369 research outputs found

    Estabelecimento, multiplicação e alongamento in vitro de Eucalyptus benthamii Maiden & Cambage x Eucalyptus dunnii Maiden.

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    Neste trabalho foram testadas diferentes concentrações de cloro ativo (NaOCl) na assepsia de explantes para o estabelecimento in vitro, bem como benzilaminopurina (BAP) e ácido naftalenoacético (ANA) para a multiplicação e alongamento de Eucalyptus benthamii x Eucalyptus dunnii. As minicepas fornecedoras de propágulos para introdução in vitro foram conduzidas em minijardim clonal sob sistema semi-hidropônico. Segmentos nodais dos clones H12, H19 e H20 foram desinfestados com 0,5; 1,0; 1,5; e 2,0% (v/v) de cloro ativo durante 10 min e inoculados em meio de cultura MS. Na obtenção de brotações múltiplas, utilizou-se o meio de cultura ½MS suplementado com 0; 0,25; 0,50; 0,75; e 1,0 mg L-1 de BAP. Na fase de alongamento, utilizou-se o meio de cultura ½MS com 0; 0,25; 0,50; 0,75; e 1,0 mg L-1 de ANA. Não houve interação entre os fatores estudados, obtendo-se 45%, 46% e 66% de estabelecimento do clone H12, H19 e H20, respectivamente. A concentração de BAP que resultou na maior proliferação de gemas axilares para o clone H12 aos 60 dias foi estimada na faixa de 0,25 e 0,30 mg L-1. Aos 60 dias, a faixa entre 0,25 e 0,75 mg L-1 de ANA promoveu o maior número de brotações alongadas do clone H12

    Recessive germline SDHA and SDHB mutations causing leukodystrophy and isolated mitochondrial complex II deficiency

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    Background Isolated complex II deficiency is a rare form of mitochondrial disease, accounting for approximately 2% of all respiratory chain deficiency diagnoses. The succinate dehydrogenase (SDH) genes (SDHA, SDHB, SDHC and SDHD) are autosomally-encoded and transcribe the conjugated heterotetramers of complex II via the action of two known assembly factors (SDHAF1 and SDHAF2). Only a handful of reports describe inherited SDH gene defects as a cause of paediatric mitochondrial disease, involving either SDHA (Leigh syndrome, cardiomyopathy) or SDHAF1 (infantile leukoencephalopathy). However, all four SDH genes, together with SDHAF2, have known tumour suppressor functions, with numerous germline and somatic mutations reported in association with hereditary cancer syndromes, including paraganglioma and pheochromocytoma. Methods and results Here, we report the clinical and molecular investigations of two patients with histochemical and biochemical evidence of a severe, isolated complex II deficiency due to novel SDH gene mutations; the first patient presented with cardiomyopathy and leukodystrophy due to compound heterozygous p.Thr508Ile and p.Ser509Leu SDHA mutations, while the second patient presented with hypotonia and leukodystrophy with elevated brain succinate demonstrated by MR spectroscopy due to a novel, homozygous p.Asp48Val SDHB mutation. Western blotting and BN-PAGE studies confirmed decreased steady-state levels of the relevant SDH subunits and impairment of complex II assembly. Evidence from yeast complementation studies provided additional support for pathogenicity of the SDHB mutation. Conclusions Our report represents the first example of SDHB mutation as a cause of inherited mitochondrial respiratory chain disease and extends the SDHA mutation spectrum in patients with isolated complex II deficiency

    Jet Substructure at the Tevatron and LHC: New results, new tools, new benchmarks

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    In this report we review recent theoretical progress and the latest experimental results in jet substructure from the Tevatron and the LHC. We review the status of and outlook for calculation and simulation tools for studying jet substructure. Following up on the report of the Boost 2010 workshop, we present a new set of benchmark comparisons of substructure techniques, focusing on the set of variables and grooming methods that are collectively known as "top taggers". To facilitate further exploration, we have attempted to collect, harmonise, and publish software implementations of these techniques.Comment: 53 pages, 17 figures. L. Asquith, S. Rappoccio, C. K. Vermilion, editors; v2: minor edits from journal revision

    Epidemiologic investigation of immune-mediated polyradiculoneuropathy among abattoir workers exposed to porcine brain

