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31 results on '"Sansanwal P"'

1. Targeting Pancreatic Cancer Cell Stemness by Blocking Fibronectin-Binding Integrins on Cancer-Associated Fibroblasts

Author

Wu, Chengsheng, Von Schalscha, Tami, Sansanwal, Diva, Qian, Chen, Jiang, Qinlin, Shepard, Ryan M, Wettersten, Hiromi I, McCormack, Stephen J, Weis, Sara M, and Cheresh, David A

Subjects
Biochemistry and Cell Biology, Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Biological Sciences, Rare Diseases, Digestive Diseases, Cancer, Pancreatic Cancer, Prevention, Humans, Pancreatic Neoplasms, Cancer-Associated Fibroblasts, Fibronectins, Neoplastic Stem Cells, Cell Line, Tumor, Integrins, Animals
Abstract

SignificanceSimultaneous targeting of two integrins that function as receptors for FN, a protumor ECM protein, can prevent fibroblasts from supporting the malignant behavior of pancreatic cancer cells.

Published
2025

4. Fibronectin-Binding Integrins Alpha-5 Beta-1 and Alpha-v Beta-3 on Cancer-Associated Fibroblasts Block Fibronectin Collagen Matrix Assembly, Tumor Initiation and Tissue Stiffness

Author

Sansanwal, Diva

Subjects
Bioengineering
Abstract

Pancreatic cancer is characterized by a dense fibrotic stroma, consisting of cancer-associated fibroblasts (CAFs), immune cells, and extracellular matrix (ECM) that promote tumor growth and treatment resistance. CAFs secrete and organize on their surface ECM proteins, including fibronectin (FN) which coordinates the assembly of collagen fibrils that promote matrix stiffness. Since CAFs are a major contributor to fibrosis and the progression of pancreatic cancer, novel approaches to target their function could have a significant impact on patient outcome. This research demonstrates that the ability of pancreatic cancer cells to initiate tumors in mice is greatly enhanced by co-injection of CAFs. Targeting FN via FN-binding integrins α5β1 and αvβ3 that are highly expressed on CAFs disrupts CAF-induced fibrosis, decreases tumor stiffness, and prevents the initiation of pancreas tumors in mice. These results highlight the therapeutic potential of targeting fibronectin-binding integrins, α5β1 and αvβ3, on CAFs to disrupt the fibrotic stroma in pancreatic cancer.

Published
2024

5. Comparing the reliability of physical activity questionnaires in community-dwelling adults with stroke.

Author

Noguchi, Kenneth S., Sansanwal, Sohnia, Mehdipour, Ava, and Tang, Ada

Subjects
REPEATED measures design, INDEPENDENT living, CRONBACH'S alpha, SECONDARY analysis, RESEARCH methodology evaluation, QUESTIONNAIRES, RESEARCH evaluation, DESCRIPTIVE statistics, STATISTICAL reliability, MEASUREMENT errors, RESEARCH methodology, ANALYSIS of variance, INTRACLASS correlation, STROKE patients, SOCIODEMOGRAPHIC factors, CONFIDENCE intervals, PHYSICAL activity, EVALUATION
Abstract

