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1. Improving Rehabilitative Assessment with Statistical and Shape Preserving Surrogate Data and Singular Spectrum Analysis

Author

Lee, T. K. M., Chan, H. W., Leo, K. H., Chew, E., Zhao, Ling, and Sanei, S.

Subjects
Electrical Engineering and Systems Science - Signal Processing
Abstract

Time series data are collected in temporal order and are widely used to train systems for prediction, modeling and classification to name a few. These systems require large amounts of data to improve generalization and prevent over-fitting. However there is a comparative lack of time series data due to operational constraints. This situation is alleviated by synthesizing data which have a suitable spread of features yet retain the distinctive features of the original data. These would be its basic statistical properties and overall shape which are important for short time series such as in rehabilitative applications or in quickly changing portions of lengthy data. In our earlier work synthesized surrogate time series were used to augment rehabilitative data. This gave good results in classification but the resulting waveforms did not preserve the original signal shape. To remedy this, we use singular spectrum analysis (SSA) to separate a signal into trends and cycles to describe the shape of the signal and low level components. In a novel way we subject the low level component to randomizing processes then recombine this with the original trend and cycle components to form a synthetic time series. We compare our approach with other methods, using statistical and shape measures and demonstrate its effectiveness in classification., Comment: This version of the paper under the same title, acknowledges the data source and the funding for current research using this data. arXiv admin note: substantial text overlap with arXiv:2404.14211

Published
2024
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4. The True Teamwork Model: Blending the Liberal Arts and International Business Education

Author

McInnis-Bowers, Cecilia and Chew, E. Byron

Abstract

As crucial stakeholders in higher education, employers have long requested, demanded, and implored that colleges and universities help students develop the team skills needed to address challenges posed by innovation. Employers seek college graduates who, in the face of persistent ambiguity and within increasingly complex environments, are able to collaborate with people with a broad diversity of backgrounds, cultural origins, attitudes, beliefs, and behaviors. In this article, the authors describe the True Teamwork Model which blends concepts from psychology, anthropology, management, and philosophy. The model represents a cohesive teaching and learning strategy designed to enable students to develop teamwork skills through a three-pronged approach: (1) knowing self; (2) understanding others; and (3) collaborating to solve complex problems. The self-guided format of the model ensures that its use by students does not compete with time for in-class content delivery by faculty. The True Teamwork Model can readily be replicated or adapted to emphasize any of the three elements, and it is transferable across programs of study.

Published
2008

5. Blending Liberal Art and Business Education

Author

Chew, E. Byron and McInnis-Bowers, Cecilia

Abstract

Business educators and colleagues in the liberal arts have not found the ideal bridge, from the student's perspective, that provides a meaningful connection between the two domains. Over the years, challenges to effectively bridge the divide between liberal arts and business have come from leaders in education, the professional business community, and from business education accrediting organizations. Words like bridging and embedding have been used to conceptually suggest the constructs of association. Most recently, the need to go beyond bridging or embedding to a more seamless approach to blending the domains has been asserted. Professional studies, such as business, should be approached as liberal education. Using one small, traditional liberal arts college's experience as an example, ways of blending these domains, rather than bridging the phantom yet palpable chasm between, are discussed here.

Published
2004

7. A Cross-Cultural Exploration of Parental Involvement and Child-Rearing Beliefs in Asian Cultures

Author

Frewen, A. R., Chew, E., Carter, M., Chunn, J., and Jotanovic, D.

Abstract

Parental involvement (PI) and child-rearing beliefs were examined amongst parents whose children attended state-run kindergartens across Singapore. A total of 244 parents completed an online survey consisting of a Child-Rearing Beliefs Scale, a PI Scale, and demographic details. Results indicated respondents were generally low-income earners with high rates of bilingualism. Two-thirds of parents had enrolled their kindergarten children in extra classes, with half of parents indicating that academic achievement was their highest priority. Ethnic differences were noted, with Chinese parents showing less involvement at home and school and less emphasis on the development of creative and practical skills and conforming behaviors than parents from other Asian backgrounds. This effect was independent from the effects of gender, parental education, and income. These results confirm the importance parents place on academic achievement in Singapore, but also, along with, extend prior research to suggest that inter Asian differences exist.

