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1. Effect of Scrape-Off-Layer Current on Reconstructed Tokamak Equilibrium

Author

King, J. R., Kruger, S. E., Groebner, R. J., Hanson, J. D., Hebert, J. D., Held, E. D., and Jepson, J. R.

Subjects
Physics - Plasma Physics
Abstract

Methods are described that extend fields from reconstructed equilibria to include scrape-off-layer current through extrapolated parametrized and experimental fits. The extrapolation includes both the effects of the toroidal-field and pressure gradients which produce scrape-off-layer current after recomputation of the Grad-Shafranov solution. To quantify the degree that inclusion of scrape-off-layer current modifies the equilibrium, the $\chi$-squared goodness-of-fit parameter is calculated for cases with and without scrape-off-layer current. The change in $\chi$-squared is found to be minor when scrape-off-layer current is included however flux surfaces are shifted by up to 3 cm. The impact on edge modes of these scrape-off-layer modifications is also found to be small and the importance of these methods to nonlinear computation is discussed., Comment: 14 pages

Published
2017
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2. What I want my Neighbors to Know about my Mental Illness

Author

Jepson J

Abstract

I live in an apartment complex in a busy part of my town. From my second-floor balcony, I can see my neighbors coming and going from their jobs, appointments, and other activities. I don't really know any of my neighbors on a personal level. I live a rather isolated life except for occasional visits from my family. So, my interactions with my neighbors consist of a polite "Hello, how are you?" or "Have a nice day," exchanges. I sometimes wonder how they would react towards me if they knew I have a diagnosed severe mental illness.

Published
2022

5. PDXK mutations cause polyneuropathy responsive to pyridoxal 5'-phosphate supplementation

Author

Chelban, V., Wilson, M. P., Warman Chardon, J., Vandrovcova, J., Zanetti, M. N., Zamba-Papanicolaou, E., Efthymiou, S., Pope, S., Conte, M. R., Abis, G., Liu, Y. -T., Tribollet, E., Haridy, N. A., Botia, J. A., Ryten, M., Nicolaou, P., Minaidou, A., Christodoulou, K., Kernohan, K. D., Eaton, A., Osmond, M., Ito, Y., Bourque, P., Jepson, J. E. C., Bello, O., Bremner, F., Cordivari, C., Reilly, M. M., Foiani, M., Heslegrave, A., Zetterberg, H., Heales, S. J. R., Wood, N. W., Rothman, J. E., Boycott, K. M., Mills, P. B., Clayton, P. T., Houlden, H., Kriouile, Y., Khorassani, M. E., Aguennouz, M., Groppa, S., Marinova Karashova, B., Van Maldergem, L., Nachbauer, W., Boesch, S., Arning, L., Timmann, D., Cormand, B., Perez-Duenas, B., Di Rosa, G., Goraya, J. S., Sultan, T., Mine, J., Avdjieva, D., Kathom, H., Tincheva, R., Banu, S., Pineda-Marfa, M., Veggiotti, P., Ferrari, M. D., van den Maagdenberg, A. M. J. M., Verrotti, A., Marseglia, G., Savasta, S., Garcia-Silva, M., Ruiz, A. M., Garavaglia, B., Borgione, E., Portaro, S., Sanchez, B. M., Boles, R., Papacostas, S., Vikelis, M., Giunti, P., Salpietro, V., Oconnor, E., Kullmann, D., Kaiyrzhanov, R., Sullivan, R., Khan, A. M., Yau, W. Y., Hostettler, I., Papanicolaou, E. Z., Dardiotis, E., Maqbool, S., Ibrahim, S., Kirmani, S., Rana, N. N., Atawneh, O., Lim, S. -Y., Shaikh, F., Koutsis, G., Breza, M., Mangano, S., Scuderi, C., Morello, G., Stojkovic, T., Torti, E., Zollo, M., Heimer, G., Dauvilliers, Y. A., Striano, P., Al-Khawaja, I., Al-Mutairi, F., Alkuraya, F. S., Sherifa, H., Rizig, M., Okubadejo, N. U., Ojo, O. O., Oshinaike, O. O., Wahab, K., Bello, A. H., Abubakar, S., Obiabo, Y., Nwazor, E., Ekenze, O., Williams, U., Iyagba, A., Taiwo, L., Komolafe, M., Oguntunde, O., Pchelina, S., Senkevich, K., Shashkin, C., Zharkynbekova, N., Koneyev, K., Manizha, G., Isrofilov, M., Guliyeva, U., Salayev, K., Khachatryan, S., Rossi, S., Silvestri, Gabriella, Bourinaris, T., Xiromerisiou, G., Fidani, L., Spanaki, C., Tucci, A., Silvestri G. (ORCID:0000-0002-1950-1468), Chelban, V., Wilson, M. P., Warman Chardon, J., Vandrovcova, J., Zanetti, M. N., Zamba-Papanicolaou, E., Efthymiou, S., Pope, S., Conte, M. R., Abis, G., Liu, Y. -T., Tribollet, E., Haridy, N. A., Botia, J. A., Ryten, M., Nicolaou, P., Minaidou, A., Christodoulou, K., Kernohan, K. D., Eaton, A., Osmond, M., Ito, Y., Bourque, P., Jepson, J. E. C., Bello, O., Bremner, F., Cordivari, C., Reilly, M. M., Foiani, M., Heslegrave, A., Zetterberg, H., Heales, S. J. R., Wood, N. W., Rothman, J. E., Boycott, K. M., Mills, P. B., Clayton, P. T., Houlden, H., Kriouile, Y., Khorassani, M. E., Aguennouz, M., Groppa, S., Marinova Karashova, B., Van Maldergem, L., Nachbauer, W., Boesch, S., Arning, L., Timmann, D., Cormand, B., Perez-Duenas, B., Di Rosa, G., Goraya, J. S., Sultan, T., Mine, J., Avdjieva, D., Kathom, H., Tincheva, R., Banu, S., Pineda-Marfa, M., Veggiotti, P., Ferrari, M. D., van den Maagdenberg, A. M. J. M., Verrotti, A., Marseglia, G., Savasta, S., Garcia-Silva, M., Ruiz, A. M., Garavaglia, B., Borgione, E., Portaro, S., Sanchez, B. M., Boles, R., Papacostas, S., Vikelis, M., Giunti, P., Salpietro, V., Oconnor, E., Kullmann, D., Kaiyrzhanov, R., Sullivan, R., Khan, A. M., Yau, W. Y., Hostettler, I., Papanicolaou, E. Z., Dardiotis, E., Maqbool, S., Ibrahim, S., Kirmani, S., Rana, N. N., Atawneh, O., Lim, S. -Y., Shaikh, F., Koutsis, G., Breza, M., Mangano, S., Scuderi, C., Morello, G., Stojkovic, T., Torti, E., Zollo, M., Heimer, G., Dauvilliers, Y. A., Striano, P., Al-Khawaja, I., Al-Mutairi, F., Alkuraya, F. S., Sherifa, H., Rizig, M., Okubadejo, N. U., Ojo, O. O., Oshinaike, O. O., Wahab, K., Bello, A. H., Abubakar, S., Obiabo, Y., Nwazor, E., Ekenze, O., Williams, U., Iyagba, A., Taiwo, L., Komolafe, M., Oguntunde, O., Pchelina, S., Senkevich, K., Shashkin, C., Zharkynbekova, N., Koneyev, K., Manizha, G., Isrofilov, M., Guliyeva, U., Salayev, K., Khachatryan, S., Rossi, S., Silvestri, Gabriella, Bourinaris, T., Xiromerisiou, G., Fidani, L., Spanaki, C., Tucci, A., and Silvestri G. (ORCID:0000-0002-1950-1468)

