EFFECT OF THE STACKING SEQUENCE ON THE IMPACT RESPONSE OF CARBON-GLASS/EPOXY HYBRID COMPOSITES

This paper investigates low-velocity impact response of Quasi Isotropic (QI) hybrid carbon/glass fiber reinforced polymer composites with alternate stacking sequences. Cross-ply woven carbon and glass fibers were used as reinforcing materials to fabricate sandwiched and interlayer hybrid composites. For comparison, the laminates containing only-carbon and only-glass fibers were also studied. Drop weight test was used to impact the samples. The images captured by a normal camera demonstrated that localized damages (delamination) existed within plies. The hybrid laminates had smaller load drops, smaller maximum deflection, and higher maximum load compared to the single fiber laminates. In addition, carbon outside interlayer hybrid laminate showed the highest maximum load and energy absorption, showing the significant dependence of the impact performance on hybridization and stacking sequence. It was concluded that a hybrid composite would help improve impact performance of laminated composites compared to non-hybrid composites if they are properly designed

Haemogenic endocardium contributes to transient definitive haematopoiesis.

Haematopoietic cells arise from spatiotemporally restricted domains in the developing embryo. Although studies of non-mammalian animal and in vitro embryonic stem cell models suggest a close relationship among cardiac, endocardial and haematopoietic lineages, it remains unknown whether the mammalian heart tube serves as a haemogenic organ akin to the dorsal aorta. Here we examine the haemogenic activity of the developing endocardium. Mouse heart explants generate myeloid and erythroid colonies in the absence of circulation. Haemogenic activity arises from a subset of endocardial cells in the outflow cushion and atria earlier than in the aorta-gonad-mesonephros region, and is transient and definitive in nature. Interestingly, key cardiac transcription factors, Nkx2-5 and Isl1, are expressed in and required for the haemogenic population of the endocardium. Together, these data suggest that a subset of endocardial/endothelial cells serve as a de novo source for transient definitive haematopoietic progenitors

Endothelial Neuropilin Disruption in Mice Causes DiGeorge Syndrome-Like Malformations via Mechanisms Distinct to Those Caused by Loss of Tbx1

The spectrum of human congenital malformations known as DiGeorge syndrome (DGS) is replicated in mice by mutation of Tbx1. Vegfa has been proposed as a modifier of DGS, based in part on the occurrence of comparable phenotypes in Tbx1 and Vegfa mutant mice. Many additional genes have been shown to cause DGS-like phenotypes in mice when mutated; these generally intersect in some manner with Tbx1, and therefore impact the same developmental processes in which Tbx1 itself is involved. In this study, using Tie2Cre, we show that endothelial-specific mutation of the gene encoding the VEGFA coreceptor neuropilin-1 (Nrp1) also replicates the most prominent terminal phenotypes that typify DGS. However, the developmental etiologies of these defects are fundamentally different from those caused by absence of TBX1. In Tie2Cre/Nrp1 mutants, initial pharyngeal organization is normal but subsequent pharyngeal organ growth is impaired, second heart field differentiation is normal but cardiac outflow tract cushion organization is distorted, neural crest cell migration is normal, and palatal mesenchyme proliferation is impaired with no change in apoptosis. Our results demonstrate that impairment of VEGF-dependent endothelial pathways leads to a spectrum of DiGeorge syndrome-type malformations, through processes that are distinguishable from those controlled by Tbx1

Expression of the human HPRT gene in neural tissue.

The human hypoxanthine guanine phosphoribosyltransferase (HPRT, EC 2.4.2.8.) is a purine salvage enzyme that catalyzes the condensation of 5\sp\prime-phophoribosyl-pyrophosphate (PRPP) and the purine bases hypoxanthine and guanine in the formation of 5\sp\prime-IMP and 5\sp\prime-GMP, respectively. The HPRT gene is an X-linked, housekeeping gene that presents a remarkable tissue specific pattern of expression. It is postulated that HPRT is differentially regulated in the mammalian CNS, however, there is no conclusive evidence to support this contention. In the present study, we have compared the levels of HPRT expression in the human central nervous system by measuring the steady state levels of HPRT transcripts in the postmortem human cerebral cortex gray matter, subcortical white matter, and liver. HPRT mRNA levels were found to be 10 fold higher in gray matter when compared to other tissues. In contrast, messenger RNA levels of APRT and $\beta$-actin remain similar in all tissues. Given the distinct cellular composition of the mammalian CNS, these studies suggest that the HPRT gene is expressed at significantly higher levels in the cortical neurons. Using size and morphological criteria to separate neuronal and glial nuclei, we analyzed the entire HPRT locus for nuclease hypersensitivity. This analysis identified a single hypersensitive domain in the 5\sp\prime CpG island that was present in all nuclei. The proposed hypersensitive site was also detected by footprinting analysis with the Msp I enzyme. Furthermore, analysis of the methylation pattern in the 5\sp\prime region revealed an Msp I site that appeared to be hypomethylated in the neuronal enriched DNA. We also investigated the use of human HPRT gene regulatory sequences in the context of the herpes simplex virus genome. The HSV-1 recombinant vectors bearing the human HPRT minigene constructs were capable of delivering and expressing the minigenes in a rat neuronal cell line, as evidenced by the detection of the human HPRT transcripts and enzyme. These data suggest that the HPRT promoter might be activated in the HSV-1 chromosome.Ph.D.Biological ChemistryUniversity of Michigan, Horace H. Rackham School of Graduate Studieshttp://deepblue.lib.umich.edu/bitstream/2027.42/103290/1/9308418.pdfDescription of 9308418.pdf : Restricted to UM users only

