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2. Radiation-Induced Thyroid Cancer

Author

Figge, James J., Jennings, Timothy, Gerasimov, Gregory, Kartel, Nikolai, Yarmolinsky, Dima, Ermak, Gennady, Wartofsky, Leonard, editor, and Van Nostrand, Douglas, editor

Published
2006
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5. Mathematical Model of the Autodyne for the Analysis of its Noise Characteristics at the High Speed of Targets Motion

Author

Ignatkov Kirill Aleksandrovich, Ermak Gennady Pavlovich, Vasiliev Alexander Sergeevich, Shaidurov Kirill Dmitrievich, and Noskov Vladislav Yakovlevich

Subjects
Physics, Amplitude, Autodyne, Noise (signal processing), Acoustics, Motion (geometry), Radiation, Antenna (radio), Signal
Abstract

The paper presents the development results of an autodyne mathematical model of that is influenced by its own reflected radiation and the noise of the oscillator. The model is designed to calculate autodyne noise and signal characteristics. It provides a general case of arbitrary values of the distance between the target and the antenna and the speed of target movement. This is equivalent to an arbitrary volumes of the time delay of the radiation echoed from the target and the autodyne signal period. Expressions are developed to calculate the signal characteristics, taking into account oscillator noise, as well as without taking them into account. In this case, the signal characteristics are understood as the dependences of the autodyne changes of the frequency and amplitude of self-oscillations when the distance to the target changes. In addition, the main relations are obtained for calculating the noise characteristics of an autodyne, recorded when signal components are excluded from consideration.

Published
2020

6. Calculation of Signal and Noise Characteristics of an Autodyne at the High Speed of Targets Motion

Author

Ermak Gennady Pavlovich, Shaidurov Kirill Dmitrievich, Ignatkov Kirill Aleksandrovich, Vasiliev Alexander Sergeevich, and Noskov Vladislav Yakovlevich

Subjects
Generator (circuit theory), Physics, Radar engineering details, Autodyne, Acoustics, Phase (waves), Motion (geometry), Radiation, Signal, Noise (radio)
Abstract

The paper presents the results of calculating the signal and noise characteristics of an autodyne for the general case of arbitrary values of the distance to the target and its speed. This is equivalent to an arbitrary ratio of the delay time of the reflected radiation and the period of the autodyne signal. The laws of the change in the level of frequency and amplitude noise of the generator when changing the distance to the target are established. It is shown that the phenomenon of unsteadiness of noise is observed when the external feedback parameter of the autodyne system is comparable with unity. Moreover, in the case of slow movement of the target, the noise characteristics have a rise in the form of peaks in the vicinity of steep sections of the phase and frequency characteristics. With a significant increase in the target’s speed, the formation of noise characteristics occurs more smoothly, without peaks. Experimental data were obtained on the Ka-band Gunn-diode frequency-modulated autodyne radar sensor.

Published
2020

17. OxidativeResponsive Protein RCAN 1-4 Is Modulated By Acute Exercise In Rat Skeletal Muscles

Author

Emrani Bidi, Ramin, Rébillard, Amélie, Lefeuvre-Orfila, Luz, Gratas-Delamarche, Arlette, Ermak, Gennady, Davies, Kelvin, Cillard, Josiane, Laboratoire Mouvement Sport Santé (M2S), École normale supérieure - Cachan (ENS Cachan)-Université de Rennes (UR)-Université de Brest (UBO)-Université de Rennes 2 (UR2)-Structure Fédérative de Recherche en Biologie et Santé de Rennes ( Biosit : Biologie - Santé - Innovation Technologique ), Détoxication et réparation tissulaire, Université de Rennes (UR)-Institut National de la Santé et de la Recherche Médicale (INSERM), Laboratoire de Physiologie et de Biomécanique de l'Exercice Musculaire. UHB, Université de Rennes 2 (UR2), École normale supérieure - Cachan (ENS Cachan)-Université de Rennes 1 (UR1), Université de Rennes (UNIV-RENNES)-Université de Rennes (UNIV-RENNES)-Université de Brest (UBO)-Université de Rennes 2 (UR2), Université de Rennes (UNIV-RENNES)-Structure Fédérative de Recherche en Biologie et Santé de Rennes ( Biosit : Biologie - Santé - Innovation Technologique ), Station commune de Recherches en Ichtyophysiologie, Biodiversité et Environnement (SCRIBE), Institut National de la Recherche Agronomique (INRA)-IFR140, Université de Rennes 1 (UR1), Université de Rennes (UNIV-RENNES)-Université de Rennes (UNIV-RENNES)-IFR140-Institut National de la Santé et de la Recherche Médicale (INSERM), Université de Rennes (UNIV-RENNES)-Université de Rennes (UNIV-RENNES), Université de Rennes (UNIV-RENNES)-Université de Rennes (UNIV-RENNES)-Université de Rennes 2 (UR2), Université de Rennes (UNIV-RENNES)-Université de Brest (UBO)-Structure Fédérative de Recherche en Biologie et Santé de Rennes ( Biosit : Biologie - Santé - Innovation Technologique ), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Rennes 1 (UR1), and Jonchère, Laurent