Background: Physical activity (PA) is important for people with stroke, but the reliability of PA questionnaires used in this population has been relatively unexplored. Objective: To compare the internal consistency, test-retest, and absolute reliability of 3 commonly used PA questionnaires in adults with stroke. Methods: Participants reported their PA levels twice, 2–3 days apart, using the Physical Activity Scale for Individuals with Physical Disabilities (PASIPD), International Physical Activity Questionnaire (IPAQ), and Global Physical Activity Questionnaire (GPAQ). Intraclass correlation coefficients (ICC2,1) were calculated for test-retest reliability, Cronbach's alpha (α) for internal consistency, and standard error of measurement (SEM) and minimal detectable change (MDC95) for absolute reliability. Results: Twenty-eight people (64.4 years, 50% female, 5.2 years post-stroke) participated. Internal consistency was acceptable for total scores on the IPAQ ($\alpha $ α = 0.79) and GPAQ ($\alpha $ α = 0.74), but only domain-level scores for the GPAQ ($\alpha $ α = 0.71–0.88). In the full sample, test-retest reliability was good for the PASIPD (ICC2,1 = 0.83) but poor for the IPAQ and GPAQ (ICC2,1 <0.50). After excluding participants self-reporting true changes in PA, all questionnaires had good test-retest reliability (ICC2,1 = 0.77–0.88). SEM and MDC95 were lowest for the PASIPD (188.8 and 523.3 MET-minutes/week, respectively). Conclusions: In adults with stroke, the IPAQ and GPAQ had adequate total-questionnaire internal consistency, and the GPAQ had acceptable domain-level internal consistency. When true change in PA did not occur, test-retest reliability was good for all questionnaires. We suggest clinicians and rehabilitation scientists can use any of the three questionnaires, but may consider the GPAQ due to acceptable internal consistency and test-retest reliability. [ABSTRACT FROM AUTHOR]

Published
2025
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6. Taxonomy of Digital Forensics: Investigation Tools and Challenges

Author

Rana, Nikita, Sansanwal, Gunjan, Khatter, Kiran, and Singh, Sukhdev

Subjects
Computer Science - Computers and Society, Computer Science - Cryptography and Security
Abstract

In today's world of computers, any kind of information can be made available within few clicks for different endeavors. The information may be tampered by changing the statistical properties and can be further used for criminal activities. These days, Cyber crimes are happening at a very large scale, and possess big threats to the security of an individual, firm, industry and even to developed countries. To combat such crimes, law enforcement agencies and investment institutions are incorporating supportive examination policies, procedures and protocols to address the complete investigation process. The paper entails a detailed review of several cyber crimes followed by various digital forensics processes involved in the cyber crime investigation. Further various digital forensics tools with detail explanation are discussed with their advantages, disadvantages, challenges, and drawbacks. A comparison among all the selected tools is also presented. Finally the paper recommends the need of training programs for the first res ponder and judgement of signature based image authentication., Comment: 19 pages and 1 table

Published
2017

7. A Peripheral Blood Diagnostic Test for Acute Rejection in Renal Transplantation

Author

Li, L, Khatri, P, Sigdel, TK, Tran, T, Ying, L, Vitalone, MJ, Chen, A, Hsieh, S, Dai, H, Zhang, M, Naesens, M, Zarkhin, V, Sansanwal, P, Chen, R, Mindrinos, M, Xiao, W, Benfield, M, Ettenger, RB, Dharnidharka, V, Mathias, R, Portale, A, McDonald, R, Harmon, W, Kershaw, D, Vehaskari, VM, Kamil, E, Baluarte, HJ, Warady, B, Davis, R, Butte, AJ, Salvatierra, O, and Sarwal, MM

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, Biotechnology, Rare Diseases, Organ Transplantation, Clinical Research, Genetics, Kidney Disease, Transplantation, Pediatric, 4.2 Evaluation of markers and technologies, Detection, screening and diagnosis, 4.1 Discovery and preclinical testing of markers and technologies, Renal and urogenital, Acute Disease, Graft Rejection, Humans, Kidney Transplantation, Polymerase Chain Reaction, Sensitivity and Specificity, Acute allograft rejection, biomarker, bioinformatics, renal allograft rejection, renal transplantation, transplantation, transplantation genomics, transplant rejection, translational research, Medical and Health Sciences, Surgery, Clinical sciences, Immunology
Abstract