Published
2015
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9. Screening for von Hippel-Lindau disease by DNA polymorphism analysis.

Author

Glenn, GM, Linehan, WM, Hosoe, S, Latif, F, Yao, M, Choyke, P, Gorin, MB, Chew, E, Olfield, E, and Manolatos, C

Subjects
Humans, DNA, Risk, Prospective Studies, Pedigree, Polymorphism, Restriction Fragment Length, von Hippel-Lindau Disease, Genetic Testing, Genetic Linkage, Polymorphism, Restriction Fragment Length, Genetics, Rare Diseases, Clinical Research, Pediatric, Prevention, 2.1 Biological and endogenous factors, General & Internal Medicine, Medical and Health Sciences
Abstract

ObjectiveVon Hippel-Lindau (VHL) disease is a rare, inherited multisystem neoplastic disorder. There is no biochemical test available to distinguish VHL disease gene carriers from their healthy siblings. We evaluated DNA polymorphism analysis as a method for identifying disease gene carriers.DesignProspective comparison of the results of DNA analysis with a comprehensive clinical screening examination.SettingThe Clinical Center of the National Institutes of Health.PatientsBlood was collected from 182 members of 16 families with VHL disease. Forty-eight asymptomatic individuals, at risk of developing this hereditary illness (with an affected parent or sibling), were examined for occult disease at the Clinical Center of the National Institutes of Health and tested by DNA polymorphism analysis.ResultsDNA polymorphism analysis predicted nine disease gene carriers and 33 individuals with the wild-type (normal) allele among the 48 individuals at risk of developing VHL disease; the test was not informative in six individuals. All nine individuals predicted to carry the VHL gene had evidence of occult disease on clinical examination. There was no clinical evidence of VHL disease in 32 of 33 individuals predicted to carry the wild-type allele.ConclusionsDNA polymorphism analysis can identify individuals likely to carry the VHL disease gene among asymptomatic members of disease families. This technique serves to focus attention on those individuals who require periodic medical examination and may help to alleviate the morbidity and mortality associated with this disease.

Published
1992

16. Germline MBD4 deficiency causes a multi-tumor predisposition syndrome

Author

Palles, C, West, HD, Chew, E, Galavotti, S, Flensburg, C, Grolleman, JE, Jansen, EAM, Curley, H, Chegwidden, L, Arbe-Barnes, EH, Lander, N, Truscott, R, Pagan, J, Bajel, A, Sherwood, K, Martin, L, Thomas, H, Georgiou, D, Fostira, F, Goldberg, Y, Adams, DJ, van der Biezen, SAM, Christie, M, Clendenning, M, Thomas, LE, Deltas, C, Dimovski, AJ, Dymerska, D, Lubinski, J, Mahmood, K, van der Post, RS, Sanders, M, Weitz, J, Taylor, JC, Turnbull, C, Vreede, L, van Wezel, T, Whalley, C, Arnedo-Pac, C, Caravagna, G, Cross, W, Chubb, D, Frangou, A, Gruber, AJ, Kinnersley, B, Noyvert, B, Church, D, Graham, T, Houlston, R, Lopez-Bigas, N, Sottoriva, A, Wedge, D, Jenkins, MA, Kuiper, RP, Roberts, AW, Cheadle, JP, Ligtenberg, MJL, Hoogerbrugge, N, Koelzer, VH, Rivas, AD, Winship, IM, Ponte, CR, Buchanan, DD, Power, DG, Green, A, Tomlinson, IPM, Sampson, JR, Majewski, IJ, de Voer, RM, Palles, C, West, HD, Chew, E, Galavotti, S, Flensburg, C, Grolleman, JE, Jansen, EAM, Curley, H, Chegwidden, L, Arbe-Barnes, EH, Lander, N, Truscott, R, Pagan, J, Bajel, A, Sherwood, K, Martin, L, Thomas, H, Georgiou, D, Fostira, F, Goldberg, Y, Adams, DJ, van der Biezen, SAM, Christie, M, Clendenning, M, Thomas, LE, Deltas, C, Dimovski, AJ, Dymerska, D, Lubinski, J, Mahmood, K, van der Post, RS, Sanders, M, Weitz, J, Taylor, JC, Turnbull, C, Vreede, L, van Wezel, T, Whalley, C, Arnedo-Pac, C, Caravagna, G, Cross, W, Chubb, D, Frangou, A, Gruber, AJ, Kinnersley, B, Noyvert, B, Church, D, Graham, T, Houlston, R, Lopez-Bigas, N, Sottoriva, A, Wedge, D, Jenkins, MA, Kuiper, RP, Roberts, AW, Cheadle, JP, Ligtenberg, MJL, Hoogerbrugge, N, Koelzer, VH, Rivas, AD, Winship, IM, Ponte, CR, Buchanan, DD, Power, DG, Green, A, Tomlinson, IPM, Sampson, JR, Majewski, IJ, and de Voer, RM

