Endophilin B1 is required for the maintenance of mitochondrial morphology

We report that a fatty acyl transferase, endophilin B1, is required for maintenance of mitochondrial morphology. Down-regulation of this protein or overexpression of endophilin B1 lacking the NH2-terminal lipid-modifying domain causes striking alterations of the mitochondrial distribution and morphology. Dissociation of the outer mitochondrial membrane compartment from that of the matrix, and formation of vesicles and tubules of outer mitochondrial membrane, was also observed in both endophilin B1 knockdown cells and after overexpression of the truncated protein, indicating that endophilin B1 is required for the regulation of the outer mitochondrial membrane dynamics. We also show that endophilin B1 translocates to the mitochondria during the synchronous remodeling of the mitochondrial network that has been described to occur during apoptosis. Double knockdown of endophilin B1 and Drp1 leads to a mitochondrial phenotype identical to that of the Drp1 single knockdown, a result consistent with Drp1 acting upstream of endophilin B1 in the maintenance of morphological dynamics of mitochondria

A Case of Birt-Hogg-Dubé Syndrome

Birt-Hogg-Dubé syndrome (BHDS) is an autosomal dominant genodermatosis characterized by cutaneous hair follicle tumors (fibrofolliculoma or trichodiscoma), pulmonary cysts, and increased risk of renal neoplasia. The genetic alteration for BHDS has been mapped to chromosome 17p12q11, and the gene in this region has been cloned and believed to be responsible for the BHDS. Mutations in the BHD gene (also known as FLCN) have been described in the patients with BHDS. We present a case of a 30-yr-old Korean woman with multiple mildly pruritic papules on her face and neck area. The patient had several firm, flesh-colored, dome-shaped, papular lesions measuring between 2 to 5 mm. Except for a history of pneumothorax her medical records were not remarkable. Mutation analysis of the BHD gene was performed, and a novel deletion mutation (p.F519LfsX17 [c.1557delT]) causing truncation of the gene product, folliculin, was found in the exon 14. The actual incidence of BHDS is unknown, but it is most likely underdiagnosed. So it is imperative that doctors recognize the skin lesions of BHDS and institute proper screening to detect other manifestations of the disease. Here, we report a case of BHDS with a novel mutation, which is the first report in Korea

Optimization of extraction process for enhancement of antioxidant activity of Acer mono bark

Response surface methodology (RSM) was used for finding the optimum extraction condition of Acer mono bark. Twenty experimental conditions were set based on three key variables such as temperature, time and pressure by signalling reaction variables with 5 levels of - 2, - 1, 0, 1, 2 in accordance with central composite design for proceeding extraction and antioxidant tests. The optimized condition for the highest extraction yields was 13.10% at 83.48°C, 54.36 MPa for 13.08 minutes. For DPPH radical scavenging ability, an optimal condition was 92.89% at 88.50°C, 49.69 MPa for 15.08 minutes, and for SOD-like activity 40.69% at 85.21°C, 53.28 MPa for 15.83 minutes. The optimized condition for total polyphenol content was 4.23 mg/g at 81.51°C, 52.92 MPa for 14.79 minutes. The most optimized extraction condition was determined to be at 85°C, 52 MPa for 14 minutes for considering both extraction yield and its biological activities of this plant

Identification of single-nucleotide polymorphisms of the prion protein gene in sika deer (Cervus nippon laiouanus)

Polymorphisms of the prion protein gene (PRNP) have been detected in several cervid species. In order to confirm the genetic variations, this study examined the DNA sequences of the PRNP obtained from 33 captive sika deer (Cervus nippon laiouanus) in Korea. A total of three single-nucleotide polymorphisms (SNPs) at codons 100, 136 and 226 in the PRNP of the sika deer were identified. The polymorphic site located at codon 100 has not been reported. The SNPs detected at codons 100 and 226 induced amino acid substitutions. The SNP at codon 136 was a silent mutation that does not induce any amino acid change. The genotype and allele frequencies were determined for each of the SNPs

Age is a determinant factor in the susceptibility of domestic ducks to H5 clade 2.3.2.1c and 2.3.4.4e high pathogenicity avian influenza viruses

High pathogenicity avian influenza (HPAI) is a viral disease with devastating consequences for the poultry industry worldwide. Domestic ducks are a major source of HPAI viruses in many Eurasian countries. The infectivity and pathogenicity of HPAI viruses in ducks vary depending on host and viral factors. To assess the factors influencing the infectivity and pathogenicity of HPAI viruses in ducks, we compared the pathobiology of two HPAI viruses (H5N1 clade 2.3.2.1c and H5N6 clade 2.3.4.4e) in 5- and 25-week-old ducks. Both HPAI viruses caused mortality in a dose-dependent manner (104, 106, and 108 EID50) in young ducks. By contrast, adult ducks were infected but exhibited no mortality due to either virus. Viral excretion was higher in young ducks than in adults, regardless of the HPAI strain. These findings demonstrate the age-dependent mortality of clade 2.3.2.1c and clade 2.3.4.4e H5 HPAI viruses in ducks