A family with Xq22.3q25 interstitial deletion and normal ovarian function.

OBJECTIVE: To investigate genomic changes in a family with deletion of X chromosome q22.3-q25 associated with normal constitutional and reproductive phenotypes. DESIGN: Case report. SETTING: Academic district hospital genetic laboratory. PATIENT(S): A family incidentally found to have deletion of X chromosome q22.3-q25. INTERVENTION(S): Cytogenetic analysis and array-based comparative genomic hybridization for amniotic fluid and peripheral blood lymphocyte of family members. MAIN OUTCOME MEASURE(S): Ovarian function and menstrual cycles. RESULT(S): The proband and two daughters showed deletion of Xq22.3q25. This region spans 17.4 Mb and contains 121 genes. CONCLUSION(S): Female subjects with deletion of Xq22.3q25 may present with normal constitutional and reproductive phenotypes.

Streptococcal collagen-like surface protein 1 promotes adhesion to the respiratory epithelial cell.

BACKGROUND: Collagen-like surface proteins Scl1 and Scl2 on Streptococcus pyogenes contain contiguous Gly-X-X triplet amino acid motifs, the characteristic structure of human collagen. Although the potential role of Scl1 in adhesion has been studied, the conclusions may be affected by the use of different S. pyogenes strains and their carriages of various adhesins. To explore the bona fide nature of Scl1 in adherence to human epithelial cells without the potential interference of other streptococcal surface factors, we constructed a scl1 isogenic mutant from the Scl2-defective S. pyogenes strain and a Scl1-expressed Escherichia coli. RESULTS: Loss of Scl1 in a Scl2-defective S. pyogenes strain dramatically decreased the adhesion of bacteria to HEp-2 human epithelial cells. Expression of Scl1 on the surface of the heterologous bacteria E. coli significantly increased adhesion to HEp-2. The increase in adhesion was nullified when Scl1-expressed E. coli was pre-incubated with proteases or antibodies against recombinant Scl1 (rScl1) protein. Treatment of HEp-2 cells with rScl protein or pronase drastically reduced the binding capability of Scl1-expressed E. coli. These findings suggest that the adhesion is mediated through Scl1 on bacterial surface and protein receptor(s) on epithelial cells. Further blocking of potential integrins revealed significant contributions of α2 and ß1 integrins in Scl1-mediated binding to epithelial cells. CONCLUSIONS: Together, these results underscore the importance of Scl1 in the virulence of S. pyogenes and implicate Scl1 as an adhesin during pathogenesis of streptococcal infection.

Introduction of a laparoscopic gynecological program in a general hospital in Taiwan.

BACKGROUND AND OBJECTIVES: We reviewed the records for 571 gynecologic laparoscopies performed at a privately owned general hospital in Kaosiung Taiwan in 1998 and 1999 and discuss here the major obstacles we encountered while introducing these procedures at our institution. METHODS: Included in this series are 293 procedures performed in 1998 (149 hysterectomies, 144 adnexal procedures), and 278 procedures performed in 1999 (131 hysterectomies, 147 adnexal procedures). Thirty-nine of these patients also underwent laparoscopic appendectomy. Mean patient age was 62 years (range 28 to 82). All procedures were performed by 1 of 6 board-certified gynecologic surgeons, or by 1 of 4 residents under the direct supervision of a board-certified surgeon. RESULTS: We experienced 0% mortality and 7.2% morbidity in this series. In comparing cases from 1998 and 1999, we observed a decrease in both mean surgery time (135.4 to 123.0, P=0.032) and mean length of hospital stay (5.52 to 4.62, P=0.046) for hysterectomies and adnexal procedures combined. CONCLUSIONS: These data support ongoing efforts to incorporate gynecologic laparoscopy as an alternative to open procedures at our institution. Introduction of these procedures in privately owned hospitals in Taiwan has been limited because of the large initial investment for equipment, patient education issues, and difficulties obtaining reimbursement.