OsTIR1 and OsAFB2 Downregulation via OsmiR393 Overexpression Leads to More Tillers, Early Flowering and Less Tolerance to Salt and Drought in Rice

The microRNA miR393 has been shown to play a role in plant development and in the stress response by targeting mRNAs that code for the auxin receptors in Arabidopsis. In this study, we verified that two rice auxin receptor gene homologs (OsTIR1 and OsAFB2) could be targeted by OsmiR393 (Os for Oryza sativa). Two new phenotypes (increased tillers and early flowering) and two previously observed phenotypes (reduced tolerance to salt and drought and hyposensitivity to auxin) were observed in the OsmiR393-overexpressing rice plants. The OsmiR393-overexpressing rice demonstrated hyposensitivity to synthetic auxin-analog treatments. These data indicated that the phenotypes of OsmiR393-overexpressing rice may be caused through hyposensitivity to the auxin signal by reduced expression of two auxin receptor genes (OsTIR1 and OsAFB2). The expression of an auxin transporter (OsAUX1) and a tillering inhibitor (OsTB1) were downregulated by overexpression of OsmiR393, which suggested that a gene chain from OsmiR393 to rice tillering may be from OsTIR1 and OsAFB2 to OsAUX1, which affected the transportation of auxin, then to OsTB1, which finally controlled tillering. The positive phenotypes (increased tillers and early flowering) and negative phenotypes (reduced tolerance to salt and hyposensitivity to auxin) of OsmiR393-overexpressing rice present a dilemma for molecular breeding

The effect of diabetes mellitus on active avoidance learning in rats: the role of nitric oxide.

BACKGROUND: Growing data report memory and other cognitive problems among individuals with diabetes mellitus. Nitric oxide may play a key role in many physiological and pathological situations. The aim was to investigate the role of NO in diabetes-induced changes in learning and lipid peroxidation. MATERIAL/METHODS: Six groups of 10 rats each were formed: control (C), diabetic (D), control+L-arginine (CA), diabetic+L-arginine (DA), control+L-NAME (CN), and diabetic+L-NAME (DN) groups. Experimental diabetes mellitus was induced by injection of streptozotocin (60 mg/kg body weight). 160 mg/kg/day L-arginine or 10 mg/kg/day L-NAME were injected intraperitoneally to the relevant groups for eight weeks. Active avoidance behavior was studied in the middle of the eighth week using an automated shuttle box. Brain and hippocampal nitrite levels were measured by a fluorometric method. TBARS levels were measured fluorometrically using 1,1,3,3-tetramethoxypropane as a standard. RESULTS: The active avoidance training indicated that diabetes was associated with learning impairment. Administration of L-NAME and L-arginine significantly impaired active avoidance performance compared with the control group. They also decreased glucose level in group DA compared with the diabetic group. Brain nitrite level was significantly different in the diabetic group; hippocampus nitrite level tended to be lower in the L-NAME groups than the diabetic and control groups, although L-arginine increased hippocampal and brain nitrite values in the CA group compared with control groups. Brain and hippocampal TBARS levels were significantly higher in diabetic than in control rats. CONCLUSIONS: Imbalance related to nitric oxide production may contribute to cognitive dysfunction in diabetes mellitus

Forbidden transitions for low-lying levels in atomic boron

The multiconfiguration Hartree-Fock in the framework of the Breit-Pauli Hamiltonian (MCHF+BP), relativistic Hartree-Fock (HFR), and multiconfiguration Dirac-Fock (MCDF) calculations of the wavelengths, oscillator strengths, and transition probabilities for the magnetic dipole (Ml) and electric quadrupole (E2) forbidden transitions between low-lying levels in the atomic boron have been performed. The data for the analysis of forbidden lines in the spectrum is important for the study of the plasma in astrophysical objects and fusion devices. The data for forbidden transitions obtained from this study have been compared with experimental and other theoretical data available in the literature. Moreover, a discussion of these calculations for the boron atom (B I) has been given in view of the MCHF+BP, HFR and MCDF methods

Visual evoked potentials in normal and sulfite oxidase deficient rats exposed to ingested sulfite.

