The effect of montmorillonite and compatibilizer quantities on stiffness and toughness of polyamide nanoblends

Although polymer blend nanocomposites are widely studied, the balance between stiffness and toughness has not yet been investigated in detail. Some materials producers as well as some sectors in the automotive industry try to improve the toughness of materials without an important loss in stiffness. With this in mind, the aim of the study reported here was to obtain a good balance between toughness and stiffness of polymer blends with different amounts of clay and compatibilizer. In this context, the microstructure of polyamide 6/ethylene–propylene–diene metallocene terpolymer/(ethylene–propylene–diene copolymer)‐graft‐(maleic anhydride) blends with various amounts of clay (2, 3, 4 and 5 wt%) and compatibilizer (10 and 20 wt%) was studied to analyse the achieved morphology to understand the macroscopic properties. The morphology of the rubber phase and the dispersion of the montmorillonite (MMT) are the main factors that influence the mechanical properties. In this sense, the highest Young's modulus is achieved for nanoblends with 5 wt% of MMT, although this nanoblend has the lowest value of notched Izod impact strength. The results obtained suggest that there is a clear trade‐off between stiffness, toughness and temperature behaviour when the ratio of (ethylene–propylene–diene copolymer)‐graft‐(maleic anhydride) to MMT is 5:1. Copyright © 2009 Society of Chemical Industry     

Seizure activity and lesions of neuronal cells by intrahippocampal injection of guanidinosuccinic acid in rats]

Intrahippocampal injection(ihci) of guanidinosuccinic acid (GSA) to rats, induced typical generarized clonic seizures and epileptiform discharges in electrohippocampogram (EHG) and electrocorticogram (ECoG), degenerative changes of neuronal cells in the injected side hippocampus. The pyramidal cells in CA1 area were found to be more vulnerable to GSA than the granular cells. Phenobarbital and phenytoin are typical antiepiletics, but in no case did they successfully protect against GSA induced convulsions, epileptiform discharges in the EHG and ECoG and neurolysis. Ketamine, a selective noncompetitive NMDA receptor antagonist, was shown to protect against not only seizures, but also neuronal cell damage induced by GSA. All these results indicate that GSA very like the endogenous excitatory amino acid, glutamic acid, it also has such effects mentioned above. Therefore, the NMDA receptor may mediate both effects of GSA.     

Vitamin C elevates red blood cell glutathione in healthy adults

Pre-transplant nephrectomy was done in a 25-year-old man for calculous pyelonephritis using a retroperitoneal laparoscopic approach with a newly devised ligature applicator-dissector- kidney retractor.     

Structural modeling of the pro-ocytocin-neurophysin precursor

The hormonal precursor pro-ocytocin-neurophysin is activated by selectivecleavage at Arg2-Ala13, producing mature ocytocin and neurophysin. Tounderstand the cleavage mechanism better, and in particular the recognitionof the cleavage site, it is necessary to characterize the three-dimensionalstructure of the precursor molecule. Here we combine a variety ofexperimental data with molecular modeling and dynamics calculations toderive possible precursor conformations. In the models obtained, theN-terminus of the precursor, corresponding to the ocytocin segment, ishydrogen bonded in a pocket of the neurophysin moiety in a similar mannerto a crystallographically obtained non-covalent complex between the twomolecules. The calculations suggest that although the ocytocin segment isrelatively flexible, it adopts a stable, broad loop structure in thevicinity of the cleavage region, which may constitute the structuralelement recognized by the cleaving enzyme. The calculations also suggest apossible widening of the distance between the two neurophysin domains inthe precursor relative to that in the non-covalent neurophysin- ocytocincomplex.     

Molecular modelling of the ORL1 receptor and its complex with nociceptin

The opioid receptor like (ORL1) receptor is a G-protein coupled receptor superfamily, and regulates a plethora of neurophysiological functions. The structural requirements for receptor activation by its endogenous agonist, nociceptin (FGGFTGARKSARKLANQ), differ markedly from those of the kappa-opioid receptor and its putative peptide agonist, dynorphin A (YGGFLRRIRPKLKWDNQ). In order to probe the functional architecture of the ORL1 receptor, a molecular model of the receptor has been built, including the TM domain and the extra- and intracellular loops. An extended binding site able to accommodate nociceptin-(1-13), the shortest fully active analogue of nociceptin, has been characterized. The N-terminal FGGF tetrapeptide is proposed to bind in a highly conserved region, comprising two distinct hydrophobic pockets in a cavity formed by TM helices 3, 5, 6 and 7, capped by the acidic second extracellular (EL2) loop controlling access to the TM elements of the peptide binding site. The nociceptin conformation provides for the selective preference of the ORL1 receptor for nociceptin over dynorphin A, conferred by residue positions 5 and 6 (TG versus LR), and the favourable interaction of its highly positively charged core (residues 8-13) with the EL2 loop, thought to mediate receptor activation. The functional roles of the EL2 loop and the conserved N-terminal tetrapeptide opioid 'message' binding site are discussed in the context of the different structural requirements of the ORL1 and kappa-opioid receptors for activation.      