Effect of ply thickness on damage mechanisms of composite laminates under repeated loading

Barely visible impact damage (BVID) occurs in composite laminates subjected to low-velocity impact. They can then exhibit significant effect on mechanical performance of laminates. Previously, it is shown, analytically and experimentally, that BVID occurs at a critical energy level and below this energy level there is no induced damage. However, repeated impact may cause BVID even below the critical energy level. This paper is a novel investigation that deals with the cyclic behaviour of quasi-isotropic glass/epoxy laminated composites under indentation, which is a quasistatic version of low-velocity impact. In particular, this study aims to investigate the ply thickness effect on matrix crack-induced delamination damage in the case of laminated composites under cyclic quasi static indentation loadings. The effect of different parameters, such as load level and ply thickness, on the damage evolution were here investigated. Tests were performed according to the ASTM 7136 standard. Since the glass layer was translucent, it was also possible to visually inspect the matrix delamination during the tests. The laminates were subjected to load levels lower than the critical load level, while there was no evidence of damages when samples were indented just once. However, by increasing the number of cycles, matrix crack-induced delamination appeared in the samples. In brief, it was observed that the ply thickness and energy level have significant effects on the intensity of the induced damage

Deficient thymic growth and vascular organization in <i>Tie2Cre/Nrp1</i> mutants.

<p>Upper row in all pairs of panels is a control, lower row is a littermate <i>Tie2Cre/Nrp1</i> mutant. PECAM1 immunostained transverse sections around the developing thymus (th) are shown; all six images are at the same magnification. <b>A</b>,<b>B</b>, E12.5 embryos; <b>C</b>,<b>D</b>, E13.5 embryos; <b>E</b>,<b>F</b>, E14.5 embryos. Arrows in A and B point to nascent vessels at the periphery of the E12.5 thymus, which are similar in control vs. mutant embryos at this stage.</p

Outflow tract morphology in <i>Tbx1</i> and <i>Tie2Cre/Nrp1</i> mutants.

<p>All hearts shown are from E10.5 embryos. <b>A</b>,<b>B</b>, control and littermate <i>Tbx1</i> null hearts, showing the straight and shortened OFT and the smaller right ventricle in the <i>Tbx1</i> mutant. <b>C</b>,<b>D</b>, control (<i>Tie2Cre/R26R</i>) and littermate <i>Tie2Cre/R26R/Nrp1</i> mutant, Xgal stained in whole mount, and showing the normal looping of the OFT in <i>Tie2Cre/Nrp1</i> mutants. Panels A′,B′,C′,D′ are traced outlines of the same hearts shown in the corresponding panels to more easily compare the absence of outflow tract lengthening and looping in the <i>Tbx1</i> mutant to the normal looping in the <i>Tie2Cre/Nrp1</i> mutant.</p

Pharyngeal arch artery organization visualized by ink injection at E10.5.

<p><b>A</b>, Normal arterial pattern in a control embryo; the numbers 3, 4, and 6 indicate the respective arch arteries. <b>B</b>,<b>C</b>, Examples of arch artery abnormalities seen in mutant embryos: an extremely hypoplastic 4^th arch artery (B), and a missing 6^th arch artery (C), both indicated by asterisks.</p

Pharyngeal morphology in <i>Tbx1</i> and <i>Tie2Cre/Nrp1</i> mutants.

<p>All panels are frontal sections of E10.5 embryos. <b>A</b>,<b>B</b>, control and littermate <i>Tbx1</i> null embryos; the <i>Tbx1</i> mutant has no segmentation of the foregut (FG) pharyngeal endoderm. <b>C</b>,<b>D</b>, control and littermate <i>Tie2Cre/Nrp1</i> mutant, showing normal pharyngeal organization in mutant embryos even when arch arteries are missing (in the mutant, both 4^th arch arteries were extremely hypoplastic, indicated by the asterisks). 3p, 4p, 3^rd and 4^th pharyngeal pouches; numbers indicate pharyngeal arch arteries. A histology artifact is responsible for the broken piece of the left 3^rd arch in the mutant shown.</p