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121 results on '"Desai, N. M."'

1. SCATSAT-1 Scatterometer : an improved successor of OSCAT

Author

Misra, T., Chakraborty, P., Lad, C., Gupta, P., Rao, J., Upadhyay, G., Kumar, S. Vinay, Kumar, B. Saravana, Gangele, S., Sinha, S., Tolani, H., Vithani, V. K., Raman, B. S., Rao, C. V. N., Dave, D. B., Jyoti, R., and Desai, N. M.

Published
2019

2. Geodetic Evidence for Cascading Landslide Motion Triggered by Extreme Rain Events at Joshimath, NW Himalaya.

Author

Sreejith, K. M., Jasir, M. C. M., Sunil, P. S., Rose, M. S., Saji, Ajish P., Agrawal, R., Bushair, M. T., Vijay Kumar, K., and Desai, N. M.

Subjects
LANDSLIDES, RAINFALL, RAINFALL measurement, GLOBAL Positioning System, SYNTHETIC aperture radar, CIVILIAN evacuation, BUILDING evacuation, NATURAL disaster warning systems
Abstract

Slope instability due to tectonic, hydrological and anthropogenic activities cause severe landslides in Himalaya. Joshimath, a densely populated Himalayan town witnessed a catastrophic landslide event during December 2022 and January 2023 causing damages to ∼700 buildings. We use Interferometric synthetic aperture radar, Global Positioning System and rainfall measurements to probe the kinematics of the Joshimath landslide. We separate the seasonal and episodic deformation components using singular spectrum analysis. While the low amplitude annual landslide motions are modulated by seasonal precipitation, acceleration phases are triggered by extreme rain events. Our analysis revealed episodes of cascading motions triggered by extreme rain events resulting an overall increase in landslide velocity from −22 mm/yr during 2004–2010 to −325 mm/yr during 2022–2023. We estimate the landslide depth (∼30 m) and hydraulic diffusivity (∼3 × 10−5 m2/s) using a 1‐D pore‐water pressure diffusion model. Our study reveals the importance of systematic monitoring of ground deformation and weather parameters for landslide hazard mitigation. Plain Language Summary: The Himalayas, world's largest and youngest mountain range formed as a result of the India‐Eurasia continental collision hosts thousands of landslides each year related to tectonic and anthropogenic activities. It is important to characterize the landslide kinematics, especially the slow moving landslides at the fast‐developing Himalayan urban centers for hazard assessment. A recent catastrophic landslide event in the Joshimath town in NW Himalaya occurred between December 2022 and January 2023 caused damages to ∼700 buildings leading to mass evacuation. We map the spatio‐temporal evolution of land deformation at Joshimath using about two decades of geodetic measurements and singular spectrum analysis technique. While the decadal‐scale landslide motions match well with the overall increase in rainfall intensity, the episodic accelerations are triggered by extreme rain events. The extreme rainfall event on 19 October 2021, triggered the latest episode of landslide acceleration, which eventually led to the tragic disaster. The present study, for the first time, provides constraints on the landslide depth and hydraulic diffusivity. Our study also emphasis on the systematic monitoring of ground deformation and weather parameters at the Himalayas for an effective landslide hazard preparedness and mitigation. Key Points: Joshimath landslide displays episodic and seasonal kinematic changes; episodic accelerations are triggered by extreme rain eventsThe 19 October 2021 extreme rain event triggered the latest episode of landslide acceleration culminating to the 2022 disasterDepth and hydraulic diffusivity of the landslide is constrained using 1‐D pore‐water pressure diffusion model [ABSTRACT FROM AUTHOR]

Published
2024
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10. Advanced space rubidium atomic frequency standard for satellite navigation.

Author

Bandi, Thejesh N., Desai, N. M., Kaintura, J., Attri, D., Saiyed, M. A., Sharma-Kesarkar, R., Sinha, P., Ghoshal, B., Mandal, S., Ghosh, B., Jain, P., Priya, P., Shukla, K., Soni, A., Somani, S., Patel, A., Kuchana, R., Karthik, K., Rao, C. V. N., and Ram, T. V. S.

