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Harmon L.,Scott and White Memorial Hospital and Clinic | Boccalandro F.,Odessa Heart Institute | Boccalandro F.,Texas Tech University Health Sciences Center | Boccalandro F.,Permian Research Foundation
Journal of Clinical Ultrasound

Background: To evaluate the correlation and agreement of the carotid artery landmarks necessary for carotid artery stenting obtained by B-mode ultrasonography (BMU), and by quantitative angiography (QCA) in patients with severe carotid artery stenosis. Methods: In 75 patients undergoing carotid artery stenting, the distal common (CCA), proximal internal (ICA) carotid artery diameter, and lesion length were measured preoperatively by BMU, and intraoperatively by QCA. Results: In 96% of the subjects, BMU imaging was adequate for interpretation. BMU and QCA Pearson correlation and Lin concordance coefficients were 0.75 (p<0.001) and 0.959 (95% CI: 0.930 - 0.996), respectively, for CCA diameter, 0.88 (p<0.001) and 0.954 (95% CI: 0.928-0.983), respectively, for ICA diameter, and 0.62 (p<0.001) and 0.734 (95% CI: 0.719-0.760), respectively, for lesion length, with a 0.765 bias correction factor and a wider data scatter by Bland Altman plots showing shorter lesion length by BMU than by QCA. Conclusions: In patients with carotid artery stenosis, BMU can provide reliable distal CCA and proximal ICA diameters in comparison with QCA, whereas lesion length measured by BMU has an acceptable correlation, but a poor agreement with QCA. © 2014 Wiley Periodicals, Inc. Source

Hecht J.R.,University of California at Los Angeles | Farrell J.J.,University of California at Los Angeles | Senzer N.,Mary Crowley Medical Research Center | Nemunaitis J.,Mary Crowley Medical Research Center | And 14 more authors.
Gastrointestinal Endoscopy

Background: TNFeradeBiologic (AdGVEGR.TNF.11D) is a replication-deficient adenoviral vector that expresses tumor necrosis factor-α (TNF-α) under the control of the Egr-1 promoter, which is inducible by chemotherapy and radiation. Objective: This study was conducted to determine the maximal tolerated dose of TNFeradeBiologic with standard chemoradiotherapy and preliminary activity and safety of the combination in the treatment of locally advanced pancreatic cancer (LAPC). Design: TNFeradeBiologic was injected into locally advanced pancreatic carcinomas by using EUS or percutaneous administration once a week for 5 weeks together with 50.4 Gy radiation and 5-fluorouracil (5-FU) 200 mg/m2 daily over 5.5 weeks. Dose levels from 4 × 109 to 1 × 1012 particle units (PU) were studied. Setting: Multicentered, academic institutions. Patients: Fifty patients with LAPC were treated. Interventions: Doses of TNFerade Biologic were administered to patients. Main Outcome Measurements: Toleration of TNFerade Biologic was measured through toxicity and tumor response, by using the criteria of the Response Evaluation Criteria in Solid Tumors and the World Health Organization, and was reviewed by a central radiology facility. Overall survival and progression-free survival were also measured. Results: Dose-limiting toxicities of pancreatitis and cholangitis were observed in 3 patients at the 1 × 1012 PU dose, making 4 × 1011 PU the maximum tolerated dose. One complete response, 3 partial responses, and 12 patients with stable disease were noted. Seven patients eventually went to surgery, 6 had clear margins, and 3 survived >24 months. Limitations: This is a Phase1/2 non-randomized study. Conclusions: Intratumoral delivery of TNFerade Biologic by EUS with fine-needle viral injection or percutaneously, combined with chemoradiation, shows promise in the treatment of LAPC. There appeared to be better clinical outcome at the maximal tolerated dose than at lower doses. The dose of 4 ×1011 PU TNFerade Biologic was generally well tolerated, with encouraging indications of activity, and will be tested in the randomized phase of this study. Delivery of TNFerade Biologic did not interfere with subsequent surgical resection. © 2012 American Society for Gastrointestinal Endoscopy. Source

Papp G.,Semmelweis University | Changchien Y.-C.,Semmelweis University | Peterfia B.,Semmelweis University | Pecsenka L.,The Surgical Center | And 4 more authors.
Modern Pathology