Monitoring of renal graft status through peripheral blood (PB) rather than invasive biopsy is important as it will lessen the risk of infection and other stresses, while reducing the costs of rejection diagnosis. Blood gene biomarker panels were discovered by microarrays at a single center and subsequently validated and cross-validated by QPCR in the NIH SNSO1 randomized study from 12 US pediatric transplant programs. A total of 367 unique human PB samples, each paired with a graft biopsy for centralized, blinded phenotype classification, were analyzed (115 acute rejection (AR), 180 stable and 72 other causes of graft injury). Of the differentially expressed genes by microarray, Q-PCR analysis of a five gene-set (DUSP1, PBEF1, PSEN1, MAPK9 and NKTR) classified AR with high accuracy. A logistic regression model was built on independent training-set (n = 47) and validated on independent test-set (n = 198)samples, discriminating AR from STA with 91% sensitivity and 94% specificity and AR from all other non-AR phenotypes with 91% sensitivity and 90% specificity. The 5-gene set can diagnose AR potentially avoiding the need for invasive renal biopsy. These data support the conduct of a prospective study to validate the clinical predictive utility of this diagnostic tool.

Published
2012

12. An Improved Approach for Load Balancing among Virtual Machines in Cloud Environment.

Author

Sansanwal, Suman and Jain, Nitin

Subjects
VIRTUAL machine systems, GENETIC algorithms, INFORMATION technology, INTERNET access, CLOUD computing, MATHEMATICAL optimization, LOAD balancing (Computer networks)
Abstract

Cloud computing has shown noteworthy evolution in information technology. Users can enjoy various services of cloud technology only if internet connection is available. In cloud computing, load balancing considered as a fundamental issue that has confronted researchers in this domain. Load balancing basically works by allotting fair and efficient work among computing resources which ultimately achieve high user satisfaction and raises systems productivity. Many load-balancing techniques made efforts to resolve this problem using metaheuristics algorithm, and amplify the operation and efficiency of systems. In this paper, existing load balancing techniques has been discussed and research gaps in existing lirture hasbeeb discussed. Also a new technique has been proposed called IG-GWO - Inquisitive Genetic Grey Wolf Optimization algorithm using combination of Grey wolf optimization (GWO) algorithm and Genetic algorithm. [ABSTRACT FROM AUTHOR]

Published
2022
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13. Protective efficacy of inactivated reverse genetics based equine influenza vaccine candidate adjuvanted with MontanideTM Pet Gel in murine model.

Author

MATHEW, Manu Kurian, VIRMANI, Nitin, BERA, Bidhan Chandra, ANAND, Taruna, KUMAR, Ramesh, BALENA, Venkataramireddy, SANSANWAL, Rekha, PAVULRAJ, Selvaraj, SUNDARAM, Karthik, VIRMANI, Meenakshi, and TRIPATHI, Bhupendra Nath

Subjects
EQUINE influenza, REVERSE genetics, INFLUENZA vaccines, BASE pairs, WEIGHT loss, INFLUENZA A virus, H1N1 subtype
Abstract

Equine influenza is a leading cause for respiratory illness in equines. Major control measures involve vaccination which requires continuous harmonization owing to antigenic drift. The present study focused on assessing the protective efficacy of an inactivated recombinant equine influenza virus (rgEIV) vaccine candidate adjuvanted with MontanideTM Pet Gel in murine model. The rgEIV was generated using reverse genetics by incorporating HA and NA segments from EIV/H3N8, clade 2-Florida sublineage in an A/WSN/33 /H1N1 backbone and inactivated by formalin. The vaccine was prepared by mixing inactivated rgEIV with MontanideTM Pet Gel adjuvant followed by intranasal inoculation into BALB/c mice intranasally. The immune responses and protective efficacy of the vaccine was evaluated by measurement of antibody titer, immunoglobulin subtyping, cytokines, clinical signs and pathological lesions after immunization and challenge with wild EIV. Serology and cytokine expression pattern indicated that the vaccine activated mixed Th1- and Th2-like responses of vaccine. Booster immunization stimulated strong antibody responses (HAI titre: 192 ± 28.6) at 42 days post immunization and the predominant antibody subtype was IgG1. Upregulation of interferon (IFN)-gamma, interleukin (IL)-12 and IL-2 levels indicates effective induction of Th1 type response. We found that vaccination has protected mice against equine influenza virus challenge as adjudged through a lack of nonappearance of visible clinical signs of disease, no loss of body weight loss, reduced pathology in the lungs and markedly reduced virus shedding from the respiratory tract. Therefore, we conclude that recombinant EIV vaccine candidate adjuvanted with Montanide™ Pet Gel could aid in quick harmonization of the vaccines through replacement of HA and NA genes for control of EIV outbreaks. [ABSTRACT FROM AUTHOR]