Subjects
[SDV] Life Sciences [q-bio], [SDV]Life Sciences [q-bio], musculoskeletal system
Abstract

International audience; Regulator of Calcineurin1 isoform 4 (RCAN1-4)is an oxidative responsive endogenous intracellular phosphatase that inhibits Calcineurin (Cn). Cnis a ubiquitously expressed serine/threonine protein phosphatase under the control of calcium/calmodulin which has been identified in skeletal muscles. However, so far, RCAN1 expression has never been studied under acute exercise. Experiment: 24 Wistar ratswere grouped in three and were subjected to the same physical exercise protocoland then sacrificed either immediately, or 3 hours or 6 hours after exercise. A control group of 8 rats were sacrificed in the same condition. Three different skeletal muscles were collected: Soleus, a predominantly slow twitch muscle rich in type 1 fibers; Extensor DigitorumLongus (EDL), a fast twitch muscle rich in type 2 fibers; andGastrocnemius a ‘mixed muscle’ which contains both type 1 and type 2 fibers. Results: RCAN1-4 was expressed differently in the three muscles. The content of RCAN1-4 was highest in Soleus and remains unchanged after exercise, However RCAN1-4 increased significantly after exercise until 6 hours in EDL and Gastrocnemius. Expression of Cn decreased in all muscles after exercise. PGC-1? as a marker for mitochondrial biogenesis was assayed, although its expression does not significantly changes in any muscle, but it is more expressed in Soleus. Insight in protein and lipid peroxidation showsdifferent patterns of peroxidation of biomolecule in different muscles. Generally malondialdehydeaugments in all muscles after the exercise; however the level of protein carbonyl content increasedonly in EDL and Gastrocnemius but not in Soleus. Conclusion: Acute exercise up-regulated RCAN1-4 expression in rat EDL and Gastrocnemius. Exhaustive exercise is known to induce oxidative stressand RCAN1-4 induction has been shown to help protect against oxidative stress in other tissues. We propose that RCAN1-4 expression represents an important component of the physiological adaptation to exercise and presently we are conducting more investigation using Diabetes Mellitus and Alzheimer’s disease models.

Published
2013

18. Exhaustive exercice modulates expression of Rcan1-4 more than other Rcan1 isoforms in rat skeletal muscle

Author

Emrani Bidi, Ramin, Rébillard, Amélie, Lefeuvre-Orfila, Luz, Gratas-Delamarche, Arlette, Ermak, Gennady, David, Kelvin, Cillard, Josiane, Laboratoire Mouvement Sport Santé (M2S), École normale supérieure - Cachan (ENS Cachan)-Université de Rennes 1 (UR1), Université de Rennes (UNIV-RENNES)-Université de Rennes (UNIV-RENNES)-Université de Brest (UBO)-Université de Rennes 2 (UR2), Université de Rennes (UNIV-RENNES)-Structure Fédérative de Recherche en Biologie et Santé de Rennes ( Biosit : Biologie - Santé - Innovation Technologique ), Signalisation et Réponses aux Agents Infectieux et Chimiques (SeRAIC), Université de Rennes 1 (UR1), Université de Rennes (UNIV-RENNES)-Université de Rennes (UNIV-RENNES)-IFR140, Station commune de Recherches en Ichtyophysiologie, Biodiversité et Environnement (SCRIBE), Institut National de la Recherche Agronomique (INRA)-IFR140, Détoxication et réparation tissulaire, Université de Rennes (UNIV-RENNES)-Université de Rennes (UNIV-RENNES)-IFR140-Institut National de la Santé et de la Recherche Médicale (INSERM), Laboratoire de Physiologie et de Biomécanique de l'Exercice Musculaire. UHB, Université de Rennes 2 (UR2), Université de Rennes (UNIV-RENNES)-Université de Rennes (UNIV-RENNES), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Rennes 1 (UR1), Jonchère, Laurent, École normale supérieure - Cachan (ENS Cachan)-Université de Rennes (UR)-Université de Brest (UBO)-Université de Rennes 2 (UR2)-Structure Fédérative de Recherche en Biologie et Santé de Rennes ( Biosit : Biologie - Santé - Innovation Technologique ), Université de Rennes (UR), and Université de Rennes (UR)-Institut National de la Santé et de la Recherche Médicale (INSERM)

