Correction of Spacecraft Magnetic Field Noise: Initial Korean Pathfinder Lunar Orbiter MAGnetometer Observation in Solar Wind.

The Korean Pathfinder Lunar Orbiter (KPLO)-MAGnetometer (KMAG) consists of three triaxial fluxgate sensors (MAG1, MAG2, and MAG3) that measure the magnetic field around the Moon. The three sensors are mounted in the order MAG3, MAG2, and MAG1 inside a 1.2 m long boom, away from the satellite body. Before it arrived on the Moon, we compared the magnetic field measurements taken by DSCOVR and KPLO in solar wind to verify the measurement performance of the KMAG instrument. We found that there were artificial disturbances in the KMAG measurement data, such as step-like and spike-like disturbances, which were produced by the spacecraft body. To remove spacecraft-generated disturbances, we applied a multi-sensor method, employing the gradiometer technique and principal component analysis, using KMAG magnetic field data, and confirmed the successful elimination of spacecraft-generated disturbances. In the future, the proposed multi-sensor method is expected to clean the magnetic field data measured onboard the KPLO from the lunar orbit.

The Role of Pyruvate Metabolism in Mitochondrial Quality Control and Inflammation.

Pyruvate metabolism, a key pathway in glycolysis and oxidative phosphorylation, is crucial for energy homeostasis and mitochondrial quality control (MQC), including fusion/fission dynamics and mitophagy. Alterations in pyruvate flux and MQC are associated with reactive oxygen species accumulation and Ca2+ flux into the mitochondria, which can induce mitochondrial ultrastructural changes, mitochondrial dysfunction and metabolic dysregulation. Perturbations in MQC are emerging as a central mechanism for the pathogenesis of various metabolic diseases, such as neurodegenerative diseases, diabetes and insulin resistance-related diseases. Mitochondrial Ca2+ regulates the pyruvate dehydrogenase complex (PDC), which is central to pyruvate metabolism, by promoting its dephosphorylation. Increase of pyruvate dehydrogenase kinase (PDK) is associated with perturbation of mitochondria-associated membranes (MAMs) function and Ca2+ flux. Pyruvate metabolism also plays an important role in immune cell activation and function, dysregulation of which also leads to insulin resistance and inflammatory disease. Pyruvate metabolism affects macrophage polarization, mitochondrial dynamics and MAM formation, which are critical in determining macrophage function and immune response. MAMs and MQCs have also been intensively studied in macrophage and T cell immunity. Metabolic reprogramming connected with pyruvate metabolism, mitochondrial dynamics and MAM formation are important to macrophages polarization (M1/M2) and function. T cell differentiation is also directly linked to pyruvate metabolism, with inhibition of pyruvate oxidation by PDKs promoting proinflammatory T cell polarization. This article provides a brief review on the emerging role of pyruvate metabolism in MQC and MAM function, and how dysfunction in these processes leads to metabolic and inflammatory diseases.

Pyruvate dehydrogenase kinase 4 promotes ubiquitin-proteasome system-dependent muscle atrophy.

