Pretilachlor Releasable Polyurea Microcapsules Suspension Optimization and Its Paddy Field Weeding Investigation.

In this study, pretilachlor was encapsulated into polyurea microcapsules prepared by water-initiated polymerization of polyaryl polymethylene isocyanate and eventually made into pretilachlor microcapsules suspension (PMS). We used response surface methodology (RSM) combined with the Box-Behnken design (BBD) model to optimize the formulation of PMS. The encapsulation efficiency (EE) of PMS was investigated with respect to three independent variables including wall material dosage (X), emulsifier dosage (X), and polymerization stirring speed (X).

Degradation, adsorption and leaching of phenazine-1-carboxamide in agricultural soils.

Phenazines, a large group of nitrogen-containing heterocycles with promising bioactivities, can be widely used as medicines and pesticides. But phenazines also generate toxicity risks due to their non-selective DNA binding. The environmental fate of phenazines in soils is the key to assess their risks; however, hitherto, there have been very few related studies.

Discovery of nitropyridyl-based dichloropropene ethers as insecticides.

A series of nitropyridyl-based dichloropropene ethers were prepared and evaluated for their insecticidal activities against main lepidopteran pests such as M. separate, P. xylostella and P.

Remediation of organochlorine pesticides contaminated lake sediment using activated carbon and carbon nanotubes.

Organochlorine pesticides (OCPs) in sediment were a potential damage for humans and ecosystems. The aim of this work was to determine the effectiveness of carbon materials remedy hexachlorocyclohexane (HCH) and dichlorodiphenyltrichloroethanes (DDTs) in sediment. Two different carbon materials including activated carbon (AC) and multi-walled carbon nanotubes (MWCNTs) were used in the present research.

Up-Regulation of PKR Signaling Pathway by Ethanol Displays an Age of Onset-Dependent Relationship.

Background: Ethanol (EtOH) neurotoxicity can result in devastating effects on brain and behavior by disrupting homeostatic signaling cascades and inducing cell death. One such mechanism involves double-stranded RNA activated protein kinase (PKR), a primary regulator of protein translation and cell viability in the presence of a virus or other external stimuli. EtOH-mediated up-regulation of interferon-gamma (IFN-γ; the oxidative stress-inducible regulator of PKR), PKR, and its target, p53, are still being fully elucidated.

Easily separated silver nanoparticle-decorated magnetic graphene oxide: Synthesis and high antibacterial activity.

Silver nanoparticle-decorated magnetic graphene oxide (MGO-Ag) was synthesized by doping silver and Fe3O4 nanoparticles on the surface of GO, which was used as an antibacterial agent. MGO-Ag was characterized by scanning electron microscopy (SEM), transmission electron microscopy (TEM), Energy dispersive X-ray (EDS), X-ray diffraction (XRD), Raman spectroscopy and magnetic property tests. It can be found that magnetic iron oxide nanoparticles and nano-Ag was well dispersed on graphene oxide; and MGO-Ag exhibited excellent antibacterial activity against Escherichia coli and Staphylococcus aureus.

Binge ethanol exposure increases the Krüppel-like factor 11-monoamine oxidase (MAO) pathway in rats: Examining the use of MAO inhibitors to prevent ethanol-induced brain injury.

Binge drinking induces several neurotoxic consequences including oxidative stress and neurodegeneration. Because of these effects, drugs which prevent ethanol-induced damage to the brain may be clinically beneficial. In this study, we investigated the ethanol-mediated KLF11-MAO cell death cascade in the frontal cortex of Sprague-Dawley rats exposed to a modified Majchowicz 4-day binge ethanol model and control rats.

Magnetic chitosan-graphene oxide composite for anti-microbial and dye removal applications.

Magnetic chitosan-graphene oxide (MCGO) nanocomposite was prepared as a multi-functional nanomaterial for the applications of antibacterial and dye removal. The nanocomposite was characterized by scanning electronic microscope (SEM), transmission electron microscopy (TEM), X-ray diffraction (XRD) and Fourier transform infrared spectrometer (FTIR). The antibacterial performance for MCGO against Escherichia coli was varied depending on the concentration of MCGO.

Chronic Social Stress and Ethanol Increase Expression of KLF11, a Cell Death Mediator, in Rat Brain.

Major depressive disorder and alcoholism are significant health burdens that can affect executive functioning, cognitive ability, job responsibilities, and personal relationships. Studies in animal models related to depression or alcoholism reveal that the expression of Krüppel-like factor 11 (KLF11, also called TIEG2) is elevated in frontal cortex, which suggests that KLF11 may play a role in stress- or ethanol-induced psychiatric conditions. KLF11 is a transcriptional activator of monoamine oxidase A and B, but also serves other functions in cell cycle regulation and apoptotic cell death.

The IFNγ-PKR pathway in the prefrontal cortex reactions to chronic excessive alcohol use.

