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Articles by B Ma
Total Records ( 2 ) for B Ma
  A. C Luke , C Stehling , R Stahl , X Li , T Kay , S Takamoto , B Ma , S Majumdar and T. Link

Background: There is continuing controversy whether long-distance running results in irreversible articular cartilage damage. New quantitative magnetic resonance imaging (MRI) techniques used at 3.0 T have been developed including T1rho (T1) and T2 relaxation time measurements that detect early cartilage proteoglycan and collagen breakdown.

Hypothesis: Marathon runners will demonstrate T1 and T2 changes in articular cartilage on MRI after a marathon, which are not seen in nonrunners. These changes are reversible.

Study Design: Cohort study; Level of evidence, 2.

Methods: Ten asymptomatic marathon runners had 3-T knee MRI scans 2 weeks before, within 48 hours after, and 10 to 12 weeks after running a marathon. The T1 and T2 MRI sequences in runners were compared with those of 10 age- and gender-matched controls who had MRI performed at baseline and 10 to 12 weeks.

Results: Runners did not demonstrate any gross morphologic MRI changes after running a marathon. Postmarathon studies, however, revealed significantly higher T2 and T1 values in all articular cartilage areas of the knee (P < .01) except the lateral compartment. The T2 values recovered to baseline except in the medial femoral condyle after 3 months. Average T1 values increased after the marathon from 37.0 to 38.9 (P < .001) and remained increased at 3 months.

Conclusion: Runners showed elevated T1 and T2 values after a marathon, suggesting biochemical changes in articular cartilage, T1 values remain elevated after 3 months of reduced activity. The patellofemoral joint and medial compartment of the knee show the highest signal changes, suggesting they are at higher risk for degeneration.

  A Tanne , B Ma , F Boudou , L Tailleux , H Botella , E Badell , F Levillain , M. E Taylor , K Drickamer , J Nigou , K. M Dobos , G Puzo , D Vestweber , M. K Wild , M Marcinko , P Sobieszczuk , L Stewart , D Lebus , B Gicquel and O. Neyrolles

The C-type lectin dendritic cell–specific intercellular adhesion molecule-3 grabbing nonintegrin (DC-SIGN) mediates the innate immune recognition of microbial carbohydrates. We investigated the function of this molecule in the host response to pathogens in vivo, by generating mouse lines lacking the DC-SIGN homologues SIGNR1, SIGNR3, and SIGNR5. Resistance to Mycobacterium tuberculosis was impaired only in SIGNR3-deficient animals. SIGNR3 was expressed in lung phagocytes during infection, and interacted with M. tuberculosis bacilli and mycobacterial surface glycoconjugates to induce secretion of critical host defense inflammatory cytokines, including tumor necrosis factor (TNF). SIGNR3 signaling was dependent on an intracellular tyrosine-based motif and the tyrosine kinase Syk. Thus, the mouse DC-SIGN homologue SIGNR3 makes a unique contribution to protection of the host against a pulmonary bacterial pathogen.

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