BACKGROUND: Muscle atrophy, leading to muscular dysfunction and weakness, is an adverse outcome of sustained period of glucocorticoids usage. However, the molecular mechanism underlying this detrimental condition is currently unclear. Pyruvate dehydrogenase kinase 4 (PDK4), a central regulator of cellular energy metabolism, is highly expressed in skeletal muscle and has been implicated in the pathogenesis of several diseases. The current study was designed to investigated and delineate the role of PDK4 in the context of muscle atrophy, which could be identified as a potential therapeutic avenue to protect against dexamethasone-induced muscle wasting. METHODS: The dexamethasone-induced muscle atrophy in C2C12 myotubes was evaluated at the molecular level by expression of key genes and proteins involved in myogenesis, using immunoblotting and qPCR analyses. Muscle dysfunction was studied in vivo in wild-type and PDK4 knockout mice treated with dexamethasone (25 mg/kg body weight, i.p., 10 days). Body weight, grip strength, muscle weight and muscle histology were assessed. The expression of myogenesis markers were analysed using qPCR, immunoblotting and immunoprecipitation. The study was extended to in vitro human skeletal muscle atrophy analysis. RESULTS: Knockdown of PDK4 was found to prevent glucocorticoid-induced muscle atrophy and dysfunction in C2C12 myotubes, which was indicated by induction of myogenin (0.3271 ± 0.102 vs 2.163 ± 0.192, ****P < 0.0001) and myosin heavy chain (0.3901 ± 0.047 vs. 0.7222 ± 0.082, **P < 0.01) protein levels and reduction of muscle atrophy F-box (10.77 ± 2.674 vs. 1.518 ± 0.172, **P < 0.01) expression. In dexamethasone-induced muscle atrophy model, mice with genetic ablation of PDK4 revealed increased muscle strength (162.1 ± 22.75 vs. 200.1 ± 37.09 g, ***P < 0.001) and muscle fibres (54.20 ± 11.85% vs. 84.07 ± 28.41%, ****P < 0.0001). To explore the mechanism, we performed coimmunoprecipitation and liquid chromatography-mass spectrometry analysis and found that myogenin is novel substrate of PDK4. PDK4 phosphorylates myogenin at S43/T57 amino acid residues, which facilitates the recruitment of muscle atrophy F-box to myogenin and leads to its subsequent ubiquitination and degradation. Finally, overexpression of non-phosphorylatable myogenin mutant using intramuscular injection prevented dexamethasone-induced muscle atrophy and preserved muscle fibres. CONCLUSIONS: We have demonstrated that PDK4 mediates dexamethasone-induced skeletal muscle atrophy. Mechanistically, PDK4 phosphorylates and degrades myogenin via recruitment of E3 ubiquitin ligase, muscle atrophy F-box. Rescue of muscle regeneration by genetic ablation of PDK4 or overexpression of non-phosphorylatable myogenin mutant indicates PDK4 as an amenable therapeutic target in muscle atrophy.

Pyruvate dehydrogenase kinase 1 and 2 deficiency reduces high-fat diet-induced hypertrophic obesity and inhibits the differentiation of preadipocytes into mature adipocytes.

Obesity is now recognized as a disease. This study revealed a novel role for pyruvate dehydrogenase kinase (PDK) in diet-induced hypertrophic obesity. Mice with global or adipose tissue-specific PDK2 deficiency were protected against diet-induced obesity. The weight of adipose tissues and the size of adipocytes were reduced. Adipocyte-specific PDK2 deficiency slightly increased insulin sensitivity in HFD-fed mice. In studies with 3T3-L1 preadipocytes, PDK2 and PDK1 expression was strongly increased during adipogenesis. Evidence was found for epigenetic induction of both PDK1 and PDK2. Gain- and loss-of-function studies with 3T3-L1 cells revealed a critical role for PDK1/2 in adipocyte differentiation and lipid accumulation. PDK1/2 induction during differentiation was also accompanied by increased expression of hypoxia-inducible factor-1α (HIF1α) and enhanced lactate production, both of which were absent in the context of PDK1/2 deficiency. Exogenous lactate supplementation increased the stability of HIF1α and promoted adipogenesis. PDK1/2 overexpression-mediated adipogenesis was abolished by HIF1α inhibition, suggesting a role for the PDK-lactate-HIF1α axis during adipogenesis. In human adipose tissue, the expression of PDK1/2 was positively correlated with that of the adipogenic marker PPARγ and inversely correlated with obesity. Similarly, PDK1/2 expression in mouse adipose tissue was decreased by chronic high-fat diet feeding. We conclude that PDK1 and 2 are novel regulators of adipogenesis that play critical roles in obesity.

Therapeutic effect of dichloroacetate against atherosclerosis via hepatic FGF21 induction mediated by acute AMPK activation.

