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Thomas Wong

Publications and source records attributed to Thomas Wong.

4 recordsLinked to original sources
PubMed2003

Dipole-mode wakefields in dielectric-loaded rectangular waveguide accelerating structures.

By applying different symmetric boundary conditions, we found that the transverse wakefields generated by an electron bunch traveling through a partially loaded rectangular dielectric structure at an off center position can be decomposed into corresponding orthogonal longitudinal section electric (LSE) and longitudinal section magnetic (LSM) modes for guided waves as in the case of longitudinal wakefields treated previously. The wakefields are characterized using the normalized shunt impedance R/Q, a function of the geometry of the accelerating structure, for both LSE and LSM modes. A numerical example is given for an X-band waveguide structure and detailed results are given for the several leading transverse wakefield terms. The analytic results obtained are in agreement with the results from the time domain simulation tool MAFIA.

Journal Article↗
PubMed2003

Therapeutic implications for interferon-alpha in arthritis: a pilot study.

OBJECTIVE: To evaluate the therapeutic potential of interferon-a (IFN-a) in osteoarthritis (OA) and rheumatoid arthritis (RA) by examining regulation of cytokine antagonist expression. METHODS: Expression of interleukin 1 receptor antagonist (IL-1Ra) and soluble tumor necrosis factor receptor (sTNFR) was examined by ELISA in cells from freshly isolated synovial fluids (SF) and synovial tissues (ST) from patients with OA or RA, either left untreated or treated with IFN-a. Single (7) and paired (5) SF and ST cells from OA and RA patients were examined. As well, the ability of IFN-a to regulate gene expression levels for osteoprotegerin (OPG) and osteoprotegerin ligand (OPGL) was examined in freshly isolated SF cells from patients with RA, by reverse transcriptase polymerase chain reaction. RESULTS: IL-1Ra and sTNFR were found to be constitutively expressed in OA and RA SF and ST cells. IFN-a treatment resulted in an increase in both IL 1Ra and sTNFR production. Freshly isolated RA SF cells exhibited constitutive OPGL gene expression in both the non-T and T cell fractions of the SF. In contrast, OPG gene expression levels were undetectable or low. IFN-a treatment of RA SF cells resulted in upregulation of OPG gene expression in the T cell fraction of the RA SF cells, whereas OPGL gene expression remained unaffected. CONCLUSION: These in vitro data suggest a therapeutic role for IFN-a in the treatment of arthritis through upregulation of critical cytokine antagonists.

Adult↗
PubMed2002

Effects of bile acids on dog pancreatic duct epithelial cell secretion and monolayer resistance.

Pancreatic duct epithelial cells (PDEC) mediate the secretion of fluid and electrolytes and are exposed to refluxed bile. In nontransformed cultured dog PDEC, which express many ion transport pathways of PDEC, 1 mM taurodeoxycholic acid (TDCA) stimulated an (125)I(-) efflux inhibited by DIDS and 5-nitro-2-(3-phenylpropylamino)benzoic acid (NPPB) and a (86)Rb(+) efflux inhibited by charybdotoxin. Inhibition by 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid (BAPTA)-AM suggests mediation via increased intracellular Ca(2+) concentration, whereas the absence of lactate dehydrogenase release excludes cellular toxicity. At 1 mM, TDCA stimulated a larger (125)I(-) efflux than glycodeoxycholate; two dihydroxy bile acids, taurochenodeoxycholate and TDCA, were similarly effective, whereas a trihydroxy bile acid, taurocholate, was ineffective. In Ussing chambers, 1 mM serosal or 2 mM luminal TDCA stimulated an I(sc) increase from confluent PDEC monolayers. TDCA also stimulated 1) a short-circuit current (I(sc)) increase from basolaterally permeabilized PDEC subject to a serosal-to-luminal Cl(-) gradient that was inhibited by BAPTA-AM, DIDS, and NPPB and 2) an I(sc) increase from apically permeabilized PDEC subject to a luminal-to-serosal K(+) gradient inhibited by BAPTA-AM and charybdotoxin. Along with the efflux studies, these findings suggest that TDCA interacts directly with PDEC to stimulate Ca(2+)-activated apical Cl(-) channels and basolateral K(+) channels. Monolayer transepithelial resistance was only minimally affected by 1 mM serosal and 2 mM luminal TDCA but decreased after exposure to higher TDCA concentrations (2 mM serosal and 4 mM luminal). A secretory role for bile acids should be considered in pancreatic diseases associated with bile reflux.

Animals↗