Recipient site creation for hair transplantation: A prospective half-side comparison study of hole versus slit.

Follicular unit strip surgery and FUE (follicular unit extraction) are techniques used for donor harvesting in hair transplantation. For recipient site creation, the slit technique is now commonly used. The hole technique is an alternative technique in which holes are created in the tissue at the recipient site. This study compared these techniques in order to evaluate the effectiveness of the hole technique. Mean time for recipient site creation was significantly shorter with the hole technique than with the slit technique (95.5 s vs. 121 s; p = 0.021). This can be explained by better visibility of the holes compared with slits. This study focused on recipient site creation and found that the hole technique was a rapid and effective for recipient site creation.

Treatment of scarring alopecia from trauma and surgical procedures in young patients using follicular unit hair transplantation.

INTRODUCTION: Hair loss due to scarring as a consequence of surgical procedures and trauma can impact young patients socially and emotionally. Recently follicular unit extraction (FUE) hair transplantation has been applied to scar treatment. PATIENTS AND METHODS: This report included four patients with scarring alopecia. All patients were female with a mean age of 12.5 years. Previous operations that caused scarring were sebaceous nevus excision with direct closure (n = 2), an extensive burn scar treated using an expander (n = 1) and cauterization for a congenital pigmented nevus (n = 1). The average size of the affected area was 10.5 cm2 . The FUE transplantation procedure was performed under local anesthesia. The number of grafts was set at approximately 25-30 grafts/ cm2 of scar. An electronic punch with a diameter of 0.8 mm was used for graft harvesting, and a 0.6-mm electronic punch was used to make cylindrical holes on recipient site. The donor sites were shaved followed by graft harvesting in two cases. For the other two cases, harvesting was done without shaving. RESULTS: The number of transplanted grafts was 60 to 600 (mean 288), and surgical time was 38 to 220 minutes (mean 108). The average dose of lidocaine was 1.4 mg/kg. The average survival rate of the grafts was 85%. CONCLUSION: Our experience in these cases suggests that this technique may be a viable option for the treatment of certain causes of scarring alopecia in the pediatric age group.

Neutrophil-derived reactive oxygen species can modulate neutrophil adhesion to endothelial cells in preeclampsia.

BACKGROUND: Neutrophil activation has been implicated in the pathophysiology of preeclampsia. The aim of this study was to investigate whether neutrophil-derived reactive oxygen species (ROS) modulate adhesion to endothelial cells in preeclampsia. METHODS: We first assessed neutrophil superoxide production and neutrophil-endothelial cell adhesion in normal nonpregnant women (n = 8), normal pregnant women (n = 10), and preeclamptic pregnant women (n = 8). We then examined the effects of neutrophil-derived ROS on neutrophil-endothelial adhesion. The release of neutrophil superoxide was measured using cytochrome C reduction. RESULTS: N-formyl-methionyl-leucyl-phenylalanine (FMLP)-stimulated superoxide production by neutrophils was significantly increased in women with preeclampsia when compared with the other two groups. Neutrophils from women with preeclampsia were more likely to adhere to endothelial cells, than were those from the other two groups (mean adhesion rate +/- s.d. (%); 20.6 +/- 2.7 in preeclampsia, 10.2 +/- 1.2 in normal pregnancy, 11.0 +/- 0.9 in normal nonpregnancy, P < 0.01). Superoxide dismutase (SOD), which dismutates the excess superoxide to hydrogen peroxide, did not affect neutrophil-endothelial adhesion. In contrast, catalase, which catalyzes the conversion of hydrogen peroxide to oxygen and water, inhibited neutrophil-endothelial adhesion in the preeclamptic group (8.1 +/- 0.5%, P < 0.01). CONCLUSION: Neutrophils from women with preeclampsia demonstrate increased CD11b expression and adhesion to endothelial cells. This is likely caused by elevations in superoxide and its derivative, hydrogen peroxide.

Generation of reactive oxygen species by neutrophils and endothelial cell injury in normal and preeclamptic pregnancies.

The aim of this study was to investigate the role of neutrophil-derived reactive oxygen species on endothelial cell dysfunction in preeclampsia. We first assessed the correlation between nitrite and superoxide anion production in normal nonpregnant (n=10), normal pregnant (n=15), and preeclamptic women (n=12). We then examined neutrophil-mediated oxygen radical damage to human umbilical vein endothelial cells in vitro. Neutrophil superoxide release was measured by cytochrome C reduction; nitrite release was measured by the modified Griess reaction, and endothelial cell injury was measured by 51Cr release. N-formyl-methionyl-leucyl-phenylalanine-stimulated superoxide release by neutrophils was significantly increased in women with preeclampsia compared with the other 2 groups. Nitrite release by neutrophils was significantly decreased in preeclampsia compared with normal pregnancy. When neutrophils were pretreated with superoxide dismutase, nitrite release by neutrophils did not differ between normal pregnancy and preeclampsia, suggesting that excess superoxide anion in preeclampsia could reduce bioavailability of nitric oxide through neutrophil autocrine function. Neutrophil-mediated endothelial cell injury was significantly greater in women with preeclampsia than in the other 2 groups. Hydrogen peroxide was important in neutrophil-mediated endothelial cell injury in preeclampsia as catalase inhibited endothelial cell injury. When neutrophils were pretreated with NG-nitro-L-arginine methyl ester, neutrophil-mediated endothelial cell injury in preeclampsia was decreased, indicating a role for peroxynitrite formation as a mechanism of endothelial cell injury. In conclusion, the modulation of neutrophils causing superoxide production to dominate over nitrite release provides a reasonable explanation for endothelial cell dysfunction in preeclampsia.