Dyslipidemia-induced atherosclerosis, which has a risk of high morbidity and mortality, can be alleviated by metabolic activation associated with mitochondrial function. The effect of dichloroacetate (DCA), a general pyruvate dehydrogenase kinase (PDK) inhibitor, on in vivo energy expenditure in ApoE-/- mice fed a western diet (WD) has not yet been investigated. WD-fed ApoE-/- mice developed atherosclerotic plaques and hyperlipidemia along with obesity, which were significantly ameliorated by DCA administration. Increased oxygen consumption was associated with heat production in the DCA-treated group, with no change in food intake or physical activity compared with those of the control. These processes were correlated with the increased gene expression of Dio2 and Ucp-1, which represents brown adipose tissue (BAT) activation, in both WD-induced atherosclerosis and high-fat-induced obesity models. In addition, we found that DCA stimulated hepatic fibroblast growth factor 21 (Fgf21) mRNA expression, which might be important for lowering lipid levels and insulin sensitization via BAT activation, in a dose- and time-dependent manner associated with serum FGF21 levels. Interestingly, Fgf21 mRNA expression was mediated in an AMP-activated protein kinase (AMPK)-dependent manner within several minutes after DCA treatment independent of peroxisome proliferator-activated receptor alpha (PPARα). Taken together, the results suggest that enhanced glucose oxidation by DCA protects against atherosclerosis by inducing hepatic FGF21 expression and BAT activation, resulting in augmented energy expenditure for heat generation.

Phenylbutyrate Ameliorates High-Fat Diet-Induced Obesity via Brown Adipose Tissue Activation.

Obesity, which is characterized by an excessive accumulation of body fat, is one of the critical factors causing metabolic syndrome. Many studies have been performed to identify appropriate agents to control obesity, but toxicity remains a problem. Herein, we identified that phenylbutyrate (PBA), which has been used to treat urea cycle disorder with very low toxicity for a long time, efficiently inhibited high fat-induced body weight gain in a diet-induced obesity mouse model (DIO model). PBA treatment decreased body fat mass and increased lean composition. Moreover, PBA increased brown adipose tissue (BAT) activity by increasing glucose uptake, thereby improving glucose tolerance and insulin tolerance. Interestingly, PBA could induce the expression of liver type phosphofructokinase (PFKL), a key enzyme in the glycolytic pathway, and knocking down PFKL dramatically repressed the expression level of Ucp1 as well as those of Prdm16, Cidea, Pgc1α, and Pparγ, which are marker genes for BAT activation. These results strongly suggested that PBA could increase energy expenditure by increasing BAT activity via the induction of PFKL. Taken together, PBA could be used as a therapeutic agent for people with obesity to prevent the development of metabolic syndrome.

Pyruvate Dehydrogenase Kinase Is a Metabolic Checkpoint for Polarization of Macrophages to the M1 Phenotype.

Metabolic reprogramming during macrophage polarization supports the effector functions of these cells in health and disease. Here, we demonstrate that pyruvate dehydrogenase kinase (PDK), which inhibits the pyruvate dehydrogenase-mediated conversion of cytosolic pyruvate to mitochondrial acetyl-CoA, functions as a metabolic checkpoint in M1 macrophages. Polarization was not prevented by PDK2 or PDK4 deletion but was fully prevented by the combined deletion of PDK2 and PDK4; this lack of polarization was correlated with improved mitochondrial respiration and rewiring of metabolic breaks that are characterized by increased glycolytic intermediates and reduced metabolites in the TCA cycle. Genetic deletion or pharmacological inhibition of PDK2/4 prevents polarization of macrophages to the M1 phenotype in response to inflammatory stimuli (lipopolysaccharide plus IFN-γ). Transplantation of PDK2/4-deficient bone marrow into irradiated wild-type mice to produce mice with PDK2/4-deficient myeloid cells prevented M1 polarization, reduced obesity-associated insulin resistance, and ameliorated adipose tissue inflammation. A novel, pharmacological PDK inhibitor, KPLH1130, improved high-fat diet-induced insulin resistance; this was correlated with a reduction in the levels of pro-inflammatory markers and improved mitochondrial function. These studies identify PDK2/4 as a metabolic checkpoint for M1 phenotype polarization of macrophages, which could potentially be exploited as a novel therapeutic target for obesity-associated metabolic disorders and other inflammatory conditions.