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    Background In October 2007, a cluster of patients experiencing a novel polyradiculoneuropathy was identified at a pork abattoir (Plant A). Patients worked in the primary carcass processing area (warm room); the majority processed severed heads (head-table). An investigation was initiated to determine risk factors for illness. Methods and Results Symptoms of the reported patients were unlike previously described occupational associated illnesses. A case-control study was conducted at Plant A. A case was defined as evidence of symptoms of peripheral neuropathy and compatible electrodiagnostic testing in a pork abattoir worker. Two control groups were used - randomly selected non-ill warm-room workers (n = 49), and all non-ill head-table workers (n = 56). Consenting cases and controls were interviewed and blood and throat swabs were collected. The 26 largest U.S. pork abattoirs were surveyed to identify additional cases. Fifteen cases were identified at Plant A; illness onsets occurred during May 2004–November 2007. Median age was 32 years (range, 21–55 years). Cases were more likely than warm-room controls to have ever worked at the head-table (adjusted odds ratio [AOR], 6.6; 95% confidence interval [CI], 1.6–26.7), removed brains or removed muscle from the backs of heads (AOR, 10.3; 95% CI, 1.5–68.5), and worked within 0–10 feet of the brain removal operation (AOR, 9.9; 95% CI, 1.2–80.0). Associations remained when comparing head-table cases and head-table controls. Workers removed brains by using compressed air that liquefied brain and generated aerosolized droplets, exposing themselves and nearby workers. Eight additional cases were identified in the only two other abattoirs using this technique. The three abattoirs that used this technique have stopped brain removal, and no new cases have been reported after 24 months of follow up. Cases compared to controls had higher median interferon-gamma (IFNγ) levels (21.7 pg/ml; vs 14.8 pg/ml, P<0.001). Discussion This novel polyradiculoneuropathy was associated with removing porcine brains with compressed air. An autoimmune mechanism is supported by higher levels of IFNγ in cases than in controls consistent with other immune mediated illnesses occurring in association with neural tissue exposure. Abattoirs should not use compressed air to remove brains and should avoid procedures that aerosolize CNS tissue. This outbreak highlights the potential for respiratory or mucosal exposure to cause an immune-mediated illness in an occupational setting

    A Formalism for the Systematic Treatment of Rapidity Logarithms in Quantum Field Theory

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    Many observables in QCD rely upon the resummation of perturbation theory to retain predictive power. Resummation follows after one factorizes the cross section into the rele- vant modes. The class of observables which are sensitive to soft recoil effects are particularly challenging to factorize and resum since they involve rapidity logarithms. In this paper we will present a formalism which allows one to factorize and resum the perturbative series for such observables in a systematic fashion through the notion of a "rapidity renormalization group". That is, a Collin-Soper like equation is realized as a renormalization group equation, but has a more universal applicability to observables beyond the traditional transverse momentum dependent parton distribution functions (TMDPDFs) and the Sudakov form factor. This formalism has the feature that it allows one to track the (non-standard) scheme dependence which is inherent in any scenario where one performs a resummation of rapidity divergences. We present a pedagogical introduction to the formalism by applying it to the well-known massive Sudakov form factor. The formalism is then used to study observables of current interest. A factorization theorem for the transverse momentum distribution of Higgs production is presented along with the result for the resummed cross section at NLL. Our formalism allows one to define gauge invariant TMDPDFs which are independent of both the hard scattering amplitude and the soft function, i.e. they are uni- versal. We present details of the factorization and resummation of the jet broadening cross section including a renormalization in pT space. We furthermore show how to regulate and renormalize exclusive processes which are plagued by endpoint singularities in such a way as to allow for a consistent resummation.Comment: Typos in Appendix C corrected, as well as a typo in eq. 5.6

    Direct photon production with effective field theory

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    The production of hard photons in hadronic collisions is studied using Soft-Collinear Effective Theory (SCET). This is the first application of SCET to a physical, observable cross section involving energetic partons in more than two directions. A factorization formula is derived which involves a non-trivial interplay of the angular dependence in the hard and soft functions, both quark and gluon jet functions, and multiple partonic channels. The relevant hard, jet and soft functions are computed to one loop and their anomalous dimensions are determined to three loops. The final resummed inclusive direct photon distribution is valid to next-to-next-to-leading logarithmic order (NNLL), one order beyond previous work. The result is improved by including non-logarithmic terms and photon isolation cuts through matching, and compared to Tevatron data and to fixed order results at the Tevatron and the LHC. The resummed cross section has a significantly smaller theoretical uncertainty than the next-to-leading fixed-order result, particularly at high transverse momentum.Comment: 42 pages, 9 figures; v2: references added, minor changes; v3: typos; v4: typos, corrections in (16), (47), (72

    Bioluminescent human breast cancer cell lines that permit rapid and sensitive in vivo detection of mammary tumors and multiple metastases in immune deficient mice

