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Introduction Programmed electrical stimulation is an essential part of VT ablation procedures but VT is not always inducible, usually for reasons that are not clear. We sought to review pacing site-specific failure of programmed electrical stimulation (PES) to induce scar-related ventricular tachycardia (VT). Methods A series of patients in whom aggressive programmed stimulation from traditional RV pacing sites failed to induce VT, but VT was easily inducible from a non-traditional site are reviewed. Computer simulations in a simple 2-dimensional model of reentry were performed. Results Six patients who had no inducible sustained VT from the RV apex/outflow tract with at least 3 extrastimuli, but relatively easily induced VT from the LV, basal RV, epicardium, or atrium are described. In 5 of these patients, the site that induced VT was closer to the likely reentry circuit region based on mapping and ablation. Computer simulations illustrated that the spatial relation between the pacing site and the entrance and exits of a reentry isthmus can determine the ease of initiation of reentry by determining the time available for recovery of excitability at the initial region of block. Conclusions The site of PES has a marked effect on inducibility of VT in some patients such that PES from the RV apex and outflow regions will fail to expose clinically relevant VTs. The frequency with which this occurs is not certain. Stimulation from alternative sites is a reasonable consideration in selected patients.

The reinforcement effect of a strain gage bonded to a low modulus material is described by a simple equation that relates the assigned, calibrated gage factor, the actual gage factor at which the strain indicator may be set to record the actual strain in the test piece outside of the neighborhood of the gage site, and a certain parameter that depends on the physical and geometrical properties of the strain gage and the specimen. It is found that the interaction effects due to reinforcement by the strain gage can be reduced substantially by increasing the length or by decreasing the thickness of the gage, whereas decreasing the thickness of the adhesive layer has but little positive effect. It is shown that appreciable error may be introduced into the data if the reinforcement effect of a strain gage bonded to a soft material is neglected in experimental stress analysis studies.

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The food industry has long utilized air and water to transport products from one location to another, especially raw products. Likewise, a gas or fluid can be utilized to separate a desirable product or products from undesirable materials. When designing systems to work with a specific food material, one must know about the aero and hydrodynamic characteristics of the material. The characteristics, or primary properties, that govern the product behavior in air or water are the drag coefficient and the terminal velocity.

The reduction in the grade classification of processed fruits and vegetables is of grave concern to the food industry. Far too often this is caused by mechanical damage during handling procedures associated with processing and distribution.

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Appendicitis is a disease which has only very recently - within the last twenty years - been studied at all. The pathology of the disease shows us that it occurs in attacks of three kinds - acute, medium, and very mild. In the acute variety the disease is well under - stood and the treatment is acknowledged by everyone to be immediate operative interference. In the mild variety, the symptoms are so slight that the disease cannot be definitely recognised. Nevertheless pathological changes occur in the appendix which produce serious results later on. In the medium variety, the symptoms are definite but the treatment varies. Appendicectomy during the height of a first attar is a perfectly safe operation, as well as a simple one. Appendicectomy during the quiescent period after an attack is no safer, and is far more liable to be a difficult operation. Convalescence is prolonged. The expectant treatment of a medium attack is unsafe and unreliable. Further attacks are almost certain to occur, and operation is called for in the long run - but the operation after several attacks is attended by difficulties and dangers which are not present in an operation during the first attack. The questions set down in the Preface may therefore be answered thus: - Definite recognisable appendicitis should be transferred entirely to the domain of surgery. Appendicectomy should not however be left to the specialist. When done at the right time it is a simple operation which can and should be performed by every medical ractitioner. Appendicitis should always be treated surgically except under circumstances where extraneous considerations make the operation a greater risk than the disase. The present mortality of the disease could be firiensely reduced were all cases operated on as soon as he condition was diagnosed. Under these circumstances he mortality should not exceed 2 -3 per cent. The resent mortality of the disease being from 7 to 10 er cent in all cases. The one rule of treatment should be that directly appendicitis is diagnosed, an operation should be performed at the earliest possible moment.

