18 research outputs found

    MAKING SUCCESSFUL PERMEABILITY MEASUREMENTS WITH ASPHALTIC CRUDE OILS

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    ABSTRACT Reservoirs with asphaltic oils are notorious for being difficult to evaluate with respect to reservoir properties. This is largely due to the flocculation of dispersed asphaltenes when the rock and fluids are brought to the surface. The flocculated asphaltenes deposit on the rock surface affecting the wettability and are suspended in the oil causing problems with flow measurements. Cleaning and aging procedures attempt to restore the rock surface back to reservoir conditions. However, unless all asphaltenes are removed, flocculated material will continue to form. Complete removal of the asphaltenes would alter the chemical and physical characteristics of the oil, creating questions about the applicability of the flow tests. This paper provides successful results from relative permeability tests using asphaltic oils. Attempts to measure oil permeabilities with dead crude oil have resulted in a continually decreasing permeability. However, once the crude oil was recombined to live oil, stable oil permeability was measured. The relative permeability tests with live oil were successfully run without the sample plugging problems typical of dead oil with flocculated asphaltenes. Results are shown for both sandstone and carbonate reservoirs

    Genetic Mapping and Exome Sequencing Identify Variants Associated with Five Novel Diseases

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    The Clinic for Special Children (CSC) has integrated biochemical and molecular methods into a rural pediatric practice serving Old Order Amish and Mennonite (Plain) children. Among the Plain people, we have used single nucleotide polymorphism (SNP) microarrays to genetically map recessive disorders to large autozygous haplotype blocks (mean = 4.4 Mb) that contain many genes (mean = 79). For some, uninformative mapping or large gene lists preclude disease-gene identification by Sanger sequencing. Seven such conditions were selected for exome sequencing at the Broad Institute; all had been previously mapped at the CSC using low density SNP microarrays coupled with autozygosity and linkage analyses. Using between 1 and 5 patient samples per disorder, we identified sequence variants in the known disease-causing genes SLC6A3 and FLVCR1, and present evidence to strongly support the pathogenicity of variants identified in TUBGCP6, BRAT1, SNIP1, CRADD, and HARS. Our results reveal the power of coupling new genotyping technologies to population-specific genetic knowledge and robust clinical data

    Corticobasal degeneration in the brain of an infant who died from a homozygous <i>BRAT1</i> mutation.

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    <p>(<b>A</b>) Throughout frontal, occipital and temporal cortex, there is marked neuronal loss, gliosis with astrocytes (arrowheads) and swollen oligodendroglia. The arrow indicates a perivascular microcalcification (superior frontal gyrus, deep cortex, 10×). (<b>B</b>) The anterior hippocampus is smaller than expected and there is neuronal loss and gliosis in zone CA-1 (Sommer's sector), demarcated from the CA-2 sector by the dotted line (4×). (<b>C</b>) At 60× magnification, the putamen shows a paucity of neurons, abundant Alzheimer Type 2 astrocytes (arrowhead) and scattered microglial nodules (arrow). Heterologous overexpression of N-terminal FLAG-tagged human BRAT1 (<b>D</b>) and hBRAT1 c.638_639insA (<b>E</b>) in mouse IMCD3 cells. Wild-type Brat1 localizes to the nucleus and cytoplasm of mIMCD3 cells. Mutant Brat1 (c.638_639insA) does not localize to the nucleus and instead forms punctate aggregations in the cytoplasm. Similar results were obtained in hARPE-19 cells (data not shown). (<b>F</b>) RT-PCR demonstrating the stability of overexpressed human BRAT1 transcripts (∼2.6 kb) in hARPE-19 cells. A B-actin amplicon (∼450 bp) was used as a loading control on the same gel. (<b>G</b>) Western blot of lysates from human ARPE-19 cells transiently transfected with wt hBRAT1 displaying FLAG-hBRAT1 fusion protein at ∼90 kDa or with hBRAT1 c.638_639insA displaying the truncated FLAG-hBRAT1 mutant fusion protein at ∼44.5 kDa (FLAG-tag and linker = 3.1 kDa). B-actin was labeled as a loading control.</p

    Microcephaly and chorioretinopathy due to a homozygous <i>TUBGCP6</i> mutation.

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    <p>(<b>A</b>) An affected infant has marked microcephaly (>4SD below normal), a receding forehead, diminutive anterior fontanelle, and sutural ridging. She has cognitive delay and visual impairment but is socially engaged. (<b>B</b>) Head circumference and length plots for Mennonite microcephaly patients. (<b>C</b>) Brain magnetic resonance imaging (MRI) shows diffuse pachygyria, normal myelination, and (<b>D</b>) a hypoplastic cerebellar vermis.</p
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