415 research outputs found

    The benefit of a 1-bit jump-start, and the necessity of stochastic encoding, in jamming channels

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    We consider the problem of communicating a message mm in the presence of a malicious jamming adversary (Calvin), who can erase an arbitrary set of up to pnpn bits, out of nn transmitted bits (x1,,xn)(x_1,\ldots,x_n). The capacity of such a channel when Calvin is exactly causal, i.e. Calvin's decision of whether or not to erase bit xix_i depends on his observations (x1,,xi)(x_1,\ldots,x_i) was recently characterized to be 12p1-2p. In this work we show two (perhaps) surprising phenomena. Firstly, we demonstrate via a novel code construction that if Calvin is delayed by even a single bit, i.e. Calvin's decision of whether or not to erase bit xix_i depends only on (x1,,xi1)(x_1,\ldots,x_{i-1}) (and is independent of the "current bit" xix_i) then the capacity increases to 1p1-p when the encoder is allowed to be stochastic. Secondly, we show via a novel jamming strategy for Calvin that, in the single-bit-delay setting, if the encoding is deterministic (i.e. the transmitted codeword is a deterministic function of the message mm) then no rate asymptotically larger than 12p1-2p is possible with vanishing probability of error, hence stochastic encoding (using private randomness at the encoder) is essential to achieve the capacity of 1p1-p against a one-bit-delayed Calvin.Comment: 21 pages, 4 figures, extended draft of submission to ISIT 201

    Upper Bounds on the Capacity of Binary Channels with Causal Adversaries

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    In this work we consider the communication of information in the presence of a causal adversarial jammer. In the setting under study, a sender wishes to communicate a message to a receiver by transmitting a codeword (x1,...,xn)(x_1,...,x_n) bit-by-bit over a communication channel. The sender and the receiver do not share common randomness. The adversarial jammer can view the transmitted bits xix_i one at a time, and can change up to a pp-fraction of them. However, the decisions of the jammer must be made in a causal manner. Namely, for each bit xix_i the jammer's decision on whether to corrupt it or not must depend only on xjx_j for jij \leq i. This is in contrast to the "classical" adversarial jamming situations in which the jammer has no knowledge of (x1,...,xn)(x_1,...,x_n), or knows (x1,...,xn)(x_1,...,x_n) completely. In this work, we present upper bounds (that hold under both the average and maximal probability of error criteria) on the capacity which hold for both deterministic and stochastic encoding schemes.Comment: To appear in the IEEE Transactions on Information Theory; shortened version appeared at ISIT 201

    Zero vs. ε error in interference channels

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    Traditional studies of multi-source, multi-terminal interference channels typically allow a vanishing probability of error in communication. Motivated by the study of network coding, this work addresses the task of quantifying the loss in rate when insisting on zero error communication in the context of interference channels

    A Time-Domain Analysis of Intracardiac Electrograms for Arrhythmia Detection

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    Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/73045/1/j.1540-8159.1991.tb05116.x.pd

    Tendinopathy—from basic science to treatment

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    Chronic tendon pathology (tendinopathy), although common, is difficult to treat. Tendons possess a highly organized fibrillar matrix, consisting of type I collagen and various 'minor' collagens, proteoglycans and glycoproteins. The tendon matrix is maintained by the resident tenocytes, and there is evidence of a continuous process of matrix remodeling, although the rate of turnover varies at different sites. A change in remodeling activity is associated with the onset of tendinopathy. Major molecular changes include increased expression of type III collagen, fibronectin, tenascin C, aggrecan and biglycan. These changes are consistent with repair, but they might also be an adaptive response to changes in mechanical loading. Repeated minor strain is thought to be the major precipitating factor in tendinopathy, although further work is required to determine whether it is mechanical overstimulation or understimulation that leads to the change in tenocyte activity. Metalloproteinase enzymes have an important role in the tendon matrix, being responsible for the degradation of collagen and proteoglycan in both healthy patients and those with disease. Metalloproteinases that show increased expression in painful tendinopathy include ADAM (a disintegrin and metalloproteinase)-12 and MMP (matrix metalloproteinase)-23. The role of these enzymes in tendon pathology is unknown, and further work is required to identify novel and specific molecular targets for therapy

    Could it be advantageous to tune the temperature controller during radiofrequency ablation? A feasibility study using theoretical models