Abstract

NavIC (Navigation with Indian Constellation) is a regional satellite navigation system called Indian Regional Navigation Satellite System (IRNSS). The NavIC is presently composed of seven operational satellite configuration geometry. We present indigenously designed and developed RAFS for NavIC, named IRAFS—Indian Rubidium Atomic Frequency Standard. The IRAFS Physics Package (PP) and electronics have novel design features, as explained in this article. We present the IRAFS performances tested in thermo-vacuum conditions demonstrating < 2 × 10–12τ−1/2 stability, reaching a flicker floor of 3 × 10–14 with a drift of < 5 × 10–13/day. The IRAFS has a mass of 7.6 kg, a volume of 16 L, and consumes power of 75 W at warm-up and < 40 W in normal operation. [ABSTRACT FROM AUTHOR]

Published
2022
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22. SCATSAT-1 Scatterometer:An Improved Successor of OSCAT

Author

Misra, T., primary, Chakraborty, P., additional, Lad, C., additional, Gupta, P., additional, Rao, J., additional, Upadhyay, G., additional, Vinay Kumar, S., additional, Saravana Kumar, B., additional, Gangele, S., additional, Sinha, S., additional, Tolani, H., additional, Vithani, V. K., additional, Raman, B. S., additional, Rao, C. V. N., additional, Dave, D. B., additional, Jyoti, R., additional, and Desai, N. M., additional

Published
2019
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28. TRANSPLANTATION CLINICAL 1