Abstract

We report an autosomal recessive, multi-organ tumor predisposition syndrome, caused by bi-allelic loss-of-function germline variants in the base excision repair (BER) gene MBD4. We identified five individuals with bi-allelic MBD4 variants within four families and these individuals had a personal and/or family history of adenomatous colorectal polyposis, acute myeloid leukemia, and uveal melanoma. MBD4 encodes a glycosylase involved in repair of G:T mismatches resulting from deamination of 5'-methylcytosine. The colorectal adenomas from MBD4-deficient individuals showed a mutator phenotype attributable to mutational signature SBS1, consistent with the function of MBD4. MBD4-deficient polyps harbored somatic mutations in similar driver genes to sporadic colorectal tumors, although AMER1 mutations were more common and KRAS mutations less frequent. Our findings expand the role of BER deficiencies in tumor predisposition. Inclusion of MBD4 in genetic testing for polyposis and multi-tumor phenotypes is warranted to improve disease management.

Published
2022

17. Germline MBD4 deficiency causes a multi-tumor predisposition syndrome

Author

Palles, C., West, H.D., Chew, E., Galavotti, S., Flensburg, C., Grolleman, J.E., Jansen, E.A.M., Curley, H., Chegwidden, L., Arbe-Barnes, E.H., Lander, N., Truscott, R., Pagan, J., Bajel, A., Sherwood, K., Martin, L., Thomas, H, Georgiou, D., Fostira, F., Goldberg, Y., Adams, D.J., Biezen, S.A.M. van der, Christie, M., Clendenning, M., Thomas, L.E., Deltas, C., Dimovski, A.J., Dymerska, D., Lubinski, J., Mahmood, K., Post, R.S. van der, Sanders, M., Weitz, J., Taylor, J.C., Turnbull, C., Vreede, L., Wezel, T. van, Whalley, C., Arnedo-Pac, C., Caravagna, G., Cross, W., Chubb, D., Frangou, A., Gruber, A.J., Kinnersley, B., Noyvert, B., Church, D., Graham, T., Houlston, R., Lopez-Bigas, N., Sottoriva, A., Wedge, D., Jenkins, Mark A., Kuiper, R.P., Roberts, A.W., Cheadle, J.P., Ligtenberg, M.J.L., Hoogerbrugge, N., Koelzer, V.H., Rivas, A.D., Winship, I.M., Ponte, C.R., Buchanan, D.D., Power, D.G., Green, A., Tomlinson, I.P., Sampson, J.R., Majewski, I.J., Voer, R.M. de, Palles, C., West, H.D., Chew, E., Galavotti, S., Flensburg, C., Grolleman, J.E., Jansen, E.A.M., Curley, H., Chegwidden, L., Arbe-Barnes, E.H., Lander, N., Truscott, R., Pagan, J., Bajel, A., Sherwood, K., Martin, L., Thomas, H, Georgiou, D., Fostira, F., Goldberg, Y., Adams, D.J., Biezen, S.A.M. van der, Christie, M., Clendenning, M., Thomas, L.E., Deltas, C., Dimovski, A.J., Dymerska, D., Lubinski, J., Mahmood, K., Post, R.S. van der, Sanders, M., Weitz, J., Taylor, J.C., Turnbull, C., Vreede, L., Wezel, T. van, Whalley, C., Arnedo-Pac, C., Caravagna, G., Cross, W., Chubb, D., Frangou, A., Gruber, A.J., Kinnersley, B., Noyvert, B., Church, D., Graham, T., Houlston, R., Lopez-Bigas, N., Sottoriva, A., Wedge, D., Jenkins, Mark A., Kuiper, R.P., Roberts, A.W., Cheadle, J.P., Ligtenberg, M.J.L., Hoogerbrugge, N., Koelzer, V.H., Rivas, A.D., Winship, I.M., Ponte, C.R., Buchanan, D.D., Power, D.G., Green, A., Tomlinson, I.P., Sampson, J.R., Majewski, I.J., and Voer, R.M. de