Sulfite oxidase (SOX) is an essential enzyme in the pathway of the oxidative degradation of sulfur amino acids, and protects cells from sulfite (SO(3)(2-)) toxicity. Rats do not mimic responses seen in human, because of their relatively high SOX activity levels. Therefore, the present study used SOX deficient rats since they are a more appropriate model for studying sulfite toxicity. The aim of the study was to investigate the effect of sulfite exposure on visual evoked potentials (VEPs) and thiobarbituric acid reactive substances (TBARS) in normal and sulfite oxidase deficient rats. Rats were assigned to six groups (n=10 rats/group) as follows; control (C), sulfite (S), sulfite+vitamin E (SE), deficient (D), deficient+sulfite (DS) and deficient+sulfite+vitamin E (DSE). Sulfite oxidase deficiency was established by feeding rats a low molybdenum diet and adding to their drinking water 200 ppm tungsten (W). Sulfite (25img/kg) was administered to the animals via their drinking water. At the end of the experimental period, flash visual evoked potentials were recorded, and TBARS, hepatic sulfite oxidase levels and plasma S-sulphonate concentrations were determined. Sulfite treatment caused a significant delay in P1, N1P2, and P3 components of VEPs in the S and DS groups compared with the C group. These prolonged mean latencies of VEP components were reversed by vitamin E treatment in SE and DSE groups. In addition, the mean latencies of P1 and P3 components were increased in SOX deficient groups compared with the C group. Lipid peroxidation was increased in the brain in S, D, DS and DSE groups compared with the control group. There were also significant increases in the retina TBARS levels of S and DS groups. Vitamin E caused a significant decrease in brain and retina TBARS levels of SE and DSE groups with respect to their corresponding controls. However, there were no important changes in amplitudes of other groups. In conclusion, our results showed that sulfite treatment caused an increase in the lipid peroxidation process that was accompanied by changes in VEPs. Furthermore, sulfite exposure resulted in greater lipid peroxidation and more electrophysiological alterations in the SOX deficient rats than in the control rats. Additionally, the reduction of all VEP latencies in the DSE group with respect to the DS group clearly indicated that vitamin E has the potential to prevent sulfite induced-VEP changes arising from dysfunction of the SOX enzyme

Effect of sulfite on cognitive function in normal and sulfite oxidase deficient rats.

Sulfites, which are commonly used as preservatives, are continuously formed in the body during metabolism of sulfur-containing amino acids. Sulfite is oxidized to sulfate ion by sulfite oxidase (SOX, EC. 1.8.3.1). The aim of this study was to investigate the possible toxic effects of sulfite on neurons by measuring active avoidance learning in normal and SOX-deficient rats. For this purpose, male albino rats used in this study were divided into eight groups such as control group (C), sulfite group (25 mg/kg) (S), vitamin E group (50 mg/kg) (E), sulfite (25 mg/kg)+vitamin E group (50 mg/kg) (SE), SOX-deficient group (D), deficient+vitamin E group (50 mg/kg) (DE), deficient+sulfite group (25 mg/kg) (DS) and deficient+sulfite (25 mg/kg)+vitamin E group (50 mg/kg) (DSE). Sulfite-induced impairment of active avoidance learning in SOX-deficient rats but not in normal rats. Sulfite had no effect on hippocampus TBARS levels in SOX normal groups. In SOX-deficient rats, TBARS levels were found to be significantly increased with sulfite exposure. Vitamin E reversed the observed detrimental effects of sulfite in the SOX-deficient rats on their hippocampal TBARS but not on their active avoidance learning. In conclusion, sulfite has neurotoxic effects in sulfite oxidase deficient rats, but this effect may not depend on oxidative stress

An investigation on physical, structural and gamma ray shielding features of Dy3+ ions doped Telluroborate glasses

WOS:000488998900041Structural, physical and gamma ray shielding properties of Dy3+ doped telluroborate glasses have been discussed. The molar volume of the glasses is proportional to the TeO2 content. The FTIR studies investigate the expansion of TeO(2 )content and the dynamic change of tetrahedral [BO4] units into trigonal [BO3] units. Using the absorption spectra, optical band gap (E-g) and Urbach's energy (Delta E) values are calculated. The molar volume of oxygen (V-O) and boron-boron separation () values are increasing while there is a fall in oxygen packing density (OPD) from 0% to 40% of TeO2. The ionic nature of the present glasses is analyzed from the bonding parameter (delta), optical basicity (Lambda(th)), covalent and ionic characteristic factors. The gamma photon attenuation investigated employing GEANT4 code. The transmission factor (TF) shows that OTBD sample (0 wt% of TeO2) has the highest TF, while the 4TBD sample (40 wt% of TeO2) has the lowest TF

Evolutionary conservation of the lipopolysaccharide binding site of β₂-glycoprotein I

β₂-Glycoprotein I (β₂GPI) is a highly abundant plasma protein and the major antigen for autoantibodies in the antiphospholipid syndrome. Recently, we have described a novel function of β₂GPI as scavenger of lipopolysaccharide (LPS). With this in mind we investigated the conservation of β₂GPI in vertebrates and set out to identify the binding site of LPS within β₂GPI. The genome sequences of 42 species were surveyed. Surface plasmon resonance (SPR) was performed with peptides to characterise the binding site of β₂GPI for LPS. β₂GPI could be identified in most tested vertebrates with a high overall amino acid homology of 80% or more in mammals. SPR revealed that a synthesised peptide (LAFWKTDA) from domain V of β₂GPI was able to compete for binding of β₂GPI to LPS. The AFWKTDA sequence was completely conserved in all mammals. The peptide containing the LPS binding site attenuated the inhibition by β₂GPI in a cellular model of LPS-induced tissue factor expression. Other important sites, such as the binding site for anionic phospholipids and the antiphospholipid antibody binding epitope, were also preserved. β₂GPI is highly conserved across the animal kingdom, which suggests that the function of β₂GPI may be more important than anticipate

An experimental and theoretical study on the novel (Z)-1-((naphthalen-2-ylamino)methylene)naphthalen-2(1H)-one crystal

PMID = 2397879