About 10% of epithelioid sarcomas have biallelic mutation of the SMARCB1 (SWI/SNF-related, matrix-associated, actin-dependent regulator of chromatin, subfamily b, member 1) gene resulting in a lack of this nuclear protein. It has been suggested that SMARCB1 may be silenced by epigenetic changes in the remaining 90% of tumors. Thus, we hypothesized that the promoter of SMARCB1 is hypermethylated. We also examined SMARCB1 mRNA level to determine if a post-translational change was possible. Thirty-six cases of epithelioid sarcomas were studied. Immunohistochemistry and mutation analysis of the SMARCB1 gene were performed to select appropriate cases. Methylation status was assessed by methylation-specific PCR. Laser capture microdissection of tumor cells followed by real-time PCR was applied to examine the expression of SMARCB1 mRNA. Of 36 epithelioid sarcomas, 31 (86%) displayed a lack of SMARCB1 nuclear protein. In all, 4 (13%) of 31 SMARCB1-negative cases harbored biallelic deletion while 9 (33%) cases showed single-allelic deletion. One (4%) frameshift deletion of exon 3 and one point mutation of exon 7 were also found. In 16 (59%) cases, both alleles were intact. Altogether, 25/31 (81%) SMARCB1-negative cases had at least one intact allele. None of these cases demonstrated promoter hypermethylation. Low levels of SMARCB1 mRNA were found in all cases with tumor tissue extracted RNA (because of the minimal normal cell contamination) but no mRNA could be detected in laser dissected cases (containing only tumor cells). Enhancer of zeste homolog 2 (EZH2) overexpression was not characteristic of epithelioid sarcoma. Thus, loss of SMARCB1 expression in epithelioid sarcoma is caused neither by DNA hypermethylation nor by post-translational modifications. Most likely it is the microRNA destruction of SMARCB1 mRNA but further investigations are needed to elucidate this issue. © 2013 USCAP, Inc. All rights reserved. Source

Passman M.A.,University of Alabama at Birmingham | McLafferty R.B.,University of Illinois at Springfield | Nagre S.B.,University of Alabama at Birmingham | Iafrati M.D.,Tufts University | And 6 more authors.
Journal of Vascular Surgery

Background: Several standard venous assessment tools have been used as independent determinants of venous disease severity, but correlation between these instruments as a global venous screening tool has not been tested. The scope of this study is to assess the validity of Venous Clinical Severity Scoring (VCSS) and its integration with other venous assessment tools as a global venous screening instrument. Methods: The American Venous Forum (AVF), National Venous Screening Program (NVSP) data registry from 2007 to 2009 was queried for participants with complete datasets, including CEAP clinical staging, VCSS, modified Chronic Venous Insufficiency Quality of Life (CIVIQ) assessment, and venous ultrasound results. Statistical correlation trends were analyzed using Spearman's rank coefficient as related to VCSS. Results: Five thousand eight hundred fourteen limbs in 2,907 participants were screened and included CEAP clinical stage C0: 26%; C1: 33%; C2: 24%; C3: 9%; C4: 7%; C5: 0.5%; C6: 0.2% (mean, 1.41 ± 1.22). VCSS mean score distribution (range, 0-3) for the entire cohort included: pain 1.01 ± 0.80, varicose veins 0.61 ± 0.84, edema 0.61 ± 0.81, pigmentation 0.15 ± 0.47, inflammation 0.07 ± 0.33, induration 0.04 ± 0.27, ulcer number 0.004 ± 0.081, ulcer size 0.007 ± 0.112, ulcer duration 0.007 ± 0.134, and compression 0.30 ± 0.81. Overall correlation between CEAP and VCSS was moderately strong (r s = 0.49; P <.0001), with highest correlation for attributes reflecting more advanced disease, including varicose vein (r s = 0.51; P <.0001), pigmentation (r s = 0.39; P <.0001), inflammation (r s = 0.28; P <.0001), induration (r s = 0.22; P <.0001), and edema (r s = 0.21; P <.0001). Based on the modified CIVIQ assessment, overall mean score for each general category included: Quality of Life (QoL)-Pain 6.04 ± 3.12 (range, 3-15), QoL-Functional 9.90 ± 5.32 (range, 5-25), and QoL-Social 5.41 ± 3.09 (range, 3-15). Overall correlation between CIVIQ and VCSS was moderately strong (r s = 0.43; P <.0001), with the highest correlation noted for pain (r s = 0.55; P <.0001) and edema (r s = 0.30; P <.0001). Based on screening venous ultrasound results, 38.1% of limbs had reflux and 1.5% obstruction in the femoral, saphenous, or popliteal vein segments. Correlation between overall venous ultrasound findings (reflux + obstruction) and VCSS was slightly positive (r s = 0.23; P <.0001) but was highest for varicose vein (r s = 0.32; P <.0001) and showed no correlation to swelling (r s = 0.06; P <.0001) and pain (r s = 0.003; P =.7947). Conclusions: While there is correlation between VCSS, CEAP, modified CIVIQ, and venous ultrasound findings, subgroup analysis indicates that this correlation is driven by different components of VCSS compared with the other venous assessment tools. This observation may reflect that VCSS has more global application in determining overall severity of venous disease, while at the same time highlighting the strengths of the other venous assessment tools. © 2011 Society for Vascular Surgery. Source

Huffaker R.K.,East Tennessee State University | Handcock T.,Scott and White Memorial Hospital and Clinic | Muir T.W.,University of Texas Medical Branch
Female Pelvic Medicine and Reconstructive Surgery

A 66-year-old para III with a 20-year history of stress urinary incontinence underwent placement of tension-free vaginal tape. Intraoperative arterial bleeding occurred. An expanding hematoma was palpated postoperatively. Interventional radiology performed a pelvic arteriogram with selective bilateral internal iliac arteriograms, a supraselective anterior division and obturator arteriogram, a left external iliac arteriogram, coil embolization of a branch of the left obturator artery, and gel foam embolization of the anterior division of the left internal iliac artery. Copyright © 2010 by Lippincott Williams & Wilkins. Source

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