Author

Schachtner, T., primary, Reinke, P., additional, Dorje, C., additional, Mjoen, G., additional, Midtvedt, K., additional, Strom, E. H., additional, Oyen, O., additional, Jenssen, T., additional, Reisaeter, A. V., additional, Smedbraaten, Y. V., additional, Sagedal, S., additional, Fagerland, M. W., additional, Hartmann, A., additional, Thiel, S., additional, Zulkarnaev, A., additional, Vatazin, A., additional, Vincenti, F., additional, Harel, E., additional, Kantor, A., additional, Thurison, T., additional, Hoyer-Hansen, G., additional, Craik, C., additional, Kute, V. B., additional, Shah, P. S., additional, Vanikar, A. V., additional, Modi, P. R., additional, Shah, P. R., additional, Gumber, M. R., additional, Patel, H. V., additional, Engineer, D. P., additional, Shah, V. R., additional, Rizvi, J., additional, Trivedi, H. L., additional, Malheiro, J., additional, Dias, L., additional, Martins, L. S., additional, Fonseca, I., additional, Pedroso, S., additional, Almeida, M., additional, Castro-Henriques, A., additional, Cabrita, A., additional, Costa, C., additional, Ritta, M., additional, Sinesi, F., additional, Sidoti, F., additional, Mantovani, S., additional, Di Nauta, A., additional, Messina, M., additional, Cavallo, R., additional, Verflova, A., additional, Svobodova, E., additional, Slatinska, J., additional, Slavcev, A., additional, Pokorna, E., additional, Viklicky, O., additional, Yagan, J., additional, Chandraker, A., additional, Diena, D., additional, Tognarelli, G., additional, Ranghino, A., additional, Bussolino, S., additional, Fop, F., additional, Segoloni, G. P., additional, Biancone, L., additional, Leone, F., additional, Mauro, M. V., additional, Gigliotti, P., additional, Lofaro, D., additional, Greco, F., additional, Perugini, D., additional, Papalia, T., additional, Perri, A., additional, Vizza, D., additional, Giraldi, C., additional, Bonofilgio, R., additional, Luis-Lima, S., additional, Marrero, D., additional, Gonzalez-Rinne, A., additional, Torres, A., additional, Salido, E., additional, Jimenez-Sosa, A., additional, Aldea-Perona, A., additional, Gonzalez-Posada, J. M., additional, Perez-Tamajon, L., additional, Rodriguez-Hernandez, A., additional, Negrin-Mena, N., additional, Porrini, E., additional, Pihlstrom, H., additional, Dahle, D. O., additional, Holdaas, H., additional, Von Der Lippe, N., additional, Waldum, B., additional, Brekke, F., additional, Amro, A., additional, Os, I., additional, Klin, P., additional, Sanabria, H., additional, Bridoux, P., additional, De Francesco, J., additional, Fortunato, R. M., additional, Raffaele, P., additional, Kong, J., additional, Son, S. H., additional, Kwon, H. Y., additional, Whang, E. J., additional, Choi, W. Y., additional, Yoon, C. S., additional, Thanaraj, V., additional, Theakstone, A., additional, Stopper, K., additional, Ferraro, A., additional, Bhattacharjya, S., additional, Devonald, M., additional, Williams, A., additional, Mella, A., additional, Gallo, E., additional, Di Vico, M. C., additional, Pagani, F., additional, Gai, M., additional, Cho, H. J., additional, Nho, K. W., additional, Park, S.-K., additional, Kim, S. B., additional, Yoshida, K., additional, Ishii, D., additional, Ohyama, T., additional, Kohguchi, D., additional, Takeuchi, Y., additional, Varga, A., additional, Sandor, B., additional, Kalmar-Nagy, K., additional, Toth, A., additional, Toth, K., additional, Szakaly, P., additional, Kildushevsky, A., additional, Fedulkina, V., additional, Kantaria, R., additional, Staeck, O., additional, Halleck, F., additional, Rissling, O., additional, Naik, M., additional, Neumayer, H.-H., additional, Budde, K., additional, Khadzhynov, D., additional, Bhadauria, D., additional, Kaul, A., additional, Prasad, N., additional, Sharma, R. K., additional, Sezer, S., additional, Bal, Z., additional, Erkmen Uyar, M., additional, Guliyev, O., additional, Erdemir, B., additional, Colak, T., additional, Ozdemir, N., additional, Haberal, M., additional, Caliskan, Y., additional, Yazici, H., additional, Artan, A. S., additional, Oto, O. A., additional, Aysuna, N., additional, Bozfakioglu, S., additional, Turkmen, A., additional, Yildiz, A., additional, Sever, M. S., additional, Yagisawa, T., additional, Nukui, A., additional, Kimura, T., additional, Nannmoku, K., additional, Kurosawa, A., additional, Sakuma, Y., additional, Miki, A., additional, Damiano, F., additional, Ligabue, G., additional, De Biasi, S., additional, Granito, M., additional, Cossarizza, A., additional, Cappelli, G., additional, Henriques, A. C., additional, Davide, J., additional, Von During, M. E., additional, Jenssen, T. G., additional, Bollerslev, J., additional, Godang, K., additional, Asberg, A., additional, Bachelet, T., additional, Martinez, C., additional, Bello, A., additional, Kejji, S., additional, Couzi, L., additional, Guidicelli, G., additional, Lepreux, S., additional, Visentin, J., additional, Congy-Jolivet, N., additional, Rostaing, L., additional, Taupin, J.-L., additional, Kamar, N., additional, Merville, P., additional, Ozdemir, H., additional, Yildirim, S., additional, Tutal, E., additional, Sayin, B., additional, Ozdemir Acar, N., additional, Banasik, M., additional, Boratynska, M., additional, Koscielska-Kasprzak, K., additional, Kaminska, D., additional, Bartoszek, D., additional, Mazanowska, O., additional, Krajewska, M., additional, Zmonarski, S., additional, Chudoba, P., additional, Dawiskiba, T., additional, Protasiewicz, M., additional, Halon, A., additional, Sas, A., additional, Kaminska, M., additional, Klinger, M., additional, Stefanovic, N., additional, Cvetkovic, T., additional, Velickovic - Radovanovic, R., additional, Jevtovic - Stoimenov, T., additional, Vlahovic, P., additional, Rungta, R., additional, Das, P., additional, Ray, D. S., additional, Gupta, S., additional, Kolonko, A., additional, Szotowska, M., additional, Kuczera, P., additional, Chudek, J., additional, Wiecek, A., additional, Sikora-Grabka, E., additional, Adamczak, M., additional, Madej, P., additional, Amanova, A., additional, Kendi Celebi, Z., additional, Bakar, F., additional, Caglayan, M. G., additional, Keven, K., additional, Massimetti, C., additional, Imperato, G., additional, Zampi, G., additional, De Vincenzi, A., additional, Fabbri, G. D. D., additional, Brescia, F., additional, Feriozzi, S., additional, Filipov, J. J., additional, Zlatkov, B. K., additional, Dimitrov, E. P., additional, Svinarov, D. A., additional, Poesen, R., additional, De Vusser, K., additional, Evenepoel, P., additional, Kuypers, D., additional, Naesens, M., additional, Meijers, B., additional, Kocak, H., additional, Yilmaz, V. T., additional, Yilmaz, F., additional, Uslu, H. B., additional, Aliosmanoglu, I., additional, Ermis, H., additional, Dinckan, A., additional, Cetinkaya, R., additional, Ersoy, F. F., additional, Suleymanlar, G., additional, Oliveira, J.