SummaryBackground:Subclavian Steal Syndrome (SSS) is a fascinating vascular phenomenon in which a steno-occlusive lesion of the proximal subclavian artery causes retrograde flow in the vertebral artery away from the brain stem subsequently causing vertebrobasilar insufficiency. SSS can present with a myriad of neurological and vascular signs and symptoms, but most commonly this phenomenon presents as an incidental finding in an asymptomatic patient.Case Report:Our patient is a 73-year-old female sent to the cardiology clinic for surgical clearance in preparation for an elective cholecystectomy. Shortness of breath was her only complaint. Review of systems was remarkable for left arm pain and blurry vision with repetitive movement. Physical examination noticeable for absence of left radial pulse. Percutaneous angiography demonstrated a totally occulted left subclavian artery with collateral circulation form the vertebrobasilar apparatus.Conclusions:Atypical presentation of this unique entity represents a challenge for physicians who require a high index of suspicion to make the diagnosis. We present an atypical case with radiographical evidence of the steal syndrome, followed by an extensive literature review of the most current diagnostic methods as well as latest recommendations for treatment options and secondary prevention.

Objective: We measured the levels of mutant huntingtin (mtHtt) and total huntingtin (tHtt) in blood leukocytes from Prospective Huntington At-Risk Observational Study (PHAROS) subjects at 50% risk of carrying the Huntington disease mutation using a homogeneous time-resolved fluorescence (HTRF) assay to assess its potential as a biomarker.Methods: Peripheral blood mononuclear cells from consenting PHAROS subjects were analyzed by HTRF using antibodies that simultaneously measured mtHtt and tHtt. mtHtt levels were normalized to tHtt, double-stranded DNA, or protein and analyzed according to cytosine-adenineguanine repeat length (CAGn), demographics, predicted time to clinical onset or known time since clinical onset, and available clinical measures.Results: From 363 assayed samples, 342 met quality control standards. Levels of mtHtt and mt/tHtt were higher in 114 subjects with expanded CAG repeats (CAG $37) compared with 228 subjects with nonexpanded CAG repeats (CAG ,37) (p , 0.0001). Analysis of relationships to predicted time to onset or to phenoconversion suggested that the HTRF signal could mark changes during the Huntington disease prodrome or after clinical onset. Conclusions:The HTRF assay can effectively measure mtHtt in multicenter sample sets and may be useful in trials of therapies targeting huntingtin. Huntington disease (HD) is caused by the expression of the toxic mutant huntingtin (mtHtt) protein, which contains an expanded polyglutamine repeat sequence near its N-terminus.1 mtHtt misfolds, undergoes posttranslational modifications, fragments, and forms soluble oligomers and insoluble intracellular aggregates, 2-4 which are differentially toxic. 5,6 Huntingtin (Htt) is the most salient target for neuroprotective therapies 7-9 and it is both essential and challenging to reliably measure it 1,2,10 to enable the development of therapies. We adapted a semiquantitative cell-based immunoassay that measures soluble mtHtt and total Htt (tHtt) using homogeneous time-resolved fluorescence (HTRF) Förster resonance energy transfer. 11,12 This HTRF assay is sensitive, reliable, and specific for soluble mtHtt in tissues and blood from HD mouse models, 11 in postmortem tissue, and in single-site studies using human peripheral blood mononuclear cells (PBMCs) from subjects with premanifest and manifest HD. [11][12][13] We optimized and technically validated the HTRF assay according to Good Laboratory Practice (GLP) standards for analyzing mtHtt and tHtt in clinical PBMC samples.12 To validate the HTRF assay in the context of a blinded multicenter study encompassing subjects with and without the HD mutation, to assess normalization methods for Htt values, and to examine whether the HD prodrome or the development of clinical

, N.J.) is used for the definitive identification of Neisseria gonorrhoeae. In this test, boiled organisms are examined by using a 1-min coagglutination technique. A total of 776 Neisseria strains, confirmed to the species level by patterns of acid production from carbohydrates incorporated in cysteine-tryptose agar or morphologically consistent with Neisseria meningitidis and fluorescent antibody negative, were tested by the coagglutination technique. Of the 516 isolates of N. gonorrhoeae, 8 (1.6%) were negative with the OMNI Test. Of the 260 isolates of Neisseria spp. other than N. gonorrhoeae, none showed a positive coagglutination reaction. The Phadebact Monoclonal GC OMNI Test provided rapid, accurate identification of N. gonorrhoeae (sensitivity, 98.4%; specificity, 100%).

No abstract