Effect of mannose-binding lectin from peanut and pea on the stem borer Chilo partellus

A mannose-binding lectin found in vegetative tissues of peanut, Arachis hypogaea, was compared with mannose-binding lectin from pea, Pisum sativum, for toxic effects on larvae of the stem borer Chilo partellus (Swinhoe). After 10 days, the mortality of larvae fed on artificial diet containing 0.5% (m/m) peanut lectin was 46.2%. The mortality of larvae fed on 1.0% peanut lectin was similar (48.1%) but insects were significantly smaller than those of the 0.5% treatment. Larvae of both lectin treatments stopped feeding within three days. Larval size and mortality was not significantly reduced by 0.1% peanut lectin and 1% heat-treated lectin did not show toxic effects. The mannose-binding lectin from pea was not toxic to C. partellus at concentrations up to 1%. Peanut lectin bound to the apical membranes of columnar epithelial cells in the mid-gut of C. partellus. This suggests that peanut lectin has an antinutritive action and that it may protect vegetative tissues of peanut against insect pests.     

Role of sensory input from the lungs in control of muscle sympathetic nerve activity during and after apnea in humans.

We reasoned that, if the lung inflation reflex contributes importantly to apnea-induced sympathetic activation, such activation would be attenuated in bilateral lung transplant recipients (LTX). We measured muscle sympathetic nerve activity (MSNA; intraneural electrodes), heart rate, mean arterial pressure, tidal volume, end-tidal Pco(2), and arterial oxygen saturation in seven LTX and seven healthy control subjects (Con) before, during, and after 20-s end-expiratory breath holds. Our evidence for denervation in LTX was 1) greatly attenuated respiratory sinus arrhythmia and 2) absence of cough reflex below the level of the carina. During apnea, the temporal pattern and the peak increase in MSNA were virtually identical in LTX and Con (347 +/- 99 and 359 +/- 46% of baseline, respectively; P > 0.05). In contrast, the amount of MSNA present in the first 5 s after resumption of breathing was greater in LTX vs. Con (101 +/- 4 vs. 38 +/- 7% of baseline, respectively; P < 0.05). There were no between-group differences in apnea-induced hypoxemia or hypercapnia, hemodynamic, or ventilatory responses. Thus cessation of the rhythmic sympathoinhibitory feedback that normally accompanies eupneic breathing does not contribute importantly to sympathetic excitation during apnea. In contrast, vagal afferent input elicited by hyperventilation-induced lung stretch plays an important role in the profound, rapid sympathetic inhibition that occurs after resumption of breathing after apnea.     

Insecticides with novel modes of action: Mechanism, selectivity and cross-resistance

Efforts have been made during the past two decades to develop insecticides with selective properties that act specifically on biochemical sites present in particular insect groups, but whose properties differ from other insecticides. This approach has led to the discovery of compounds that affect the hormonal regulation of molting and developmental processes in insects; for example, ecdysone agonists, juvenile hormone mimics and chitin synthesis inhibitors. In addition, compounds that selectively interact with the insect nicotinic acetylcholine receptor, such as imidacloprid, acetamiprid and thiamethoxam, have been introduced for the control of aphids, whiteflies and other insect species. Natural products acting selectively on insect pests, such as avermectins, spinosad and azadirachtin, have been introduced for controlling selected groups of insect pests. Compounds acting on the nervous site that controls the sucking pump of aphids and whiteflies, such as pymetrozine, or respiration, such as diafenthiuron, have been introduced for controlling sucking pests. All the above compounds are important components in pest and resistance management programs.     

Angiotensin II stimulates the production of NO and peroxynitrite in endothelial cells

Angiotensin II(ANG II) produces vasoconstriction by a direct action on smooth musclecells via AT₁ receptors. Thesereceptors are also present in the endothelium, but their function ispoorly understood. This study was therefore undertaken to determinewhether ANG II elicits the release of nitric oxide (NO) from cultured rat aortic endothelial cells. NO production, measured by theaccumulation of nitrite and nitrate, was enhanced by10⁷ M ANG II. Thebiological activity of the NO released by ANG II action was evaluatedby measuring its guanylate cyclase-stimulating activity in smoothmuscle cells. The guanosine 3',5'-cyclic monophosphate (cGMP) content of smooth muscle cells was significantly increased byexposure of supernatant from ANG II-stimulated endothelial cells. Theseeffects resulted from the activation of NO synthase, as they wereinhibited by the L-arginineanalogs. These ANG II actions were mediated by theAT₁ receptor, as shown by theirinhibition by the AT₁ antagonistlosartan. The cGMP production by reporter cells was inhibited by thecalmodulin antagonist W-7, suggesting that ANG II activates endothelialcalmodulin-dependent NO synthase. This hypothesis is also supported bythe increase of intracellular free calcium induced by ANG II inendothelial cells. ANG II also stimulated luminol-enhancedchemiluminescence in endothelial cells. This effect was inhibited byN-monomethyl-L-arginine andsuperoxide dismutase, suggesting that this luminol-enhancedchemiluminescence reflected an increase in peroxynitrite production.Thus ANG II stimulates NO release from macrovascular endothelium, whichmay modulate the direct vasoconstrictor effect of ANG II on smoothmuscle cells. However, this beneficial effect may be counteracted bythe simultaneous production of peroxynitrite, which could contribute toseveral pathological processes in the vascular wall.