Recent advances in the pathogenesis of microvascular complications in diabetes.

Millions of people worldwide have diabetes, which is diagnosed by fasting blood glucose levels exceeding 126 mg/dL. Regardless of the type of diabetes, prolonged hyperglycemia is damaging to several organs including eyes, kidneys, nerve, and/or heart. The damages are associated with a high risk of morbidity and mortality. Diabetes has been implicated in ischemia in the microvasculature of the target tissues, which occurs due to the insufficient perfusion of tissues. The resulting occlusion and pain affect the quality of life. Multiple therapeutic approaches have been proposed for a long time to overcome these vascular complications. Apart from systemically controlling high glucose levels, other therapeutic strategies are not well understood. In this review, we summarize the recent literature for biochemical/cellular targets that are being utilized for the treatment of diabetic microvascular diseases. These targets, which are closely associated with mitochondrial dysfunction, include the polyol and diacylglycerol-protein kinase C pathways, oxidative stress, non-enzymatic glycation and the formation of advanced glycation end products, and immune dysregulation/inflammation.

Feasibility and safety of EUS-guided selective portal vein embolization with a coil and cyanoacrylate in a live porcine model.

BACKGROUND AND OBJECTIVES: Preoperative portal vein (PV) embolization using the percutaneous transhepatic approach has been performed in patients with hepatobiliary malignancy before extensive liver resection. The aim of this study is to evaluate the technical feasibility and initial safety of EUS-guided selective PV embolization using a coil and cyanoacrylate in a live porcine model. METHODS: EUS-guided selective intrahepatic PV embolization with a coil and cyanoacrylate was performed in 9 pigs. The selected PV was punctured with 19G fine-needle aspiration (FNA) needle, and the coil was inserted under EUS-guidance. The cyanoacrylate was then immediately injected through the same FNA needle. The blood flow change in the embolized PV was evaluated using color Doppler EUS. A necropsy was performed following the 1-week observation period. RESULTS: The success rates for the coil and cyanoacrylate delivery were 88.9% (8/9) and 87.5% (7/8), respectively. In 1 case, the coil migrated into the hepatic parenchyma. In another case, the cyanoacrylate injection failed due to early clogging in the FNA needle. There was a complete blockage of blood flow confirmed by color Doppler EUS in the embolized PV after coil and cyanoacrylate treatment. There was coil migration into the hepatic parenchyma in 1 case. There was no animal distress observed during the 1-week observation period before necropsy. The necropsy showed no evidence of damage to the intra-abdominal organs, and the selected PV was totally occluded with embolus. CONCLUSION: The study findings indicate EUS-guided selective PV embolization is both technically feasible and initially safe in an animal model.

Endoscopic ultrasonography-guided placement of a transhepatic portal vein stent in a live porcine model.

BACKGROUND AND OBJECTIVES: Percutaneous portal vein (PV) stent placement is used to manage PV occlusion or stenosis caused by malignancy. The use of endoscopic ultrasonography (EUS) has expanded to include vascular interventions. The aim of this study was to examine the technical feasibility and safety of EUS-guided transhepatic PV stent placement in a live porcine model. MATERIALS AND METHODS: EUS-guided transhepatic PV stent placement was performed in six male miniature pigs under general anesthesia using forward-viewing echoendoscope. Under EUS guidance, the left intrahepatic PV was punctured with a 19-gauge fine-needle aspiration (FNA) needle and a 0.025 inch guidewire inserted through the needle and into the main PV. The FNA needle was then withdrawn and a needle-knife inserted to dilate the tract. Under EUS and fluoroscopic guidance, a noncovered metal stent was inserted over the guidewire and released into the main PV. RESULTS: A PV stent was placed successfully in all six pigs with no technical problems or complications. The patency of the stent in the main PV was confirmed using color Doppler EUS and transhepatic portal venography. Necropsy of the first three animals revealed no evidence of bleeding and damage to intra-abdominal organs or vessels. No complications occurred in the remaining three animals during the 8 weeks observation period. CONCLUSIONS: EUS-guided transhepatic PV stent placement can be both technically feasible and safe in a live animal model.

