Wound healing is primarily controlled by the proliferation and migration of keratinocytes and fibroblasts as well as the complex interactions between these two cell types. To investigate the interactions between keratinocytes and fibroblasts and the effects of direct cell-to-cell contact on the proliferation and migration of keratinocytes, keratinocytes and fibroblasts were stained with different fluorescence dyes and co-cultured with or without transwells. During the early stage (first 5 days) of the culture, the keratinocytes in contact with fibroblasts proliferated significantly faster than those not in contact with fibroblasts, but in the late stage (11th to 15th day), keratinocyte growth slowed down in all cultures unless EGF was added. In addition, keratinocyte migration was enhanced in co-cultures with fibroblasts in direct contact, but not in the transwells. Furthermore, the effects of the fibroblasts on keratinocyte migration and growth at early culture stage correlated with heparin-binding EGF-like growth factor (HB-EGF), IL-1α and TGF-β1 levels in the cultures where the cells were grown in direct contact. These effects were inhibited by anti-HB-EGF, anti-IL-1α and anti-TGF-β1 antibodies and anti-HB-EGF showed the greatest inhibition. Co-culture of keratinocytes and IL-1α and TGF-β1 siRNA-transfected fibroblasts exhibited a significant reduction in HB-EGF production and keratinocyte proliferation. These results suggest that contact with fibroblasts stimulates the migration and proliferation of keratinocytes during wound healing, and that HB-EGF plays a central role in this process and can be up-regulated by IL-1α and TGF-β1, which also regulate keratinocyte proliferation differently during the early and late stage.

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Our study implied that multiple genes are involved in scar formation and contraction. Interferon is an autosecreted cytokine that might be responsible for self-control of overgrowth of cells in wounds. The early period of hypertrophic scar formation might be a good time for preventing overgrowth and contraction of hypertrophic scar by gene therapy.

SummaryBackgroundIncreasing complications of polyacrylamide hydrogel (PAAG) augmentation mammoplasty, such as chronic persistent infection, have recently caught the attention of both the medical field and the general public.Material/MethodsA total of 96 patients with severe chronic infection following PAAG augmentation mammoplasty were treated in the present study including 63 cases with infection confined to the breast and 33 with systemic infection. Endoscopy and surgery were performed to completely remove the materials and clear the infected tissues followed by drug-irrigation and vacuum-assisted closure for several days.ResultsIn patients with severe infection there were large amounts of PAAG, fibers and infiltration of numerous neutrophils and macrophages. The infection-inducing materials were extensively dispersed in the mammary and subcutaneous tissues, pectoral fascia and intermuscular space. In addition, there was scattered distribution of PAAG materials in the armpit, chest wall and abdominal wall, which were mixed with necrotic tissues and surrounded by lymphocytes, giant cells, macrophages and other inflammatory cells, forming chronic granulomatous and fibrous lesions. Infection was controlled following surgical intervention. No residual infectious foci or recurrent infections were noted among these patients. Although the severe infection did not result in mastectomy, patients had breast atrophy and various degrees of deformation.ConclusionsChronic infection following PAAG augmentation mammaplasty usually causes systemic infection and other devastating adverse reactions. This study confirms PAAG augmentation mammaplasty is another failed attempt. More attention should be paid to the injection of large doses of liquid filler.

Polyacrylamide hydrogel (PAAG) has been widely used for injection augmentation mammaplasty in Russia, China, and Iran for more than 2 decades. In recent years, it has been advocated as a safe permanent filler for soft-tissue augmentation. However, the complications associated with PAAG injection in soft-tissue augmentation have not been extensively investigated. Augmentation mammaplasty through PAAG injection is associated with some complications. The incidence of infection during breastfeeding was reported to be higher than 50%. Herein, we report 58 cases of infection in breastfeeding women receiving PAAG injection, including 50 with unilateral injection (36 on the right, 14 on the left) and 8 bilateral injection. They experienced large breast autoinflation and some severe symptoms, such as local and systemic fever, breast swelling, nipple bulging, tenderness, and pain, which lead to surgical removal of galactocele or intraprosthetic collection of sterile pus resulting in deformity. Operation and comprehensive measures including removal of the injected material, clearing residual cavity, and pharmacotherapy were carried out to control infection and inflammation for 1 to 2 weeks. In the following 12 months, no relapse or recurrence of residual cavity was noted. Therefore, we do not recommend PAAG injection for augmentation mammaplasty, especially in women intending to breastfeed. Patients undergoing PAAG injection for augmentation mammaplasty should avoid breastfeeding. PAAG injection will cause serious consequences resulting in tissue atrophy and breast resection if inappropriately handled.

Mesenchymal stem cells (MSCs) are promising candidates for skin wound repair due to their capabilities of accumulating at wounds and differentiating into multiple types of skin cells. However, the underlying mechanisms responsible for these processes remain unclear. In this study, we found that osteopontin (OPN) stimulated the migration of MSCs in vitro, and observed the recruitment of endogenous MSCs to a skin wound and their differentiation into keratinocytes and endothelial cells. In OPN knock-out mice, the recruitment of MSCs to the skin wound was significantly inhibited, and wound closure was hampered after an intradermal injection of exogenous MSCs compared to wild-type mice. Consistent with these observations, the expressions of adhesion molecule CD44 and its receptor E-selectin were significantly decreased in the lesions of OPN knock-out mice compared with wild-type mice suggesting that OPN may regulate the migration of MSCs through its interactions with CD44 during skin wound recovery. In summary, our data demonstrated that OPN played a critical role in activating the migration of MSCs to injured sites and their differentiation into specific skin cell types during skin wound healing.

Indium oxyhydroxide (InOOH) 1-D nanostructures have been synthesized utilizing the hexamethylene diamine (HMDA)-assisted hydrolysis of In 3+ cation method in the solvent poly(ethylene glycol 400) (PEG-400). It was found that the amount of distilled water and the solvent type were two key factors for the synthesis of high quality nanocrystals. The anisotropic growth of InOOH could be attributed to the HMDA molecule-assisted oriented attachment of nanoparticles, and the formation of tubular InOOH nanostructures could be due to ''dissolution and recrystallization''. By annealing InOOH precursors at 400 1C in air, hexagonal corundum-type indium sesquioxide (H-In 2 O 3 ), which inherits the morphologies of its precursor with a slight size shrinking, was also prepared. The photocatalytic properties of tubular and rod-like H-In 2 O 3 nanocrystals were investigated by the photodegradation of rhodamine B (RhB) molecules under ultraviolet (UV) light irradiation.

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