     

A study of extracellular matrix-cell adhesion peptidic epitopes related to human serum amyloid A (SAA)

Summary Serum amyloid A (SAA), an acute-phase protein, exists normally in the serum while complexed with high-density lipoprotein 3 (SAA-HDL₃). Its levels increase markedly during inflammatory diseases. The pentapeptide Tyr-Ile-Gly-Ser-Asp (YIGSR-like) and the tripeptide Arg-Gly-Asn (RGD-like), related to the cell adhesion domains of laminin and fibronectin, respectively, exist in SAA within close proximity (YIGSDKYFHARGNY; amino acid residues 29–42). A structure-function study of linear and head-to-tail cyclic peptides, related to the amino acid residues 29–42) and 70–76 (GRGAEDS) of human SAA, was performed in order to evaluate their ability to inhibit adhesion of human T-lymphocytes to surfaces coated with extracellular matrix purified from bovine corneal cells.     

Surface energetics to assess biomass attachment onto hydrophobic interaction adsorbents in expanded beds

Cell-to-support interaction and cell-to-cell aggregation phenomena have been studied in a model system composed of intact yeast cells and Phenyl-Streamline adsorbents. Biomass components and beaded adsorbents were characterized by contact angle determinations with three diagnostic liquids and zeta potential measurements. Subsequently, free energy of interaction vs. distance profiles between interacting surfaces was calculated in the aqueous media provided by operating mobile phases. The effect of pH and ammonium sulphate concentration within the normal operating ranges was evaluated. Calculation indicated that moderate interaction between cell particles and adsorbent beads can develop in the presence of salt. Cell-to-cell aggregation was suspected to occur at high salt concentration and neutral pH. Predictions based on the application of the XDLVO approach were confirmed by independent experimental methods like biomass deposition experiments and laser diffraction spectroscopy. Understanding biomass attachment onto hydrophobic supports can help in alleviating process limitations normally encountered during expanded bed adsorption of bioproducts.     

The immunomodulatory sphingosine 1-phosphate analog FTY720 reduces lesion size and improves neurological outcome in a mouse model of cerebral ischemia

Cerebral ischemia is accompanied by fulminant cellular and humoral inflammatory changes in the brain which contribute to lesion development after stroke. A tight interplay between the brain and the peripheral immune system leads to a biphasic immune response to stroke consisting of an early activation of peripheral immune cells with massive production of proinflammatory cytokines followed by a systemic immunosuppression within days of cerebral ischemia that is characterized by massive immune cell loss in spleen and thymus. Recent work has documented the importance of T lymphocytes in the early exacerbation of ischemic injury. The lipid signaling mediator sphingosine 1-phosphate-derived stable analog FTY720 (fingolimod) acts as an immunosuppressant and induces lymphopenia by preventing the egress of lymphocytes, especially T cells, from lymph nodes. We found that treatment with FTY720 (1 mg/kg) reduced lesion size and improved neurological function after experimental stroke in mice, decreased the numbers of infiltrating neutrophils, activated microglia/macrophages in the ischemic lesion and reduced immunohistochemical features of apoptotic cell death in the lesion.     

Impaired Antibody Response Causes Persistence of Prototypic T Cell–Contained Virus

CD8 T cells are recognized key players in control of persistent virus infections, but increasing evidence suggests that assistance from other immune mediators is also needed. Here, we investigated whether specific antibody responses contribute to control of lymphocytic choriomeningitis virus (LCMV), a prototypic mouse model of systemic persistent infection. Mice expressing transgenic B cell receptors of LCMV-unrelated specificity, and mice unable to produce soluble immunoglobulin M (IgM) exhibited protracted viremia or failed to resolve LCMV. Virus control depended on immunoglobulin class switch, but neither on complement cascades nor on Fc receptor γ chain or Fc γ receptor IIB. Cessation of viremia concurred with the emergence of viral envelope-specific antibodies, rather than with neutralizing serum activity, and even early nonneutralizing IgM impeded viral persistence. This important role for virus-specific antibodies may be similarly underappreciated in other primarily T cell–controlled infections such as HIV and hepatitis C virus, and we suggest this contribution of antibodies be given consideration in future strategies for vaccination and immunotherapy.     

Functional Anatomy of Polycomb and Trithorax Chromatin Landscapes in Drosophila Embryos

Polycomb group (PcG) and trithorax group (trxG) proteins are conserved chromatin factors that regulate key developmental genes throughout development. In Drosophila, PcG and trxG factors bind to regulatory DNA elements called PcG and trxG response elements (PREs and TREs). Several DNA binding proteins have been suggested to recruit PcG proteins to PREs, but the DNA sequences necessary and sufficient to define PREs are largely unknown. Here, we used chromatin immunoprecipitation (ChIP) on chip assays to map the chromosomal distribution of Drosophila PcG proteins, the N- and C-terminal fragments of the Trithorax (TRX) protein and four candidate DNA-binding factors for PcG recruitment. In addition, we mapped histone modifications associated with PcG-dependent silencing and TRX-mediated activation. PcG proteins colocalize in large regions that may be defined as polycomb domains and colocalize with recruiters to form several hundreds of putative PREs. Strikingly, the majority of PcG recruiter binding sites are associated with H3K4me3 and not with PcG binding, suggesting that recruiter proteins have a dual function in activation as well as silencing. One major discriminant between activation and silencing is the strong binding of Pleiohomeotic (PHO) to silenced regions, whereas its homolog Pleiohomeotic-like (PHOL) binds preferentially to active promoters. In addition, the C-terminal fragment of TRX (TRX-C) showed high affinity to PcG binding sites, whereas the N-terminal fragment (TRX-N) bound mainly to active promoter regions trimethylated on H3K4. Our results indicate that DNA binding proteins serve as platforms to assist PcG and trxG binding. Furthermore, several DNA sequence features discriminate between PcG- and TRX-N–bound regions, indicating that underlying DNA sequence contains critical information to drive PREs and TREs towards silencing or activation.