Taxonomy of the order Bunyavirales: update 2019.

In February 2019, following the annual taxon ratification vote, the order Bunyavirales was amended by creation of two new families, four new subfamilies, 11 new genera and 77 new species, merging of two species, and deletion of one species. This article presents the updated taxonomy of the order Bunyavirales now accepted by the International Committee on Taxonomy of Viruses (ICTV).

Activity of bovine lactoferrin in resistance to white spot syndrome virus infection in shrimp.

White spot syndrome virus (WSSV) is a notorious pathogen that has plagued shrimp farming worldwide for decades. To date, there are no known treatments that are effective against this virus. Lactoferrin (LF) is a protein with many bioactivities, including antiviral properties. In this study, the activities and mechanisms of bovine LF (bLF) against WSSV were analyzed. Our results showed that bLF treatment significantly reduced shrimp mortalities caused by WSSV infection. bLF was found to have the ability to bind to surfaces of both host cells and WSSV virions. These bindings may have been a result of bLF interactions with the host cellular chitin binding protein and F1 ATP synthase ß subunit protein and the WSSV structural proteins VP28, VP110, VP150 and VP160B. bLF demonstrated potential for development as an anti-WSSV agent in shrimp culture. Furthermore, these reactionary proteins may play a role in WSSV infection.

Effects of Lyrm1 knockdown on mitochondrial function in 3 T3-L1 murine adipocytes.

To explore the effects of Lyrm1 knockdown on the mitochondrial function of 3 T3-L1 adipocytes using small interfering RNA (siRNA). 3 T3-L1 preadipocytes were infected with either a negative control (NC) expression lentivirus or a Lyrm1-shRNA expression lentivirus and induced to differentiate. The knockdown efficiency of Lrym1-specific shRNA in 3 T3-L1 cells was evaluated by real-time PCR. The ultrastructure of the mitochondria in adipocytes was visualized using transmission electron microscopy after differentiation. The levels of mitochondrial DNA copy numbers and Ucp2 mRNA were detected by real-time quantitative PCR. The levels of ATP production was detected using a photon-counting luminometer. The mitochondrial membrane potential and ROS levels of cells were analyzed with a FACScan flow cytometer using Cell Quest software. Cells transfected with lentiviral-Lyrm1-shRNA showed a significantly reduced transcription of Lyrm1 mRNA compared with NC cells. The size and ultrastructure of mitochondria in Lyrm1 knockdown adipocytes was similar to those of the NC cells. There was no significant difference in mtDNA copy number between the two groups. The total level of ATP production, mitochondrial membrane potential and Ucp2 mRNA expression levels were dramatically increased in adipocytes transfected with Lyrm1 RNAi. Furthermore, the level of ROS was dramatically decreased in Lyrm1 knockdown adipocytes. Knockdown of the Lyrm1 gene in adipocytes resulted in dramatically increased cellular ATP production, mitochondrial membrane potentials and levels Ucp2 mRNA, while ROS levels were significantly decreased. These results imply that mitochondrial function is improved in adipocytes after the knockdown of Lyrm1.

α-Lipoic acid ameliorates impaired glucose uptake in LYRM1 overexpressing 3T3-L1 adipocytes through the IRS-1/Akt signaling pathway.

Overexpression of the Homo sapiens LYR motif containing 1 (LYRM1) causes mitochondrial dysfunction and induces insulin resistance in 3T3-L1 adipocytes. α-Lipoic acid (α-LA), a dithiol compound with antioxidant properties, improves glucose transport and utilization in 3T3-L1 adipocytes. The aim of this study was to investigate the direct effects of α-LA on reactive oxygen species (ROS) production and insulin sensitivity in LYRM1 overexpressing 3T3-L1 adipocytes and to explore the underlying mechanism. Pretreatment with α-LA significantly increased both basal and insulin-stimulated glucose uptake and insulin-stimulated GLUT4 translocation, while intracellular ROS levels in LYRM1 overexpressing 3T3-L1 adipocytes were decreased. These changes were accompanied by a marked upregulation in expression of insulin-stimulated tyrosine phosphorylation of IRS-1 and serine phosphorylation of Akt following treatment with α-LA. These results indicated that α-LA protects 3T3-L1 adipocytes from LYRM1-induced insulin resistance partially via its capacity to restore mitochondrial function and/or increase phosphorylation of IRS-1 and Akt.

Effects of embryonic exposure to polychlorinated biphenyls on zebrafish (Danio rerio) retinal development.

