94 research outputs found
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
Effect of quercetin on capacitation status and lipid peroxidation of stallion spermatozoa
No full textLower fertility of preserved stallion semen may be caused by damage to the spermatozoa or premature capacitation during storage. We investigated the use of the flavonoid, quercetin, with a standard skim milk extender for storage of stallion spermatozoa to prevent premature capacitation and acrosome reaction and to reduce the damage to spermatozoa from lipid peroxidation. Several concentrations of quercetin (0.05, 0.1, 0.2, 0.3 mM) were mixed with skim milk-glucose extender, and the antioxidant effectiveness was assessed using xanthine-xanthine oxidase challenge for 21 h. The effect of quercetin on capacitation status of sperm was assessed during a 4 h incubation at 33 C, and a storage trial at 5 C for 6 days. In addition, the ability of sperm stored in quercetin extender to undergo capacitation and acrosome reaction was assessed using heparin and A23187. Lipid peroxidation in the sperm after challenge was inhibited by any concentration of quercetin in the medium, while 0.1 and 0.3 mM queicetin were most effective at preventing capacitation and acrosome reaction during a 33 C incubation. During storage at 5 degrees C for 6 d, quercetin addition to the extender significantly reduced the proportion of sperm capacitation. Heparin had no effect on capacitation status in either extender, but A23187 increased the proportion of sperm stored in the quercetin extender undergoing capacitation and acrosome reaction. In conclusion, quercetin in the standard skim milk-glucose extender for equine semen during storage reduces lipid peroxidation of the sperm, maintains internal adenosine triphosphate (ATP) concentration, and prevents premature capacitation of sperm cells before insemination while still allowing the sperm to capacitate and acrosome react after insemination.PT: J; CR: ADEOYAOSIGUWA SA, 1993, J REPROD FERTIL, V99, P187 AITKEN RJ, 1988, J ANDROL, V9, P367 AITKEN RJ, 1989, BIOL REPROD, V40, P183 AITKEN RJ, 1993, MOL REPROD DEV, V35, P302 AITKEN RJ, 1995, REPROD FERT DEVELOP, V7, P659 ALVAREZ JG, 1983, BIOL REPROD, V29, P548 BLUE BJ, 1989, EQUINE VET J S, V8, P111 BRZEZINSKASLEBO.E, 1995, BIOL TRACE ELEM RES, V47, P69 DASGUPTA S, 1994, J REPROD FERTIL, V102, P107 DELAMIRANDE E, 1992, J ANDROL, V13, P379 DELAMIRANDE E, 1993, FREE RADICAL BIO MED, V14, P157 DELAMIRANDE E, 1995, FREE RADICAL BIO MED, V18, P487 DELAMIRANDE E, 1997, MOL HUM REPROD, V3, P175 DELAMIRANDE E, 1998, J ANDROL, V19, P585 FARLIN ME, 1993, EQUINE VET J S, V15, P49 FRASER LR, 1992, J REPROD FERTIL, V96, P363 FRASER LR, 1995, MOL REPROD DEV, V40, P233 GILLAN L, 1997, REPROD FERT DEVELOP, V9, P481 GREEN CE, 2001, REPRODUCTION, V122, P889 HAMMERSTEDT RH, 1983, BIOCH METABOLIC PROC, P29 HAMMERSTEDT RH, 1988, ARCH BIOCHEM BIOPHYS, V266, P111 HAMMERSTEDT RH, 1993, REPROD FERT DEVELOP, V5, P675 HAN HL, 1990, FERTIL STERIL, V54, P1177 HARRISON RAP, 1996, REPROD FERT DEVELOP, V8, P581 KALAB P, 1998, MOL REPROD DEV, V51, P304 KANKOFER M, 2005, THERIOGENOLOGY, V63, P1354 KENNEY RM, 1975, P ANN CONV AM ASS EQ, V21, P327 KHANDUJA KL, 2001, ANDROLOGIA, V33, P277 KODAMA H, 1996, J ANDROL, V17, P151 LECLERC P, 1997, FREE RADICAL BIO MED, V22, P643 LENZ RW, 1983, GAMETE RES, V8, P11 LENZI A, 1996, HUM REPROD UPDATE, V2, P246 MCNIVEN MA, 2003, CELL PRES TECH, V1, P165 MOSKAUG JO, 2004, MECH AGEING DEV, V125, P315 NASSARDEN L, 1990, MOL REPROD DEV, V25, P369 OHTA A, 1989, BIOCHIM BIOPHYS ACTA, V984, P151 PARRISH JJ, 1988, BIOL REPROD, V38, P1171 POMMER AC, 2002, THERIOGENOLOGY, V57, P1493 ROLDAN ERS, 1989, J REPROD FERTIL, V85, P297 ROY JB, 1985, P 41 ANN M AM FERT S, P75 VARNER DD, 1993, ARCH ANDROLOGY, V31, P199 WATSON PF, 1990, MARSHALLS PHYSL REPR, V2, P747 WATSON PF, 1995, REPROD FERT DEVELOP, V7, P871 ZHANG JJ, 1990, MOL REPROD DEV, V26, P361; NR: 44; TC: 0; J9: CELL PRESERV TECHNOL; PG: 9; GA: 106OESource type: Electronic(1
Are EU spatial ex ante coexistence regulations proportional?
