Growth,Physiological and Biochemical Traits of Sage under the Exogenous Stimulating and Stress Factors

Russian Journal of Plant Physiology - Sage (Salvia officinalis L.) belonging to the Lamiaceae family, as the main herb in the world is cultivated in many countries for extraction of essential oil...     

Growth-promoting bacteria and natural regulators mitigate salt toxicity and improve rapeseed plant performance

Salinity is a major environmental stress that limits plant production and portraits a critical challenge to food security in the world. In this research, the impacts of plant growth–promoting bacteria (Pseudomonas RS-198 and Azospirillum brasilense RS-SP7) and foliar application of plant hormones (salicylic acid 1 mM and jasmonic acid 0.5 mM) on alleviating the harmful effects of salt stress in rapeseed plants (Brassica napus cv. okapi) were examined under greenhouse condition. Salt stress diminished rapeseed biomass, leaf area, water content, nitrogen, phosphorus, potassium, calcium, magnesium, and chlorophyll content, while it increased sodium content, endogenous salicylic and jasmonic acids, osmolyte production, H₂O₂ and O₂^•− generations, TBARS content, and antioxidant enzyme activities. Plant growth, nutrient content, leaf expansion, osmolyte production, and antioxidant enzyme activities were increased, but oxidative and osmotic stress indicators were decreased by bacteria inoculation + salicylic acid under salt stress. Antioxidant enzyme activities were amplified by jasmonic acid treatments under salt stress, although rapeseed growth was not generally affected by jasmonic acid. Bacterial + hormonal treatments were superior to individual treatments in reducing detrimental effects of salt stress. The best treatment in rectifying rapeseed growth under salt stress was combination of Pseudomonas and salicylic acid. This combination attenuated destructive salinity properties and subsequently amended rapeseed growth via enhancing endogenous salicylic acid content and some essential nutrients such as potassium, phosphorus, and magnesium.

     

Electrochemical impedimetric immunosensor for insulin like growth factor-1 using specific monoclonal antibody-nanogold modified electrode

An electrochemical impedimetric immunosensor was developed for ultrasensitive determination of insulin-like growth factor-1 (IGF-1) based on immobilization of a specific monoclonal antibody on gold nanoparticles (GNPs) modified gold electrode. Self-assembly of colloidal gold nanoparticles on the gold electrode was conducted through the thiol groups of 1,6-hexanedithiol (HDT) monolayer as a cross linker. The redox reactions of [Fe(CN)(6)](4-)/[Fe(CN)(6)](3-) on the electrode surface was probed for studying the immobilization and determination processes, using cyclic voltammetry (CV) and electrochemical impedance spectroscopy (EIS). The interaction of antigen with grafted antibody recognition layer was carried out by soaking the modified electrode into antigen solution at 37°C for 3 h. The immunosensor showed linearity over 1.0-180.0 pg mL(-1) and the limit of detection was 0.15 pg mL(-1). The association constant between IGF-1 and immobilized antibody was calculated to be 9.17×10(11) M(-1). The proposed method is a useful tool for screening picogram amounts of IGF-1 in clinical laboratory as a diagnostic test.     

Histamine controls food intake in sheep via H1 receptors

Histamine is a well known amine which controls many physiological functions of the CNS, including fluid balance, appetite, thermoregulation, cardiovascular control, learning and the stress response. All these functions are mediated via three well known membrane receptors (H₁, H₂ and H₃) and, in laboratory animals, feeding behavior is under the control of H₁ type. In order to investigate the central effect of histamine on feeding behavior in sheep and the characterization of the receptor involved, two Latin square design experiments were undertaken using four Iranian Nainee rams implanted with intracerebroventricular cannulae. In the first experiment, 12 h fasted (7:00 p.m.–7:00 a.m.) rams in individual pens were infused with 0 (control), 100, 400 and 800 nM of histamine such that each ram received each dose four times on different days. Ten minutes after injection (7:00 a.m.) water and a food container were put in the pens and the consumption of water and food were recorded at 0.5, 1, 3 and 12 h. Results from this experiment revealed that histamine significantly (P < 0.01) suppressed food intake with no effect on water consumption. In the second experiment the use of three specific histamine antagonists: chloropheniramine, ranitidine and thioperamide, showed that the anorexic effect of histamine was significantly (P < 0.01) blocked by chloropheniramine. It is concluded that feeding behavior in sheep is inhibited by histamine acting via H₁ receptors.     