Background: Brain cell death is a major pathological consequence of alcohol neurotoxicity. However, the molecular cascades in alcohol-induced brain tissue injury are unclear.

Methods: Using Western blot and double immunofluorescence, we examined the expression of interferon (IFN)-induced protein kinase R (PKR), phosphorylated-PKR (p-PKR), and IFN gamma (IFNγ) in the prefrontal cortex (PFC) of postmortem brains from subjects with alcohol use disorders (AUD).

Evidence revealing deregulation of the KLF11-MAO A pathway in association with chronic stress and depressive disorders.

The biochemical pathways underlying major depressive disorder (MDD) and chronic stress are not well understood. However, it has been reported that monoamine oxidase A (MAO A, a major neurotransmitter-degrading enzyme) is significantly increased in the brains of human subjects affected with MDD and rats exposed to chronic social defeat (CSD) stress, which is used to model depression. In the current study, we compared the protein levels of a MAO A-transcriptional activator, Kruppel-like factor 11 (KLF11 , also recognized as transforming growth factor-beta-inducible early gene 2) between the brains of 18 human subjects with MDD and 18 control subjects.

Diabetes-causing gene, kruppel-like factor 11, modulates the antinociceptive response of chronic ethanol intake.

Background: Alcohol (EtOH [ethanol]) is an antinociceptive agent, working in part, by reducing sensitivity to painful stimuli. The transcription factor Kruppel-like factor 11 (KLF11), a human diabetes-causing gene that also regulates the neurotransmitter metabolic enzymes monoamine oxidase (MAO), has recently been identified as an EtOH-inducible gene. However, its role in antinociception remains unknown.

A microchip electrophoresis-mass spectrometric platform for fast separation and identification of enantiomers employing the partial filling technique.

A microchip electrophoresis-mass spectrometric (MCE-MS) method was developed for fast chiral analysis. The proposed MCE-MS platform deployed a glass/PDMS hybrid microchip with an easy-to-fabricate monolithic nanoelectrospray emitter. Enantiomeric MCE separation was achieved by means of the partial filling technique.

Cognitive deficits and disruption of neurogenesis in a mouse model of apolipoprotein E4 domain interaction.

Apolipoprotein E4 (apoE4) allele is the major genetic risk factor for sporadic Alzheimer disease (AD) due to the higher prevalence and earlier onset of AD in apoE4 carriers. Accumulating data suggest that the interaction between the N- and the C-terminal domains in the protein may be the main pathologic feature of apoE4. To test this hypothesis, we used Arg-61 mice, a model of apoE4 domain interaction, by introducing the domain interaction feature of human apoE4 into native mouse apoE.

Elevated monoamine oxidase a binding during major depressive episodes is associated with greater severity and reversed neurovegetative symptoms.

Inadequate treatment response occurs in approximately 40% of major depressive episodes (MDEs), and one approach to solve this is careful matching of treatment to the specific pathologies of MDE. One such biological abnormality is elevated monoamine oxidase A (MAO-A) levels, which occurs in the prefrontal and anterior cingulate cortex (PFC and ACC) during MDE; however, the subtypes for which this abnormality is most prominent are unknown. We hypothesized that MAO-A levels in the PFC and ACC are most elevated in MDE with greater severity and reversed neurovegetative symptoms (hypersomnia and either hyperphagia or weight gain).

Expression of autophagy and UPR genes in the developing brain during ethanol-sensitive and resistant periods.

Fetal alcohol spectrum disorders (FASD) results from ethanol exposure to the developing fetus and is the leading cause of mental retardation. FASD is associated with a broad range of neurobehavioral deficits which may be mediated by ethanol-induced neurodegeneration in the developing brain. An immature brain is more susceptible to ethanol neurotoxicity.

The expression of KLF11 (TIEG2), a monoamine oxidase B transcriptional activator in the prefrontal cortex of human alcohol dependence.

Background: The biochemical pathways underlying alcohol abuse and dependence are not well understood, although brain cell loss and neurotoxicity have been reported in subjects with alcohol dependence. Monoamine oxidase B (MAO B; an enzyme that catabolizes neurotransmitters such as dopamine) is consistently increased in this psychiatric illness. MAO B has been implicated in the pathogenesis of alcohol dependence and alcohol-induced brain neurotoxicity.

Epigenetics: a promising paradigm for better understanding and managing pain.

Unlabelled: Epigenetic regulation of gene expression is a rapidly growing area of research. Considering the longevity and plasticity of neurons, the studies on epigenetic pathways in the nervous system should be of special interest for both epigeneticists and neuroscientists. Activation or inactivation of different epigenetic pathways becomes more pronounced when the cells experience rapid changes in their environment, and such changes can be easily caused by injury and inflammation, resulting in pain perception or distortion of pain perception (eg, hyperalgesia).

Synthesis and antifungal activities of trichodermin derivatives as fungicides on rice.