Inhibition of Pyruvate Dehydrogenase Kinase 2 Protects Against Hepatic Steatosis Through Modulation of Tricarboxylic Acid Cycle Anaplerosis and Ketogenesis.

Hepatic steatosis is associated with increased insulin resistance and tricarboxylic acid (TCA) cycle flux, but decreased ketogenesis and pyruvate dehydrogenase complex (PDC) flux. This study examined whether hepatic PDC activation by inhibition of pyruvate dehydrogenase kinase 2 (PDK2) ameliorates these metabolic abnormalities. Wild-type mice fed a high-fat diet exhibited hepatic steatosis, insulin resistance, and increased levels of pyruvate, TCA cycle intermediates, and malonyl-CoA but reduced ketogenesis and PDC activity due to PDK2 induction. Hepatic PDC activation by PDK2 inhibition attenuated hepatic steatosis, improved hepatic insulin sensitivity, reduced hepatic glucose production, increased capacity for ß-oxidation and ketogenesis, and decreased the capacity for lipogenesis. These results were attributed to altered enzymatic capacities and a reduction in TCA anaplerosis that limited the availability of oxaloacetate for the TCA cycle, which promoted ketogenesis. The current study reports that increasing hepatic PDC activity by inhibition of PDK2 ameliorates hepatic steatosis and insulin sensitivity by regulating TCA cycle anaplerosis and ketogenesis. The findings suggest PDK2 is a potential therapeutic target for nonalcoholic fatty liver disease.

Roseovarius aquimarinus sp. nov., a slightly halophilic bacterium isolated from seawater.

A Gram-stain-negative, non-spore-forming, rod-shaped, motile, facultatively anaerobic bacterium, designated CAU 1059T, was isolated from a seawater sample from Jeju Island, Republic of Korea. The bacterium grew optimally at 37 °C, at pH 7.0 and in the presence of 2 % (w/v) NaCl. Phylogenetic analysis based on 16S rRNA gene sequences revealed that strain CAU 1059T belonged to the genus Roseovarius. It exhibited only 91.5-96.9 % sequence similarity to the type strains of recognized Roseovarius species. Similar to other species of the genus Roseovarius, strain CAU 1059T had ubiquinone-10 (Q-10) as the predominant ubiquinone and C16 : 0 and summed feature 8 (C18 : 1ω7c/ω6c) as the major fatty acids. The polar lipid pattern consisted of diphosphatidylglycerol, phosphatidylglycerol, phosphatidylethanolamine and phosphatidylcholine; three unidentified phospholipids, two aminolipids, an aminophospholipid and nine other lipids were also found. The G+C content of the genomic DNA was 61.9 mol%. On the basis of the data provided, strain CAU 1059T should be classified as representing a novel species of the genus Roseovarius, for which the name Roseovarius aquimarinus sp. nov. is proposed. The type strain is CAU 1059T ( = KCTC 32014T = CCUG 64792T).

Paenibacillus doosanensis sp. nov., isolated from soil.