Abstract

Objective: To identify disease-causing variants in autosomal recessive axonal polyneuropathy with optic atrophy and provide targeted replacement therapy. Methods: We performed genome-wide sequencing, homozygosity mapping, and segregation analysis for novel disease-causing gene discovery. We used circular dichroism to show secondary structure changes and isothermal titration calorimetry to investigate the impact of variants on adenosine triphosphate (ATP) binding. Pathogenicity was further supported by enzymatic assays and mass spectroscopy on recombinant protein, patient-derived fibroblasts, plasma, and erythrocytes. Response to supplementation was measured with clinical validated rating scales, electrophysiology, and biochemical quantification. Results: We identified biallelic mutations in PDXK in 5 individuals from 2 unrelated families with primary axonal polyneuropathy and optic atrophy. The natural history of this disorder suggests that untreated, affected individuals become wheelchair-bound and blind. We identified conformational rearrangement in the mutant enzyme around the ATP-binding pocket. Low PDXK ATP binding resulted in decreased erythrocyte PDXK activity and low pyridoxal 5′-phosphate (PLP) concentrations. We rescued the clinical and biochemical profile with PLP supplementation in 1 family, improvement in power, pain, and fatigue contributing to patients regaining their ability to walk independently during the first year of PLP normalization. Interpretation: We show that mutations in PDXK cause autosomal recessive axonal peripheral polyneuropathy leading to disease via reduced PDXK enzymatic activity and low PLP. We show that the biochemical profile can be rescued with PLP supplementation associated with clinical improvement. As B6 is a cofactor in diverse essential biological pathways, our findings may have direct implications for neuropathies of unknown etiology characterized by reduced PLP levels. ANN NEUROL 2019;86:225–240.