Published
2019
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14. Guidelines for the use and interpretation of assays for monitoring autophagy

Author

Klionsky, D.J. Abdalla, F.C. Abeliovich, H. Abraham, R.T. Acevedo-Arozena, A. Adeli, K. Agholme, L. Agnello, M. Agostinis, P. Aguirre-Ghiso, J.A. Ahn, H.J. Ait-Mohamed, O. Ait-Si-Ali, S. Akematsu, T. Akira, S. Al-Younes, H.M. Al-Zeer, M.A. Albert, M.L. Albin, R.L. Alegre-Abarrategui, J. Aleo, M.F. Alirezaei, M. Almasan, A. Almonte-Becerril, M. Amano, A. Amaravadi, R. Amarnath, S. Amer, A.O. Andrieu-Abadie, N. Anantharam, V. Ann, D.K. Anoopkumar-Dukie, S. Aoki, H. Apostolova, N. Arancia, G. Aris, J.P. Asanuma, K. Asare, N.Y.O. Ashida, H. Askanas, V. Askew, D.S. Auberger, P. Baba, M. Backues, S.K. Baehrecke, E.H. Bahr, B.A. Bai, X.-Y. Bailly, Y. Baiocchi, R. Baldini, G. Balduini, W. Ballabio, A. Bamber, B.A. Bampton, E.T.W. Bánhegyi, G. Bartholomew, C.R. Bassham, D.C. Bast Jr., R.C. Batoko, H. Bay, B.-H. Beau, I. Béchet, D.M. Begley, T.J. Behl, C. Behrends, C. Bekri, S. Bellaire, B. Bendall, L.J. Benetti, L. Berliocchi, L. Bernardi, H. Bernassola, F. Besteiro, S. Bhatia-Kissova, I. Bi, X. Biard-Piechaczyk, M. Blum, J.S. Boise, L.H. Bonaldo, P. Boone, D.L. Bornhauser, B.C. Bortoluci, K.R. Bossis, I. Bost, F. Bourquin, J.-P. Boya, P. Boyer-Guittaut, M. Bozhkov, P.V. Brady, N.R. Brancolini, C. Brech, A. Brenman, J.E. Brennand, A. Bresnick, E.H. Brest, P. Bridges, D. Bristol, M.L. Brookes, P.S. Brown, E.J. Brumell, J.H. Brunetti-Pierri, N. Brunk, U.T. Bulman, D.E. Bultman, S.J. Bultynck, G. Burbulla, L.F. Bursch, W. Butchar, J.P. Buzgariu, W. Bydlowski, S.P. Cadwell, K. Cahová, M. Cai, D. Cai, J. Cai, Q. Calabretta, B. Calvo-Garrido, J. Camougrand, N. Campanella, M. Campos-Salinas, J. Candi, E. Cao, L. Caplan, A.B. Carding, S.R. Cardoso, S.M. Carew, J.S. Carlin, C.R. Carmignac, V. Carneiro, L.A.M. Carra, S. Caruso, R.A. Casari, G. Casas, C. Castino, R. Cebollero, E. Cecconi, F. Celli, J. Chaachouay, H. Chae, H.-J. Chai, C.-Y. Chan, D.C. Chan, E.Y. Chang, R.C.-C. Che, C.-M. Chen, C.-C. Chen, G.-C. Chen, G.-Q. Chen, M. Chen, Q. Chen, S.S.-L. Chen, W. Chen, X. Chen, X. Chen, X. Chen, Y.-G. Chen, Y. Chen, Y. Chen, Y.-J. Chen, Z. Cheng, A. Cheng, C.H.K. Cheng, Y. Cheong, H. Cheong, J.-H. Cherry, S. Chess-Williams, R. Cheung, Z.H. Chevet, E. Chiang, H.-L. Chiarelli, R. Chiba, T. Chin, L.-S. Chiou, S.-H. Chisari, F.V. Cho, C.H. Cho, D.-H. Choi, A.M.K. Choi, D. Choi, K.S. Choi, M.E. Chouaib, S. Choubey, D. Choubey, V. Chu, C.T. Chuang, T.-H. Chueh, S.