Twenty new trichodermin derivatives, 2a-5, containing alkoxy, acyloxy, and Br groups in 4-, 8-, 9-, 10- and 16-positions were synthesized and characterized. The antifungal activities of the new compounds against rice false smut (Ustilaginoidea virens), rice sheath blight (Rhizoctonia solani), and rice blast (Magnaporthe grisea) were evaluated. The results of bioassays indicated that the antifungal activities were particularly susceptible to changes at 4-, 8-, and 16-positions, but low to changes at 9- and 10-positions.

Allopregnanolone reinstates tyrosine hydroxylase immunoreactive neurons and motor performance in an MPTP-lesioned mouse model of Parkinson's disease.

Restorative/protective therapies to restore dopamine neurons in the substantia nigra pars compacta (SNpc) are greatly needed to effectively change the debilitating course of Parkinson's disease. In this study, we tested the therapeutic potential of a neurogenic neurosteroid, allopregnanolone, in the restoration of the components of the nigrostriatal pathway in MPTP-lesioned mice by measuring striatal dopamine levels, total and tyrosine hydroxylase immunoreactive neuron numbers and BrdU-positive cells in the SNpc. An acute treatment (once/week for two weeks) with allopregnanolone restored the number of tyrosine hydroxylase-positive and total cell numbers in the SNpc of MPTP-lesioned mice, even though this did not increase striatal dopamine.

Convergent effects of acute stress and glucocorticoid exposure upon MAO-A in humans.

Monoamine oxidase-A (MAO-A), a key brain enzyme which metabolizes monoamines, is implicated in the pathophysiology of stress-related illnesses, including major depressive disorder, addiction, and violent behavior. Chronic stressors and glucocorticoid-administration typically associate with elevated MAO-A levels/activity. However, the relationship of shorter stress or glucocorticoid exposures and MAO-A levels/activity is not well established.

Monoamine oxidases in major depressive disorder and alcoholism.

Monoamine oxidases play an integral role in brain function. Both monoamine oxidase A (MAO-A) and monoamine oxidase B (MAO-B) regulate neurochemistry by degrading monoamine neurotransmitters (serotonin, dopamine, and norepinephrine). Any alteration in MAO levels can have devastating effects on the brain and behavior by lowering or raising neurotransmitter levels and producing toxic reactive oxygen species.

Synthesis and fungicidal activity of novel 2,3-disubstituted-1,3-benzoxazines.

A series of new 2,3-disubstituted-3,4-dihydro-2H-1,3-benzoxazines were prepared in moderate to excellent yields by aza-acetalizations of aromatic aldehydes with 2-(N-substituted aminomethyl)phenols in the presence of TMSCl. Their structures were confirmed by IR, ¹H-NMR, ¹³C-NMR, MS and elemental analysis. The fungicidal activities of the target compounds were preliminarily evaluated, and some compounds exhibited good activity against Rhizoctonia solani.

Mechanistic role for a novel glucocorticoid-KLF11 (TIEG2) protein pathway in stress-induced monoamine oxidase A expression.

Chronic stress is a risk factor for psychiatric illnesses, including depressive disorders, and is characterized by increased blood glucocorticoids and brain monoamine oxidase A (MAO A, which degrades monoamine neurotransmitters). This study elucidates the relationship between stress-induced MAO A and the transcription factor Kruppel-like factor 11 (KLF11, also called TIEG2, a member of the Sp/KLF- family), which inhibits cell growth. We report that 1) a glucocorticoid (dexamethasone) increases KLF11 mRNA and protein levels in cultured neuronal cells; 2) overexpressing KLF11 increases levels of MAO A mRNA and enzymatic activity, which is further enhanced by glucocorticoids; in contrast, siRNA-mediated KLF11 knockdown reduces glucocorticoid-induced MAO A expression in cultured neurons; 3) induction of KLF11 and translocation of KLF11 from the cytoplasm to the nucleus are key regulatory mechanisms leading to increased MAO A catalytic activity and mRNA levels because of direct activation of the MAO A promoter via Sp/KLF-binding sites; 4) KLF11 knockout mice show reduced MAO A mRNA and catalytic activity in the brain cortex compared with wild-type mice; and 5) exposure to chronic social defeat stress induces blood glucocorticoids and activates the KLF11 pathway in the rat brain, which results in increased MAO A mRNA and enzymatic activity.

A dominant negative ERβ splice variant determines the effectiveness of early or late estrogen therapy after ovariectomy in rats.

The molecular mechanisms for the discrepancy in outcome of initiating estrogen therapy (ET) around peri-menopause or several years after menopause in women are unknown. We hypothesize that the level of expression of a dominant negative estrogen receptor (ER) β variant, ERβ2, may be a key factor determining the effectiveness of ET in post-menopausal women. We tested this hypothesis in ovariectomized nine month-old (an age when irregular estrous cycles occur) female Sprague Dawley rats.