Published
2019

6. Clinical, pathological and functional characterization of riboflavin-responsive neuropathy

Author

Manole, A, Jaunmuktane, Z, Hargreaves, I, Ludtmann, M H R, Pandraud, A, Salpietro, V, Pope, S, Horga, A, Scalco, R S, Li, A, Ashokkumar, B, Lourenço, C M, Horvath, R, Chinnery, P F, Toro, C, Singleton, A B, Abramov, A Y, Muntoni, F, Hanna, F G, Reilly, M M, Revesz, T, Kullman, N D M, Jepson, J E C, and Houlden, H

Abstract

Brown-Vialetto-Van Laere syndrome represents a phenotypic spectrum of motor, sensory, and cranial nerve neuropathy, often with ataxia, optic atrophy and respiratory problems leading to ventilator-dependence. Loss-of-function mutations in two riboflavin transporter genes, SLC52A2 and SLC52A3, have recently been linked to Brown-Vialetto-Van Laere syndrome. However, the genetic frequency, neuropathology and downstream consequences of riboflavin transporter mutations are unclear. By screening a large cohort of 132 patients with early-onset severe sensory, motor and cranial nerve neuropathy we confirmed the strong genetic link between riboflavin transporter mutations and Brown-Vialetto-Van Laere syndrome, identifying 22 pathogenic mutations in SLC52A2 and SLC52A3, 14 of which were novel. Brain and spinal cord neuropathological examination of two cases with SLC52A3 mutations showed classical symmetrical brainstem lesions resembling pathology seen in mitochondrial disease, including severe neuronal loss in the lower cranial nerve nuclei, anterior horns and corresponding nerves, atrophy of the spinothalamic and spinocerebellar tracts and posterior column–medial lemniscus pathways. Mitochondrial dysfunction has previously been implicated in an array of neurodegenerative disorders. Since riboflavin metabolites are critical components of the mitochondrial electron transport chain, we hypothesized that reduced riboflavin transport would result in impaired mitochondrial activity, and confirmed this using in vitro and in vivo models. Electron transport chain complex I and complex II activity were decreased in SLC52A2 patient fibroblasts, while global knockdown of the single Drosophila melanogaster riboflavin transporter homologue revealed reduced levels of riboflavin, downstream metabolites, and electron transport chain complex I activity. This in turn led to abnormal mitochondrial membrane potential, respiratory chain activity and morphology. Riboflavin transporter knockdown in Drosophila also resulted in severely impaired locomotor activity and reduced lifespan, mirroring patient pathology, and these phenotypes could be partially rescued using a novel esterified derivative of riboflavin. Our findings expand the genetic, clinical and neuropathological features of Brown-Vialetto-Van Laere syndrome, implicate mitochondrial dysfunction as a downstream consequence of riboflavin transporter gene defects, and validate riboflavin esters as a potential therapeutic strategy.

Published
2017

9. UTAH

Author

Jepson, J. Ellwood

Published
1956

10. UTAH

Author

Jepson, J. Ellwood

Published
1957

14. PBPK MODELING OF SHORT-TERM (0 TO 5 MIN) HUMAN INHALATION EXPOSURES TO HALOGENATED HYDROCARBONS

Author

A. Vinegar G. W. Jepson J. H. Overton

Subjects
Toxicology, Physiologically based pharmacokinetic modelling, medicine.anatomical_structure, Inhalation, Chemistry, Human exposure, Health, Toxicology and Mutagenesis, Environmental chemistry, medicine, Animal testing, Sensitization
Abstract

Allowable human exposure to Halons and Halon replacement chemicals is often regulated on the basis of cardiac sensitization potential. Exposure guidelines are established using dose-response data obtained from animal testing. Results from animal tests are often summarized by no-observable-adverse-effect level and lowest-observable-adverseeffect level values. This threshold approach alone does not provide the information necessary to evaluate the cardiac sensitization potential for the chemical of interest under a variety of exposure concentrations and durations. In order to provide a tool for decision makers and regulators tasked with setting exposure guidelines for Halon replacement chem icals, a quantitative approach was established that allows exposures to be assessed in terms of the chemical concentrations in blood during the exposure. A physiologically based pharmacokinetic model was modified to include a respiratory-tract compartment containing a dead-space region and a pulmonary exchange area. The ...

Published
1998

29. Sympathetic Bias.

Author

Levy Sandra, David M. and Jepson, J. Peart

Subjects
*STATISTICIANS, *STATISTICAL bias, *QUANTITATIVE research, *TEXTBOOKS, *PROFESSIONAL-client communication
Abstract

We wish to deal with investigator bias in a statistical context. We sketch how a textbook solution to the problem of "outliers" which avoids one sort of investigator bias, creates the temptation for another sort. We write down a model of the approbation seeking statistician who is tempted by sympathy for client to violate the disciplinary standards. We give a simple account of one context in which we might expect investigator bias to flourish. Finally, we offer tentative suggestions to deal with the problem of investigator bias which follow from our account. As we have given a very sparse and stylized account of investigator bias, we ask what might be done to overcome this limitation. [ABSTRACT FROM AUTHOR]

Published
2008
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31. Professional issues. Do not attempt resuscitation decisions: the nursing role.