-H. Chun, T. Chwae, Y.-J. Chye, M.-L. Ciarcia, R. Ciriolo, M.R. Clague, M.J. Clark, R.S.B. Clarke, P.G.H. Clarke, R. Codogno, P. Coller, H.A. Colombo, M.I. Comincini, S. Condello, M. Condorelli, F. Cookson, M.R. Coombs, G.H. Coppens, I. Corbalan, R. Cossart, P. Costelli, P. Costes, S. Coto-Montes, A. Couve, E. Coxon, F.P. Cregg, J.M. Crespo, J.L. Cronjé, M.J. Cuervo, A.M. Cullen, J.J. Czaja, M.J. D'Amelio, M. Darfeuille-Michaud, A. Davids, L.M. Davies, F.E. De Felici, M. De Groot, J.F. De Haan, C.A.M. De Martino, L. De Milito, A. De Tata, V. Debnath, J. Degterev, A. Dehay, B. Delbridge, L.M.D. Demarchi, F. Deng, Y.Z. Dengjel, J. Dent, P. Denton, D. Deretic, V. Desai, S.D. Devenish, R.J. Di Gioacchino, M. Di Paolo, G. Di Pietro, C. Díaz-Araya, G. Díaz-Laviada, I. Diaz-Meco, M.T. Diaz-Nido, J. Dikic, I. Dinesh-Kumar, S.P. Ding, W.-X. Distelhorst, C.W. Diwan, A. Djavaheri-Mergny, M. Dokudovskaya, S. Dong, Z. Dorsey, F.C. Dosenko, V. Dowling, J.J. Doxsey, S. Dreux, M. Drew, M.E. Duan, Q. Duchosal, M.A. Duff, K. Dugail, I. Durbeej, M. Duszenko, M. Edelstein, C.L. Edinger, A.L. Egea, G. Eichinger, L. Eissa, N.T. Ekmekcioglu, S. El-Deiry, W.S. Elazar, Z. Elgendy, M. Ellerby, L.M. Er Eng, K. Engelbrecht, A.-M. Engelender, S. Erenpreisa, J. Escalante, R. Esclatine, A. Eskelinen, E.-L. Espert, L. Espina, V. Fan, H. Fan, J. Fan, Q.-W. Fan, Z. Fang, S. Fang, Y. Fanto, M. Fanzani, A. Farkas, T. Farré, J.-C. Faure, M. Fechheimer, M. Feng, C.G. Feng, J. Feng, Q. Feng, Y. Fésüs, L. Feuer, R. Figueiredo-Pereira, M.E. Fimia, G.M. Fingar, D.C. Finkbeiner, S. Finkel, T. Finley, K.D. Fiorito, F. Fisher, E.A. Fisher, P.B. Flajolet, M. Florez-McClure, M.L. Florio, S. Fon, E.A. Fornai, F. Fortunato, F. Fotedar, R. Fowler, D.H. Fox, H.S. Franco, R. Frankel, L.B. Fransen, M. Fuentes, J.M. Fueyo, J. Fujii, J. Fujisaki, K. Fujita, E. Fukuda, M. Furukawa, R.H. Gaestel, M. Gailly, P. Gajewska, M. Galliot, B. Galy, V. Ganesh, S. Ganetzky, B. Ganley, I.G. Gao, F.-B. Gao, G.F. Gao, J. Garcia, L. Garcia-Manero, G. Garcia-Marcos, M. Garmyn, M. Gartel, A.L. Gatti, E. Gautel, M. Gawriluk, T.R. Gegg, M.E. Geng, J. Germain, M. Gestwicki, J.E. Gewirtz, D.A. Ghavami, S. Ghosh, P. Giammarioli, A.M. Giatromanolaki, A.N. Gibson, S.B. Gilkerson, R.W. Ginger, M.L. Ginsberg, H.N. Golab, J. Goligorsky, M.S. Golstein, P. Gomez-Manzano, C. Goncu, E. Gongora, C. Gonzalez, C.D. Gonzalez, R. González-Estévez, C. González-Polo, R.A. Gonzalez-Rey, E. Gorbunov, N.V. Gorski, S. Goruppi, S. Gottlieb, R.A. Gozuacik, D. Granato, G.E. Grant, G.D. Green, K.N. Gregorc, A. Gros, F. Grose, C. Grunt, T.W. Gual, P. Guan, J.