A Gram-stain-positive, aerobic, endospore-forming bacterium, designated CAU 1055(T), was isolated from soil and its taxonomic position was investigated using a polyphasic approach. Phylogenetic analysis based on 16S rRNA gene sequence comparison revealed that the strain formed a distinct lineage within the genus Paenibacillus and was most closely related to Paenibacillus contaminans CKOBP-6(T) (similarity, 95.2 %) and Paenibacillus terrigena A35(T) (similarity, 95.2 %). The levels of 16S rRNA gene sequence similarity with other species of the genus Paenibacillus, including the type species of the genus, Paenibacillus polymyxa IAM 13419(T) (similarity, 91.7 %), were all <94.6 %. Strain CAU 1055(T) contained MK-7 as the only isoprenoid quinone and anteiso-C15 : 0 and iso-C16 : 0 as the major fatty acids. The cell-wall peptidoglycan of strain CAU 1055(T) contained meso-diaminopimelic acid. The polar lipids were composed of diphosphatidylglycerol, phosphatidylethanolamine, phosphatidylglycerol, lysyl-phospatidylglycerol and three unidentified aminophospholipids. The DNA G+C content was 48.3 mol%. The results of physiological and biochemical tests allowed phenotypic differentiation of strain CAU 1055(T) from closely related recognized species. On the basis of phenotypic data and phylogenetic inference, strain CAU 1055(T) should be classified in the genus Paenibacillus, as a member of a novel species, for which the name Paenibacillus doosanensis sp. nov. is proposed. The type strain is CAU 1055(T) ( = KCTC 33036(T) = CCUG 63270(T)).

Bacillus songklensis sp. nov., isolated from soil.

A Gram-stain-positive, spore-forming, rod-shaped, motile, strictly aerobic bacterial strain, designated CAU 1033(T), was isolated from soil and its taxonomic position was investigated using a polyphasic approach. Phylogenetic analysis based on 16S rRNA gene sequences revealed that strain CAU 1033(T) formed a distinct lineage within the genus Bacillus and was most closely related to Bacillus drentensis KCTC 13025(T) (similarity 95.9 %). CAU 1033(T) contained MK-7 as the only isoprenoid quinone and iso-C15 : 0 and anteiso-C15 : 0 as the major fatty acids. The cell wall peptidoglycan of strain CAU 1033(T) contained meso-diaminopimelic acid and the major whole-cell sugars were arabinose, sucrose and ribose. The polar lipids were composed of diphosphatidylglycerol, phosphatidylglycerol, phosphatidylethanolamine, two unidentified phospholipids, four unidentified aminophospholipids, an unidentified aminolipid, two unidentified glycolipids and another unidentified polar lipid. The DNA G+C content was 41.4 mol%. On the basis of phenotypic data and phylogenetic inference, strain CAU 1033(T) was classified as a representative of a novel species in the genus Bacillus for which the name Bacillus songklensis sp. nov. is proposed. The type strain is CAU 1033(T) ( = KCTC 13881(T) = CCUG 61889(T)).

Dimethylfumarate suppresses adipogenic differentiation in 3T3-L1 preadipocytes through inhibition of STAT3 activity.

The excessive accumulation of adipocytes contributes to the development of obesity and obesity-related diseases. The interactions of several transcription factors, such as C/EBPß, PPARγ, C/EBPα, Nrf2, and STAT3, are required for adipogenic differentiation. Dimethylfumarate (DMF), an immune modulator and antioxidant, may function as an inhibitor of STAT3 and an activator of Nrf2. This study examined whether DMF inhibits adipogenic differentiation of 3T3-L1 preadipocytes by inhibiting STAT3 or activating Nrf2. DMF suppressed 3T3-L1 preadipocyte differentiation to mature adipocytes in a dose-dependent manner as determined by Oil Red O staining. The mRNA and protein levels of adipogenic genes, including C/EBPß, C/EBPα, PPARγ, SREBP-1c, FAS, and aP2, were significantly lower in DMF-treated 3T3-L1 preadipocytes. Suppression of adipogenic differentiation by DMF treatment resulted primarily from inhibition of the early stages of differentiation. DMF inhibits clonal expansion during adipogenic differentiation through induction of a G1 cell cycle arrest. Additionally, DMF regulates cell cycle-related proteins, such as p21, pRb, and cyclin D. DMF treatment markedly inhibited differentiation medium-induced STAT3 phosphorylation and inhibited STAT3 transcriptional activation of a reporter construct composed of four synthetic STAT3-response elements. Moreover, inhibition of endogenous Nrf2 activity using a dominant negative Nrf2 did not abolish the DMF-induced inhibition of adipogenic differentiation of 3T3-L1 preadipocytes. In summary, DMF is a negative regulator of adipogenic differentiation based on its regulation of adipogenic transcription factors and cell cycle proteins. This negative regulation by DMF is mediated by STAT3 inhibition, but is unlikely to involve Nrf2 activation.

