1,530 research outputs found
Experimental investigation on aluminium composite surface machined by electrical discharge machining process using response surface methodology / R. Rajesh and M. Dev Anand
No full textindustry. Nowadays there is a critical need for cost-effective machining processes for this material. Not much work has been reported for machining of Aluminum based composite with Electrical Discharge Machining (EDM) process. In this work, an attempt has been made to model the machinability evaluation through the Response Surface Methodology (RSM) while machining of Al-10% SiCp Metal Matrix Composite (MMC) was manufactured through stir casting method. The experimental results obtained aims at the selection of optimal machining conditions for EDM of Aluminum based MMC. The work piece material has been cleverly considered as control factor along with the combined effect of six controllable input variables and its effect on the surface roughness has been investigated with the minimum number of experiments. Analysis of variance is performed to get contribution of each parameter on the performance characteristics and it was observed that the discharge current is the significant process parameter that affects the EDM robustness. The contour plots were generated to study the effect of process parameters as well as their interactions. The experimental analysis for the optimal setting shows that there is considerable improvement in the process. The application of this technique converts the response variable to a single response process parameters which are optimized using Box Behnken based approach RSM and thus simplifies the optimization procedure. Result of confirmation experiments shows that the established mathematical models can predict the output response which satisfy the real requirement in practice
Corrigendum to Programmed cell death in the lithium pilocarpine model: Evidence for NMDA receptor and ceramide-mediated mechanisms [Brain Dev 30 (2008) 513-519] (DOI:10.1016-j.braindev.2008.01.002)
No full text[No abstract available]Mikati MA, 2008, BRAIN DEV-JPN, V30, P513, DOI 10.1016-j.braindev.2008.01.0020
The Cryosphere Discussions
No full textwww.geosci-model-dev-discuss.net/6/3003/2013/ doi:10.5194/gmdd-6-3003-2013 © Author(s) 2013. CC Attribution 3.0 License
A role for SUMO modification in transcriptional repression and activation
No full textSince the discovery of the SUMO (small ubiquitin-related modifier) family of proteins just over a decade ago, a plethora of substrates have been uncovered including many regulators of transcription. Conjugation of SUMO to target proteins has generally been considered as a repressive modification. However, there are now a growing number of examples where SUMOylation has been shown to activate transcription. Here, we discuss whether there is something intrinsically repressive about SUMOylation, or if the outcome of this modification in the context of transcription will prove to be largely substrate-dependent. We highlight some of the technical challenges that will be faced by attempting to answer this question
Transformation of mucocartilage to a definitive cartilage during metamorphosis in the sea lamprey, Petromyzon-marinus
No full textPT: J; CR: ARCHER CW, 1982, CELL DIFFER, V11, P245 BROWDER LW, 1980, DEV BIOL, P577 CAPLAN AI, 1973, J EMBRYOL EXP MORPH, V29, P571 DAMAS H, 1935, ARCH BIOL, V46, P171 DARNELL J, 1986, MOL CELL BIOL EDE DA, 1983, CARTILAGE, V2, P143 EIKENBERRY EF, 1984, J MOL BIOL, V176, P261 FOX H, 1975, J EMBRYOL EXP MORPH, V34, P191 FUKUDA Y, 1984, AM J ANAT, V170, P597 GODMAN GC, 1960, J BIOPHYS BIOCHEM CY, V8, P719 GOEL SC, 1970, J EMBRYOL EXPTL MORP, V23, P169 GOSS RJ, 1972, AM ZOOL, V12, P151 GOULD RP, 1972, EXP CELL RES, V72, P325 HALL BK, 1978, DEV CELLULAR SKELETA, P86 HAM AW, 1979, HISTOLOGY HARDISTY MW, 1971, BIOL LAMPREYS, V1, P127 HARDISTY MW, 1971, BIOL LAMPREYS, V1, P85 HARDISTY MW, 1981, BIOL LAMPREYS, V3, P333 HASTY KA, 1981, DEV BIOL, V86, P198 HASTY KA, 1983, J HISTOCHEM CYTOCHEM, V31, P1367 HEASMAN J, 1978, J EMBRYOL EXP MORPH, V46, P119 HORNBRUCH A, 1970, NATURE, V226, P764 HUNZIKER EB, 1982, J ULTRASTRUCT RES, V81, P1 JANNERS MY, 1970, DEV BIOL, V23, P136 JOHNELS A, 1948, ACTA ZOOL-STOCKHOLM, V29, P139 JURAND A, 1965, P ROY SOC B, V162, P387 KIMURA S, 1982, COMP BIOCH PHYSL, V73, P335 KOSHER RA, 1980, J EMBRYOL EXP MORPH, V56, P91 KOSHER RA, 1983, CARTILAGE, V1, P59 LASH JW, 1978, DEV BIOL, V66, P151 LINSENMAYER TF, 1981, CELL BIOL EXTRACELLU, P5 MANGIA F, 1970, ARCH ANAT MICROSC MO, V59, P283 MARTIN GR, 1985, TRENDS BIOCHEM SCI, V10, P285 MILLER EJ, 1969, P NATL ACAD SCI USA, V64, P1264 NATHANSON MA, 1980, DEV BIOL, V78, P301 OLSON M, 1971, AM J ANAT, V131, P197 POTTER IC, 1978, CAN J ZOOL, V56, P561 SCHMIDT AJ, 