-C., additional, Santos, J., additional, Lobato, L., additional, Mendonca, D., additional, Watarai, Y., additional, Yamamoto, T., additional, Tsujita, M., additional, Hiramitsu, T., additional, Goto, N., additional, Narumi, S., additional, Kobayashi, T., additional, Line, P.-D., additional, Housawi, A., additional, House, A., additional, Ng, C., additional, Denesyk, K., additional, Rehman, F., additional, Moist, L., additional, Musetti, C., additional, Battista, M., additional, Izzo, C., additional, Guglielmetti, G., additional, Airoldi, A., additional, Stratta, P., additional, Cena, T., additional, Quaglia, M., additional, Fenoglio, R., additional, Cagna, D., additional, Amoroso, A., additional, Palmisano, A., additional, Degli Antoni, A. M., additional, Vaglio, A., additional, Piotti, G., additional, Cremaschi, E., additional, Buzio, C., additional, Maggiore, U., additional, Lee, M.-C., additional, Hsu, B.-G., additional, Zalamea Jarrin, F., additional, Sanchez Sobrino, B., additional, Lafuente Covarrubias, O., additional, Karsten Alvarez, S., additional, Dominguez Apinaniz, P., additional, Llopez Carratala, R., additional, Portoles Perez, J., additional, Yildirim, T., additional, Yilmaz, R., additional, Turkmen, E., additional, Altindal, M., additional, Arici, M., additional, Altun, B., additional, Erdem, Y., additional, Dounousi, E., additional, Mitsis, M., additional, Naka, K., additional, Pappas, H., additional, Lakkas, L., additional, Harisis, H., additional, Pappas, K., additional, Koutlas, V., additional, Tzalavra, I., additional, Spanos, G., additional, Michalis, L., additional, Siamopoulos, K., additional, Iwabuchi, T., additional, Nanmoku, K., additional, Yasunaru, S., additional, Yoshikawa, M., additional, Kitamura, K., additional, Fuji, H., additional, Fujisawa, M., additional, Nishi, S., additional, Carta, P., additional, Zanazzi, M., additional, Buti, E., additional, Larti, A., additional, Caroti, L., additional, Di Maria, L., additional, Minetti, E. E., additional, Shi, Y., additional, Luo, L., additional, Cai, B., additional, Wang, T., additional, Zou, Y., additional, Wang, L., additional, Kim, Y., additional, Kim, H. S., additional, Choi, B. S., additional, Park, C. W., additional, Yang, C. W., additional, Kim, Y.-S., additional, Chung, B. H., additional, Baek, C. H., additional, Kim, M., additional, Kim, J.-S., additional, Yang, W. S., additional, Han, D. J., additional, Mikolasevic, I., additional, Racki, S., additional, Lukenda, V., additional, Persic, M. P., additional, Colic, M., additional, Devcic, B., additional, Orlic, L., additional, Gurlek Demirci, B., additional, Say N, C. B., additional, Ozdemir Acar, F. N., additional, Vali, S., additional, Ismal, K., additional, Sahay, M., additional, Civiletti, F., additional, Cantaluppi, V., additional, Medica, D., additional, Mazzeo, A. T., additional, Assenzio, B., additional, Mastromauro, I., additional, Deambrosis, I., additional, Giaretta, F., additional, Fanelli, V., additional, Mascia, L., additional, Gkirdis, I., additional, Bechlioulis, A., additional, Evangelou, D., additional, Zarzoulas, F., additional, Kotsia, A., additional, Balafa, O., additional, Tzeltzes, G., additional, Nakas, G., additional, Kalaitzidis, R., additional, Katsouras, C., additional, Uyanik, S., additional, Toprak, S. K., additional, Ilhan, O., additional, Ekmen Uyar, M., additional, Hernandez Vargas, H., additional, Artamendi Larranaga, M., additional, Ramalle Gomara, E., additional, Gil Catalinas, F., additional, Bello Ovalle, A., additional, Pimentel Guzman, G., additional, Coloma Lopez, A., additional, Sierra Carpio, M., additional, Gil Paraiso, A., additional, Dall Anesse, C., additional, Beired Val, I., additional, Huarte Loza, E., additional, Choy, B. Y., additional, Kwan, L., additional, Mok, M., additional, Chan, T. M., additional, Yamakawa, T., additional, Kobayashi, A., additional, Yamamoto, I., additional, Mafune, A., additional, Nakada, Y., additional, Tannno, Y., additional, Tsuboi, N., additional, Yamamoto, H., additional, Yokoyama, K., additional, Ohkido, I., additional, Yokoo, T., additional, Luque, Y., additional, Anglicheau, D., additional, Rabant, M., additional, Clement, R., additional, Kreis, H., additional, Sartorius, A., additional, Noel, L.-H., additional, Timsit, M.-O., additional, Legendre, C., additional, Rancic, N., additional, Vavic, N., additional, Dragojevic-Simic, V., additional, Katic, J., additional, Jacimovic, N., additional, Kovacevic, A., additional, Mikov, M., additional, Veldhuijzen, N. M. H., additional, Rookmaaker, M. B., additional, Van Zuilen, A. D., additional, Nquyen, T. Q., additional, Boer, W. H., additional, Sahtout, W., additional, Ghezaiel, H., additional, Azzebi, A., additional, Ben Abdelkrim, S., additional, Guedri, Y., additional, Mrabet, S., additional, Nouira, S., additional, Ferdaws, S., additional, Amor, S., additional, Belarbia, A., additional, Zellama, D., additional, Mokni, M., additional, Achour, A., additional, Parikova, A., additional, Hanzal, V., additional, Fronek, J., additional, Orandi, B. J., additional, James, N. T., additional, Montgomery, R. A., additional, Desai, N. M., additional, Segev, D. L., additional, Fontana, F., additional, Ballestri, M., additional, and Magistroni, R., additional