Oceanobacillus chungangensis sp. nov., isolated from a sand dune.

A Gram-stain-positive, spore-forming, rod-shaped, motile, strictly aerobic bacterial strain, designated CAU 1051(T), was isolated from a sand dune and its taxonomic position was investigated using a polyphasic approach. Strain CAU 1051(T) grew optimally at pH 5.0 and 30 °C. NaCl was not required for growth but up to 10.0 % (w/v) NaCl was tolerated. Phylogenetic analysis based on 16S rRNA gene sequences revealed that strain CAU 1051(T) formed a distinct lineage within the genus Oceanobacillus and was most closely related to Oceanobacillus profundus CL-MP28(T), Oceanobacillus caeni S-11(T), and Oceanobacillus picturae LMG 19492(T) (96.8 %, 95.6 % and 95.3 % similarity, respectively). DNA-DNA reassociation analysis showed that strain CAU 1051(T) displayed 28.2±0.7 % relatedness to O. profundus KCTC 13625(T). Strain CAU 1051(T) contained MK-7 as the only isoprenoid quinone and anteiso-C15 : 0 as the major fatty acid. The cell wall peptidoglycan of strain CAU 1051(T) contained meso-diaminopimelic acid. The polar lipids were composed of diphosphatidylglycerol, phosphatidylglycerol, six unidentified phospholipids, an unidentified glycolipid, and six unidentified polar lipids. The major whole-cell sugars were glucose and ribose. The DNA G+C content was 36.3 mol%. On the basis of phenotypic data and phylogenetic inference, strain CAU 1051(T) represents a novel species of the genus Oceanobacillus for which the name Oceanobacillus chungangensis sp. nov. is proposed. The type strain is CAU 1051(T) ( = KCTC 33035(T) = CCUG 63270(T)).

Haloferula chungangensis sp. nov., isolated from marine sediment.

A Gram-stain-negative, non-spore-forming, non-motile, strictly aerobic, rod-shaped bacterial strain, designated CAU 1074(T), was isolated from marine sediment and its taxonomic position was investigated using a polyphasic approach. Strain CAU 1074(T) grew optimally at 30 °C and pH 6.5. Phylogenetic analysis based on 16S rRNA gene sequences revealed that strain CAU 1074(T) formed a distinct lineage within the genus Haloferula and was most closely related to Haloferula harenae KCTC 22198(T) (96.0% similarity). Strain CAU 1074(T) contained MK-9 as the major isoprenoid quinone, and iso-C(14:0,) C(16:1)ω9c and C(16:0) as the major fatty acids. The cell wall peptidoglycan contained meso-diaminopimelic acid. The major whole-cell sugars were glucose, xylose, mannose and ribose. The polar lipids were composed of diphosphatidylglycerol, phosphatidylethanolamine, phosphatidylglycerol, aminoglycolipid and two unidentified phospholipids. The DNA G+C content of the strain was 64.0 mol%. On the basis of phenotypic and chemotaxonomic data, and phylogenetic inference, strain CAU 1074(T) should be classified as a member of a novel species in the genus Haloferula, for which the name Haloferula chungangensis sp. nov. is proposed; the type strain is CAU 1074(T) (= KCTC 23578(T) = CCUG 61920(T)). An emended description of the genus Haloferula is also provided.

Algoriphagus chungangensis sp. nov., isolated from a tidal flat sediment.