Author

Jepson J

Abstract

This exploratory study examines the roles of practice nurses with regard to do not attempt resuscitation (DNAR) decisions. The British Medical Association (BMA) and the Royal College of Nursing (RCN) have published joint DNAR guidelines. One NHS trust responded by developing a local DNAR policy written for use in hospital and general practice. The study focuses on aspects of compliance with the policy and hence DNAR decision-making, in particular, the nurse's involvement in the decision-making process. The response rate to self-administered questionnaires to practice nurses was 52% (n = 45). Hospital nurses (n = 49) were selected for interview using a quota-sampling technique. Comparisons were made of the views of acute and community staff in their use of the DNAR policy. A clear finding is that hospital nurses wish for more autonomy in DNAR decision-making and improved methods of communicating with medical colleagues when decisions are made. Practice nurses are currently not involved in DNAR decisions. The appropriateness of developing policies for such complex issues as DNAR, when compliance remains low, questions their validity. This study raises awareness, and adds to the discussion for the need for a multidisciplinary approach to DNAR policy. [ABSTRACT FROM AUTHOR]

Published
2003
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32. Treatment of uterine sarcomas.

Author

Echt, Gregory, Jepson, Joanne, Steel, John, Langholz, Bryan, Luxton, Gary, Hernandez, Wilfredo, Astrahan, Melvin, Petrovich, Zbigniew, Echt, G, Jepson, J, Steel, J, Langholz, B, Luxton, G, Hernandez, W, Astrahan, M, and Petrovich, Z

Published
1990
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42. Hemopoiesis in Pituitary Dwarfs Treated With Human Growth Hormone and Testosterone

Author

Jepson, J. H. and McGarry, E. E.

Abstract

Prepubertal hypopituitary dwarfs are anemic and have reduced levels of erythropoietin-stimulating factor (ESF) in the urine. Treatment with human growth hormone (HGH) in doses sufficient to produce linear growth and weight gain induces bone marrow lymphocytosis, increased erythropoiesis indicated by an increase of the red cell mass (RCM) and improved iron kinetic studies. This was associated with increased concentrations of ESF in the urine, increased transferrin levels, and expansion of the plasma volume. The combination of testosterone and HGH increased further erythropoiesis but could not be specifically ascribed to testosterone, since the continued action of HGH could be responsible for the observed effects. The excretion of ESF was not increased further. Testosterone did, however, maintain ESF excretion on deletion of HGH from the regimen, suggesting at least one common mode of action for these hormones in the hypoanabolic subject. In contrast, testosterone failed to maintain the plasma volume increase induced by HGH and did not further effect the observed bone marrow lymphocytosis.

Published
1972
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43. Effect of Prolactin on Erythropoiesis in the Mouse

Author

JEPSON, J. H. and LOWENSTEIN, L.

Abstract

The effect of prolactin, growth hormone, progesterone, testosterone, lactating mouse plasma (fifth postpartum day), pregnant mouse plasma (sixteenth to nineteenth day of pregnancy) on erythropoiesis in the polycythemic mouse has been studied and compared. Prolactin was found to stimulate erythropoiesis in the intact mouse. Also, pregnant mouse plasma and lactating mouse plasma had an erythropoietic stimulating effect. Prolactin produced an increase in the red cell mass when administered over a prolonged period to normal and orchidectomized mice. This suggests that the testes are not necessary for the action of prolactin. It is suggested that prolactin could function as an erythropoietic stimulatory component in pregnant and lactating mouse plasma.

Published
1964
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44. Polycythemia and Increased Erythropoietin Production in a Patient with Hypertrophy of the Juxta-Glomerular Appartus

Author

JEPSON, J. and MCGARRY, E. E.

Abstract

A patient with proven hypertrophy of the juxtaglomerular apparatus was found to be polycythemic and hypervolemic. Increased levels of erythropoietin were present in the urine and plasma collected from the patient. The associated increase in aldosterone secretion rate, elevated blood renin and angiotensin levels suggest the juxtaglomerular apparatus may directly or indirectly play a role in the production of erythropoietin.

Published
1968
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50. Correspondence. The Construction of Iron and Steel Railway-Wagons

Author

Angus, J., Jones, W. R. S., Shackleford, A. L., Lart, F. A., Jepson, J. T., Leslie, B., Annan, W. C., Miller, R., Bamber, H., Sheffield, G. H., Cardew, C. E., Thwaite, B. H., Cowan, P. J., Dobson, J. M., Twinberrow, J. D., Hack, H., Head, A. P., and Hyde, P. A.

Abstract

n/a

Published
1904

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