Abstract

Contains fulltext : 251996.pdf (Publisher’s version ) (Open Access), We report an autosomal recessive, multi-organ tumor predisposition syndrome, caused by bi-allelic loss-of-function germline variants in the base excision repair (BER) gene MBD4. We identified five individuals with bi-allelic MBD4 variants within four families and these individuals had a personal and/or family history of adenomatous colorectal polyposis, acute myeloid leukemia, and uveal melanoma. MBD4 encodes a glycosylase involved in repair of G:T mismatches resulting from deamination of 5'-methylcytosine. The colorectal adenomas from MBD4-deficient individuals showed a mutator phenotype attributable to mutational signature SBS1, consistent with the function of MBD4. MBD4-deficient polyps harbored somatic mutations in similar driver genes to sporadic colorectal tumors, although AMER1 mutations were more common and KRAS mutations less frequent. Our findings expand the role of BER deficiencies in tumor predisposition. Inclusion of MBD4 in genetic testing for polyposis and multi-tumor phenotypes is warranted to improve disease management.

Published
2022

18. Ganciclovir-induced mutations are present in a diverse spectrum of post-transplant malignancies

Author

Fang, H, Yan, HHN, Bilardi, RA, Flensburg, C, Yang, H, Barbour, JA, Siu, HC, Turski, M, Chew, E, Xu, Z, Lam, ST, Sharma, R, Xu, M, Li, J, Ip, HW, Cheung, CYM, Huen, MSY, Sweet-Cordero, EA, Majewski, IJ, Leung, SY, Wong, JWH, Fang, H, Yan, HHN, Bilardi, RA, Flensburg, C, Yang, H, Barbour, JA, Siu, HC, Turski, M, Chew, E, Xu, Z, Lam, ST, Sharma, R, Xu, M, Li, J, Ip, HW, Cheung, CYM, Huen, MSY, Sweet-Cordero, EA, Majewski, IJ, Leung, SY, and Wong, JWH

Abstract

BACKGROUND: Ganciclovir (GCV) is widely used in solid organ and haematopoietic stem cell transplant patients for prophylaxis and treatment of cytomegalovirus. It has long been considered a mutagen and carcinogen. However, the contribution of GCV to cancer incidence and other factors that influence its mutagenicity remains unknown. METHODS: This retrospective cohort study analysed genomics data for 121,771 patients who had undergone targeted sequencing compiled by the Genomics Evidence Neoplasia Information Exchange (GENIE) or Foundation Medicine (FM). A statistical approach was developed to identify patients with GCV-associated mutational signature (GCVsig) from targeted sequenced data of tumour samples. Cell line exposure models were further used to quantify mutation burden and DNA damage caused by GCV and other antiviral and immunosuppressive drugs. RESULTS: Mutational profiles from 22 of 121,771 patient samples in the GENIE and FM cohorts showed evidence of GCVsig. A diverse range of cancers was represented. All patients with detailed clinical history available had previously undergone solid organ transplantation and received GCV and mycophenolate treatment. RAS hotspot mutations associated with GCVsig were present in 9 of the 22 samples, with all samples harbouring multiple GCV-associated protein-altering mutations in cancer driver genes. In vitro testing in cell lines showed that elevated DNA damage response and GCVsig are uniquely associated with GCV but not acyclovir, a structurally similar antiviral. Combination treatment of GCV with the immunosuppressant, mycophenolate mofetil (MMF), increased the misincorporation of GCV in genomic DNA and mutations attributed to GCVsig in cell lines and organoids. CONCLUSIONS: In summary, GCV can cause a diverse range of cancers. Its mutagenicity may be potentiated by other therapies, such as mycophenolate, commonly co-prescribed with GCV for post-transplant patients. Further investigation of the optimal use of these drugs