Gallium uptake by transferrin and interaction with receptor 1

The kinetics and thermodynamics of Ga(III) exchange between gallium mononitrilotriacetate and human serum transferrin as well as those of the interaction between gallium-loaded transferrin and the transferrin receptor 1 were investigated in neutral media. Gallium is exchanged between the chelate and the C-site of human serum apotransferrin in interaction with bicarbonate in about 50 s to yield an intermediate complex with an equilibrium constant K ₁ = (3.9 ± 1.2) × 10⁻², a direct second-order rate constant k ₁ = 425 ± 50 M⁻¹ s⁻¹ and a reverse second-order rate constant k ₋₁ = (1.1 ± 3) × 10⁴ M⁻¹ s⁻¹. The intermediate complex loses a single proton with proton dissociation constant K _1a = 80 ± 40 nM to yield a first kinetic product. This product then undergoes a modification in its conformation which lasts about 500 s to produce a second kinetic intermediate, which in turn undergoes a final extremely slow (several hours) modification in its conformation to yield the gallium-saturated transferrin in its final state. The mechanism of gallium uptake differs from that of iron and does not involve the same transitions in conformation reported during iron uptake. The interaction of gallium-loaded transferrin with the transferrin receptor occurs in a single very fast kinetic step with a dissociation constant K _d = 1.10 ± 0.12 μM and a second-order rate constant k _d = (1.15 ± 0.3) × 10¹⁰ M⁻¹ s⁻¹. This mechanism is different from that observed with the ferric holotransferrin and suggests that the interaction between the receptor and gallium-loaded transferrin probably takes place on the helical domain of the receptor which is specific for the C-site of transferrin and HFE. The relevance of gallium incorporation by the transferrin receptor-mediated iron-acquisition pathway is discussed.     

Multiple cyclin kinase inhibitors promote bile acid-induced apoptosis and autophagy in primary hepatocytes via p53-CD95-dependent signaling

Previously, using primary hepatocytes residing in early G(1) phase, we demonstrated that expression of the cyclin-dependent kinase (CDK) inhibitor protein p21(Cip-1/WAF1/mda6) (p21) enhanced the toxicity of deoxycholic acid (DCA) + MEK1/2 inhibitor. This study examined the mechanisms regulating this apoptotic process. Overexpression of p21 or p27(Kip-1) (p27) enhanced DCA + MEK1/2 inhibitor toxicity in primary hepatocytes that was dependent on expression of acidic sphingomyelinase and CD95. Overexpression of p21 suppressed MDM2, elevated p53 levels, and enhanced CD95, BAX, NOXA, and PUMA expression; knockdown of BAX/NOXA/PUMA reduced CDK inhibitor-stimulated cell killing. Parallel to cell death processes, overexpression of p21 or p27 profoundly enhanced DCA + MEK1/2 inhibitor-induced expression of ATG5 and GRP78/BiP and phosphorylation of PKR-like endoplasmic reticulum kinase (PERK) and eIF2alpha, and it increased the numbers of vesicles containing a transfected LC3-GFP construct. Incubation of cells with 3-methyladenine or knockdown of ATG5 suppressed DCA + MEK1/2 inhibitor-induced LC3-GFP vesicularization and enhanced DCA + MEK1/2 inhibitor-induced toxicity. Expression of dominant negative PERK blocked DCA + MEK1/2 inhibitor-induced expression of ATG5, GRP78/BiP, and eIF2alpha phosphorylation and prevented LC3-GFP vesicularization. Knock-out or knockdown of p53 or CD95 abolished DCA + MEK1/2 inhibitor-induced PERK phosphorylation and prevented LC3-GFP vesicularization. Thus, CDK inhibitors suppress MDM2 levels and enhance p53 expression that facilitates bile acid-induced, ceramide-dependent CD95 activation to induce both apoptosis and autophagy in primary hepatocytes.     

Differentiation of presumptive lens ectoderm of the chick in vitro studied with immunofluorescence techniques

The differentiation capacity of presumptive lens ectoderm was studied in the chick by an in vitro technique using the appearance of central nervous system or lens-specific antigens as indicators of differentiation. Handling the explants resulted in 'autodifferentiation' of both antigens, but co-culture with alcohol-killed primitive node or optic cup material could induce much stronger differentiation. Little specificity exists in the reaction and a hypothesis is presented whereby selection between the two differentiation pathways is thought to be due mainly to maturation within the ectoderm and the inducing tissue plays a minor qualitative role.