1968, CELLULAR BIOL VERTEB SCHNEIDER A, 1879, ANATOMIE ENTWICKELUN, P85 SEARLS RL, 1972, DEV BIOL, V28, P123 SHEEHAN DC, 1980, THEORY PRACTICE HIST SHELDON H, 1983, CARTILAGE, V1, P87 SHEREN SB, 1986, COMP BIOCHEM PHYS B, V85, P5 SHORE RC, 1981, J ANAT, V133, P67 STOCKWELL RA, 1979, BIOL CARTILAGE CELLS STUDNICKA FK, 1897, ARCH MIKROSK ANAT, V48, P606 SUMMERBELL D, 1973, NATURE, V244, P492 THOROGOOD PV, 1975, J EMBRYOL EXP MORPH, V33, P581 VONDERMARK K, 1979, CLIN ORTHOP RELAT R, V139, P185 WATENABE K, 1974, CELL TISS RES, V155, P321 WRIGHT GM, 1982, AM J ANAT, V165, P39 WRIGHT GM, 1983, AM J ANAT, V167, P59 WRIGHT GM, 1983, EXPERIENTIA, V39, P495 WRIGHT GM, 1984, CAN J ZOOL, V62, P2445 YOUSON JH, 1979, CAN J ZOOL, V57, P1808 YOUSON JH, 1982, J MORPHOL, V171, P89; NR: 56; TC: 10; J9: J MORPHOL; PG: 21; GA: K6234Source type: Electronic(1
HIGH-STABILITY BIMORPH SCANNING TUNNELING MICROSCOPE
No full textPT: J; CR: BINNIG G, 1983, SURF SCI, V126, P236 BINNIG G, 1986, IBM J RES DEV, V30, P355 BINNIG G, 1986, PHYS REV LETT, V56, P930 BRYANT A, 1986, APPL PHYS LETT, V48, P832 DEMUTH JE, 1986, J VAC SCI TECHNOL 2, V4, P1320 DRAKE B, 1986, REV SCI INSTRUM, V57, P441 DURIG U, 1986, IBM J RES DEV, V30, P478 GERBER C, 1986, REV SCI INSTRUM, V57, P221 GIMZEWSKI JK, 1985, PHYS REV LETT, V55, P951 JERICHO MH, 1987, REV SCI INSTRUM, V58, P1349 MAMIN HJ, 1985, REV SCI INSTRUM, V56, P2168 MAMIN HJ, 1986, IBM J RES DEV, V30, P492 MCKENNA R, 1987, HONOURS PROJECT DALH MURALT P, 1986, IBM J RES DEV, V30, P443 SMITH DPE, 1986, APPL PHYS LETT, V49, P1166 VANDEWALLE GFA, 1985, REV SCI INSTRUM, V56, P1573; NR: 16; TC: 27; J9: REV SCI INSTR; PG: 6; GA: J6076Source type: Electronic(1
Special issue on human resource strategies for small states
No full textPT: J; NR: 0; TC: 0; J9: INT J EDUC DEV; PG: 2; GA: 415XGSource type: Electronic(1
Functional neurons and melanocytes induced from immortal lines of postnatal neural crest-like stem cells
No full textStem cells, that is, cells that can both reproduce themselves and differentiate into functional cell types, attract much interest as potential aids to healing and disease therapy. Embryonic neural crest is pluripotent and generates the peripheral nervous system, melanocytes, and some connective tissues. Neural-crest-related stem cells have been reported previously in postnatal skin: committed melanocytic stem cells in the hair follicle, and pluripotent cell types from the hair follicle and papilla that can produce various sets of lineages. Here we describe novel pluripotent neural crest-like stem cells from neonatal mouse epidermis, with different potencies, isolated as 3 independent immortal lines. Using alternative regulatory factors, they could be converted to large numbers of either Schwann precursor cells, pigmented melanocytes, chondrocytes, or functional sensory neurons showing voltage-gated sodium channels. Some of the neurons displayed abundant active TRPV1 and TRPA1 receptors. Such functional neurons have previously been obtained in culture only with difficulty, by explantation. The system was also used to generate comparative gene expression data for the stem cells, melanocytes, and melanoblasts that sufficiently explain the lack of pigment in melanoblasts and provide a rationale for some genes expressed apparently ectopically in melanomas, such as ephrin receptors.—Sviderskaya, E. V., Easty, D. J., Lawrence, M. A., Sánchez, D. P., Negulyaev, Y. A., Patel, R. H., Anand, P., Korchev, Y. E., Bennett, D. C. Functional neurons and melanocytes induced from immortal lines of postnatal neural crest-like stem cells
Retinitis Pigmentosa GTPase Regulator (RPGR) protein isoforms in mammalian retina:insights into X-linked Retinitis Pigmentosa and associated ciliopathies
No full textMutations in the cilia-centrosomal protein Retinitis Pigmentosa GTPase Regulator (RPGR) are a frequent cause of retinal degeneration. The RPGR gene undergoes complex alternative splicing and encodes multiple protein isoforms. To elucidate the function of major RPGR isoforms (RPGR 1-19 and RPGR ORF15), we have generated isoform-specific antibodies and examined their expression and localization in the retina. Using sucrose-gradient centrifugation, immunofluorescence and co-immunoprecipitation methods, we show that RPGR isoforms localize to distinct sub-cellular compartments in mammalian photoreceptors and associate with a number of cilia-centrosomal proteins. The RCC1-like domain of RPGR, which is present in all major RPGR isoforms, is sufficient to target it to the cilia and centrosomes in cultured cells. Our findings indicate that multiple isotypes of RPGR may perform overlapping yet somewhat distinct transport-related functions in photoreceptors
Poverty
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