Published
2022

20. The Business Administration Capstone: Assessment and Integrative Learning.

Author

Chew, E. Byron

Abstract

At Birmingham-Southern College (Alabama), the business administration program's senior year capstone course in strategic business management serves three purposes: allows evaluation of the school's academic program; helps assess student capabilities; and allows integration of learning across disciplines. The course occurs during the January interim term and provides intensive teamwork and interaction between students and faculty. (MSE)

Published
1996

23. Germline loss-of-function variants in the base-excision repair gene MBD4 cause a Mendelian recessive syndrome of adenomatous colorectal polyposis and acute myeloid leukaemia

Author

Khalid Mahmood, Chew E, Dagmara Dymerska, Roberts Aw, Mark Clendenning, Christoffer Flensburg, Nicoline Hoogerbrugge, Ben Kinnersley, Goldberg Y, Boris Noyvert, Jenny C. Taylor, Mathijs A. Sanders, van Wezel T, Lilian Vreede, Giulio Caravagna, Daniel D. Buchanan, Curley H, van der Biezen Sa, Richard S. Houlston, Celina Whalley, Michael Christie, Laura Chegwidden, Georgiou D, Judith E. Grolleman, Huw Thomas, Galavotti S, Sherwood K, Sottoriva A, Erik A. M. Jansen, Aleksandar Dimovski, Mark A. Jenkins, M.J.L. Ligtenberg, Roland P. Kuiper, Ian J. Majewski, Bajel A, Jakub Lubiński, Ian Tomlinson, Anna Frangou, Claire Palles, Pac Ca, Florentia Fostira, Deltas C, Clare Turnbull, Ingrid Winship, David N. Church, Lynn Martin, William Cross, Jürgen Weitz, David C. Wedge, Koelzer Vh, Rivas Ad, Barnes Ea, Nuria Lopez-Bigas, David J. Adams, van der Post Rs, Daniel Chubb, de Voer Rm, Trevor A. Graham, Andreas J. Gruber, and Ponte Cr

Subjects
Myeloid, Colorectal cancer, DNA Repair Pathway, Colorectal polyposis, Base excision repair, Biology, medicine.disease, medicine.disease_cause, Germline, MBD4, medicine.anatomical_structure, Cancer research, medicine, KRAS
Abstract

Inherited defects in base-excision repair (BER) predispose to adenomatous polyposis and colorectal cancer (CRC), yet our understanding of this important DNA repair pathway remains incomplete. By combining detailed clinical, histological and molecular profiling, we reveal biallelic germline loss-of-function (LOF) variants in the BER gene MBD4 to predispose to adenomatous polyposis and –uniquely amongst CRC predisposition syndromes– to myeloid neoplasms. Neoplasms from MBD4-deficient patients almost exclusively accumulate somatic CpG>TpG mutations, resembling mutational signature SBS1. MBD4-deficient adenomas harbour mutations in known CRC driver genes, although AMER1 mutations were more common and KRAS mutations less frequent. We did not find an increased risk for colorectal tumours in individuals with a monoallelic MBD4 LOF variant. We suggest that this condition should be termed MBD4-associated neoplasia syndrome (MANS) and that MBD4 is included in testing for the genetic diagnosis of polyposis and/or early-onset AML.

Published
2021

25. Assessment of the lower ureteric excision technique associated oncological outcomes for upper urinary tract urothelial carcinoma: Retrospective, updated interim analysis from the Scottish Renal Cancer Network

Author

Blackmur, J.P., primary, Chew, E., additional, Trail, M., additional, Brodie, K., additional, Santoni, N., additional, Rodger, F., additional, Hamilton, D., additional, Gaba, F., additional, Randall, S., additional, Chapman, A., additional, and Laird, A., additional

Published
2021
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26. Intact TP-53 function is essential for sustaining durable responses to BH3-mimetic drugs in leukemias