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    Purpose: To assess whether tailoring the Kp and Ki values of a proportional-integral (PI) controller during radiofrequency (RF) cardiac ablation could be advantageous from the point of view of the dynamic behaviour of the controller, in particular, whether control action could be speeded up and larger lesions obtained. Methods: Theoretical models were built and solved by the finite element method. RF cardiac ablations were simulated with temperature controlled at 55 degrees C. Specific PI controllers were implemented with Kp and Ki parameters adapted to cases with different tissue values (specific heat, thermal conductivity and electrical conductivity) electrode-tissue contact characteristics (insertion depth, cooling effect of circulating blood) and electrode characteristics (size, location and arrangement of the temperature sensor in the electrode). Results: The lesion dimensions and T(max) remained almost unchanged when the specific PI controller was used instead of one tuned for the standard case: T(max) varied less than 1.9 degrees C, lesion width less than 0.2 mm, and lesion depth less than 0.3 mm. As expected, we did observe a direct logical relationship between the response time of each controller and the transient value of electrode temperature. Conclusion: The results suggest that a PI controller designed for a standard case (such as that described in this study), could offer benefits under different tissue conditions, electrode-tissue contact, and electrode characteristics.This work received financial support from the Spanish 'Plan Nacional de I+D+I del Ministerio de Ciencia e Innovacion' Grant no. TEC2008-01369/TEC and FEDER Project MTM2010-14909. The translation of this paper was funded by the Universitat Politecnica de Valencia, Spain. The authors alone are responsible for the content and writing of the paperAlba Martínez, J.; Trujillo Guillen, M.; Blasco Giménez, RM.; Berjano Zanón, E. (2011). Could it be advantageous to tune the temperature controller during radiofrequency ablation? A feasibility study using theoretical models. International Journal of Hyperthermia. 27(6):539-548. https://doi.org/10.3109/02656736.2011.586665S539548276Gaita, F., Caponi, D., Pianelli, M., Scaglione, M., Toso, E., Cesarani, F., … Leclercq, J. F. (2010). Radiofrequency Catheter Ablation of Atrial Fibrillation: A Cause of Silent Thromboembolism? Circulation, 122(17), 1667-1673. doi:10.1161/circulationaha.110.937953Anfinsen, O.-G., Aass, H., Kongsgaard, E., Foerster, A., Scott, H., & Amlie, J. P. (1999). Journal of Interventional Cardiac Electrophysiology, 3(4), 343-351. doi:10.1023/a:1009840004782PETERSEN, H. H., CHEN, X., PIETERSEN, A., SVENDSEN, J. H., & HAUNSO, S. (2000). Tissue Temperatures and Lesion Size During Irrigated Tip Catheter Radiofrequency Ablation: An In Vitro Comparison of Temperature-Controlled Irrigated Tip Ablation, Power-Controlled Irrigated Tip Ablation, and Standard Temperature-Controlled Ablation. Pacing and Clinical Electrophysiology, 23(1), 8-17. doi:10.1111/j.1540-8159.2000.tb00644.xTungjitkusolmun, S., Woo, E. J., Cao, H., Tsai, J. Z., Vorperian, V. R., & Webster, J. G. (2000). Thermal—electrical finite element modelling for radio frequency cardiac ablation: Effects of changes in myocardial properties. Medical & Biological Engineering & Computing, 38(5), 562-568. doi:10.1007/bf02345754Lai, Y.-C., Choy, Y. B., Haemmerich, D., Vorperian, V. R., & Webster, J. G. (2004). Lesion Size Estimator of Cardiac Radiofrequency Ablation at Different Common Locations With Different Tip Temperatures. IEEE Transactions on Biomedical Engineering, 51(10), 1859-1864. doi:10.1109/tbme.2004.831529Jain, M. K., & Wolf, P. D. (1999). Temperature-controlled and constant-power radio-frequency ablation: what affects lesion growth? IEEE Transactions on Biomedical Engineering, 46(12), 1405-1412. doi:10.1109/10.804568Panescu, D., Whayne, J. G., Fleischman, S. D., Mirotznik, M. S., Swanson, D. K., & Webster, J. G. (1995). Three-dimensional finite element analysis of current density and temperature distributions during radio-frequency ablation. IEEE Transactions on Biomedical Engineering, 42(9), 879-890. doi:10.1109/10.412649Hong Cao, Vorperian, V. R., Tungjitkusolmun, S., Jan-Zern Tsai, Haemmerich, D., Young Bin Choy, & Webster, J. G. (2001). Flow effect on lesion formation in RF cardiac catheter ablation. IEEE Transactions on Biomedical Engineering, 48(4), 425-433. doi:10.1109/10.915708Tungjitkusolmun, S., Vorperian, V. R., Bhavaraju, N., Cao, H., Tsai, J.