No full textThe EU is currently struggling to implement coherent coexistence regulations on genetically modified (GM) and non-GM crops in all member states. While it stresses that any approach needs to be “proportionate to the aim of achieving coexistence”, very few studies have actually attempted to assess whether the proposed spatial ex ante coexistence regulations (SEACERs) satisfy this proportionality condition. In this article, we define proportionality as a functional relationship which is weakly increasing in the incentives for coexistence. We propose a spatial framework based on an existing landscape and introduce the new concept of shadow factor as a measure for the opportunity costs induced by SEACERs. This enables comparing the proportionality of (i) rigid SEACERs which are based on large isolation distances imposed on GM farmers versus (ii) flexible SEACERs based on pollen barrier agreements between neighboring farmers. Our theoretical and empirical findings argue for flexibility as rigid SEACERs violate the proportionality condition and, hence, are not consistent with the objectives of the EU.policy analysis, GIS, shadow factor, Agricultural and Food Policy, Crop Production/Industries,
RNAseq analysis of fast skeletal muscle in restriction-fed transgenic coho salmon (Oncorhynchus kisutch) : an experimental model uncoupling the growth hormone and nutritional signals regulating growth
No full textBackground Coho salmon (Oncorhynchus kisutch) transgenic for growth hormone (Gh) express Gh in multiple tissues which results in increased appetite and continuous high growth with satiation feeding. Restricting Gh-transgenics to the same lower ration (TR) as wild-type fish (WT) results in similar growth, but with the recruitment of fewer, larger diameter, muscle skeletal fibres to reach a given body size. In order to better understand the genetic mechanisms behind these different patterns of muscle growth and to investigate how the decoupling of Gh and nutritional signals affects gene regulation we used RNA-seq to compare the fast skeletal muscle transcriptome in TR and WT coho salmon. Results Illumina sequencing of individually barcoded libraries from 6 WT and 6 TR coho salmon yielded 704,550,985 paired end reads which were used to construct 323,115 contigs containing 19,093 unique genes of which >10,000 contained >90 % of the coding sequence. Transcripts coding for 31 genes required for myoblast fusion were identified with 22 significantly downregulated in TR relative to WT fish, including 10 (vaspa, cdh15, graf1, crk, crkl, dock1, trio, plekho1a, cdc42a and dock5) associated with signaling through the cell surface protein cadherin. Nineteen out of 44 (43 %) translation initiation factors and 14 of 47 (30 %) protein chaperones were upregulated in TR relative to WT fish. Conclusions TR coho salmon showed increased growth hormone transcripts and gene expression associated with protein synthesis and folding than WT fish even though net rates of protein accretion were similar. The uncoupling of Gh and amino acid signals likely results in additional costs of transcription associated with protein turnover in TR fish. The predicted reduction in the ionic costs of homeostasis in TR fish associated with increased fibre size were shown to involve multiple pathways regulating myotube fusion, particularly cadherin signaling.Peer reviewe
Intrapartum-related neonatal encephalopathy incidence and impairment at regional and global levels for 2010 with trends from 1990.