Subjects
[SDV] Life Sciences [q-bio], [SDV]Life Sciences [q-bio], ComputingMilieux_MISCELLANEOUS
Abstract

International audience; no abstract

Published
2012

29. Renaming theDSCR1 / Adapt78gene family asRCAN: regulators of calcineurin

Author

Davies, Kelvin J. A., primary, Ermak, Gennady, additional, Rothermel, Beverley A., additional, Pritchard, Melanie, additional, Heitman, Joseph, additional, Ahnn, Joohong, additional, Henrique‐Silva, Flavio, additional, Crawford, Dana, additional, Canaider, Silvia, additional, Strippoli, Pierluigi, additional, Carinci, Paolo, additional, Min, Kyung‐Tai, additional, Fox, Deborah S., additional, Cunningham, Kyle W., additional, Bassel‐Duby, Rhonda, additional, Olson, Eric N., additional, Zhang, Zhuohua, additional, Williams, R. Sanders, additional, Gerber, Hans‐Peter, additional, Pérez‐Riba, Mercè, additional, Seo, Hisao, additional, Cao, Xia, additional, Klee, Claude B., additional, Redondo, Juan Miguel, additional, Maltais, Lois J., additional, Bruford, Elspeth A., additional, Povey, Sue, additional, Molkentin, Jeffery D., additional, McKeon, Frank D., additional, Duh, Elia J., additional, Crabtree, Gerald R., additional, Cyert, Martha S., additional, Luna, Susana, additional, and Estivill, Xavier, additional

Published
2007
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34. Molecular Pathogenesis of Thyroid Cancer.

Author

Wartofsky, Leonard, Van Nostrand, Douglas, Figge, James J., Kartel, Nikolai A., Yarmolinsky, Dima, and Ermak, Gennady

Abstract

The thyroid follicular epithelial cell (thyrocyte) responds to myriad growth-stimulating substances, including hormones, growth factors, cytokines, and other mitogens (1-15), as exemplified in Table 1. Thyrocyte responses to these factors are mediated by distinct signal transduction pathways (Figs. 1-3). Each pathway features a cell surface receptor that is linked to a specific cytoplasmic signal transduction cascade: 1.Receptor tyrosine kinase (RTK)/RAS/RAF/MEK/mitogenactivated protein kinase (MAPK) pathway (Fig. 1).2.Thyrotropin (TSH) receptor/adenylate cyclase/protein kinase A (PKA) pathway (Fig. 2).3.Receptor/phospholipase C (PLC)/protein kinase C (PKC) pathway (Fig. 3). [ABSTRACT FROM AUTHOR]

Published
2006
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35. Radiation-Induced Thyroid Cancer.

Author

Wartofsky, Leonard, Van Nostrand, Douglas, Figge, James J., Jennings, Timothy, Gerasimov, Gregory, Kartel, Nikolai, Yarmolinsky, Dima, and Ermak, Gennady

Abstract

Radiation is one of the few accepted risk factors for thyroid cancer. Numerous studies have confirmed that the thyroid gland is one of the most radiation-sensitive human organs and that thyroid cancer is one of the most common radiogenic malignancies. Analysis of these studies is problematic, however, owing to difficulties in dose assessment, long-term follow-up of thousands of exposed subjects, definition and confirmation of pathological diagnoses, and differences in exposure modalities. [ABSTRACT FROM AUTHOR]

Published
2006
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45. Renaming the DSCR1/Adapt78 gene family as RCAN: regulators of calcineurin.