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Phrenic Nerve Injury (PNI) has been well studied by cardiac surgeons. More recently it has been recognized as a potential complication of catheter ablation with a prevalence of 0.11 to 0.48 % after atrial fibrillation (AF) ablation. This review will focus on PNI after AF ablation. Anatomical studies have shown a close relationship between the right phrenic nerve and it's proximity to the superior vena cava (SVC), and the antero-inferior part of the right superior pulmonary vein (RSPV). In addition, the proximity of the left phrenic nerve to the left atrial appendage has been well established. Independent of the type of ablation catheter (4mm, 8 mm, irrigated tip, balloon) or energy source used (radiofrequency (RF), ultrasound, cryothermia, and laser); the risk of PNI exists during ablation at the critical areas listed above. Although up to thirty-one percent of patients with PNI after AF ablation remain asymptomatic, dyspnea remain the cardinal symptom and is present in all symptomatic patients. Despite the theoretical risk for significant adverse effect on functional status and quality of life, short-term outcomes from published studies appear favorable with 81% of patients with PNI having a complete recovery after 7 ± 7 months.Conclusion: Existing studies have described PNI as an uncommon but avoidable complication in patients undergoing pulmonary vein isolation for AF. Prior to ablation at the SVC, antero-inferior RSPV ostium or the left atrial appendage, pacing should be performed before energy delivery. If phrenic nerve capture is documented, energy delivery should be avoided at this site. Electrophysiologist's vigilance as well as pacing prior to ablation at high risk sites in close proximity to the phrenic nerve are the currently available tools to avoid the complication of PNI.

In the initial phases of angiogenesis, endothelial cells must degrade and cross the vessel basement membrane, as do tumor cells during invasion and metastasis formation. Various metalloproteinases have been implicated in tumor cell invasion, in particular MMP-2 (72 kDa collagenase IV, gelatinase A), which has been demonstrated to be associated with tumor metastasis formation. Supernatants from AIDS-Kaposi sarcoma (KS) cells induce normal endothelial cells to invade through a reconstituted basement membrane (Matrigel) in vitro, which correlates with the angiogenic potential of KS cells in vivo. Here we demonstrate that two specific inhibitors of MMP-2, TIMP-2 and a peptide from the MMP-2 propeptide region (peptide 74), inhibit endothelial cell invasion induced by AIDS-KS cell supernatants. Smooth muscle cells were much less sensitive to these inhibitors. These data suggest that MMP-2 activation is a key event in endothelial cell invasion, the initial phase of tumor-associated neoangiogenesis. Inhibition of this enzyme could be an effective treatment for KS and tumor-associated angiogenesis.

The objective of the present study was to measure preoperative plasma tissue inhibitor of metalloproteinase (TIMP)-1 levels in colorectal cancer patients and relate these values to clinical and biochemical patient characteristics. TIMP-1 levels were determined by ELISA in EDTA plasma samples collected preoperatively from 588 colorectal cancer patients. Plasma TIMP-1 levels were distributed with a median value of 141.1 microg/liter (range, 53.7-788.7 microg/liter). Whereas no significant differences were found in the median plasma TIMP-1 levels among patients with Dukes' stage A, B, and C disease, patients with Dukes' stage D disease had significantly higher plasma TIMP-1 levels (P0.0001); however, high plasma TIMP-1 levels were not restricted to advanced disease. A relatively weak correlation between plasma TIMP-1 level and age was found (r = 0.35; P0.0001). There was no significant difference in TIMP-1 levels between males and females (P = 0.97). Univariate analysis demonstrated an increasing risk of mortality with increasing TIMP-1 levels [scored as the log(e)(TIMP-1); hazard ratio = 3.3; 95% confidence interval, 2.6-4.2; P0.0001]. Including covariates (Dukes' stage, primary tumor location, gender, age, plasminogen activator inhibitor type 1, and soluble urokinase plasminogen activator receptor) in a multivariate analysis, TIMP-1 was retained in the final model (hazard ratio = 2.5; 95% confidence interval, 1.7-3.7; P0.0001). This study showed a highly significant association between preoperative plasma TIMP-1 levels and survival in colorectal cancer patients, with higher plasma TIMP-1 levels being associated with poor outcome. Independent of clinical parameters including Dukes' stage, plasma TIMP-1 levels were found to strongly predict prognosis of colorectal cancer patients. Additional studies are needed to validate the clinical usefulness of plasma TIMP-1 measurements.