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    INTRODUCTION: Our goal was to generate xenograft mouse models of human breast cancer based on luciferase-expressing MDA-MB-231 tumor cells that would provide rapid mammary tumor growth; produce metastasis to clinically relevant tissues such as lymph nodes, lung, and bone; and permit sensitive in vivo detection of both primary and secondary tumor sites by bioluminescent imaging. METHOD: Two clonal cell sublines of human MDA-MB-231 cells that stably expressed firefly luciferase were isolated following transfection of the parental cells with luciferase cDNA. Each subline was passaged once or twice in vivo to enhance primary tumor growth and to increase metastasis. The resulting luciferase-expressing D3H1 and D3H2LN cells were analyzed for long-term bioluminescent stability, primary tumor growth, and distal metastasis to lymph nodes, lungs, bone and soft tissues by bioluminescent imaging. Cells were injected into the mammary fat pad of nude and nude-beige mice or were delivered systemically via intracardiac injection. Metastasis was also evaluated by ex vivo imaging and histologic analysis postmortem. RESULTS: The D3H1 and D3H2LN cell lines exhibited long-term stable luciferase expression for up to 4–6 months of accumulative tumor growth time in vivo. Bioluminescent imaging quantified primary mammary fat pad tumor development and detected early spontaneous lymph node metastasis in vivo. Increased frequency of spontaneous lymph node metastasis was observed with D3H2LN tumors as compared with D3H1 tumors. With postmortem ex vivo imaging, we detected additional lung micrometastasis in mice with D3H2LN mammary tumors. Subsequent histologic evaluation of tissue sections from lymph nodes and lung lobes confirmed spontaneous tumor metastasis at these sites. Following intracardiac injection of the MDA-MB-231-luc tumor cells, early metastasis to skeletal tissues, lymph nodes, brain and various visceral organs was detected. Weekly in vivo imaging data permitted longitudinal analysis of metastasis at multiple sites simultaneously. Ex vivo imaging data from sampled tissues verified both skeletal and multiple soft tissue tumor metastasis. CONCLUSION: This study characterized two new bioluminescent MDA-MB-231-luc human breast carcinoma cell lines with enhanced tumor growth and widespread metastasis in mice. Their application to current xenograft models of breast cancer offers rapid and highly sensitive detection options for preclinical assessment of anticancer therapies in vivo

    Do current and magnetic helicities have the same sign?

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    Current helicity, H c , and magnetic helicity, H m , are two main quantities used to characterize magnetic fields. For example, such quantities have been widely used to characterize solar active regions and their ejecta (magnetic clouds). It is commonly assumed that H c and H m have the same sign, but this has not been rigorously addressed beyond the simple case of linear force-free fields. We aim to answer whether H m H c ≥ 0 in general, and whether it is true over some useful set of magnetic fields. This question is addressed analytically and with numerical examples. The main focus is on cylindrically symmetric straight flux tubes, referred to as flux ropes (FRs), using the relative magnetic helicity with respect to a straight (untwisted) reference field. Counterexamples with H m H c &lt; 0 have been found for cylindrically symmetric FRs with finite plasma pressure, and for force-free cylindrically symmetric FRs in which the poloidal field component changes direction. Our main result is a proof that H m H c ≥ 0 is true for force-free cylindrically symmetric FRs where the toroidal field and poloidal field components are each of a single sign, and the poloidal component does not exceed the toroidal component. We conclude that the conjecture that current and magnetic helicities have the same sign is not true in general, but it is true for a set of FRs of importance to coronal and heliospheric physics

    Fragilities Caused by Dosage Imbalance in Regulation of the Budding Yeast Cell Cycle

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    Cells can maintain their functions despite fluctuations in intracellular parameters, such as protein activities and gene expression levels. This commonly observed biological property of cells is called robustness. On the other hand, these parameters have different limitations, each reflecting the property of the subsystem containing the parameter. The budding yeast cell cycle is quite fragile upon overexpression of CDC14, but is robust upon overexpression of ESP1. The gene products of both CDC14 and ESP1 are regulated by 1∶1 binding with their inhibitors (Net1 and Pds1), and a mathematical model predicts the extreme fragility of the cell cycle upon overexpression of CDC14 and ESP1 caused by dosage imbalance between these genes. However, it has not been experimentally shown that dosage imbalance causes fragility of the cell cycle. In this study, we measured the quantitative genetic interactions of these genes by performing combinatorial “genetic tug-of-war” experiments. We first showed experimental evidence that dosage imbalance between CDC14 and NET1 causes fragility. We also showed that fragility arising from dosage imbalance between ESP1 and PDS1 is masked by CDH1 and CLB2. The masking function of CLB2 was stabilization of Pds1 by its phosphorylation. We finally modified Chen's model according to our findings. We thus propose that dosage imbalance causes fragility in biological systems
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