of IBD is based upon adult studies. Symptoms include abdominal pain, cramping, fatigue and diarrhea. Genetic factors play a significant role in determining IBD susceptibility. Epidemiological data support a genetic contribution to the pathogenesis of IBD. Recently, numerous new genes have been identified as being involved in the genetic susceptibility to IBD: TNF- 308A, CARD15 (NOD2), MIF-173, N-acetyltransferase 2 (NAT2), NKG2D (natural killer cell 2D), STAT6 (signal transducer and activator of transcription 6), CTLA-4 (cytotoxic T lymphocyte antigen-4), MICA-MICB (major histocompatibility complex A and B), HLA-DRB1, HLA class-Ⅱ, IL-18, IL-4, MICA-A5, CD14, TI R4, Fas-670, p53 and NF-kB. The characterization of these novel genes has the potential to identify therapeutic agents and aid clinical assessment of phenotype and prognosis in patients with IBD (UC and CD).
文摘Objective: The aim of our study was to analyze the long-term results of rituximab combined with temozolomide in treatment of elderly patients (> 60 years) with relapsed primary central nervous system lymphoma (PCNSL). Methods: Twelve postoperative elderly patients (> 60 years) were treated between August 2004 and October 2009. Temozolomide 100 mg/m2 to 200 mg/m2 days 1 to 7 and 15 to 21 and rituximab 375 mg/m2 days 1, 5, 8, 22. The maximum number of rituximab cycles was two. After one or two cycles of this combination, patients with an objective response and an acceptable level of toxicity continued treatment with single agent temozolomide (days 1 to 5, every 28 days). The overall survival was analyzed by using Kaplan-Meier. Results: The overall survival was 9 months. Toxicity was very mild with no grade 3-4 neurotoxicity toxic events. Conclusion: Rituximab combined with temozolomide seems to yields substantial long-term survival with moderate toxicity for the treatment of elderly relapsed PCNSL.
文摘Objective: Detecting the expression and mutation of human telomeric repeat binding factor (hTRF1) in 10 malignant hematopoietic cell line cells on the base of determining its genomic structure and its four pseudogenes to clarify ifhTRF1 mutation is one of the factors of the activation of telomerase. Methods: hTRFlcDNA sequences were obtained from GenBank, its genome structure and pseudogenes were forecasted by BLAST and other biology information programs and then testified by sequencing. Real-time RT-PCR was used to detect the expression of h TRFlmRNA in 10 cell line cells, including myelogenous leukemia cell lines K562, HL-60, U-937, NB4, THP-I, HEL and Dami; lymphoblastic leukemia cell lines 6T-CEM, Jurkat and Raji. Telomerase activities of cells were detected by using telomeric repeat amplification (TRAP)-ELISA protocol. PCR and sequencing were used to detect mutation of each exon ofhTRF1 in 10 cell line cells. Results: hTRF1 gene, mapped to 8q13, was divided into 10 exons and spans 38.6 kb. Four processed pseudogenes ofhTRF1 located on chromosome 13, 18, 21 and X respectively, was named as ψhTRFI-13, ψhTRFI-18, ψhTRF1-21 and ψhTRFI-X respectively. All cell line cells showed positive telomerase activity. The expression of hTRF1 was significantly lower in malignant hematopoietic cell lines cells (0.0338, 0.0108-0.0749) than in normal mononuclear cells (0.0493, 0.0369-0.128) (P=0.004). But no significant mutation was found in all exons of hTRF1 in 10 cell line cells. Four variants were found in part ofintron 1, 2 and 8 ofhTRF1. Their infection on gene function is unknown and needs further studies. Conclusion: hTRF1 mutation is probably not one of the main factors for telomerase activation in malignant hematopoietic disease.
基金Innovative Team Project of Science and Technology Commission of Shanghai, China(No.06DZ05902)
文摘Nano-ZrO2 particles were modified by poly(ethylene terephalate) prepolymer(pre-PET) via polycondensation.FT-IR,TEM,and TGA results showed that pre-PET was successfully grafted on the surface of nano-ZrO2particles.Compared to the original nano-ZrO2,the grafted nano-ZrO2 had better compatibility with the polycarbonate(PC) matrix and could be dispersed more homogeneously in PC.Hence,interfacial adhesion between ZrO2 and PC was enhanced.The mechanical properties of the resultant PC/nano-ZrO2 composite like tensile strength and notched impact strength were greatly improved.Calculated respectively from tensile yield stress PC/nano-ZrO2 composites,the interfacial interaction parameter B was employed to quantitatively characterize the effective interfacial interaction between the nano-ZrO2 and PC matrix.