Polychlorinated biphenyls (PCBs) are persistent environmental pollutants that affect embryonic development. The purpose of this study was to examine the effects of embryonic exposure to PCBs on early retinal development in zebrafish, Danio rerio. Zebrafish embryos were immediately exposed to different concentrations (0, 0.125, 0.25, 0.5, 1.0 and 2.0 mg) of PCBs per liter of medium at 28.5 °C. Embryos were assessed at 30, 48, 72 and 96 h post-fertilization (hpf) for changes in embryonic survival rate, development, larval retinal morphology and ultrastructure of the retina. The results show that PCB exposure decreased the survival rate of embryos in a time- and dose-dependent manner. Embryos exposed to the higher concentrations of PCBs (0.5, 1.0 and 2.0 mg l(-1) ) displayed obvious gross morphological deformities. At 72 hpf, the retinal layer development of zebrafish was delayed at higher PCB concentrations (1.0 mg l(-1) ). At 96 hpf, irregularity of photoreceptor cells arrangement and thickening of photoreceptor and ganglionic layers were observed in PCB-treated larvae at concentrations of 0.25-1 mg l(-1) . Ultrastructural examination showed signs of growth inhibition of the photoreceptor outer segment at 0.25-1 mg l(-1) PCB exposure at 72 hpf, as well as the appearance of massive vacuoles and holes inside the outer segments in the PCB exposure group at 96 hpf. These results suggest that embryonic exposure to moderate and high levels of PCBs induced developmental deficits in zebrafish retinas, particularly in photoreceptor cells.

Stability analysis of Hadamard and Caputo-Hadamard fractional nonlinear systems without and with delay.

This paper handles with the Hadamard and the Caputo-Hadamard fractional derivative and stability of related systems without and with delay. Firstly, the derivative inequalities are obtained, which is indispensable in applying the theorems derived in this paper. Then, for systems without delay, we get the stability results by using the Lyapunov direct method and for systems with delay, we explore two useful inequalities to verify the stability. Examples are presented with numerical simulations to illustrate the effectiveness of our results.

Monoclonal antibody to six transmembrane epithelial antigen of prostate-4 influences insulin sensitivity by attenuating phosphorylation of P13K (P85) and Akt: possible mitochondrial mechanism.

We examined the effects of anti-six-transmembrane epithelial antigen of the prostate-4 (STEAP4) antibodies on glucose transport in mature adipocytes and determined the mechanism of insulin resistance in obesity. Western blotting was performed to determine STEAP4 expression, to assess translocation of insulin-sensitive glucose transporter 4 (GLUT4), and to measure phosphorylation and total protein content of insulin-signaling proteins. Confocal laser microscopy and flow cytometry were used to detect intracellular reactive oxygen species (ROS) and fluctuations in mitochondrial membrane potential (ΔΨ). ATP production was measured by using a luciferase-based luminescence assay kit. After the application of anti-STEAP4 antibodies at 0.002 mg/mL, adipocytes exhibited reduced insulin-stimulated glucose transport by attenuating the phosphorylation of IRS-1, PI3K (p85), and Akt. The antibodies also potentially increase the level of ROS and decrease cellular ATP production and ΔΨ. In conclusion, (i) STEAP4 regulates the function of IRS-1, PI3K, and Akt and decreases insulin-induced GLUT4 translocation and glucose uptake; (ii) ROS-related mitochondrial dysfunction may be related to a reduced IRS-1 correlation with the PI3K signaling pathway, leading to insulin resistance. These observations highlight the potential role of STEAP4 in glucose homeostasis and possibly in the pathophysiology of type 2 diabetes related to obesity and may provide new insights into the mechanisms of insulin resistance in obesity.

UCP4 overexpression improves fatty acid oxidation and insulin sensitivity in L6 myocytes.

Obesity, which is caused by energy uptake being greater than energy expenditure, is widely prevalent today. Currently, only a limited number of efficient interventional strategies are available for the prevention of obesity. Previous studies have shown that UCP4 transcription occurs at a considerable level in mouse skeletal muscle; however, the exact functions of UCP4 remain unclear. In this study, we investigated the effect of UCP4 on mitochondrial function and insulin sensitivity in mature L6 myocytes. UCP4 overexpression in L6 myocytes induced increased mitochondrial carnitine palmitoyltransferase 1A (CPT1A) and decreased citrate synthase (CS) mRNA in the basal condition (i.e., in the absence of insulin). UCP4 overexpression significantly improved insulin sensitivity, increased tyrosine phosphorylation of IRS-1 in the presence of insulin, and significantly reduced intracellular triglyceride (TG). Additionally, intracellular ATP content and mitochondrial membrane potential were downregulated. We also observed that intracellular ROS, mitochondrial morphology, and mitochondrial mtDNA copy number were maintained upon UCP4 expression, with no change in mitochondrial fusion and fission. In summary, our findings provide evidence to show that UCP4 overexpression reduced the insulin sensitivity and mitochondrial fatty acid oxidation of L6 myocytes. These findings support the notion that UCPs are ideal targets for treatment of insulin resistance.