Author

Thijssen, R, Diepstraten, ST, Moujalled, D, Chew, E, Flensburg, C, Shi, MX, Dengler, MA, Litalien, V, MacRaild, S, Chen, M, Anstee, NS, Reljic, B, Gabriel, SS, Djajawi, TM, Riffkin, CD, Aubrey, BJ, Chang, C, Tai, L, Xu, Z, Morley, T, Pomilio, G, Bruedigam, C, Kallies, A, Stroud, DA, Bajel, A, Kluck, RM, Lane, SW, Schoumacher, M, Banquet, S, Majewski, IJ, Strasser, A, Roberts, AW, Huang, DCS, Brown, FC, Kelly, GL, Wei, AH, Thijssen, R, Diepstraten, ST, Moujalled, D, Chew, E, Flensburg, C, Shi, MX, Dengler, MA, Litalien, V, MacRaild, S, Chen, M, Anstee, NS, Reljic, B, Gabriel, SS, Djajawi, TM, Riffkin, CD, Aubrey, BJ, Chang, C, Tai, L, Xu, Z, Morley, T, Pomilio, G, Bruedigam, C, Kallies, A, Stroud, DA, Bajel, A, Kluck, RM, Lane, SW, Schoumacher, M, Banquet, S, Majewski, IJ, Strasser, A, Roberts, AW, Huang, DCS, Brown, FC, Kelly, GL, and Wei, AH

Abstract

Selective targeting of BCL-2 with the BH3-mimetic venetoclax has been a transformative treatment for patients with various leukemias. TP-53 controls apoptosis upstream of where BCL-2 and its prosurvival relatives, such as MCL-1, act. Therefore, targeting these prosurvival proteins could trigger apoptosis across diverse blood cancers, irrespective of TP53 mutation status. Indeed, targeting BCL-2 has produced clinically relevant responses in blood cancers with aberrant TP-53. However, in our study, TP53-mutated or -deficient myeloid and lymphoid leukemias outcompeted isogenic controls with intact TP-53, unless sufficient concentrations of BH3-mimetics targeting BCL-2 or MCL-1 were applied. Strikingly, tumor cells with TP-53 dysfunction escaped and thrived over time if inhibition of BCL-2 or MCL-1 was sublethal, in part because of an increased threshold for BAX/BAK activation in these cells. Our study revealed the key role of TP-53 in shaping long-term responses to BH3-mimetic drugs and reconciled the disparate pattern of initial clinical response to venetoclax, followed by subsequent treatment failure among patients with TP53-mutant chronic lymphocytic leukemia or acute myeloid leukemia. In contrast to BH3-mimetics targeting just BCL-2 or MCL-1 at doses that are individually sublethal, a combined BH3-mimetic approach targeting both prosurvival proteins enhanced lethality and durably suppressed the leukemia burden, regardless of TP53 mutation status. Our findings highlight the importance of using sufficiently lethal treatment strategies to maximize outcomes of patients with TP53-mutant disease. In addition, our findings caution against use of sublethal BH3-mimetic drug regimens that may enhance the risk of disease progression driven by emergent TP53-mutant clones.

Published
2021

32. Using Transcranial Direct Current Stimulation to Augment the Effect of Motor Imagery-Assisted Brain-Computer Interface Training in Chronic Stroke Patients—Cortical Reorganization Considerations

Author

Chew, E, Teo, Wei-Peng, Tang, N, Ang, KK, Ng, YS, Zhou, JH, Teh, I, Phua, KS, Zhao, L, Guan, C, Chew, E, Teo, Wei-Peng, Tang, N, Ang, KK, Ng, YS, Zhou, JH, Teh, I, Phua, KS, Zhao, L, and Guan, C