-L. Guan, K.-L. Guichard, S.M. Gukovskaya, A.S. Gukovsky, I. Gunst, J. Gustafsson, A.B. Halayko, A.J. Hale, A.N. Halonen, S.K. Hamasaki, M. Han, F. Han, T. Hancock, M.K. Hansen, M. Harada, H. Harada, M. Hardt, S.E. Harper, J.W. Harris, A.L. Harris, J. Harris, S.D. Hashimoto, M. Haspel, J.A. Hayashi, S.-I. Hazelhurst, L.A. He, C. He, Y.-W. Hébert, M.-J. Heidenreich, K.A. Helfrich, M.H. Helgason, G.V. Henske, E.P. Herman, B. Herman, P.K. Hetz, C. Hilfiker, S. Hill, J.A. Hocking, L.J. Hofman, P. Hofmann, T.G. Höhfeld, J. Holyoake, T.L. Hong, M.-H. Hood, D.A. Hotamisligil, G.S. Houwerzijl, E.J. Høyer-Hansen, M. Hu, B. Hu, C.-A.A. Hu, H.-M. Hua, Y. Huang, C. Huang, J. Huang, S. Huang, W.-P. Huber, T.B. Huh, W.-K. Hung, T.-H. Hupp, T.R. Hur, G.M. Hurley, J.B. Hussain, S.N.A. Hussey, P.J. Hwang, J.J. Hwang, S. Ichihara, A. Ilkhanizadeh, S. Inoki, K. Into, T. Iovane, V. Iovanna, J.L. Ip, N.Y. Isaka, Y. Ishida, H. Isidoro, C. Isobe, K.-I. Iwasaki, A. Izquierdo, M. Izumi, Y. Jaakkola, P.M. Jäättelä, M. Jackson, G.R. Jackson, W.T. Janji, B. Jendrach, M. Jeon, J.-H. Jeung, E.-B. Jiang, H. Jiang, H. Jiang, J.X. Jiang, M. Jiang, Q. Jiang, X. Jiménez, A. Jin, M. Jin, S. Joe, C.O. Johansen, T. Johnson, D.E. Johnson, G.V.W. Jones, N.L. Joseph, B. Joseph, S.K. Joubert, A.M. Juhász, G. Juillerat-Jeanneret, L. Jung, C.H. Jung, Y.-K. Kaarniranta, K. Kaasik, A. Kabuta, T. Kadowaki, M. Kagedal, K. Kamada, Y. Kaminskyy, V.O. Kampinga, H.H. Kanamori, H. Kang, C. Kang, K.B. Il Kang, K. Kang, R. Kang, Y.-A. Kanki, T. Kanneganti, T.-D. Kanno, H. Kanthasamy, A.G. Kanthasamy, A. Karantza, V. Kaushal, G.P. Kaushik, S. Kawazoe, Y. Ke, P.-Y. Kehrl, J.H. Kelekar, A. Kerkhoff, C. Kessel, D.H. Khalil, H. Kiel, J.A.K.W. Kiger, A.A. Kihara, A. Kim, D.R. Kim, D.-H. Kim, D.-H. Kim, E.-K. Kim, H.-R. Kim, J.-S. Kim, J.H. Kim, J.C. Kim, J.K. Kim, P.K. Kim, S.W. Kim, Y.-S. Kim, Y. Kimchi, A. Kimmelman, A.C. King, J.S. Kinsella, T.J. Kirkin, V. Kirshenbaum, L.A. Kitamoto, K. Kitazato, K. Klein, L. Klimecki, W.T. Klucken, J. Knecht, E. Ko, B.C.B. Koch, J.C. Koga, H. Koh, J.-Y. Koh, Y.H. Koike, M. Komatsu, M. Kominami, E. Kong, H.J. Kong, W.-J. Korolchuk, V.I. Kotake, Y. Koukourakis, M.I. Kouri Flores, J.B. Kovács, A.L. Kraft, C. Krainc, D. Krämer, H. Kretz-Remy, C. Krichevsky, A.M. Kroemer, G. Krüger, R. Krut, O. Ktistakis, N.T. Kuan, C.-Y. Kucharczyk, R. Kumar, A. Kumar, R. Kumar, S. Kundu, M. Kung, H.