Published
2014
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29. C5 Complement Protein Inhibition as Salvage Therapy for Severe Antibody-Mediated Rejection Following HLA-Incompatible Renal Transplantation

Author

Orandi, B. J., primary, Garonzik-Wang, J. M., additional, Gupta, N., additional, Van Arendonk, K. J., additional, Lonze, B. E., additional, Zachary, A., additional, Alachkar, N., additional, Kraus, E. S., additional, Locke, J. E., additional, Nazarian, S. M., additional, Dagher, N. N., additional, Desai, N. M., additional, Segev, D. L., additional, and Montgomery, R. A., additional

Published
2012
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30. Outcomes of 262 Consecutive HLA-incompatible Renal Transplants

Author

Lonze, B. E., primary, Zachary, A., additional, Alachkar, N., additional, Kraus, E. S., additional, Locke, J. E., additional, Nazarian, S. M., additional, Orandi, B. J., additional, Garonzik-Wang, J. M., additional, Warren, D. S., additional, Dagher, N. N., additional, Singer, A. L., additional, Desai, N. M., additional, Segev, D. L., additional, and Montgomery, R. A., additional

Published
2012
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33. A Risk Index for Living Donor Kidney Transplantation

Author

Massie, A. B., Leanza, J., Fahmy, L. M., Chow, E. K. H., Desai, N. M., Luo, X., King, E. A., Bowring, M. G., and Segev, D. L.

