1,605 research outputs found

    Unusual formation and sub-omohyoid course of external jugular vein.

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    Variations in the origin and termination of external jugular vein are common and are reported in the past. However, variations in the course of external jugular vein are uncommon. During routine dissection classes for medical undergraduates, we came across the unusual formation and course of right external jugular vein and absence of common facial vein, in an approximately 60-year-old male cadaver of Indian origin. External jugular vein was formed by the continuation of undivided trunk of retromandibular vein. Following its formation, it passed vertically superficial to sternocleidomastoid muscle to the lower part of occipital triangle. In the occipital triangle it pierced the investing layer of deep cervical fascia and passed deep to the inferior belly of omohyoid muscle and coursed through the subclavian triangle. Then, it terminated at the junction of subclavian vein with internal jugular vein. Facial vein joined with submental vein and finally drained into internal jugular vein. Further, the posterior auricular vein and anterior jugular veins were absent. Knowledge about the variations of the retromandibular vein, common facial vein and external jugular vein observed in this study, may be important for the surgeons, to prevent inadvertent injury and excessive bleeding during diagnostic and therapeutic procedures

    Beneficial Role of Hydro-alcoholic Seed Extract of Trigonella foenum graecum on Bone Structure and Strength in Menopause Induced Osteopenia

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    BACKGROUND: The current strategies to prevent and treat menopausal osteoporosis are hormone replacement therapy (HRT). However, the long-term use of hormone replacement therapy is limited due to its side-effects. Alternately, use of phytoestrogens has been implicated. Trigonella foenum graecum (TFG) seeds are rich in phytoestrogen and known traditional medicine to treat menopause induced hyperlipidemia. Therefore, in this study, we evaluated the role of dietary TFG seed extract on bone structure and mechanical properties in ovariectomized rats.METHODS: Twenty four female Wistar rats were randomly allocated into four groups; 1) control, 2) ovariectomized, 3) ovariectomized + TFG seed extract and 4) ovariectomized + 17β-estradiol. TFG seed extract/17β-estradiol was administered for 30 days, 14 days after ovariectomy. After the treatment, right femora were collected to measure the length and biomechanical properties, and left femora were gathered to study the micro architectural changes while tibia were collected to measure the dry weight.RESULTS: Maximum flexor load to break femur bone was significantly low in ovariectomized rats in comparison with control rats (P<0.05). Supplementation with TFG significantly improved the maximum flexor load (P<0.05) and tibia dry weight (P<0.01) compared to ovariectomized untreated rats. TFG administration also significantly preserved the trabecular (P<0.01) and cortical bone (P<0.05) thickness compared to ovariectomized rats.CONCLUSION: This study found that dietary intake of TFG seeds can improve the bone structure and biomechanical properties in ovariectomized rats indicating that TFG may be an alternative treatment strategy to prevent the menopause induced osteopenia.

    Trim17, novel E3 ubiquitin-ligase, initiates neuronal apoptosis

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    Accumulating data indicate that the ubiquitin-proteasome system controls apoptosis by regulating the level and the function of key regulatory proteins. In this study, we identified Trim17, a member of the TRIM/RBCC protein family, as one of the critical E3 ubiquitin ligases involved in the control of neuronal apoptosis upstream of mitochondria. We show that expression of Trim17 is increased both at the mRNA and protein level in several in vitro models of transcription-dependent neuronal apoptosis. Expression of Trim17 is controlled by the PI3K/Akt/GSK3 pathway in cerebellar granule neurons (CGN). Moreover, the Trim17 protein is expressed in vivo, in apoptotic neurons that naturally die during post-natal cerebellar development. Overexpression of active Trim17 in primary CGN was sufficient to induce the intrinsic pathway of apoptosis in survival conditions. This pro-apoptotic effect was abolished in Bax(-/-) neurons and depended on the E3 activity of Trim17 conferred by its RING domain. Furthermore, knock-down of endogenous Trim17 and overexpression of dominant-negative mutants of Trim17 blocked trophic factor withdrawal-induced apoptosis both in CGN and in sympathetic neurons. Collectively, our data are the first to assign a cellular function to Trim17 by showing that its E3 activity is both necessary and sufficient for the initiation of neuronal apoptosis. Cell Death and Differentiation (2010) 17, 1928-1941; doi: 10.1038/cdd.2010.73; published online 18 June 201

    Bioactive Compounds of Rambutan (Nephelium lappaceum L.)

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    Rambutan, a widely popular tropical fruit encompasses rich amount of bioactive compounds. All parts of this plant (leaves, bark, root, fruits, fruit skin, pulp and seeds) finds traditional usage, and are linked with high therapeutic values. Rambutan fruits parts like that of peel, pulp and seeds have been scientifically investigated in-depth and is reported to encompass high amounts of bioactive compounds (such as polyphenol, flavonoid, alkaloid, essential mineral, dietary fiber). These compounds contribute towards antioxidant, antimicrobial, anticancer, antidiabetic and anti-obesity activities. However, literature pertaining towards potential industrial applications (food, cosmetics, pharmaceutical) of rambutan fruits are limited. In the present chapter, it is intended to document some of the interesting research themes published on rambutan fruits, and identify the existing gaps to open up arena for future research work.This chapter theme is based on our ongoing project—VALORTECH, which has received funding from the European Union’s Horizon 2020 research and innovation program under grant agreement No 810630

    Neuromyelitis optica MOG-IgG causes reversible lesions in mouse brain.

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    INTRODUCTION: Antibodies against myelin oligodendrocyte glycoprotein (MOG-IgG) are present in some neuromyelitis optica patients who lack antibodies against aquaporin-4 (AQP4-IgG). The effects of neuromyelitis optica MOG-IgG in the central nervous system have not been investigated in vivo. We microinjected MOG-IgG, obtained from patients with neuromyelitis optica, into mouse brains and compared the results with AQP4-IgG. RESULTS: MOG-IgG caused myelin changes and altered the expression of axonal proteins that are essential for action potential firing, but did not produce inflammation, axonal loss, neuronal or astrocyte death. These changes were independent of complement and recovered within two weeks. By contrast, AQP4-IgG produced complement-mediated myelin loss, neuronal and astrocyte death with limited recovery at two weeks. CONCLUSIONS: These differences mirror the better outcomes for MOG-IgG compared with AQP4-IgG patients and raise the possibility that MOG-IgG contributes to pathology in some neuromyelitis optica patients

    Neuromyelitis optica MOG-IgG causes reversible lesions in mouse brain.

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    INTRODUCTION: Antibodies against myelin oligodendrocyte glycoprotein (MOG-IgG) are present in some neuromyelitis optica patients who lack antibodies against aquaporin-4 (AQP4-IgG). The effects of neuromyelitis optica MOG-IgG in the central nervous system have not been investigated in vivo. We microinjected MOG-IgG, obtained from patients with neuromyelitis optica, into mouse brains and compared the results with AQP4-IgG. RESULTS: MOG-IgG caused myelin changes and altered the expression of axonal proteins that are essential for action potential firing, but did not produce inflammation, axonal loss, neuronal or astrocyte death. These changes were independent of complement and recovered within two weeks. By contrast, AQP4-IgG produced complement-mediated myelin loss, neuronal and astrocyte death with limited recovery at two weeks. CONCLUSIONS: These differences mirror the better outcomes for MOG-IgG compared with AQP4-IgG patients and raise the possibility that MOG-IgG contributes to pathology in some neuromyelitis optica patients

    Interplay between estrogen receptor and AKT in estradiol-induced alternative splicing.

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    BACKGROUND: Alternative splicing is critical for generating complex proteomes in response to extracellular signals. Nuclear receptors including estrogen receptor alpha (ERα) and their ligands promote alternative splicing. The endogenous targets of ERα:estradiol (E2)-mediated alternative splicing and the influence of extracellular kinases that phosphorylate ERα on E2-induced splicing are unknown. METHODS: MCF-7 and its anti-estrogen derivatives were used for the majority of the assays. CD44 mini gene was used to measure the effect of E2 and AKT on alternative splicing. ExonHit array analysis was performed to identify E2 and AKT-regulated endogenous alternatively spliced apoptosis-related genes. Quantitative reverse transcription polymerase chain reaction was performed to verify alternative splicing. ERα binding to alternatively spliced genes was verified by chromatin immunoprecipitation assay. Bromodeoxyuridine incorporation-ELISA and Annexin V labeling assays were done to measure cell proliferation and apoptosis, respectively. RESULTS: We identified the targets of E2-induced alternative splicing and deconstructed some of the mechanisms surrounding E2-induced splicing by combining splice array with ERα cistrome and gene expression array. E2-induced alternatively spliced genes fall into at least two subgroups: coupled to E2-regulated transcription and ERα binding to the gene without an effect on rate of transcription. Further, AKT, which phosphorylates both ERα and splicing factors, influenced ERα:E2 dependent splicing in a gene-specific manner. Genes that are alternatively spliced include FAS/CD95, FGFR2, and AXIN-1. E2 increased the expression of FGFR2 C1 isoform but reduced C3 isoform at mRNA level. E2-induced alternative splicing of FAS and FGFR2 in MCF-7 cells correlated with resistance to FAS activation-induced apoptosis and response to keratinocyte growth factor (KGF), respectively. Resistance of MCF-7 breast cancer cells to the anti-estrogen tamoxifen was associated with ERα-dependent overexpression of FGFR2, whereas resistance to fulvestrant was associated with ERα-dependent isoform switching, which correlated with altered response to KGF. CONCLUSION: E2 may partly alter cellular proteome through alternative splicing uncoupled to its effects on transcription initiation and aberration in E2-induced alternative splicing events may influence response to anti-estrogens.RIGHTS : This article is licensed under the BioMed Central licence at http://www.biomedcentral.com/about/license which is similar to the 'Creative Commons Attribution Licence'. In brief you may : copy, distribute, and display the work; make derivative works; or make commercial use of the work - under the following conditions: the original author must be given credit; for any reuse or distribution, it must be made clear to others what the license terms of this work are

    Limits on WWZ and WW\gamma couplings from p\bar{p}\to e\nu jj X events at \sqrt{s} = 1.8 TeV

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    We present limits on anomalous WWZ and WW-gamma couplings from a search for WW and WZ production in p-bar p collisions at sqrt(s)=1.8 TeV. We use p-bar p -> e-nu jjX events recorded with the D0 detector at the Fermilab Tevatron Collider during the 1992-1995 run. The data sample corresponds to an integrated luminosity of 96.0+-5.1 pb^(-1). Assuming identical WWZ and WW-gamma coupling parameters, the 95% CL limits on the CP-conserving couplings are -0.33<lambda<0.36 (Delta-kappa=0) and -0.43<Delta-kappa<0.59 (lambda=0), for a form factor scale Lambda = 2.0 TeV. Limits based on other assumptions are also presented.Comment: 11 pages, 2 figures, 2 table

    Search for New Physics in e mu X Data at D0 Using Sleuth: A Quasi-Model-Independent Search Strategy for New Physics

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    We present a quasi-model-independent search for the physics responsible for electroweak symmetry breaking. We define final states to be studied, and construct a rule that identifies a set of relevant variables for any particular final state. A new algorithm ("Sleuth") searches for regions of excess in those variables and quantifies the significance of any detected excess. After demonstrating the sensitivity of the method, we apply it to the semi-inclusive channel e mu X collected in 108 pb^-1 of ppbar collisions at sqrt(s) = 1.8 TeV at the D0 experiment during 1992-1996 at the Fermilab Tevatron. We find no evidence of new high p_T physics in this sample.Comment: 23 pages, 12 figures. Submitted to Physical Review
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