-Z., & Webster, J. G. (2001). Guidelines for predicting lesion size at common endocardial locations during radio-frequency ablation. IEEE Transactions on Biomedical Engineering, 48(2), 194-201. doi:10.1109/10.909640Schutt, D., Berjano, E. J., & Haemmerich, D. (2009). Effect of electrode thermal conductivity in cardiac radiofrequency catheter ablation: A computational modeling study. International Journal of Hyperthermia, 25(2), 99-107. doi:10.1080/02656730802563051Langberg, J. J., Calkins, H., el-Atassi, R., Borganelli, M., Leon, A., Kalbfleisch, S. J., & Morady, F. (1992). Temperature monitoring during radiofrequency catheter ablation of accessory pathways. Circulation, 86(5), 1469-1474. doi:10.1161/01.cir.86.5.1469Calkins, H., Prystowsky, E., Carlson, M., Klein, L. S., Saul, J. P., & Gillette, P. (1994). Temperature monitoring during radiofrequency catheter ablation procedures using closed loop control. Atakr Multicenter Investigators Group. Circulation, 90(3), 1279-1286. doi:10.1161/01.cir.90.3.1279Lennox CD, Temperature controlled RF coagulation. Patent number: 5.122.137 Hudson NHEdwards SD, Stern RA, Electrode and associated system using thermally insulated temperature sensing elements. Patent number: US Patent 5,456,682Panescu D, Fleischman SD, Whayne JG, Swanson DK, (EP Technology. Effects of temperature sensor placement on performance of temperature-controlled ablation. IEEE 17th Annual Conference, Engineering in Medicine and Biology Society, Montreal, Canada (1995)BLOUIN, L. T., MARCUS, F. I., & LAMPE, L. (1991). Assessment of Effects of a Radiofrequency Energy Field and Thermistor Location in an Electrode Catheter on the Accuracy of Temperature Measurement. Pacing and Clinical Electrophysiology, 14(5), 807-813. doi:10.1111/j.1540-8159.1991.tb04111.xBerjano, E. J. (2006). BioMedical Engineering OnLine, 5(1), 24. doi:10.1186/1475-925x-5-24Bhavaraju, N. C., Cao, H., Yuan, D. Y., Valvano, J. W., & Webster, J. G. (2001). Measurement of directional thermal properties of biomaterials. IEEE Transactions on Biomedical Engineering, 48(2), 261-267. doi:10.1109/10.909647Hong Cao, Tungjitkusolmun, S., Young Bin Choy, Jang-Zern Tsai, Vorperian, V. R., & Webster, J. G. (2002). Using electrical impedance to predict catheter-endocardial contact during RF cardiac ablation. IEEE Transactions on Biomedical Engineering, 49(3), 247-253. doi:10.1109/10.983459PETERSEN, H. H., & SVENDSEN, J. H. (2003). Can Lesion Size During Radiofrequency Ablation Be Predicted By the Temperature Rise to a Low Power Test Pulse in Vitro? Pacing and Clinical Electrophysiology, 26(8), 1653-1659. doi:10.1046/j.1460-9592.2003.t01-1-00248.xLANGBERG, J. J., LEE, M. A., CHIN, M. C., & ROSENQVIST, M. (1990). Radiofrequency Catheter Ablation: The Effect of Electrode Size on Lesion Volume In Vivo. Pacing and Clinical Electrophysiology, 13(10), 1242-1248. doi:10.1111/j.1540-8159.1990.tb02022.

    Gene expression and matrix turnover in overused and damaged tendons

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    Chronic, painful conditions affecting tendons, frequently known as tendinopathy, are very common types of sporting injury. The tendon extracellular matrix is substantially altered in tendinopathy, and these changes are thought to precede and underlie the clinical condition. The tendon cell response to repeated minor injuries or “overuse” is thought to be a major factor in the development of tendinopathy. Changes in matrix turnover may also be effected by the cellular response to physical load, altering the balance of matrix turnover and changing the structure and composition of the tendon. Matrix turnover is relatively high in tendons exposed to high mechanical demands, such as the supraspinatus and Achilles, and this is thought to represent either a repair or tissue maintenance function. Metalloproteinases are a large family of enzymes capable of degrading all of the tendon matrix components, and these are thought to play a major role in the degradation of matrix during development, adaptation and repair. It is proposed that some metalloproteinase enzymes are required for the health of the tendon, and others may be damaging, leading to degeneration of the tissue. Further research is required to investigate how these enzyme activities are regulated in tendon and altered in tendinopathy. A profile of all the metalloproteinases expressed and active in healthy and degenerate tendon is required and may lead to the development of new drug therapies for these common and debilitating sports injuries
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