Abstract

Introduction: Transcranial direct current stimulation (tDCS) has been shown to modulate cortical plasticity, enhance motor learning and post-stroke upper extremity motor recovery. It has also been demonstrated to facilitate activation of brain-computer interface (BCI) in stroke patients. We had previously demonstrated that BCI-assisted motor imagery (MI-BCI) can improve upper extremity impairment in chronic stroke participants. This study was carried out to investigate the effects of priming with tDCS prior to MI-BCI training in chronic stroke patients with moderate to severe upper extremity paresis and to investigate the cortical activity changes associated with training. Methods: This is a double-blinded randomized clinical trial. Participants were randomized to receive 10 sessions of 20-min 1 mA tDCS or sham-tDCS before MI-BCI, with the anode applied to the ipsilesional, and the cathode to the contralesional primary motor cortex (M1). Upper extremity sub-scale of the Fugl-Meyer Assessment (UE-FM) and corticospinal excitability measured by transcranial magnetic stimulation (TMS) were assessed before, after and 4 weeks after intervention. Results: Ten participants received real tDCS and nine received sham tDCS. UE-FM improved significantly in both groups after intervention. Of those with unrecordable motor evoked potential (MEP-) to the ipsilesional M1, significant improvement in UE-FM was found in the real-tDCS group, but not in the sham group. Resting motor threshold (RMT) of ipsilesional M1 decreased significantly after intervention in the real-tDCS group. Short intra-cortical inhibition (SICI) in the contralesional M1 was reduced significantly following intervention in the sham group. Correlation was found between baseline UE-FM score and changes in the contralesional SICI for all, as well as between changes in UE-FM and changes in contralesional RMT in the MEP- group. Conclusion: MI-BCI improved the motor function of the stroke-affected arm in chronic stroke p

Published
2020

34. A Smart Service Platform for Cost Efficient Cardiac Health Monitoring.

Author

Faust, O, Lei, N, Chew, E, Ciaccio, EJ, Acharya, UR, Faust, O, Lei, N, Chew, E, Ciaccio, EJ, and Acharya, UR

Abstract

Aim

In this study we have investigated the problem of cost effective wireless heart health monitoring from a service design perspective.

Subject and methods

There is a great medical and economic need to support the diagnosis of a wide range of debilitating and indeed fatal non-communicable diseases, like Cardiovascular Disease (CVD), Atrial Fibrillation (AF), diabetes, and sleep disorders. To address this need, we put forward the idea that the combination of Heart Rate (HR) measurements, Internet of Things (IoT), and advanced Artificial Intelligence (AI), forms a Heart Health Monitoring Service Platform (HHMSP). This service platform can be used for multi-disease monitoring, where a distinct service meets the needs of patients having a specific disease. The service functionality is realized by combining common and distinct modules. This forms the technological basis which facilitates a hybrid diagnosis process where machines and practitioners work cooperatively to improve outcomes for patients.

Results

Human checks and balances on independent machine decisions maintain safety and reliability of the diagnosis. Cost efficiency comes from efficient signal processing and replacing manual analysis with AI based machine classification. To show the practicality of the proposed service platform, we have implemented an AF monitoring service.

Conclusion

Having common modules allows us to harvest the economies of scale. That is an advantage, because the fixed cost for the infrastructure is shared among a large group of customers. Distinct modules define which AI models are used and how the communication with practitioners, caregivers and patients is handled. That makes the proposed HHMSP agile enough to address safety, reliability and functionality needs from healthcare providers.