Author

Davies, Kelvin J. A., Ermak, Gennady, Rothermel, Beverley A., Pritchard, Melanie, Heitman, Joseph, Joohong Ahnn, Henrique-Silva, Flavio, Crawford, Dana, Canaider, Silvia, Strippoli, Pierluigi, Carinci, Paolo, Kyung-Tai Min, Fox, Deborah S., Cunningham, Kyle W., Bassel-Duby, Rhonda, Olson, Erie N., Zhuohua Zhang, Williams, R. Sanders, Gerber, Hans-Peter, and Pérez-Riba, Mercè

Subjects
*NAMES, *GENES, *PHOSPHOPROTEIN phosphatases, *PHOSPHATASES, *ENZYMES
Abstract

The article proposes a new name for DSCR1/Adapt78 gene family. It is suggested that this gene family should be called as regulators of calcineurin (RCAN) to indicate their ability to bond and modulate the protein phosphatase enzyme, calcineurin. The RCAN gene family and its regulation of calcineurin are discussed.

Published
2007
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46. The DSCR1(Adapt78) isoform 1 protein calcipressin 1 inhibits calcineurin and protects against acute calcium‐mediated stress damage, including transient oxidative stress

Author

Ermak, Gennady, Harris, Cathryn D., and Davies, Kelvin J. A.

Abstract

Although DSCR1(Adapt78) has been associated with successful adaptation to oxidative stress and calcium stress and with devastating diseases such as Alzheimer's and Down syndrome, no rationale for these apparently contradictory findings has been tested. In fact, DSCR1 (Adapt78)has not yet been proved to provide protection against acute oxidative stress or calcium stress. We have addressed this question using cross‐adaptation to H2O2and the calcium ionophore A23187, stable DSCR1(Adapt78) transfection and over‐expression in hamster HA‐1 cells, ‘tet‐off’ regulated DSCR1(Adapt78) isoform 1 transgene expression in human PC‐12 cells, and DSCR1(Adapt78) antisense oligonucleotides to test the ability of the DSCR1(Adapt78) protein product calcipressin 1 (a calcineurin inhibitor) to protect against oxidative stress and calcium stress. Under all conditions, resistance to oxidative stress and calcium stress increased as a function of DSCR1(Adapt78)/calcipressin 1 expression and decreased as gene/protein expression diminished. We conclude that cells may transiently use increased expression of the DSCR1(Adapt78) gene product calcipressin 1 to provide short‐term protection against acute oxidative stress and other calcium‐mediated stresses, whereas chronic overexpression may be associated with Alzheimer disease progression.—Ermak, G., Harris, C. D., Davies, K. J. A. The DSCR1(Adapt78) isoform 1 protein calcipressin 1 inhibits calcineurin and protects against acute calcium‐mediated stress damage, including transient oxidative stress. FASEB J.16, 814–824 (2002)

Published
2002
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48. Gene expression in Alzheimer's disease.

Author

Ermak G and Davies KJ

Subjects
Alzheimer Disease pathology, Humans, Presenilin-1, Presenilin-2, Alzheimer Disease genetics, Amyloid beta-Protein Precursor analogs & derivatives, Amyloid beta-Protein Precursor genetics, Apolipoproteins E genetics, Membrane Proteins genetics
Abstract

Even though the exact cause of Alzheimer's disease is not known, it is clear that genetic factors play a major role. Screening of familial cases has so far linked four genes to Alzheimer's disease: amyloid precursor protein, presenilin 1, presenilin 2 and apolipoprotein E. Mutations in the amyloid precursor protein, presenilin 1 and presenilin 2 genes cause the enhanced production of b amyloid that is found in neuritic plaques. While apolipoprotein E allele e4 does not cause enhanced production of amyloid, it does enhance its deposition. The genes identified so far are linked to only about 10% of total Alzheimer's disease cases, and there are a number of familial cases that are not linked to any of the four genes. This suggests that important genetic factors have yet to be identified. The key events in Alzheimer's disease are cytoskeletal changes and the formation of paired helical filaments, and these are common to the two hallmarks of Alzheimer's disease: neuritic plaques and neurofibrillary tangles. So far there is no explanation as to how the identified genes cause these events. Here we speculate that paired helical filaments can form as a result of overexpression of the DSCR1 (Adap78) gene. b Amyloids and/or other stress factors can induce DSCR1 (Adap78) and cause decreased activity of calcineurin. Chronic downregulation of calcineurin can lead to gradual accumulation of hyperphosphorylated tau, the formation of paired helical filaments and Alzheimer's disease-like cytoskeletal changes., (Copyright 2002 Prous Science)

Published
2002
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