-J. Kurz, T. Kwon, H.J. La Spada, A.R. Lafont, F. Lamark, T. Landry, J. Lane, J.D. Lapaquette, P. Laporte, J.F. László, L. Lavandero, S. Lavoie, J.N. Layfield, R. Lazo, P.A. Le, W. Le Cam, L. Ledbetter, D.J. Lee, A.J.X. Lee, B.-W. Lee, G.M. Lee, J. Lee, J.-H. Lee, M. Lee, M.-S. Lee, S.H. Leeuwenburgh, C. Legembre, P. Legouis, R. Lehmann, M. Lei, H.-Y. Lei, Q.-Y. Leib, D.A. Leiro, J. Lemasters, J.J. Lemoine, A. Lesniak, M.S. Lev, D. Levenson, V.V. Levine, B. Levy, E. Li, F. Li, J.-L. Li, L. Li, S. Li, W. Li, X.-J. Li, Y.-B. Li, Y.-P. Liang, C. Liang, Q. Liao, Y.-F. Liberski, P.P. Lieberman, A. Lim, H.J. Lim, K.-L. Lim, K. Lin, C.-F. Lin, F.-C. Lin, J. Lin, J.D. Lin, K. Lin, W.-W. Lin, W.-C. Lin, Y.-L. Linden, R. Lingor, P. Lippincott-Schwartz, J. Lisanti, M.P. Liton, P.B. Liu, B. Liu, C.-F. Liu, K. Liu, L. Liu, Q.A. Liu, W. Liu, Y.-C. Liu, Y. Lockshin, R.A. Lok, C.-N. Lonial, S. Loos, B. Lopez-Berestein, G. López-Otín, C. Lossi, L. Lotze, M.T. Lõw, P. Lu, B. Lu, B. Lu, B. Lu, Z. Luciano, F. Lukacs, N.W. Lund, A.H. Lynch-Day, M.A. Ma, Y. Macian, F. MacKeigan, J.P. Macleod, K.F. Madeo, F. Maiuri, L. Maiuri, M.C. Malagoli, D. Malicdan, M.C.V. Malorni, W. Man, N. Mandelkow, E.-M. Manon, S. Manov, I. Mao, K. Mao, X. Mao, Z. Marambaud, P. Marazziti, D. Marcel, Y.L. Marchbank, K. Marchetti, P. Marciniak, S.J. Marcondes, M. Mardi, M. Marfe, G. Mariño, G. Markaki, M. Marten, M.R. Martin, S.J. Martinand-Mari, C. Martinet, W. Martinez-Vicente, M. Masini, M. Matarrese, P. Matsuo, S. Matteoni, R. Mayer, A. Mazure, N.M. McConkey, D.J. McConnell, M.J. McDermott, C. McDonald, C. McInerney, G.M. McKenna, S.L. McLaughlin, B. McLean, P.J. McMaster, C.R. McQuibban, G.A. Meijer, A.J. Meisler, M.H. Meléndez, A. Melia, T.J. Melino, G. Mena, M.A. Menendez, J.A. Menna-Barreto, R.F.S. Menon, M.B. Menzies, F.M. Mercer, C.A. Merighi, A. Merry, D.E. Meschini, S. Meyer, C.G. Meyer, T.F. Miao, C.-Y. Miao, J.-Y. Michels, P.A.M. Michiels, C. Mijaljica, D. Milojkovic, A. Minucci, S. Miracco, C. Miranti, C.K. Mitroulis, I. Miyazawa, K. Mizushima, N. Mograbi, B. Mohseni, S. Molero, X. Mollereau, B. Mollinedo, F. Momoi, T. Monastyrska, I. Monick, M.M. Monteiro, M.J. Moore, M.N. Mora, R. Moreau, K. Moreira, P.I. Moriyasu, Y. Moscat, J. Mostowy, S. Mottram, J.C. Motyl, T. Moussa, C.E.-H. Müller, S. Muller, S. Münger, K. Münz, C. Murphy, L.O. Murphy, M.E. Musarò, A. Mysorekar, I. Nagata, E. Nagata, K. Nahimana, A. Nair, U. Nakagawa, T. Nakahira, K. Nakano, H. Nakatogawa, H. Nanjundan, M. Naqvi, N.I. Narendra, D.P. Narita, M. Navarro, M. Nawrocki, S.T. 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Abstract

