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Biomedical subjects

C L Zheng

Publications and source records attributed to C L Zheng.

5 recordsLinked to original sources
PubMed2004

A database designed to computationally aid an experimental approach to alternative splicing.

A unique microarray approach has been developed to profile alternative splicing in the cell. To support the development of this approach, we have developed the Manually Annotated Alternatively Spliced Events (MAASE) database system, which is a unique alternative splicing information resource designed specifically with experimentalists in mind. MAASE is an online resource for the convenient access, identification, and annotation of alternative splicing events (ASEs). MAASE consists of two components: an annotation system and a curated database. The annotation system is a web-based workspace that combines manual and computational approaches to identifying and annotating ASEs, a combination that is vital if a comprehensive collection is to be obtained. The annotation system is publicly available and provides a scalable solution to acquiring as well as contributing to annotated ASEs. MAASE annotated ASEs are deposited into the database component, which can either be queried one entry at a time or multiple entries at a time with convenient access to alternatively spliced junctional and surrounding sequences to facilitate the design of microarray experiments.

Alternative Splicing↗
PubMed2001

Balance of Th1/Th2 cytokines associated with the preventive effect of incomplete Freund's adjuvant on the development of adjuvant arthritis in LEW rats.

Complete Freund's adjuvant (CFA) could induce adjuvant arthritis (AA) in LEW rats and incomplete Freund's adjuvant (IFA) could induce oil induced arthritis (OIA) in DA but not in LEW rats. Lymph node cells (LNCs) from these AA and OIA rats showed increased mRNA expression of IFN-gamma, IL-2 and TNF-alpha but not IL-4. LNCs from IFA immunized LEW rats showed increased expression of IL-4, reduced expression of IFN-gamma and TNF-alpha and no IL-2, in contrast to IFA immunized DA rats. The pretreatment of IFA before CFA challenge could completely prevent AA in LEW rats and their LNCs showed increased expression of IL-4 and IFN-gamma but not IL-2 and TNF-alpha. In F1 (LEW x DA) rats, IFA could not induce OIA but the pretreatment of IFA before CFA challenge could induce very mild AA with 80% incidence, LNCs showing an elevated expression of all the above cytokines. These findings suggest that increased Th1 cytokine expression is associated with disease development and that increased IL-4 expression or the balance of Th2 over Th1 cytokine expression plays an important regulatory role in disease development.

Animals↗
PubMed2000

Dimethyl dioctadecyl ammonium bromide (DDA)-induced arthritis in rats: a model of experimental arthritis.

A single intradermal injection of 2 mg of dimethyl dioctadecyl ammonium bromide (DDA) in phosphate buffered saline (PBS) could induce polyarthritis in both LEW and DA rats with low incidence and severity whereas 2 mg of DDA in incomplete Freund's adjuvant (IFA) could induce very severe polyarthritis with 100% incidence in LEW rats. Histology of DDA-induced arthritis (DIA) revealed cellular infiltration, synovial hypertrophy, development of granulation tissue, destruction of cartilage and bone deformation in the articular joints. Lymph node cells (LNCs) but not immunoglobulin fractions from the DIA rats successfully transferred the severe disease into the naive recipients. A challenge injection of DDA in IFA in the rats, which had recovered from the DIA, could reactivate the disease. It is thus concluded that DDA has arthritis-inducing ability in the rats which is potentiated by IFA and the DIA is a cell-mediated immune disease which might be a model of experimental arthritis.

Adjuvants, Immunologic↗
PubMed1999

The preventive effects of incomplete Freund's adjuvant and other vehicles on the development of adjuvant-induced arthritis in Lewis rats.

The present study showed a novel finding that the development of adjuvant-induced arthritis (AA) in Lewis rats was completely prevented by incomplete Freund's adjuvant (IFA) injected 21 or 28 days before complete Freund's adjuvant (CFA) challenge. Hexadecane also completely prevented AA and squalane, methyl oleate and pristane moderately prevented AA, though pristane by itself induced mild arthritis in two out of five rats. Concanavalin A-stimulated lymph node cells (LNCs) isolated from AA rats were able to adoptively transfer the severe polyarthritis to all the naive recipients or even to the IFA pretreated recipients with earlier onset and more rapid progression than those of AA. The LNCs from the donors who had been pretreated with IFA and subsequently challenged with CFA could induce mild arthritis in only two out of eight naive recipients, whereas all the recipients who were challenged with CFA immediately after intravenous injection of these LNCs developed significantly less severe arthritis. However, the LNCs from IFA-pretreated donors failed to prevent AA. According to the T helper type 1 (Th1)/Th2 paradigm, it was suggested that the adjuvant-active vehicles such as IFA, hexadecane, squalane, methyl oleate and pristane, can affect and deviate the Th1/Th2 balance of immune responses in host. CFA could promote the propagation of Th2 cells rather than Th1 cells in these vehicle-pretreated rats through as yet undetermined mechanisms, eventually resulting in the prevention of AA. Finally, we discussed a regulatory role of adjuvant vehicles for induction and suppression of AA.

Adoptive Transfer↗