Abstract

Choosing between multiple living kidney donors, or evaluating offers in kidney paired donation, can be challenging because no metric currently exists for living donor quality. Furthermore, some deceased donor (DD) kidneys can result in better outcomes than some living donor kidneys, yet there is no way to compare them on the same scale. To better inform clinical decision‐making, we created a living kidney donor profile index (LKDPI) on the same scale as the DD KDPI, using Cox regression and adjusting for recipient characteristics. Donor age over 50 (hazard ratio [HR] per 10 years = 1.151.241.33), elevated BMI (HR per 10 units = 1.011.091.16), African‐American race (HR = 1.151.251.37), cigarette use (HR = 1.091.161.23), as well as ABO incompatibility (HR = 1.031.271.58), HLA B (HR = 1.031.081.14) mismatches, and DR (HR = 1.041.091.15) mismatches were associated with greater risk of graft loss after living donor transplantation (all p < 0.05). Median (interquartile range) LKDPI score was 13 (1–27); 24.2% of donors had LKDPI < 0 (less risk than any DD kidney), and 4.4% of donors had LKDPI > 50 (more risk than the median DD kidney). The LKDPI is a useful tool for comparing living donor kidneys to each other and to deceased donor kidneys. This study proposes a risk index for living donor kidney transplant recipients, the LKDPI, which quantifies the risk of graft loss on the same scale as the KDPI. See editorial on page 1951from Schold and Kaplan.

Published
2016
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34. Changes in Discard Rate After the Introduction of the Kidney Donor Profile Index (KDPI)

Author

Bae, S., Massie, A. B., Luo, X., Anjum, S., Desai, N. M., and Segev, D. L.

Abstract

Since March 26, 2012, the Kidney Donor Profile Index (KDPI) has been provided with all deceased‐donor kidney offers, with the goal of improving the expanded criteria donor (ECD) indicator. Although an improved risk index may facilitate identification and transplantation of marginal yet viable kidneys, a granular percentile system may reduce provider–patient communication flexibility, paradoxically leading to more discards (“labeling effect”). We studied the discard rates of the kidneys recovered for transplantation between March 26, 2010 and March 25, 2012 (“ECDera,” N = 28 636) and March 26, 2012 and March 25, 2014 (“KDPIera,” N = 29 021) using Scientific Registry of Transplant Recipients (SRTR) data. There was no significant change in discard rate from ECDera (18.1%) to KDPIera (18.3%) among the entire population (adjusted odds ratio [aOR] = 0.971.041.10, p = 0.3), or in any KDPIstratum. However, among kidneys in which ECDand KDPIindicators were discordant, “high risk” standard criteria donor (SCD) kidneys (with KDPI> 85) were at increased risk of discard in the KDPIera (aOR= 1.071.421.89, p = 0.02). Yet, recipients of these kidneys were at much lower risk of death (adjusted Risk Ratio [aRR] = 0.560.770.94at 2 years posttransplant) compared to those remaining on dialysis waiting for low‐KDPIkidneys. Our findings suggest that there might be an unexpected, harmful labeling effect of reporting a high KDPIfor SCDkidneys, without the expected advantage of providing a more granular risk index. Providing the Kidney Donor Profile Index (KDPI) with deceased donor kidney offers is associated with increased discards of standard criteria donor kidneys with KDPI > 85, a subgroup where the old standard/extended criteria donor designation and the new KDPI scoring deliver opposing messages, suggesting the possibility of a labeling effect.

Published
2016
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41. Selectivity Engineering of Phase Transfer Catalyzed Alkylation of 2‘-Hydroxyacetophenone:  Enhancement in Rates and Selectivity by Creation of a Third Liquid Phase

Author

Yadav, G. D. and Desai, N. M.