Overexpression of LYRM1 induces mitochondrial impairment in 3T3-L1 adipocytes.

Homo sapiens LYR motif containing 1 (LYRM1) is a recently discovered gene involved in adipose tissue homeostasis and obesity-associated insulin resistance. The exact mechanism by which LYRM1 induces insulin resistance has not yet been fully elucidated. In this study, we demonstrated that the overexpression of LYRM1 in 3T3-L1 adipocytes resulted in reduced insulin-stimulated glucose uptake, an abnormal mitochondrial morphology, and a decrease in intracellular ATP synthesis and mitochondrial membrane potential. In addition, LYRM1 overexpression led to excessive production of intracellular of reactive oxygen species. Collectively, our results indicated that the overexpression of LYRM1 caused mitochondrial dysfunction in adipocytes, which might be responsible for the development of LYRM1-induced insulin resistance.

Short report: Tissue-specific expression profiles of the uncoupling protein family in normal control mice and genetically ob/ob mice.

Uncoupling proteins (UCPs) located in the inner mitochondrial membrane are involved in the regulation of energy balance. Thus far, 5 UCP isoforms have been identified, but controversies exist in the research focused on the function of the UCPs (except UCP1) in the pathogenesis of obesity. Because of the known cross-reactivity of the antibodies presently available for the detection of UCP proteins, this study systematically analyzed the differential tissue expression profiles of the 5 UCP isoforms in lean control mice and ob/ob mice by using real-time polymerase chain reaction (PCR) analysis. The results show that the tissue-specific expression patterns of individual isoforms in normal and ob/ob mice are considerably different; this will provide new insights into the functions of UCPs in the pathogenesis of genetic obesity.

Gene expression profiles of adipose tissue of high-fat diet-induced obese rats by cDNA microarrays.

To better understand the molecular basis of dietary obesity, we examined adipose tissue genes differentially expressed in a well-characterized rat model of high-fat diet (HFD)-induced obesity using cDNA microarrays. Male Sprague-Dawley rats were fed either the HFD or the normal diet. Seven weeks later, the weights of obese models (362.92 ± 39.65 g) were significantly higher than those of normal control rats (315.22 ± 42.30 g, P < 0.01) and the wet weights of adipose tissue of rats fed with HFD (9.29 ± 5.14 g) were significantly higher than those of normal control rats (4.09 ± 2.69 g, P < 0.01), which confirmed the successful preparation of obese models. cDNA microarrays containing 9 216 genes/Ests were used to investigate gene expression of adipose tissue. Autoradiographic analysis showed that 532, 154, and 22 genes were differently expressed over 2-, 3-, and 5-fold, respectively. The analysis of gene expression profiles indicated that 276 genes were up-regulated and 432 genes were down-regulated in response to HFD-induced obesity. Different clusters of genes associated with lipid metabolism, extracellular matrix, signal transduction, cytoskeleton, cell apoptosis, etc., such as VLCS-H2, DGAT, ACADVL, PHYH, SCD, ACACA, ACS, MMP-2, MMP-15, CD38, CAMK2D, CACNA1F, CAPZA2, TMOD3, ARPC2, KNS2, TPM1, MAPK8, GADD45B, DAXX, TOK-1, PRKACA, STAT6, were concerned.

The lin-4 gene controls fat accumulation and longevity in Caenorhabditis elegans.

Previous studies have determined that lin-4, which was the first miRNA to be discovered, controls the timing of cell fate determination and life span in Caenorhabditis elegans. However, the mechanism of lin-4 involvement in these processes remains poorly understood. Fat storage is an essential aspect of the life cycle of organisms, and the function of lin-4 in fat accumulation is not clear. In this study, we showed that the fat content is reduced remarkably in C. elegans lin-4 mutants. Quantitative RT-PCR analysis revealed a considerable decrease in the levels of SBP-1 and OGA-1 mRNA in lin-4 mutants. We also showed that lin-4 mutants have a significantly shorter life span than wild-type worms. DCF assay experiments showed that the reactive oxygen species (ROS) levels increased and mitochondrial DNA (mtDNA) copy number decreased in loss-of-function lin-4 mutants. These mutants also showed attenuation of locomotion. Taken together, our findings suggest that lin-4 may play an important role in regulating fat accumulation and locomotion and that lin-4 may control the life span of C. elegans by mediating ROS production.

