MOSQUITO NET WITH DINOTEFURAN AND PBO FOR KILLING MOSQUITOES, ESPECIALLY MOSQUITOES WITH PYRETHROID RESISTANCE

Dinotefuran and PBO is used for killing mosquitoes, as PBO increases the knockdown speed of Dinotefuran. The present invention relates to insecticidal mosquito nets containing PBO in combination with an insecticide. One of the methods to counteract malaria is the use of commercially available long lasting insecticidal mosquito nets for protecting humans from the bite of Anopheline mosquitoes that carry malaria. Whereas the typically applied pyrethroids have been used successfully as insecticides on such nets due to their rapid knockdown effect, there is currently a critical increased resistance to pyrethroids observed among those mosquitoes. One type of resistance is metabolic, which is counteracted by applying piperonyl butoxide (PBO) simultaneously with a pyrethroid to the mosquito when resting on the net. The PBO works as an inhibitor of the resistance associated metabolic enzymes and increases the mortality rate of the pyrethroid resistant mosquitoes. Another type of resistance is through a mutation at the target site of the pyrethroid, known as knockdown-resistance (kdr), which significantly slows the knockdown effect when the mosquito rests on the net and gives the mosquito the possibility to bite before paralysis (followed by death)

Presence of 5-hydroxyguaiacyl units as native lignin constituents in plants as seen by Py-GC/MS

Instituto de Recursos Naturales y Agrobiología de Sevilla, CSIC, P.O. Box 1052, 41080-Seville, Spain 2Centro de Investigaciones Biológicas, CSIC, Ramiro de Maeztu 9, E-28040 Madrid, Spain E-mail address: [email protected] (J.C. del Río)The presence of 5-hydroxyguaiacyl moieties in the lignin from several plants has been assessed by Py-GC/MS. Different woody (eucalypt) and nonwoody (flax, hemp, kenaf, jute, sisal and abaca) angiosperms were selected for this study. The pyrolysis of whole fibers released lignin-derived products with p-hydroxyphenyl, guaiacyl and syringyl structures. Indeed, a series of compounds having a 5-hydroxyguaiacyl nuclei, including 3-methoxycatechol, 5-vinyl-3-methoxycatechol and 5-propenyl-3-methoxycatechol, were detected and identified in all samples, although in lower amounts than the normal guaiacyl and syringyl compounds. The analysis of the lignins isolated from the same plants also indicated the presence of 5-hydroxyguaiacyl moieties in the isolated lignins. These compounds are supposed to arise from the pyrolysis of 5-hydroxyguaiacyl moieties, which are supposed to be native constituents of lignin in plants forming benzodioxane substructures.This study has been supported by the Spanish Ministerio de Ciencia y Tecnología (MCyT) and FEDER funds (project AGL2005-01748) and the EU project BIORENEW (NMP2-CT-2006-026456). We thank CELESA S.A. (Tortosa, Spain) for providing the nonwoody plant samples, and ENCE for providing the eucalypt wood sample.Peer reviewe

Oxygen Tension and the VHL-Hif1α Pathway Determine Onset of Neuronal Polarization and Cerebellar Germinal Zone Exit.

Postnatal brain circuit assembly is driven by temporally regulated intrinsic and cell-extrinsic cues that organize neurogenesis, migration, and axo-dendritic specification in post-mitotic neurons. While cell polarity is an intrinsic organizer of morphogenic events, environmental cues in the germinal zone (GZ) instructing neuron polarization and their coupling during postnatal development are unclear. We report that oxygen tension, which rises at birth, and the von Hippel-Lindau (VHL)-hypoxia-inducible factor 1α (Hif1α) pathway regulate polarization and maturation of post-mitotic cerebellar granule neurons (CGNs). At early postnatal stages with low GZ vascularization, Hif1α restrains CGN-progenitor cell-cycle exit. Unexpectedly, cell-intrinsic VHL-Hif1α pathway activation also delays the timing of CGN differentiation, germinal zone exit, and migration initiation through transcriptional repression of the partitioning-defective (Pard) complex. As vascularization proceeds, these inhibitory mechanisms are downregulated, implicating increasing oxygen tension as a critical switch for neuronal polarization and cerebellar GZ exit

Exenatide Improves Bone Quality in a Murine Model of Genetically Inherited Type 2 Diabetes Mellitus