Abstract

Enhancements in rate of reaction and selectivity of the desired product in biphasic reactions are achieved by creating a third liquid phase, under appropriate conditions, where the third liquid phase is the locale of the main reaction, having a dramatic effect on product distribution in complex chemical reactions. Thus, in the case of phase transfer catalysis (PTC), conversion of liquid−liquid (L−L) PTC into liquid−liquid−liquid (L−L−L) PTC is of considerable techno-commercial interest resulting in waste minimization which is a major theme of green chemistry. Etherification of 2‘-hydroxyacetophenone with 1-bromopentane, under traditional liquid−liquid phase transfer catalysis, results in loss of catalyst. However, the transformation of two liquid phases into three liquid phases (L−L−L) PTC leads enhancement in rates by orders of magnitude, with 100% conversion of the limiting reactant 1-bromopentane and 100% selectivity to 2‘-pentyloxyacetophenone. This strategy eliminates separation problems and results in high reaction rates reducing the total reaction time. Moreover, the catalyst-rich third phase is recycled more than 7 times without loss in activity. The kinetics of the reaction are studied in great detail. There is a substantial reduction in activation energy under L−L−L PTC vis-à-vis L−L PTC, where the locale of the reaction is shifted from the organic phase to the third phase.

Published
2005

43. Cloning and sequence of rat myoadenylate deaminase cDNA. Evidence for tissue-specific and developmental regulation.

Author

Sabina, R L, Marquetant, R, Desai, N M, Kaletha, K, and Holmes, E W

Abstract

Myoadenylate deaminase is the muscle-specific isoform of AMP deaminase (EC 3.5.4.6), an enzyme which plays a special role in energy metabolism in skeletal muscle. A 2.3-kilobase cDNA encoding this enzyme has been cloned from a lambda gt10 library prepared from rat skeletal muscle using oligonucleotide probes designed from AMP deaminase peptide sequences. This cDNA was sequenced, and the amino acid sequence of this isoform of AMP deaminase was deduced. Sequences homologous to this cDNA are identified in the genome of eukaryotes as diverse as yeast and man. Tissue-specific expression of a 2.5-kilobase AMP deaminase transcript is demonstrated, and the abundance of this transcript as well as the 80-kDa adult, muscle-specific peptide of AMP deaminase increase in parallel during postnatal skeletal muscle development. In the adult animal, the abundance of this transcript and AMP deaminase activity are differentially expressed in various skeletal muscle fiber types. We conclude that AMP deaminase sequences have been highly conserved during evolution, and in mammals there is developmental and tissue-specific control of expression of this gene.

Published
1987
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44. Evidence for sequential expression of multiple AMP deaminase isoforms during skeletal muscle development.

Author

Marquetant, R, Desai, N M, Sabina, R L, and Holmes, E W

Abstract

AMP deaminase (myoadenylate deaminase; EC 3.5.4.6) is an integral part of the myofibril in skeletal muscle, and this enzyme plays an important role in energy metabolism in this tissue. We report here the identification of three AMP deaminase isoforms during skeletal muscle development in the rat. An embryonic isoform is expressed in the developing hindlimb of the rat between 7 and 14 days of gestation. This isoform is not unique to skeletal muscle or the embryo as it is also expressed in many nonmuscle tissues of the perinatal and adult rat. A perinatal isoform of AMP deaminase that is restricted to skeletal muscle is produced 4-6 days before birth and persists for 2-3 weeks of postnatal life. An adult, skeletal muscle-specific isoform of AMP deaminase appears at birth and reaches maximal levels after 3 weeks of postnatal development. We conclude from these studies there is a developmentally controlled program that leads to the sequential expression of AMP deaminase isoforms during the transition from embryonic to adult skeletal muscle.

Published
1987
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49. Recurrent IgA Nephropathy After Kidney Transplantation.