No full textBACKGROUND: Intrapartum hypoxic events ("birth asphyxia") may result in stillbirth, neonatal or postneonatal mortality, and impairment. Systematic morbidity estimates for the burden of impairment outcomes are currently limited. Neonatal encephalopathy (NE) following an intrapartum hypoxic event is a strong predictor of long-term impairment. METHODS: Linear regression modeling was conducted on data identified through systematic reviews to estimate NE incidence and time trends for 184 countries. Meta-analyses were undertaken to estimate the risk of NE by sex of the newborn, neonatal case fatality rate, and impairment risk. A compartmental model estimated postneonatal survivors of NE, depending on access to care, and then the proportion of survivors with impairment. Separate modeling for the Global Burden of Disease 2010 (GBD2010) study estimated disability adjusted life years (DALYs), years of life with disability (YLDs), and years of life lost (YLLs) attributed to intrapartum-related events. RESULTS: In 2010, 1.15 million babies (uncertainty range: 0.89-1.60 million; 8.5 cases per 1,000 live births) were estimated to have developed NE associated with intrapartum events, with 96% born in low- and middle-income countries, as compared with 1.60 million in 1990 (11.7 cases per 1,000 live births). An estimated 287,000 (181,000-440,000) neonates with NE died in 2010; 233,000 (163,000-342,000) survived with moderate or severe neurodevelopmental impairment; and 181,000 (82,000-319,000) had mild impairment. In GBD2010, intrapartum-related conditions comprised 50.2 million DALYs (2.4% of total) and 6.1 million YLDs. CONCLUSION: Intrapartum-related conditions are a large global burden, mostly due to high mortality in low-income countries. Universal coverage of obstetric care and neonatal resuscitation would prevent most of these deaths and disabilities. Rates of impairment are highest in middle-income countries where neonatal intensive care was more recently introduced, but quality may be poor. In settings without neonatal intensive care, the impairment rate is low due to high mortality, which is relevant for the scale-up of basic neonatal resuscitation
Pure Mafia - a novel about child labour, plus thesis and commentary
No full textThis thesis was submitted for the degree of Doctor of Philosophy and awarded by Brunel University.This PhD in Creative Writing consists of three parts. The first part is a full-length novel, approximately 80K words, entitled Pure
Mafia. It is a drama about child labour and the Pakistani “carpet mafia”. This is
intertwined with the story of an unhappily married man undergoing a midlife crisis who
has an affair with a younger woman; the latter is instrumental to the main plot about
child labour. The book’s second main theme is British Pakistanis. An overarching theme
is abuse and exploitation, both personal and global, but ultimately of redemption and
renewal. The story is set in 2010/2011, mainly in London, England, with a middle
section in Lahore, Pakistan. The second part is an academic thesis, approximately 20K words, entitled Cheap Labour = Child Labour, on the main theme of the novel, child labour. It attempts to show that child labour is an inevitable consequence of cheap labour generally, and that the only way to tackle child labour is to address cheap labour. The thesis has been consciously and deliberately written as an objective, third person, standalone document and for this reason does not mention the novel. It is partly designed to fulfil the general
PhD criterion of demonstrating scholarship and research. The third part is a subjective, first person critical commentary, approximately 15K words, on the writing of the novel and the thesis, the connection between them, and the research context; it is entitled Pure Mafia: A critical commentary. It explains why
the main thesis is on child labour, rather than on the creative process or an English
Literature thesis; however, the commentary does include in some detail an insight into
the creative process, as well as a discussion of influences and tradition of writing. The final section of the commentary summarises this entire PhD’s original
contribution to knowledge
Sentimentality or speculation? Diaspora investment, crisis economies and urban transformation
No full textThis article explores political and moral economies of diasporic investment in urban property. It challenges uncritical policy discourses on migrant investment that romanticise transnational family and entrepreneurial networks by assuming diasporic social embeddedness, mutual trust, risk-reduction and socio-economic benefits, often founded in neo-liberal assumptions. The article elaborates alternate starting propositions emphasising the conflicting interests and predatory business practices that characterise informalised state governance and episodes of crisis. It stresses the importance of understanding changing regulatory regimes over finance and urban property. Migrants’ desires need to be scrutinised in relation to those of a range of other actors who cannot be assumed to have convergent interests – including relatives, investment advisors, money transfer companies, estate agents, property developers. The article takes the case of hyperinflationary Zimbabwe, where remittances from the displaced middle classes not only provided essential familial support, but were also materialised in urban real estate, contributing to inflated property prices and a residential construction boom in the capital city. Diasporic investors were vulnerable to fraud due to the combination of effects of fantasies of successful return to dream homes and irregular regimes for remittances and property. But there were notable speculative opportunities for those with government connections. New diaspora suburbs and homes that have transformed the landscape of the Harare periphery stand as material testimony to the intersection of emigré sentimentality and the speculative informalised economy of the crisis years
