Biomedical subjects

Qingjun Ma

Publications and source records attributed to Qingjun Ma.

24 records · Page 2Linked to original sources

PubMed2003

In-house measurement of the sulfur anomalous signal and its use for phasing.

Five test structures (orthorhombic and trigonal trypsin, cubic and rhombohedral insulin and thaumatin) have been solved by the SAD (single-wavelength anomalous diffraction) method using highly redundant data collected at 100 K with a CCD detector, rotating-anode generator and three-circle goniometer. The very weak anomalous scattering (primarily from sulfur) was sufficient to locate all the anomalous scatterers using the integrated direct and Patterson methods in SHELXD. These positions and occupancies were used without further refinement to estimate phases that were extended to native (in-house) resolution by the sphere of influence algorithm in SHELXE. The final map correlation coefficients relative to the anisotropically refined structures were in the range 0.81-0.97. The use of highly redundant medium-resolution laboratory data for sulfur-SAD phasing combined with high-resolution synchrotron native data for phase expansion and structure refinement clearly has considerable potential.

Algorithms↗

PubMed2003

Diagnosis of severe acute respiratory syndrome (SARS) by detection of SARS coronavirus nucleocapsid antibodies in an antigen-capturing enzyme-linked immunosorbent assay.

Recombinant severe acute respiratory syndrome (SARS) coronavirus nucleocapsid protein was employed to establish an antigen-capturing enzyme-linked immunosorbent assay (ELISA). Antinucleocapsid protein antibodies could be detected in 68.4% of probable SARS patients 6 to 10 days after illness and in 89.6% of the patients 11 to 61 days after illness. No false-positive results were observed in 20 non-SARS fever patients, 24 non-SARS respiratory illness patients, and 20 health care workers. Among 940 other non-SARS clinical serum samples, only 1 was found to be weakly positive. This method provides a new, sensitive, and specific approach for SARS diagnosis.

Antibodies, Viral↗

PubMed2003

[Simvastatin induces osteoblastic differentiation of bone marrow stromal cells].

OBJECTIVE: To observe the effect of simvastatin on osteoblastic cell differentiation of bone marrow stromal cells in vitro, and to elucidate the mechanisms of anabolic effect of simvastatin on bone formation. METHODS: Bone marrow stromal cells from femur and tibia of adult female BALB-C mice were cultured in vitro, after being treated with different concentrations of simvastatin for 72 h, changes of mRNA level of osteocalcin (OCN) were detected by RT-PCR, change of OCN, and osteopontin (OPN) expression were examined by Western blot, and the changes of cellular alkaline phosphatase activity (ALP) were examined by histochemistry and enzymologic measurement. RESULTS: After bone marrow stromal cells were treated with different concentration of simvastatin for 72 h, level of OCN mRNA increased, and expression of OCN and OPN also increased in a concentration-dependent manner, and cellular ALP activity significantly increased in a concentration-dependent manner. CONCLUSION: Simvastatin can stimulate osteoblastic differentiation, and improve cellular ALPase activity with high expression of osteocalcin and osteopontin in vitro. These may be parts of the mechanism of anabolic effect of simvastatin on bone formation.

Alkaline Phosphatase↗

PubMed2002

Synthesis and structures of [[HC(CMeNAr)(2)]Ge(S)X] (Ar = 2,6-iPr(2)C(6)H(3), X = F, Cl, Me): structurally characterized examples with a formal double bond between group 14 and 16 elements bearing a halide.

Treatment of [{HC(CMeNAr)2}GeX] (Ar = 2,6-iPr2C6H3, X = Cl (1), F (2)), with elemental sulfur at room temperature smoothly afforded the [{HC(CMeNAr)2}Ge(S)X] (X = Cl (3), F (4)). Compound 4 can also be obtained from 3 with the fluorination reagent Me3SnF. Reaction of 3 with MeLi led to the formation of [{HC(CMeNAr)2}Ge(S)Me] (5). Single-crystal X-ray structural analyses indicate compounds 3-5 are monomeric. The germanium centers adopt four coordinated sites and reside in distorted tetrahedral environment. Compounds 3 and 4 are structurally characterized examples with a formal double bond between group 14 and 16 elements bearing a halide.

Journal Article↗

PubMed2002

Expression of human VEGF(121) cDNA in mouse bone marrow stromal cells.

OBJECTIVE: To construct a retroviral vector carrying human vascular endothelial growth factor (hVEGF (121)) cDNA for evaluation of the possibility of VEGF gene therapy in ischemic bone disease. METHODS: hVEGF(121) cDNA was obtained from the plasmid pCDI/VEGF(121) and cloned into retroviral plasmid pLXSN. Recombinant plasmid was transferred to the retro virus packaging cell, PT-67, by lipofectamine mediated gene transfer. Mouse bone marrow stromal cells (MSCs) were transfected by the retrovirus. The integration of the hVEGF(121) cDNA into MSC genomic DNA and expression of the VEGF gene was detected. Proliferation assays of human umbilical vein endothelial cells (HUVECs) by VEGF(121) in culture medium were performed. RESULTS: Recombinant pLXSN/VEGF(121) was correctly constructed and confirmed by restriction endonuclease analysis and DNA sequencing analysis. hVEGF(121) gene was integrated into MSC genomic DNA after transfection, and the VEGF(121) protein was expressed. Proliferation assays showed VEGF(121) in culture medium was a biologically active protein and had a mitogenic effect on HUVEC. CONCLUSIONS: Recombinant retroviral vector carrying hVEGF(121) cDNA was successfully constructed. VEGF (121) protein expressed by MSCs had mitogenic effect biologically. This provides a further foundation for VEGF gene therapy for bone ischemic disease and bone tissue engineering.

Animals↗

PubMed2002

[Construction of adenoviral vector encoding human VEGF(121) cDNA and its expression in vitro].

OBJECTIVE: To construct the adenoviral vector bringing hVEGF(121) cDNA for evaluation of the possibility of VEGF gene therapy in ischemic bone disease. METHODS: Human vascular endothelial growth factor (hVEGF(121)) cDNA obtained from the plasmid pCDI/VEGF(121) was cloned into plasmid pshuttle and further cloned to Adeno-X Viral DNA. The recombinant adenoviral plasmid was identified and then transferred to the adenoviral packaging cell HEK293 by lipofectamine mediated gene transfer method to pack the virus. After titilating the virus, the mouse bone marrow stromal cells (MSC) were transfected by the adenovirus and the expression of VEGF gene was detected. RESULTS: The recombinant Adeno-VEGF(121) was correctly constructed and confirmed by restriction endonuclease analysis and DNA sequencing analysis. After MSCs were tranfected by the virus, RT-PCR showed that hVEGF(121) mRNA was transcripted from the hVEGF(121) gene. Western blot and immune histochemistry showed VEGF(121) protein was expressed in transgene MSCs. CONCLUSION: The recombinant adenoviral vector bringing hVEGF(121) cDNA was successfully constructed and the transgene MSC expressed hVEGF gene in vitro, it provided the further foundation of VEGF gene therapy for bone ischemic diseases.

Adenoviridae↗