A stair-like two-dimensional silver(I) coordination polymer of N'-(3-cyanobenzylidene)nicotinohydrazide.

The structure of the title compound, poly[[[mu3-N'-(3-cyanobenzylidene)nicotinohydrazide]silver(I)] hexafluoroarsenate], {[Ag(C14H10N4O)](AsF6)}n, at 173 K exhibits a novel stair-like two-dimensional layer and a three-dimensional supramolecular framework through C-H...Ag hydrogen bonds. The Ag(I) cation is coordinated by three N atoms and one O atom from N'-(3-cyanobenzylidene)nicotinohydrazide (L) ligands, resulting in a distorted tetrahedral coordination geometry. The organic ligand acts as a mu3-bridging ligand through the pyridyl and carbonitrile N atoms and deviates from planarity in order to adapt to the coordination geometry. Two ligands bridge two Ag(I) cations to construct a small 2+2 Ag2L2 ring. Four ligands bridge one Ag(I) cation from each of four of these small rings to form a large grid. An interesting stair-like two-dimensional (3,6)-net is formed through Ag(I) metal centres acting as three-connection nodes and through L molecules as tri-linkage spacers.

Dichlorido(2,9-dimeth-oxy-1,10-phenanthroline-κN,N')zinc(II).

In the crystal structure of the title compound, [ZnCl(2)(C(14)H(12)N(2)O(2))], the Zn(II) center is four-coordinated by two N atoms from one 2,9-dimeth-oxy-1,10-phenanthroline ligand and two Cl atoms. The coordination geometry is distorted tetra-hedral, as the Zn-N bond distances are shorter than the Zn-Cl distances, and the Cl-Zn-N and Cl-Zn-Cl bond angles are much larger than the N-Zn-N angle. For the ligand, the O and C atoms of the meth-oxy groups are almost in the plane defined by the phenanthroline ring. The two O atoms deviate from the phenanthroline mean plane by 0.076 (2) and 0.084 (2) Å, and the two methyl C atoms deviate from the phenanthroline mean plane by 0.035 (3) and 0.361 (3) Å. There are medium π-π stacking interactions between two parallel phenanthroline rings with a centroid-centroid distance of 3.7860 (2) Šand a dihedral angle between the plane defined by the two parallel phenanthroline rings of 1.13 (5)°.

Dichlorido(2,9-dieth-oxy-1,10-phenanthroline-κN,N')zinc(II).

All non-H atoms except for the Cl atoms lie on a mirror plane in the title complex, [ZnCl(2)(C(16)H(16)N(2)O(2))]. The Zn(II) ion is coordinated by two N atoms from a bis-chelating 2,9-dieth-oxy-1,10-phenanthroline ligand and two symmetry-related Cl atoms in a distorted tetra-hedral environment. The two Zn-N bond lengths are significantly different from each other and the N-Zn-N angle is acute. In the crystal structure, there are weak but significant π-π stacking inter-actions between phenanthroline rings, with a centroid-centroid distance of 3.764 (1) Å.

catena-Poly[[[[N'-(4-cyano-benzyl-idene)nicotinohydrazide]silver(I)]-µ-[N'-4-cyano-benzyl-idene)nicotinohydrazide]] hexa-fluoridoarsenate].

In the title compound, {[Ag(C(14)H(10)N(4)O)(2)]AsF(6)}(n), the Ag(I) ion is coordinated by two N atoms from two different pyridyl rings and one N atom from one carbonitrile group of three different N'-(4-cyano-benzyl-idene)nicotinohydrazide ligands in a distorted T-shaped geometry. The Ag-N(carbonitrile) bond distance is significant longer than those of Ag-N(pyrid-yl). The bond angles around the Ag(I) atom are also not in line with those in an ideal T-shaped geometry. One type of ligand acts as the bridge that connects Ag(I) atoms into chains along [01]. These chains are linked to each other via N-H⋯O hydrogen bonds and Ag⋯O inter-actions with an Ag⋯O separation of 2.869 (2) Å. In addition, the [AsF(6)](-) counter-anions are linked to the hydrazone groups through N-H⋯F hydrogen bonds. Four of the F atoms of the [AsF(6)](-) anion are disordered over two sets of sites with occupancies of 0.732 (9) and 0.268 (9).

