Use of Septal Cartilage in Rhinoplasty to Correct Nasal Deformity After Unilateral Cleft Lip and Palate Surgery.

Background: The most common facial defect is the congenital cleft lip (CL), which can occur with or without a cleft palate (CP). Patients need primary plastic surgery for rehabilitation and esthetics; nevertheless, secondary abnormalities of the lip and nose may develop after primary surgery. These deformities are complex and involve all tissue layers, including the skeletal platform, inner lining, osseocartilaginous structure, and overlying skin. This study evaluated the results of nasal deformity rhinoplasty using septal cartilage in patients with nasal deformities after plastic surgery for unilateral CL and CP. Methods: This retrospective study was conducted on 21 patients with secondary unilateral CL nasal deformity between June 2015 and August 2016. All patients underwent rhinoplasty with the use of septal cartilage grafts. Pre- and post-operative nasal forms were measured. Results: The patients had cosmetic problems and impaired nasal airflow due to distorted anatomy. The postoperative nasal forms were improved in all patients. Rhinoplasty using septal cartilage effectively increased the height of the columella and nose and improved the balance of the base width and the length of both sides of the nose. Excellent results were achieved in 18 patients. Three patients showed good results. No patient showed a fair result. Conclusion: This study demonstrated an effective correction of esthetic deformities and significant improvement in airway patency. A long-term longitudinal study is still required to evaluate the influence of septal cartilage harvesting on face and nasal development until children reach their late teens.

Overexpression of the ZmDEF1 gene increases the resistance to weevil larvae in transgenic maize seeds.

Plant defensins are divided into 18 groups and are multifunctional proteins. The Zea mays defensin 1 (ZmDEF1) gene encodes the defensin 1 protein, which can inhibit alpha-amylase in the insect gut. In this study, the ZmDEF1 gene was transferred into two maize cultivars, LC1 and LVN99, to improve weevil resistance in maize. The recombinant ZmDEF1 protein was assessed for its ability to inhibit alpha-amylase in the gut of the larvae of the maize weevil (Sitophilus zeamais Motsch.). ZmDEF1 was cloned into a pBetaPhaso-dest vector, which harbours phaseolin, a seed-specific promoter, and the Agrobacterium tumefaciens strain C58 harbouring the pBetaPhaso-ZmDEF1 vector was used to transfer the ZmDEF1 gene into two maize cultivars using immature embryos. Transformed calluses were selected on selection media containing kanamycin. The stable integration of the ZmDEF1 transgene into the transgenic maize plant genome was confirmed using Southern blotting. The recombinant ZmDEF1 protein of approximately 10 kDa was expressed in three transgenic maize lines from the LC1 cultivar (C1, C3, and C5) and two transgenic maize lines from the LVN99 cultivar (L1 and L3). The ZmDEF1 transgenic efficiency based on the results of PCR, as well as Southern and Western blotting, was 1.32% and 0.82%, respectively, which depends on the genotypes of LC1 and LVN99. The recombinant ZmDEF1 protein inhibited the alpha-amylase activity of the maize weevil larvae, and its ability to inhibit alpha-amylase is 54.52-63.09% greater than the ZmDEF1 protein extracted from non-transgenic plants.

Aryl hydrocarbon receptor antagonism and its role in rheumatoid arthritis.

Although rheumatoid arthritis (RA) is the most common autoimmune disease, affecting approximately 1% of the population worldwide, its pathogenic mechanisms are poorly understood. Tobacco smoke, an environmental risk factor for RA, contains several ligands of aryl hydrocarbon receptor (Ahr), also known as dioxin receptor. Ahr plays critical roles in the immune system. We previously demonstrated that Ahr in helper T-cells contributes to development of collagen-induced arthritis, a mouse model of RA. Other studies have shown that cigarette smoke condensate and pure Ahr ligands exacerbate RA by altering bone metabolism and inducing proinflammatory responses in fibroblast-like synoviocytes. Consistent with these findings, several Ahr antagonists such as α-naphthoflavone, resveratrol, and GNF351 reverse the effect of Ahr ligands in RA pathogenesis. In this review, we summarize the current knowledge of Ahr function in the immune system and the potential clinical benefits of Ahr antagonism in treating RA.