62 research outputs found

    How does a cadaver model work for testing ultrasound diagnostic capability for rheumatic-like tendon damage?

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    To establish whether a cadaver model can serve as an effective surrogate for the detection of tendon damage characteristic of rheumatoid arthritis (RA). In addition, we evaluated intraobserver and interobserver agreement in the grading of RA-like tendon tears shown by US, as well as the concordance between the US findings and the surgically induced lesions in the cadaver model. RA-like tendon damage was surgically induced in the tibialis anterior tendon (TAT) and tibialis posterior tendon (TPT) of ten ankle/foot fresh-frozen cadaveric specimens. Of the 20 tendons examined, six were randomly assigned a surgically induced partial tear; six a complete tear; and eight left undamaged. Three rheumatologists, experts in musculoskeletal US, assessed from 1 to 5 the quality of US imaging of the cadaveric models on a Likert scale. Tendons were then categorized as having either no damage, (0); partial tear, (1); or complete tear (2). All 20 tendons were blindly and independently evaluated twice, over two rounds, by each of the three observers. Overall, technical performance was satisfactory for all items in the two rounds (all values over 2.9 in a Likert scale 1-5). Intraobserver and interobserver agreement for US grading of tendon damage was good (mean κ values 0.62 and 0.71, respectively), with greater reliability found in the TAT than the TPT. Concordance between US findings and experimental tendon lesions was acceptable (70-100 %), again greater for the TAT than for the TPT. A cadaver model with surgically created tendon damage can be useful in evaluating US metric properties of RA tendon lesions

    Characterization of an activated human ros gene.

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    A human oncogene, mcf3, previously detected by a combination of DNA-mediated gene transfer and a tumorigenicity assay, derives from a human homology of the avian v-ros oncogene. Both v-ros and mcf3 can encode a protein with homology to tyrosine-specific protein kinases, and both mcf3 and v-ros encode a potential transmembrane domain N terminal to the kinase domain. mcf3 probably arose during gene transfer from a normal human ros gene by the loss of a putative extracellular domain. There do not appear to be any other gross rearrangements in the structure of mcf3

    Characterization of an activated human ros gene.

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    Isolation and characterization of a new cellular oncogene encoding a protein with multiple potential transmembrane domains

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    We have cloned and sequenced a new human oncogene and have named it mas. This oncogene was detected by its tumorigenicity in nude mice using the cotransfection and tumorigenicity assay previously described. The mas oncogene has a weak focus-inducing activity in transfected NIH 3T3 cells. A DNA rearrangement in the 5' noncoding sequence, which occurred during transfection, is probably rsponsible for activation of the mas gene. The cDNA sequence of the mas oncogene reveals a long open reading frame that codes for a 325 amino acid protein. This protein is very hydrophobic and has seven potential transmembrane domains. In this respect, the structure of the mas protein is novel among cellular oncogene products and may reflect a new functional class of oncogenes

    Hysterosonographically Guided Endometrial Biopsy

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    Paradoxical Embolization in Patients with Cryptogenic Stroke

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    BACKGROUND: The increased prevalence of patent foramen ovale (PFO) in patients with cryptogenic stroke suggests the occurrence of paradoxical embolism. Previous studies have found paradoxical embolism to be uncommon in stroke, but few have focussed on patients with cryptogenic stroke. We therefore evaluated pelvic veins and leg veins in this population. METHODS: Eighteen patients (median age 45 years) with a cryptogenic brain ischemic event (stroke 16, TIA 2) underwent magnetic resonance venography (MRV). Evaluation consisted of time-of-flight (TOF) and phase contrast images through the pelvis. A positive MRV was defined as an intravascular decrease in signal intensity at least 15 millimeters (mm) in length contacting the wall of a vein and showing matching abnormalities on both pulse sequences. Lower extremity venous duplex examination was also performed in 17/18. RESULTS: All patients had normal cranial arteries, apart from the artery referable to the index stroke. A right-to-left intracardiac shunt was identified in 16/18. MRV was performed a median of 22 days (range, 2–416) post-event. In three patients, only the TOF was performed (all negative studies). There were three patients who had evidence for paradoxical embolism. Patient 1 had sickle cell disease and two small cortical emboli, a PFO, a 30 mm left external iliac vein clot three days post-stroke, and a right calf vein clot diagnosed 23 days post-stroke. Patient 2 had a history of right knee injury and surgery, top of the basilar embolus, a PFO, and a chronic clot in the distal right popliteal vein. Patient 3 had several hours of sudden dysarthria and confusion after pelvic surgery, a PFO, and a right calf vein clot two days post-TIA. One patient had a basilar artery embolus and a 20 mm right external iliac vein clot, but no PFO. Another patient had no DVT day 2 post-stroke, but bilateral calf vein DVT on day 10. CONCLUSIONS: Pelvic MRV has diagnostic utility in the evaluation of patients with cryptogenic stroke. Pelvic vein and calf vein thrombosis are a source of paradoxical embolism in some patients with cryptogenic stroke. The incidence of thrombus in these two sites requires further evaluation in this population

    Bullous Lung Disease

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