A Multivariate Surface-Based Analysis of the Putamen in Premature Newborns: Regional Differences within the Ventral Striatum
No full textMany children born preterm exhibit frontal executive dysfunction, behavioral problems including attentional deficit/hyperactivity disorder and attention related learning disabilities. Anomalies in regional specificity of cortico-striato-thalamo-cortical circuits may underlie deficits in these disorders. Nonspecific volumetric deficits of striatal structures have been documented in these subjects, but little is known about surface deformation in these structures. For the first time, here we found regional surface morphological differences in the preterm neonatal ventral striatum. We performed regional group comparisons of the surface anatomy of the striatum (putamen and globus pallidus) between 17 preterm and 19 term-born neonates at term-equivalent age. We reconstructed striatal surfaces from manually segmented brain magnetic resonance images and analyzed them using our in-house conformal mapping program. All surfaces were registered to a template with a new surface fluid registration method. Vertex-based statistical comparisons between the two groups were performed via four methods: univariate and multivariate tensor-based morphometry, the commonly used medial axis distance, and a combination of the last two statistics. We found statistically significant differences in regional morphology between the two groups that are consistent across statistics, but more extensive for multivariate measures. Differences were localized to the ventral aspect of the striatum. In particular, we found abnormalities in the preterm anterior/inferior putamen, which is interconnected with the medial orbital/prefrontal cortex and the midline thalamic nuclei including the medial dorsal nucleus and pulvinar. These findings support the hypothesis that the ventral striatum is vulnerable, within the cortico-stiato-thalamo-cortical neural circuitry, which may underlie the risk for long-term development of frontal executive dysfunction, attention deficit hyperactivity disorder and attention-related learning disabilities in preterm neonates. © 2013 Shi et al
Embryonic stem cells: modelling effects ofearly embryo environment
No full textThe Developmental Origins of Health and Disease (DOHaD) hypothesis proposes that embryonic environment can induce permanent changes in metabolism during development, increasing the risk of disease in adults. Adverse environments during critical stages of gestation are sufficient to induce adaptations in offspring and disease susceptibility in later life. Rodent models show that maternal diet exclusively during preimplantation development induces cardiovascular and metabolic disease in adult offspring. Changes must therefore occur within the distinct cell populations of the early embryo and be maintained throughout development. Determining adaptive mechanisms has been challenging due to the small size of the early embryo, and genetic variability in outbred strains previously used. We generated mouse embryonic stem (ES) cells from inbred C57BL/6 mice as a model to overcome these problems. These were used to characterise mechanisms associated with the embryo’s adaptive responses to maternal diet. ES cell lines were derived from blastocysts of C57BL/6 mice assigned to either an isocaloric low protein diet (LPD), or a control diet exclusively through preimplantation development. ES cell lines were characterised for karyotype, sex, gene expression, and functional characteristics including proliferation, death, and metabolism at standardised passages. LPD had no impact on blastocyst formation in vivo or blastocyst cell lineage allocation. Experimental conditions did affect blastocyst outgrowth development in vitro. LPDoutgrowths cultured with less feeder fibroblasts showed slower development than controls. Although LPD blastocyst outgrowth was comparable to controls under high feeder growth conditions, there was a significant reduction in the capacity for ES cell derivation. There was a prominent sex bias towards male ES cell lines. These ES cells retained similar levels of gene expression related to pluripotency, housekeeping and developmental functions irrespective of diet. LPD did not affect growth or metabolism. These cells however showed increased basal apoptosis, and reduced levels of phosphorylated Extracellular signal-regulated kinase (ERK). The reduced ES cell isolation efficiency may indicate a reduced number of pluripotent cells present within the early embryo or increased sensitivity of these cells in response to maternal LPD. Increased apoptosis in ES cells derived from LPD-blastocysts reveal that these cells are indeed more sensitive. Reduced activated ERK may suggest that dysregulated ERK-mediated survival signalling causes enhanced apoptosis. Such adaptations in the early embryo may impact on lineage allocation as differentiation occurs. These ES cell lines may provide a model to investigate such mechanistic adaptations in post-implantation tissues providing further insight into foetal responses to poor nutrition and the induction of adult onset disease
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