Bis[N'-(3-cyano-benzyl-idene)isonicotino-hydrazide]silver(I) trifluoro-acetate.

In the title compound, [Ag(C(14)H(10)N(4)O)(2)]CF(3)CO(2), the Ag(I) ion is coordinated by two N atoms of the pyridine rings of two N'-(3-cyano-benzyl-idene)isonicotinohydrazide ligands in a nearly linear geometry. In the crystal structure, a combination of close contacts formed via Ag⋯N inter-actions [Ag⋯N = 3.098 (2) and 3.261 (2) Å] from symmetry-related mol-ecules and inter-molecular N-H⋯O hydrogen bonds between CF(3)CO(2) (-) anions and the hydrazone groups of two ligands give rise to chains. Furthermore, there are Ag⋯O inter-actions with a separation of 2.765 (2) Šbetween chains. The F atoms of the CF(3)CO(2) (-) anion are disordered over two sites with refined occupancies of 0.593 (5) and 0.407 (5).

A grid-like two-dimensional Ag(I)coordination polymer: poly[[[mu3-N'-(4-cyanobenzylidene)isonicotinohydrazide]silver(I)] perchlorate].

This study presents new coordinating modes of a Schiff base with three coordinating groups and an interesting two-dimensional framework based on two types of constructing units. In the title compound, {[Ag(C(14)H(10)N(4)O)]ClO(4)}(n), the Ag(I) ion is coordinated by three N atoms and one O atom from three different N'-(4-cyanobenzylidene)isonicotinohydrazide (L) ligands, forming a primary distorted square-planar coordination geometry. Two ligands each bridge two metal centres through one carbonitrile N atom in a monodentate mode and the hydrazide N and O atoms in a bidentate mode to form a small centrosymmetric (2+2)-Ag(2)L(2) ring as a principal constructing unit. The pyridyl N atoms from four ligands in four of these small rings coordinate to Ag atoms in adjacent rings to form a large hexanuclear silver grid. A two-dimensional framework of rectangular grids is constructed from these small rings and large grids. Two perchlorate anions are located in each large grid and are bound to the grid by N-H...O hydrogen bonding. Crosslinking between the layers is achieved through long Ag...O interactions between the perchlorate anions and Ag atoms in adjacent layers.

Bis[µ-3-(1H-pyrazol-1-yl)benzonitrile-κN:N']bis-[perchloratosilver(I)].

In the title centrosymmetric complex, [Ag(2)(ClO(4))(2)(C(10)H(7)N(3))(2)], the unique Ag(I) ion is coordinated by an N atom from a carbonitrile group, an N atom from a symmetry-related pyrazole group and an O atom of a perchlorate ligand to form a distorted T-shaped environment. Two 3-(1H-pyrazol-1-yl)benzonitrile ligands each bridge two Ag(I) ions to form a dinuclear complex. In the crystal structure, there are weak Ag⋯O inter-actions within the range 2.70-3.01 Šlinking dimeric units into layers approximately parallel to (100). The O atoms of the perchlorate ligand are disordered over two sites with occupancies of 0.570 (11) and 0.430 (11), respectively.

catena-Poly[[(2,9-dieth-oxy-1,10-phen-anthroline-κN,N')cadmium(II)]-di-µ-dicyan-amido-κN:N].

In the title polymer, [Cd(C(2)N(3))(2)(C(16)H(16)N(2)O(2))](n), the Cd(II) ion is coordinated by two N atoms from one 2,9-dieth-oxy-1,10-phenanthroline mol-ecule and four N atoms from four symmetry-related dicyanamide ions in a distorted octa-hedral geometry. In the 2,9-dieth-oxy-1,10-phenanthroline ligand, the O and C atoms of the eth-oxy groups are located almost in the plane defined by the phenanthroline ring system. Two dicyanamide ions bridge two Cd(II) ions, which are located on a twofold axis, forming a one-dimensional zigzag chain along the [001] direction. The 2,9-dieth-oxy-1,10-phenanthroline mol-ecules act as bidentate terminal ligands. There are π-π inter-actions between polymeric chains, characterized by a centroid-centroid distance of 3.7624 (2) Šbetween the phenanthroline rings of two neighbouring chains.