The Efficacy of CT-Based Conformal Electron Beam Radiation Therapy After Keloid Excision.

BACKGROUND: Adjuvant computed tomography-based conformal electron beam radiation therapy (RT) for patients with keloids enables radiation oncologists to customize the target volume with precision and deliver the maximal prescription dose while sparing normal surrounding tissues. OBJECTIVE: To report treatment and cosmetic outcomes by the patient's self-assessment survey. METHODS: Medical records of patients with keloids, who were treated with postoperative electron beam RT between January 2015 and December 2020, were reviewed. A total of 85 consecutive patients with 136 keloids were included in this study. Subjective cosmetic outcomes were scored by each patient using a 5-point Likert scale survey. RESULTS: The median follow-up time was 29.0 months (range, 12.1-77.9 months), and local recurrence was observed in 10 lesions (7.4%). The recurrence rate of keloids occurring in the ear was 5.4%, whereas the recurrence rate of keloids occurring at other body sites was 11.4%. Among the patients who responded to the questionnaire about the cosmetic outcome, 70.2% of patients declared being either very satisfied (44.7%) or satisfied (25.5%). CONCLUSION: Surgical excision, followed by CT-based conformal electron beam RT, for patients with keloids ensures a high degree of local control resulting in good cosmetic outcomes.

Inhibition of proinflammatory cytokine expression by NF-kappaB (p65) antisense oligonucleotide in Helicobacter pylori-infected mice.

BACKGROUND: Helicobacter pylori induces the expression of proinflammatory cytokines in vitro by activating nuclear factor-kappaB, a transcriptional regulator. However, it has not been clarified whether H. pylori-induced proinflammatory cytokines are also mediated through nuclear factor-kappaB in vivo. The aim of this study was to evaluate the role of nuclear factor-kappaB on the expressions of proinflammatory cytokines in H. pylori-infected mice. MATERIALS AND METHODS: We evaluated nuclear factor-kappaB (p65) activation in the H. pylori-infected gastric mucosa of mice by immunofluorescent staining using antip65 polyclonal antibody, and the expressions of proinflammatory cytokines with inhibition of nuclear factor-kappaB pathway by using phosphorothioate antisense and sense oligonucleotide against the nuclear factor-kappaB (p65). RESULTS: In the H. pylori-infected gastric mucosa of mice, immunofluorescent staining using antip65 polyclonal antibody showed nuclear factor-kappaB (p65) activation, which was particularly localized to epithelial cells. Tumor necrosis factor-alpha and interleukin-1beta concentrations in gastric mucosa by enzyme-linked immunosorbent assay (ELISA) were elevated in the infected group versus the uninfected group. Pretreatment with nuclear factor-kappaB (p65) antisense oligonucleotide inhibited the activation of nuclear factor-kappaB and the expressions of tumor necrosis factor-alpha and interleukin-1beta in H. pylori-infected gastric mucosa. Sense oligonucleotide did not influence on the expression of proinflammatory cytokines. CONCLUSIONS: H. pylori infection was found to activate the expressions of proinflammatory cytokines via nuclear factor-kappaB in vivo, and this may play an important role in the initiation of H. pylori-induced gastric inflammation.