Klotho mice: a novel wound model of aged skin.

BackgroundAs the elderly population continues to expand, it becomes increasingly important to develop treatments to improve wound healing in the elderly. One problem limiting the research is the lack of appropriate animal models for wound healing in elderly patients. We hypothesized that the Klotho mouse of premature aging is a suitable animal model to shed light on many of the biological processes involved in aging skin.MethodsKlotho mice (kl/kl), Klotho-heterozygous mice (kl/+), and wild-type mice (+/+) were wounded, and the area of the wound was measured every 3 days until the wound was healed. To compare the klotho phenotype with wild-type mice, wounds were also harvested at 4 and 7 days after wounding. For histological examination, paraffin-embedded sections were stained with hematoxylin and eosin and Masson trichrome. Collagen expression in the wound was also studied by analyzing messenger RNA using real-time polymerase chain reaction.ResultsKlotho mice showed a significantly slower rate of wound closure compared with Klotho-heterozygous mice and wild-type mice. Histology showed substantial less healing and collagen deposition in the wounds of the Klotho mice. The expression of collagen messenger RNA in Klotho mice was also less than that in heterozygous and wild-type mice. The Klotho mice exhibited significant phenotypic similarities with aged skin, such as atrophy and delayed wound healing.ConclusionThese preliminary data suggest that the Klotho mouse may be a model to further investigate wound healing in the elderly

Cryptococcus gattii Genotype VGIIa Infection in Man, Japan, 2007

We report a patient in Japan infected with Cryptococcus gattii genotype VGIIa who had no recent history of travel to disease-endemic areas. This strain was identical to the Vancouver Island outbreak strain R265. Our results suggest that this virulent strain has spread to regions outside North America

Altered regulation of mesenchymal cell senescence in adipose tissue promotes pathological changes associated with diabetic wound healing

Pathologic diabetic wound healing is caused by sequential and progressive deterioration of hemostasis, inflammation, proliferation, and resolution/remodeling. Cellular senescence promotes wound healing; however, diabetic wounds exhibit low levels of senescent factors and accumulate senescent cells, which impair the healing process. Here we show that the number of p15(INK4B) + PDGFR alpha + senescent mesenchymal cells in adipose tissue increases transiently during early phases of wound healing in both non-diabetic mice and humans. Transplantation of adipose tissue from diabetic mice into non-diabetic mice results in impaired wound healing and an altered cellular senescence-associated secretory phenotype (SASP), suggesting that insufficient induction of adipose tissue senescence after injury is a pathological mechanism of diabetic wound healing. These results provide insight into how regulation of senescence in adipose tissue contributes to wound healing and could constitute a basis for developing therapeutic treatment for wound healing impairment in diabetes. Type-2 diabetic adipose tissue impairs transient senescence during wound healing with expression of different components of the senescence-associated secretory phenotype (SASP), and this is associated with deteriorated wound healing

Correction of Lobule-type Microtia: Part 2: The Stage of Ear Elevation

Background: Here, we introduce our recent operative technique for ear elevation that results in (1) minimal morbidity for patients, (2) symmetric appearance, (3) clearer 3-dimensional structure with a deep concha, (4) good aesthetic appearance by hiding the grafted area behind the ear, and (5) maintenance of deep temporoauricular sulcus and angle. Methods: After a skin incision, the ear is elevated with temporoparietal fascia underlying the cartilage. On the conchal area, undermining is performed just below the skin so that the deep concavity can be maintained. Scalp and neck skin behind the ear is undermined subcutaneously and lifted up cranially to hide the entire area of grafted skin behind the ear. The postauricular surface is covered by full-thickness skin from the lower abdomen. A protective splint is applied for 3 months while sleeping. Results: A total of 137 ears in 121 patients were corrected with our technique and followed up for at least 3 years. All of the scar tissue could be hidden behind the ear, an aesthetically excellent result. Conclusions: Our technique made it possible to acquire an excellent and symmetrical shape of the ear. The important points in our procedure are as follows: (1) subcutaneous posterior undermining to enlarge the conchal cavity, (2) careful arrangement of the temporoauricular angle and auriculo-earlobe angle, (3) reduction in the area of temporally grafted skin to hide all scars behind the ear, and (4) protection of the ear to maintain the shape using a postoperative splint