Type 2 diabetes mellitus (T2DM) is associated with skeletal complications, including an increased risk of fractures. Reduced blood supply and bone strength may contribute to this skeletal fragility. We hypothesized that long-term administration of Exenatide, a glucagon- like peptide-1 receptor agonist, would improve bone architecture and strength of T2DM mice by increasing blood flow to bone, thereby stimulating bone formation. In this study, we used a model of obesity and severe T2DM, the leptin receptor-deficient db/db mouse to assess alterations in bone quality and hindlimb blood flow and to examine the beneficial effects of 4 weeks administration of Exenatide. As expected, diabetic mice showed marked alterations in bone structure, remodeling and strength, and basal vascular tone compared with lean mice. Exenatide treatment improved trabecular bone mass and architecture by increasing bone formation rate, but only in diabetic mice. Although there was no effect on hindlimb perfusion at the end of this treatment, exenatide administration acutely increased tibial blood flow. While Exenatide treatment did not restore the impaired bone strength, intrinsic properties of the matrix, such as collagen maturity, were improved. The effects of Exenatide on in vitro bone formation were further investigated in primary osteoblasts cultured under high-glucose conditions, showing that Exenatide reversed the impairment in bone formation induced by glucose. In conclusion, Exenatide improves trabecular bone mass by increasing bone formation and could protect against the development of skeletal complications associated with T2DM

Mutations impairing GSK3-mediated MAF phosphorylation cause cataract, deafness, intellectual disability, seizures, and a down syndrome-like facies

Transcription factors operate in developmental processes to mediate inductive events and cell competence, and perturbation of their function or regulation can dramatically affect morphogenesis, organogenesis, and growth. We report that a narrow spectrum of amino-acid substitutions within the transactivation domain of the v-maf avian musculoaponeurotic fibrosarcoma oncogene homolog (MAF), a leucine zipper-containing transcription factor of the AP1 superfamily, profoundly affect development. Seven different de novo missense mutations involving conserved residues of the four GSK3 phosphorylation motifs were identified in eight unrelated individuals. The distinctive clinical phenotype, for which we propose the eponym Aymé-Gripp syndrome, is not limited to lens and eye defects as previously reported for MAF/Maf loss of function but includes sensorineural deafness, intellectual disability, seizures, brachycephaly, distinctive flat facial appearance, skeletal anomalies, mammary gland hypoplasia, and reduced growth. Disease-causing mutations were demonstrated to impair proper MAF phosphorylation, ubiquitination and proteasomal degradation, perturbed gene expression in primary skin fibroblasts, and induced neurodevelopmental defects in an in vivo model. Our findings nosologically and clinically delineate a previously poorly understood recognizable multisystem disorder, provide evidence for MAF governing a wider range of developmental programs than previously appreciated, and describe a novel instance of protein dosage effect severely perturbing developmen

Zinc Intake and Biochemical Markers of Bone Turnover in Type 1 Diabetes

OBJECTIVE—To examine the relationship between Zn nutritive status and biochemical markers of bone turnover in type 1 diabetes

Expression profiling of Castanea genes during resistant and susceptible interactions with the Oomycete pathogen Phytophthora cinnamomi reveal possible mechanisms of immunity

The most dangerous pathogen affecting the production of chestnuts is Phytophthora cinnamomi a hemibiotrophic that causes root rot, also known as ink disease. Little information has been acquired in chestnut on the molecular defense strategies against this pathogen. The expression of eight candidate genes potentially involved in the defense to P. cinnamomi was quantified by digital PCR in Castanea genotypes showing different susceptibility to the pathogen. Seven of the eight candidate genes displayed differentially expressed levels depending on genotype and time-point after inoculation. Cast_Gnk2-like revealed to be the most expressed gene across all experiments and the one that best discriminates between susceptible and resistant genotypes. Our data suggest that the pre-formed defenses are crucial for the resistance of C. crenata to P. cinnamomi. A lower and delayed expression of the eight studied genes was found in the susceptible Castanea sativa, which may be related with the establishment and spread of the disease in this species. A working model integrating the obtained results is presentedinfo:eu-repo/semantics/publishedVersio

Deleterious Effects of Simulated Spaceflight on Bone and Microvasculature in Adult Mice

Long-term spaceflight leads to extensive changes in the musculoskeletal system attributable, in part, to unloading during microgravity exposure. Additionally, irradiation at doses similar to that of a solar flare or a round-trip sojourn to Mars may cause significant depletion of stem/progenitor cell pools throughout the body as well as inflammation associated with prompt skeletal-tissue degradation. Previously, we demonstrated that irradiation leads to rapid bone loss, which can be mitigated in the short term by injection of a potent antioxidant (-lipoic acid). Furthermore, simulated weightlessness in adult mice adversely affects skeletal responses to low linear energy transfer (LET) radiation (137Cs). Here, we hypothesized that simulated weightlessness exacerbates the adverse effects of simulated space radiation (including both protons and 56Fe ions) by adversely affecting skeletal structure and functions as well as associated vasculature. Furthermore, we hypothesized that an antioxidant cocktail, which has been shown to be protective in other tissues, mitigates space radiation induced bone loss