Published
2020

48. Irish cardiac society: Proceedings of annual general meeting held 1st November, 1997

Author

Seifer, C., McNeill, B., O’Donnell, M., Daly, K., Kellett, J., McGee, H. M., Montogomery, A. J., O’Callaghan, D., Horgan, J. H., Mahon, N. G., Codd, M., Brennan, J., Egan, B., McCann, H. A., Sugrue, D. D., Menown, I. B. A., Patterson, R. S. H. W., McMechan, S. R., Hameed, S., Adgey, A. A. J., Baird, S. H., McBride, S. J., Trouton, T. G., Wilson, C., McRedmond, J. P., Fitzgerald, D. J., Crowley, J. J., Tanguay, J-F., Santos, R. M., Stack, R. S., Mahon, N. G., Keelan, P., McCann, H. A., Sugrue, D. D., McKenna, C. J., AuBuchon, R., Camrud, A. R., Holmes, D. R., Schwartz, R. S., McKenna, C. J., Camrud, A. R., Wolff, R., Edwards, W. D., Holmes, D. R., Schwartz, R. S., Hanratty, C., McAuley, D., Young, I., Murtagh, G., O’Keeffe, B., Richardson, G., Scott, M., Chew, E. W., Bailie, N. A., Graham, A. M. J., O’Kane, H., McKenna, C. J., Kwon, H. M., Ellis, L., Holmes, D. R., Virmani, R., Schwartz, R. S., Noelke, L., Wood, A. E., Javadpour, H., Veerasingham, D., Wood, A. E., O’Kane, D., Allen, J. D., Adgey, A. A. J., Hennessy, T., Johnson, P., Hildick-Smith, D., Winter, E., Shapiro, L., McKenna, C. J., Edwards, W. D., Lerman, A., Holmes, D. R., Schwartz, R. S., McGrath, L. T., Passmore, P., Silke, B., McAuley, D., Nugent, A. G., McGurk, C., Hanratty, C., Maguire, S., Johnston, G. D., McAuley, D., Nugent, A. G., McGurk, C., Hanratty, C., Maguire, S., Johnston, G. D., Lovell, S. L., McDowell, G., McEneany, D., Riley, M. S., Nicholls, D. P., Gilligan, D., Sargent, D., Dan, D., Gilligan, D., Elam, G., Rhee, B., Keane, D., Zhou, L., McGovern, B., Garan, H., Ruskin, J., O’Shea, J. C., Tan, H-C., Zidar, J. P., Stack, R. S., Crowley, J. J., O’Keeffe, D. B., Graffin, S., Fitzsimmons, D., Brown, S., Duff, D., Denham, B., Woods, F., Neligan, M., Oslizlok, P., Connolly, C. K., Danton, M. H. D., O’Kane, H., Danton, M., Gladstone, D. J., Craig, B., Mulholland, H. C., Casey, F., Chaudhuri, S., Hinchion, J., Wood, A. E., Hinchion, J., Wood, A. E., Menown, I. B. A., Patterson, R. H. S. W., MacKenzie, G., Adgey, A. A. J., Harbinson, M. T., Burgess, L. M., Moohan, V., McEneaney, D. J., Adgey, A. A. J., Menown, I. B. A., MacKenzie, G., Patterson, R. S. H. W., Adgey, A. A. J., Finnegan, O. C., Doherty, L., Silke, B., Riddell, J. G., Meleady, R., Daly, L., Graham, I., Quinn, M., Foley, B., Lee, J., Mulvihill, N., Crean, P., Walsh, M., O’Morain, C., Quinn, M., Crean, P., Foley, B., Walsh, M., Hynes, C., King, S. M., David, S., Newton, H., Maguire, M., Rafferty, F., Horgan, J. H., Sullivan, P. A., Murphy, D., Gallagher, S., Menown, I. B. A., Allen, J., Anderson, J. McC, Adgey, A. A. J., Dan, D., Hoag, J., Eckberg, D., Gilligan, D., Galvin, J., Garan, H., McGovern, B., Ruskin, J., Mahon, N. G., Diamond, P., Neilan, T., Keelan, E., H. A., McCarthy, C., Sugrue, D. D., Harbinson, M. T., Moohan, V. P., McEneaney, D. J., Burgess, L. M., Anderson, J. McC, Ayers, G. M., Adgey, A. A. J., Roberts, M., Burgess, L., Anderson, C., Wilson, C., Khan, M., Clements, I. P., Miller, W. L., Seifer, C., O’Donnell, M., McNeill, B., Daly, K., Turtle, F., McDowell, G., Long, H., McNair, W., Campbell, N. P. S., Mathew, T. P., Turtle, F., Smye, M., Nesbitt, G. S., Young, I. S., Adgey, A. A. J., Meleady, R., Mulcahy, D., Graham, I. M., Moore, D., Menown, I. B. A., McMechan, S. R., MacKenzie, G., Adgey, A. A. J., Diamond, P., Sugrue, D., Codd, M. B., Galvin, J., Zimmerman, P., Winget, J., Capeless, M., Galvin, J., Garan, H., McGovern, B., Ruskin, J., McKelvey, T. A., Danton, M. H. D., Sarsam, M. I. A., McEneaney, D., Roberts, M., Burgess, L., Anderson, C., Wilson, C., and Khan, M.

Published
1998
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