A Gram-stain-negative, non-spore-forming, non-motile, strictly aerobic, rod-shaped bacterial strain, designated CAU 1002(T), was isolated from a tidal flat sediment and its taxonomic position was investigated using a polyphasic approach. Strain CAU 1002(T) grew optimally at 30 °C and pH 7.5. Phylogenetic analysis based on 16S rRNA gene sequences revealed that strain CAU 1002(T) formed a distinct lineage within the genus Algoriphagus and was most closely related to Algoriphagus lutimaris KCTC 22630(T) and Algoriphagus halophilus KCTC 12051(T) (97.75 and 97.74 % 16S rRNA gene sequence similarity, respectively). The strain contained MK-7 as the major isoprenoid quinone and iso-C(15 : 0) and C(16 : 1)ω7c and/or iso-C(15 : 0) 2-OH (summed feature 3) as the major fatty acids. The cell-wall peptidoglycan of strain CAU 1002(T) contained meso-diaminopimelic acids. The major whole-cell sugars were glucose, arabinose, sucrose, and ribose. The polar lipid profile was composed of phosphatidylethanolamine, five unidentified aminolipids, one unidentified aminophospholipid, one unidentified phospholipid, one unidentified aminoglycolipid, one unidentified glycolipid and twelve unidentified lipids. The DNA G+C content of strain CAU 1002(T) was 38.0 mol%. On the basis of phylogenetic inference, phenotypic, chemotaxonomic and genotypic data, strain CAU 1002(T) should be classified into the genus Algoriphagus as a member of a novel species, for which the name Algoriphagus chungangensis sp. nov. is proposed. The type strain is CAU 1002(T) ( = KCTC 23759(T) = CCUG 61890(T)). The description of the genus Algoriphagus is emended.

Molecular characterization of serotype G9 rotaviruses circulating in South Korea between 2005 and 2010.

A total of 18 rotavirus G9 strains in South Korea were collected during five rotavirus seasons between 2005 and 2010. The relationship between these strains was examined by analyzing the genetic variation of two major structural genes, VP7 and VP4. All the rotavirus isolates were of the G9P[8] genotype. The VP7 phylogenetic analysis demonstrated that all of the G9 rotaviruses circulating in South Korea belonged to lineage IIId and were within three single clusters. The amino acid comparison of the antigenic regions of the VP7 gene suggests possible common progenitors of these strains. Phylogenetic analysis of P[8] VP4 genotypes indicated three lineages, P[8]-2, P[8]-3, and P[8]-4, with P[8]-3 being the most common. The results of this study provide information on the genetic relatedness of rotavirus G9 strains circulating in South Korea over recent years and can be utilized for the development of effective vaccines and the identification of reference strains for future efficacy studies.

Maribacter chungangensis sp. nov., isolated from a green seaweed, and emended descriptions of the genus Maribacter and Maribacter arcticus.

A Gram-stain-negative, non-spore-forming, strictly aerobic, orange-pigmented bacterial strain, motile by gliding, designated CAU 1044(T), was isolated from a green seaweed and its taxonomic position was investigated using a polyphasic approach. Phylogenetic analysis based on 16S rRNA gene sequences revealed that strain CAU 1044(T) formed a distinct lineage within the genus Maribacter and was most closely related to Maribacter antarcticus JCM 15445(T) and Maribacter arcticus KOPRI 20941(T) (96.3 and 95.7 % similarity, respectively). Strain CAU 1044(T) contained menaquinone 6 as the only isoprenoid quinone and iso-C15 : 0, summed feature 3 (comprising C16 : 1ω7c and/or C16 : 1ω6c and/or iso-C15 : 0 2-OH), iso-C17 : 0 3-OH and iso-C15 : 1 G as the major fatty acids. The cell wall peptidoglycan of strain CAU 1044(T) contained meso-diaminopimelic acid and the major whole-cell sugars were glucose and ribose. The polar lipids were composed of phosphatidylethanolamine, one unidentified phospholipid, six unidentified aminolipids and four unidentified lipids. The DNA G+C content was 40.2 mol%. On the basis of phenotypic data and phylogenetic inference, strain CAU 1044(T) should be classified as a representative of a novel species in the genus Maribacter for which the name Maribacter chungangensis sp. nov. is proposed. The type strain is CAU 1044(T) ( = KCTC 23735(T) = CCUG 61948(T)). Emended descriptions of the genus Maribacter and the species M. arcticus KCTC 22053(T) are also proposed.