Author

Nijim S, Vujjini V, Alasfar S, Luo X, Orandi B, Delp C, Desai NM, Montgomery RA, Lonze BE, and Alachkar N

Subjects
Adult, Female, Glomerulonephritis, IGA complications, Graft Survival, Humans, Male, Middle Aged, Recurrence, Retrospective Studies, Risk Factors, Glomerulonephritis, IGA pathology, Glomerulonephritis, IGA surgery, Kidney Transplantation
Abstract

Background: Immunoglobulin (Ig)A nephropathy is the most common primary glomerulonephritis worldwide, with a high recurrence rate after kidney transplantation. The aim of this study was to assess allograft survival, impact of recurrence on allograft function, and risk factors for post-transplant IgA recurrence., Methods: We identified 104 patients with IgA nephropathy who underwent kidney transplantation at our center between 1993 and 2014. Fourteen patients underwent more than one allograft., Results: IgA recurrence was documented in 23 (19%) allografts. Median time to recurrence was 6.75 years (interquartile range, 1.4-9.2 years). Twelve of the 23 recurrences were from living related donors (P = .07), and those with younger age at transplantation (37.7 ± 2.3 vs 44 ± 1.3, P = .05) were at higher risk of recurrence. Mean allograft survival was reduced in those with recurrence (6.5 ± 5.1 years) compared with those without recurrence (10.4 ± 7.5 years). At 6 years after transplant, allograft failure was documented in 52% of the recurrence group compared with 10% in the non-recurrence group (P = .002)., Conclusions: IgA recurrence after transplant is an important cause of allograft loss. Living related donors and younger age at transplantation are associated with high recurrence rate. Close monitoring and treatment of recurrence are crucial., (Copyright © 2016 Elsevier Inc. All rights reserved.)

Published
2016
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50. Novel mechanism of increased Ca2+ release following oxidative stress in neuronal cells involves type 2 inositol-1,4,5-trisphosphate receptors.

Author

Kaja S, Duncan RS, Longoria S, Hilgenberg JD, Payne AJ, Desai NM, Parikh RA, Burroughs SL, Gregg EV, Goad DL, and Koulen P

Subjects
Animals, Calcium physiology, Calcium Signaling drug effects, Cell Line, Inositol 1,4,5-Trisphosphate Receptors biosynthesis, Inositol 1,4,5-Trisphosphate Receptors genetics, Intracellular Fluid drug effects, Intracellular Fluid metabolism, Intracellular Space drug effects, Intracellular Space physiology, Mice, Models, Neurological, Nerve Degeneration etiology, Nerve Degeneration physiopathology, Neurons drug effects, Oxidative Stress drug effects, Up-Regulation drug effects, tert-Butylhydroperoxide toxicity, Calcium metabolism, Calcium Signaling physiology, Inositol 1,4,5-Trisphosphate Receptors physiology, Nerve Degeneration metabolism, Neurons metabolism, Oxidative Stress physiology, Up-Regulation physiology
Abstract

Dysregulation of Ca(2+) signaling following oxidative stress is an important pathophysiological mechanism of many chronic neurodegenerative disorders, including Alzheimer's disease, age-related macular degeneration, glaucomatous and diabetic retinopathies. However, the underlying mechanisms of disturbed intracellular Ca(2+) signaling remain largely unknown. We here describe a novel mechanism for increased intracellular Ca(2+) release following oxidative stress in a neuronal cell line. Using an experimental approach that included quantitative polymerase chain reaction, quantitative immunoblotting, microfluorimetry and the optical imaging of intracellular Ca(2+) release, we show that sub-lethal tert-butyl hydroperoxide-mediated oxidative stress result in a selective up-regulation of type-2 inositol-1,4,5,-trisphophate receptors. This oxidative stress mediated change was detected both at the transcriptional and translational level and functionally resulted in increased Ca(2+) release into the nucleoplasm from the membranes of the nuclear envelope at a given receptor-specific stimulus. Our data describe a novel source of Ca(2+) dysregulation induced by oxidative stress with potential relevance for differential subcellular Ca(2+) signaling specifically within the nucleus and the development of novel neuroprotective strategies in neurodegenerative disorders., (Copyright © 2011 IBRO. Published by Elsevier Ltd. All rights reserved.)

Published
2011
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