In 2008 we published the first set of guidelines for standardizing research in autophagy. Since then, research on this topic has continued to accelerate, and many new scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Accordingly, it is important to update these guidelines for monitoring autophagy in different organisms. Various reviews have described the range of assays that have been used for this purpose. Nevertheless, there continues to be confusion regarding acceptable methods to measure autophagy, especially in multicellular eukaryotes. A key point that needs to be emphasized is that there is a difference between measurements that monitor the numbers or volume of autophagic elements (e.g., autophagosomes or autolysosomes) at any stage of the autophagic process vs. those that measure flux through the autophagy pathway (i.e., the complete process); thus, a block in macroautophagy that results in autophagosome accumulation needs to be differentiated from stimuli that result in increased autophagic activity, defined as increased autophagy induction coupled with increased delivery to, and degradation within, lysosomes (in most higher eukaryotes and some protists such as Dictyostelium) or the vacuole (in plants and fungi). In other words, it is especially important that investigators new to the field understand that the appearance of more autophagosomes does not necessarily equate with more autophagy. In fact, in many cases, autophagosomes accumulate because of a block in trafficking to lysosomes without a concomitant change in autophagosome biogenesis, whereas an increase in autolysosomes may reflect a reduction in degradative activity. Here, we present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macroautophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes. These guidelines are not meant to be a formulaic set of rules, because the appropriate assays depend in part on the question being asked and the system being used. In addition, we emphasize that no individual assay is guaranteed to be the most appropriate one in every situation, and we strongly recommend the use of multiple assays to monitor autophagy. In these guidelines, we consider these various methods of assessing autophagy and what information can, or cannot, be obtained from them. Finally, by discussing the merits and limits of particular autophagy assays, we hope to encourage technical innovation in the field. © 2012 Landes Bioscience.

Published
2012

15. Measurement of the bottom-strange meson mixing phase in the full CDF data set

Author

Aaltonen, T., Alvarez, González, