32 research outputs found

    Dichloridobis(N,N,N′,N′-tetra­methyl­thio­urea-κS)mercury(II)

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    In the title compound, [HgCl2(C5H12N2S)2], the HgII atom is located on a twofold rotation axis and is bonded in a distorted tetra­hedral coordination mode to two chloride ions and to two tetra­methyl­thio­urea (tmtu) mol­ecules through their S atoms. The crystal structure is stabilized by C—H⋯N and C—H⋯S hydrogen bonds

    Diiodidobis(N,N,N′,N′-tetra­methyl­thio­urea-κS)cadmium(II)

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    In the title compound, [CdI2(C5H12N2S)2], the CdII ion is located on a twofold rotation axis and is coordinated in a distorted tetra­hedral mode by two iodide ions and by two tetra­methyl­thio­urea (tmtu) ligands through their S atoms. The crystal structure is stabilized by C—H⋯N and C—H⋯S hydrogen bonds

    Racemic methyl 3,10-dioxa-2-aza­tri­cyclo­[6.2.1.02,6]undecane-4-carboxyl­ate

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    The structure of the racemic title compound, C10H15NO4, consists of a tricyclic skeleton comprising a six-membered piperidine ring and five-membered isoxazolidine and tetra­hydro­furan rings. The piperidine ring adopts a distorted chair conformation, while the isoxazolidine and tetra­hydro­furan rings have envelope conformations

    Tissue characterization of benign cardiac tumors by cardiac magnetic resonance imaging, a review of core imaging protocol and benign cardiac tumors

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    Generally, cardiac masses are initially suspected on routine echocardiography. Cardiac magnetic resonance (CMR) imaging is further performed to differentiate tumors from pseudo-tumors and to characterize the cardiac masses based on their appearance on T1/T2-weighted images, detection of perfusion and demonstration of gadolinium-based contrast agent uptake on early and late gadolinium enhancement images. Further evaluation of cardiac masses by CMR is critical because unnecessary surgery can be avoided by better tissue characterization. Different cardiac tissues have different T1 and T2 relaxation times, principally owing to different internal biochemical environments surrounding the protons. In CMR, the signal intensity from a particular tissue depends on its T1 and T2 relaxation times and its proton density. CMR uses this principle to differentiate between various tissue types by weighting images based on their T1 or T2 relaxation times. Generally, tumor cells are larger, edematous, and have associated inflammatory reactions. Higher free water content of the neoplastic cells and other changes in tissue composition lead to prolonged T1/T2 relaxation times and thus an inherent contrast between tumors and normal tissue exists. Overall, these biochemical changes create an environment where different cardiac masses produce different signal intensity on their T1- weighted and T2- weighted images that help to discriminate between them. In this review article, we have provided a detailed description of the core CMR imaging protocol for evaluation of cardiac masses. We have also discussed the basic features of benign cardiac tumors as well as the role of CMR in evaluation and further tissue characterization of these tumors

    Human knockouts and phenotypic analysis in a cohort with a high rate of consanguinity

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    A major goal of biomedicine is to understand the function of every gene in the human genome. Loss-of-function mutations can disrupt both copies of a given gene in humans and phenotypic analysis of such 'human knockouts' can provide insight into gene function. Consanguineous unions are more likely to result in offspring carrying homozygous loss-of-function mutations. In Pakistan, consanguinity rates are notably high. Here we sequence the protein-coding regions of 10,503 adult participants in the Pakistan Risk of Myocardial Infarction Study (PROMIS), designed to understand the determinants of cardiometabolic diseases in individuals from South Asia. We identified individuals carrying homozygous predicted loss-of-function (pLoF) mutations, and performed phenotypic analysis involving more than 200 biochemical and disease traits. We enumerated 49,138 rare (<1% minor allele frequency) pLoF mutations. These pLoF mutations are estimated to knock out 1,317 genes, each in at least one participant. Homozygosity for pLoF mutations at PLA2G7 was associated with absent enzymatic activity of soluble lipoprotein-associated phospholipase A2; at CYP2F1, with higher plasma interleukin-8 concentrations; at TREH, with lower concentrations of apoB-containing lipoprotein subfractions; at either A3GALT2 or NRG4, with markedly reduced plasma insulin C-peptide concentrations; and at SLC9A3R1, with mediators of calcium and phosphate signalling. Heterozygous deficiency of APOC3 has been shown to protect against coronary heart disease; we identified APOC3 homozygous pLoF carriers in our cohort. We recruited these human knockouts and challenged them with an oral fat load. Compared with family members lacking the mutation, individuals with APOC3 knocked out displayed marked blunting of the usual post-prandial rise in plasma triglycerides. Overall, these observations provide a roadmap for a 'human knockout project', a systematic effort to understand the phenotypic consequences of complete disruption of genes in humans.D.S. is supported by grants from the National Institutes of Health, the Fogarty International, the Wellcome Trust, the British Heart Foundation, and Pfizer. P.N. is supported by the John S. LaDue Memorial Fellowship in Cardiology from Harvard Medical School. H.-H.W. is supported by a grant from the Samsung Medical Center, Korea (SMO116163). S.K. is supported by the Ofer and Shelly Nemirovsky MGH Research Scholar Award and by grants from the National Institutes of Health (R01HL107816), the Donovan Family Foundation, and Fondation Leducq. Exome sequencing was supported by a grant from the NHGRI (5U54HG003067-11) to S.G. and E.S.L. D.G.M. is supported by a grant from the National Institutes of Health (R01GM104371). J.D. holds a British Heart Foundation Chair, European Research Council Senior Investigator Award, and NIHR Senior Investigator Award. The Cardiovascular Epidemiology Unit at the University of Cambridge, which supported the field work and genotyping of PROMIS, is funded by the UK Medical Research Council, British Heart Foundation, and NIHR Cambridge Biomedical Research Centre ... Fieldwork in the PROMIS study has been supported through funds available to investigators at the Center for Non-Communicable Diseases, Pakistan and the University of Cambridge, UK

    Rhodium-catalyzed polymerization of phenylacetylene and its derivatives

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    The present report overviews relevant aspects of rhodium-catalyzed polymerization of phenylacetylenes and substituted acetylene monomers. The π-conjugated polymers obtained through this catalytic homogeneous process are very interesting because of their outstanding electronic, optical and structural properties. The employed rhodium-based catalysts span from simple and well-defined mononuclear complexes to complex binary or even ternary catalytic systems. Extensive fine-tuning of the electronic and steric properties of the catalysts has allowed tailoring the synthesis of conjugated polymers using living polymerization processes. Additionally, recent detailed studies concerning the mechanism of phenylacetylene polymerization are enlightened. © 2013 King Fahd University of Petroleum and Minerals.The authors express their appreciation to the support from the Ministry of Higher Education, Saudi Arabia, in establishment of the Center of Research Excellence in Petroleum Refining and Petrochemicals at King Fahd University of Petroleum and Minerals (KFUPM). The support of KFUPM under the KACST funded project (630-11- ) is also highly appreciated.Peer Reviewe
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