Biomedical subjects

Lihui Qin

Publications and source records attributed to Lihui Qin.

4 recordsLinked to original sources

PubMed2005

Pathology of the NovaSure (radio-frequency) impedance-controlled endometrial ablation system.

The widespread use of increasingly novel diagnostic and neoadjuvant therapeutic modalities necessitates that contemporary pathologists familiarize themselves with the spectrum of tissue derangements that may be seen in the eventual surgical specimens. In the management of endometrial lesions, for example, a variety of endometrial ablation technologies, such as cryosurgery, balloon therapy, microwave, hot circulating saline, and bipolar impedance technology, have been introduced in the past decade and are being utilized with increasing frequency. We describe herein pathologic changes associated with one such technology, the NovaSure impedance-controlled endometrial ablation system. The US Food and Drug Administration approved NovaSure in 2001 for ablation of the endometrial lining in premenopausal women with menorrhagia. The ablation is accomplished by the delivery of radio-frequency energy for a period of approximately 90 seconds through a device inserted transcervically into the endometrial cavity. Our patient, a 54-year-old with menorrhagia, had undergone the NovaSure ablative treatment 38 days prior to her eventual hysterectomy. The resultant changes were quite distinctive: in a uterine wall that was 20 to 30 mm thick, a 3- to 6-mm-thick, hyalinized, subendometrial bandlike zone was apparent throughout the uterus even on macroscopic examination of the slides. This zone was sharply demarcated from the subjacent myometrium and from the endometrium; the latter displayed severe stromal fibrosis, some myxoid change, and sparse glands that were largely confined to the basalis. Paradoxically, scattered aggregates of stromal cells in the endometrium remained relatively viable. Adenomyotic aggregates and leiomyomata in the myometrium beneath the hyalinized zone were unaffected by this treatment. Practitioners evaluating hysterectomy specimens should be aware of changes such as those described herein, not only to better understand the specimens they evaluate but to avoid potentially misinterpreting grotesque alterations caused by benign processes.

Catheter Ablation↗

PubMed2003

Suppressor of cytokine signaling 1 inhibits IL-10-mediated immune responses.

IL-10 has proved to be a key cytokine in regulating inflammatory responses by controlling the production and function of various other cytokines. The suppressor of cytokine signaling (SOCS) gene products are a family of cytoplasmic molecules that are essential mediators for negatively regulating cytokine signaling. It has been previously shown that IL-10 induced SOCS3 expression and that forced constitutive expression of SOCS3 inhibits IL-10/STAT3 activation and LPS-induced macrophage activation. In this report, we show that, in addition to SOCS3 expression, IL-10 induces SOCS1 up-regulation in all cell lines tested, including Ba/F3 pro-B cells, MC/9 mast cells, M1 leukemia cells, U3A human fibroblasts, and primary mouse CD4(+) T cells. Induction of SOCS molecules is dependent on STAT3 activation by IL-10R1. Cell lines constitutively overexpressing SOCS proteins demonstrated that SOCS1 and SOCS3, but not SOCS2, are able to partially inhibit IL-10-mediated STAT3 activation and proliferative responses. Pretreatment of M1 cells with IFN-gamma resulted in SOCS1 induction and a reduction of IL-10-mediated STAT3 activation and cell growth inhibition. IL-10-induced SOCS is associated with the inhibition of IFN-gamma signaling in various cell types, and this inhibition is independent of C-terminal serine residues of the IL-10R, previously shown to be required for other anti-inflammatory responses. Thus, the present results show that both SOCS1 and SOCS3 are induced by IL-10 and may be important inhibitors of both IL-10 and IFN-gamma signaling. IL-10-induced SOCS1 may directly inhibit IL-10 IFN-gamma signaling, while inhibition of other proinflammatory cytokine responses may use additional IL-10R1-mediated mechanisms.

Animals↗

PubMed2002

L-selectin-dependent lymphoid occupancy is required to induce alloantigen-specific tolerance.

Maneuvers that interfere with signals 1, 2, 3, or Ag processing can result in indefinite allograft survival. However, they are not applicable to all tissues, strains, or species, suggesting that there are additional levels of immune regulation. We hypothesized that secondary lymphoid organs are important for interactions among lymphocytes, alloantigen, and immunosuppressants that lead to tolerance. To explore this, cardiac allografts were performed with a tolerogenic immunosuppressive regimen. Concurrent administration of anti-L-selectin (CD62L) Ab, which prevents lymph node homing, prevents indefinite allograft survival and tolerance. Anti-CD62L Ab is not costimulatory, and Fab and F(ab')(2) anti-CD62L have similar activities. Flow cytometry and histologic examination show that Ab shifts T cells away from lymph nodes and into spleen, peripheral blood, and graft. Tolerance is not induced in CD62L(-/-) mice, and adoptive transfer of CD62L(-/-), but not CD62L(+/+), T cells prevents tolerization in wild-type recipients. FTY720, an immunosuppressant that promotes chemokine-dependent, but CD62L-independent, lymph node homing, reverses the Ab effect. Blockade of other homing receptors also prevents tolerization. These results indicate that T lymphocytes use CD62L-dependent migration for alloantigen-specific tolerance, and suggest that lymph nodes or other lymphoid tissues are an important site for peripheral tolerization to alloantigen.

Animals↗

PubMed2002

CD2 is a dominant target for allogeneic responses.

CD2 and 2B4 (CD244) are members of the immunoglobulin gene superfamily and are both ligands for another family member, CD48. CD2 is widely distributed on T, NK, and B cells and some antigen-presenting cells, while 2B4 is expressed on NK and some T cells and monocytes and is known to participate in NK cytotoxicity. Since indefinite allograft survival could be obtained by a combination of anti-CD48 plus anti-CD2 mAb administration, it was important to determine the role of 2B4 blockade in allograft rejection. MAbs directed against CD2, CD48, or 2B4 were administered singly or in pairs to cardiac allograft recipients. The experiments show that only anti-CD2 plus anti-CD48 mAbs result in indefinite allograft survival, while anti-CD2 plus anti-2B4 mAbs substantially prolong graft survival, and anti-CD48 plus anti-2B4 mAbs were no better than each mAb alone. The effect of these mAbs on anti-CD3 mAb and alloantigen-driven proliferation and IFN-gamma production were also assessed. In general, anti-CD2 inhibited both anti-CD3 mAb and alloantigen-driven responses, while anti-CD48 inhibited only anti-CD3 mAb but not alloantigen-driven proliferative and cytokine responses. Anti-2B4 mAbs were generally ineffective alone. Combinations of mAbs were more effective than single mAbs only in alloantigen-driven proliferation, commensurate with allograft survival results. Using CD2-/- and CD48-/- T cells and antigen-presenting cells, we also demonstrate that these inhibitory mAbs act primarily by blocking intercellular interactions, rather than directly delivering negative signals to T cells. These results suggest that, unlike CD2, 2B4 is not a potent regulatory molecule or ligand for CD48 in the response to alloantigen. Blocking the 2B4-CD48 receptor-ligand pair does not inhibit T-cell responses and alloreactivity to the same degree as CD2-CD48 blockade.

Animals↗