Analysis of the number of enlarged pores according to site, age, and sex.

BACKGROUND: Increasing the number of enlarged pores causes cosmetic problems. The difference in the number of enlarged pores according to facial site, age, and sex is unclear. OBJECTIVE: To analyze the distribution of the number of enlarged pores according to facial site, age, and sex. METHODS AND MATERIALS: We analyzed the number of the enlarged pores and the percentage of wrinkles in the nose, forehead, and cheek from 434 polarized images. The measurement results were analyzed according to site, age, and sex. Relationship between enlarged pore counts and wrinkle severity was also analyzed. The study was conducted by using DermaVision,™ which can take cross-polarization, parallel polarization, and ultraviolet light images. RESULTS: The enlarged pores of the nose and forehead were more prominent than in the cheeks. Pore counts were increased with age, and the increment was significant between the 30's and 40's. There was no significant difference by gender. Enlarged pore counts were related to wrinkle severity. CONCLUSIONS: The number of enlarged pores differs depending on body site and increased with age. The enlarged pore counts correlate with wrinkle severity and the correlation varies depending on the body site.

Activation of matrix metalloproteinase-2 by a novel oral spirochetal species Treponema lecithinolyticum.

BACKGROUND: Periodontal tissue destruction is a characteristic of periodontitis. This can be caused by either bacterial enzymes or host cell-derived matrix metalloproteinases (MMPs). In order to elucidate the etiologic role of oral spirochetes, we investigated the effects of Treponema lecithinolyticum, a novel saccharolytic species, on MMP-2 activation. METHODS: Gingival fibroblasts (GFs) and periodontal ligament (PDL) cells obtained from healthy human subjects were cultured to confluence in alpha-minimal essential medium (alpha-MEM) supplemented with 10% fetal bovine serum. After serum starvation for a day, the cultures were treated with whole cell sonicates, heat-denatured whole cell sonicates, outer membrane fraction (OMF) or formaldehyde-fixed cells of T. lecithinolyticum. Culture supernatants were collected after incubation for 24 to 48 hours and analyzed for MMP-2 activation by gelatin zymography. Collagenolytic activity was quantitatively measured using human [3H] type IV collagen as a substrate. RESULTS: Treatment of GFs and PDL cells with whole cell sonicates, formaldehyde-fixed whole cells, or the OMF of T. lecithinolyticum resulted in the production of MMP-2 partly in the fully active form with a molecular mass of 62 kDa, whereas non-treated control cultures and cultures treated with a heat-denatured fraction did not show the active form. Cultures exposed to T. lecithinolyticum had higher collagenolytic activity than non-treated cultures. CONCLUSIONS: Our results demonstrate that T. lecithinolyticum, possibly mediated by proteinaceous cell surface-associated components, may participate in extracellular matrix degradation by activation of MMP-2 during periodontal inflammation.

The effect of the scid mutation on mechanism and control of immunoglobulin heavy and light chain gene rearrangement.

Most Abelson murine leukemia virus (A-MuLV)-transformed cell lines derived from scid (severe combined immune deficient) mice actively rearrange their endogenous immunoglobulin (Ig) heavy (H), but not light (L) chain variable region genes. Such cell lines express germline VH segments and other RNA transcripts that are characteristically produced by early precursor (pre)-B lymphocytes, but do not express high levels of transcripts from the germline kappa (k) constant region (C kappa) locus. However, we have derived scid A-MuLV transformants that express germline C kappa transcripts and attempt kappa gene assembly. In one case kappa gene expression and rearrangement occurred in the absence of mu H chain expression, and in another was not induced efficiently by introduction of a mu-expression vector. Although the vast majority of scid H and L chain coding sequence joins are grossly aberrant, scid A-MuLV transformants can form normal coding joints at a very low frequency. In contrast, these cells form generally normal signal sequence joins at an approximately normal efficiency. Thus, these findings mechanistically distinguish coding and signal join formation. Subcloning analyses suggest that scid A-MuLV transformants that do not attempt chromosomal coding sequence joining may have a relative survival advantage, and therefore that these events may often result in unrepaired chromosomal breakage and cell death.