The purpose of this study is to determine the effect of systemic blockade of Interleukin-6 (IL-6) on allosensitization, regulatory T cell frequencies and suppressive phenotype, and allograft survival rates in a mouse model of corneal transplantation. Allogeneic corneal transplantation was performed using C57BL/6 mice as donors and BALB/c mice as recipients. Graft recipients were injected daily with either anti-IL-6 antibody or an isotype control antibody (1.25 mg/ml) for the first 7 days and on alternate days thereafter until week 8 after transplantation. Allograft survival was evaluated for 8 weeks using Kaplan-Meier survival analysis. Draining lymph nodes (DLN) were harvested at week 3 after transplantation, and proliferation of isolated recipient T cells through direct and indirect pathways was determined using mixed lymphocyte reaction assay. Frequencies of CD4(+)CD25(+)Foxp3(+) regulatory T cells, their expression of Foxp3, and frequencies of IFNy(+)CD4(+) Th1 cells were determined in DLN using flow cytometry. Finally, CD4(+) T cells were cultured with bone marrow-derived dendritic cells from either C57BL/6 or BALB/c mice in the presence of IL-6-blocking antibody to determine Treg induction through direct and indirect pathways, respectively. Treatment with anti-IL-6 antibody suppressed both the direct and indirect pathways of allosensitization in graft recipients and significantly improved allograft survival rates. Furthermore, in vivo blockade of IL-6 enhanced Foxp3 expression by Tregs in graft recipients undergoing rejection, but did not exert a significant effect on Treg frequencies. Finally, IL-6 neutralization in vitro enhanced the differentiation of Tregs from CD4(+) T cells through both direct and indirect pathways. Our results demonstrate that systemic administration of IL-6-blocking antibody to corneal allograft recipients suppresses direct and indirect routes of allosensitization, is associated with increased expression of Foxp3 by Tregs, and improves allograft survival rates.