Increased number of cardiomyocytes in cross-sections from tachycardia-induced cardiomyopathic hearts

Based on positive identification of DNA replication and mitotic division in cardiomyocytes isolated from failing hearts, it has been proposed that adult ventricular cardiomyocytes can gain the capacity to proliferate with progression of heart failure. However, due to the lack of a reliable method to distinctly image individual cardiac cells within the myocardial syntitium, such a concept still remains largely controversial. In the present study, we used laser confocal microscopy, to image cross-sections of intact myocardium stained with fluorescein-conjugated wheat germ agglutinin and propidium iodide. This approach allowed to clearly separate the profile of individual myocytes within cardiac tissue sections. We found that in the left ventricles of dogs, subjected to tachycardia-induced cardiomyopathy, the number of cells was significantly increased in both longitudinal and transversal sections. Treatment with the angiotensin-converting enzyme inhibitor, enalapril, reversed these changes to values similar to those found in controls. Therefore, this study provides evidence, at the in situ level, for cellular hyperplasia in heart failure. This supports the more general notion that adult cardiomyocytes may not be terminally differentiated, and that an increase in cell number could contribute to the increase in left ventricular mass observed with progression of disease.     

Molecular typing of Neisseria gonorrhoeae causing repeated infections: evolution of porin during passage within a community

Thirty-three Neisseria gonorrhoeae isolates from 15 persons infected multiple times with the same serovar were compared using por gene sequencing, opa-typing, and arbitrarily primed-polymerase chain reaction. All three molecular techniques were more discriminatory than serotyping and identified differences between some isolates belonging to the same serovar. Although there were differences among Por sequences within some serovars, 10 of 15 subjects became reinfected with gonococci expressing identical Por proteins. Sequence analysis of por genes revealed evidence of horizontal genetic exchange and point mutations in potential surface-exposed regions during passage in the community.     

Organized cell swimming motions in Bacillus subtilis colonies: patterns of short-lived whirls and jets

The swimming motions of cells within Bacillus subtilis colonies, as well as the associated fluid flows, were analyzed from video films produced during colony growth and expansion on wet agar surfaces. Individual cells in very wet dense populations moved at rates between 76 and 116 microm/s. Swimming cells were organized into patterns of whirls, each approximately 1,000 microm2, and jets of about 95 by 12 microm. Whirls and jets were short-lived, lasting only about 0.25 s. Patterns within given areas constantly repeated with a periodicity of approximately 1 s. Whirls of a given direction became disorganized and then re-formed, usually into whirls moving in the opposite direction. Pattern elements were also organized with respect to one another in the colony. Neighboring whirls usually turned in opposite directions. This correlation decreased as a function of distance between whirls. Fluid flows associated with whirls and jets were measured by observing the movement of marker latex spheres added to colonies. The average velocity of markers traveling in whirls was 19 microm/s, whereas those traveling in jets moved at 27 microm/s. The paths followed by markers were aligned with the direction of cell motion, suggesting that cells create flows moving with them into whirls and along jets. When colonies became dry, swimming motions ceased except in regions close to the periphery and in isolated islands where cells traveled in slow whirls at about 4 microm/s. The addition of water resulted in immediate though transient rapid swimming (> 80 microm/s) in characteristic whirl and jet patterns. The rate of swimming decreased to 13 microm/s within 2 min, however, as the water diffused into the agar. Organized swimming patterns were nevertheless preserved throughout this period. These findings show that cell swimming in colonies is highly organized.     

Severe leukopenia and dysregulated erythropoiesis in SCID mice persistently infected with the parvovirus minute virus of mice

Parvovirus minute virus of mice strain i (MVMi) infects committed granulocyte-macrophage CFU and erythroid burst-forming unit (CFU-GM and BFU-E, respectively) and pluripotent (CFU-S) mouse hematopoietic progenitors in vitro. To study the effects of MVMi infection on mouse hemopoiesis in the absence of a specific immune response, adult SCID mice were inoculated by the natural intranasal route of infection and monitored for hematopoietic and viral multiplication parameters. Infected animals developed a very severe viral-dose-dependent leukopenia by 30 days postinfection (d.p.i.) that led to death within 100 days, even though the number of circulating platelets and erythrocytes remained unaltered throughout the disease. In the bone marrow of every lethally inoculated mouse, a deep suppression of CFU-GM and BFU-E clonogenic progenitors occurring during the 20- to 35-d.p.i. interval corresponded with the maximal MVMi production, as determined by the accumulation of virus DNA replicative intermediates and the yield of infectious virus. Viral productive infection was limited to a small subset of primitive cells expressing the major replicative viral antigen (NS-1 protein), the numbers of which declined with the disease. However, the infection induced a sharp and lasting unbalance of the marrow hemopoiesis, denoted by a marked depletion of granulomacrophagic cells (GR-1(+) and MAC-1(+)) concomitant with a twofold absolute increase in erythroid cells (TER-119(+)). A stimulated definitive erythropoiesis in the infected mice was further evidenced by a 12-fold increase per femur of recognizable proerythroblasts, a quantitative apoptosis confined to uninfected TER-119(+) cells, as well as by a 4-fold elevation in the number of circulating reticulocytes. Therefore, MVMi targets and suppresses primitive hemopoietic progenitors leading to a very severe leukopenia, but compensatory mechanisms are mounted specifically by the erythroid lineage that maintain an effective erythropoiesis. The results show that infection of SCID mice with the parvovirus MVMi causes a novel dysregulation of murine hemopoiesis in vivo.