Background: A bilayered skin substitute composed of allogeneic keratinocytes and fibroblasts in a collagen gel has been approved by the US Food and Drug Administration for the treatment of venous and diabetic ulcers. Its mechanism of action has not been fully determined. Objective: To determine the longevity of allogeneic fibroblasts and keratinocytes in a bilayered skin substitute in patients with venous leg ulcers. Methods: Ten patients with venous leg ulcers were treated with a bilayered skin substitute on day 0, days 3 to 5, and weeks 1 through 3. Biopsy specimens of the grafted wound were taken. We used polymerase chain reaction analysis to determine whether allogeneic DNA was present in the biopsy specimens. Results: We detected allogeneic DNA in 2 of 8 specimens at 1 month after initial grafting. Neither of the 2 patients showed persistence of allogeneic DNA at 2 months after initial grafting. Conclusions: Allogeneic cells from a bilayered skin substitute do not appear to survive permanently after grafting for treatment of venous leg ulcers. Other mechanisms of action might include cytokine release, structural support, or provision of a moist wound environment.

A scar from an acute surgical wound becomes softer, more elastic, dryer, less erythematous, and less pigmented as it ages. In contrast, chronic wound scars become harder as they age. These different properties of healed acute wounds and healed chronic wounds may be a result of the different healing processes in each wound type.

Introduction: Human papillomavirus (HPV) association in genital wart is well known, however, data are mostly from developed countries and no data from Bangladesh is yet available. Methods: In order to see the HPV association and type distribution in genital warts in Bangladeshi patients, we screened DNA from warts and checked presence of HPV by real time polymerase chain reaction (PCR). Results: Out of 44 wart specimens from 44 patients, 30(68.18%) were found positive for HPV. Out of these 30 positive patients low risk HPVs were 25 (83.33%) and high risk HPVs were 3(10%) and co-infection with low risk and high risk HPVs were 2(6.66%). Among the low risk HPVs, type 6 was found in 23(85.18%) and type 11 was found in 4(14.8%) indicating high dominance of HPV type 6. Among the high risk HPVs, type 16 was found in one, type 18 was found in one and HPV other than type 16 and 18 was found in three patients. Though the number of male patients in this study was smaller than female patients (10 vs 34) type distribution of HPVs in warts from male and female are similar. Conclusion: Although it is accepted that HPV 6 and 11 genotypes are main causes of warts, our findings show non-negligible incidence of multiple infections and high-risk genotypes in both male and female with benign HPV manifestations (warts). This is the first report of HPV documentation and type distribution in genital warts in Bangladesh and hence demand further large scale study.