Venice Chart International Consensus Document on Ventricular Tachycardia/Ventricular Fibrillation Ablation ANDREA NATALE, M.D.,∗ ANTONIO RAVIELE, M.D.,† AMIN AL-AHMAD, M.D.,‡ OTTAVIO ALFIERI, M.D.,¶ ETIENNE ALIOT, M.D.,∗∗ JESUS ALMENDRAL, M.D.,†† GUNTER BREITHARDT, M.D.,‡‡ JOSEP BRUGADA, M.D.,¶¶ HUGH CALKINS, M.D.,∗∗∗ DAVID CALLANS, M.D.,††† RICCARDO CAPPATO, M.D.,‡‡‡ JOHN A. CAMM, M.D.,¶¶¶ PAOLO DELLA BELLA, M.D.,∗∗∗∗ GERARD M. GUIRAUDON, M.D.,†††† MICHEL HAISSAGUERRE, M.D.,‡‡‡‡ GERHARD HINDRICKS, M.D.,¶¶¶¶ SIEW YEN HO, M.D.,∗∗∗∗∗ KARL H. KUCK, M.D.,††††† FRANCIS MARCHLINSKI, M.D.,‡‡‡‡‡ DOUGLAS L. PACKER, M.D.,¶¶¶¶¶ ERIC N. PRYSTOWSKY, M.D.,∗∗∗∗∗∗ VIVEK Y. REDDY, M.D.,†††††† JEREMY N. RUSKIN, M.D.,‡‡‡‡‡‡ MAURICIO SCANAVACCA, M.D.,¶¶¶¶¶¶ KALYANAM SHIVKUMAR, M.D.,∗∗∗∗∗∗∗ KYOKO SOEJIMA, M.D.,††††††† WILLIAM J. STEVENSON, M.D.,‡‡‡‡‡‡‡ SAKIS THEMISTOCLAKIS, M.D.,¶¶¶¶¶¶¶ ATUL VERMA, M.D.,∗∗∗∗∗∗∗∗ and DAVID WILBER, M.D.,†††††††† for the Venice Chart members From the ∗Texas Cardiac Arrhythmia Institute, St. David’s Medical Center, Austin, TX, USA; †Cardiovascular Department, Ospedale dell’Angelo, Mestre-Venice, Italy; ‡Cardiac Arrhythmia Service, Stanford University Medical School, Stanford, USA; ¶Department of Cardiac Surgery, Ospedale San Raffaele, Milan, Italy; ∗∗Department of Cardio-Vascular Diseases, CHU de Nancy, Hopital de Brabois, Vandoeuvre-les-Nancy, France; ††Division of Cardiology, Hospital General Gregorio Maranon, Madrid, Spain; ‡‡Department of Cardiology and Angiology, University Hospital of Munster, Munster, Germany; ¶¶Thorax Institute-Cardiology, Hospital Clinic, University of Barcelona, Barcelona, Spain; ∗∗∗Department of Cardiology, The Johns Hopkins Hospital, Baltimore, MD, USA; †††Department of Medicine, Section of Cardiovascular Disease, Hospital of the University of Pennsylvania, Philadelphia, PA, USA; ‡‡‡Department of Electrophysiology, Policlinico San Donato, San Donato Milanese, Italy; ¶¶¶Cardiac and Vascular Sciences, St. George’s Hospital Medical School, London, UK; ∗∗∗∗Cardiology Division, Centro Cardiologico Monzino, Milan, Italy; ††††Cardiac Surgery, University of Western Ontario, London, Canada; ‡‡‡‡Hopital Cardiologique du Haut Leveque, Bordeaux, France; ¶¶¶¶Heart Center, Department of Cardiology, University of Leipzig, Leipzig, Germany; ∗∗∗∗∗Cardiac Morphology Unit, Royal Brompton Hospital, London and Imperial College, London, UK; †††††Department of Cardiology, Asklepios Klinik St. Georg, Hamburg, Germany; ‡‡‡‡‡Department of Medicine, Section of Cardiovascular Disease, University of Pennsylvania, Philadelphia, PA, USA; ¶¶¶¶¶Cardiac Translational and Electrophysiology Laboratory, Saint Mary’s Hospital Complex, Mayo Clinic Foundation, Rochester, NY, USA; ∗∗∗∗∗∗The Care Group, Indianapolis, IN, USA; ††††††Cardiac Arrhythmia Service, Miller School of Medicine, University of Miami, Miami, USA; ‡‡‡‡‡‡Arrhythmia Service, Massachusetts General Hospital, Boston, MA, USA; ¶¶¶¶¶¶Heart Institute, University of San Paulo Medical School, San Paulo, Brazil; ∗∗∗∗∗∗∗Cardiac Arrhythmia Center, David Geffen School of Medicine at UCLA, Los Angeles, CA, USA; †††††††Cardiovascular Division, University of Miami Hospital, Miami USA; ‡‡‡‡‡‡‡Cardiovascular Division, Brigham and Women’s Hospital, Boston, MA, USA; ¶¶¶¶¶¶¶Cardiovascular Department, Ospedale dell’Angelo, Mestre-Venice, Italy; ∗∗∗∗∗∗∗∗Cardiology, Southlake Regional Health Center, Toronto, Canada; and ††††††††Department of Cardiology, Loyola University Medical Center, Chicago, IL, USA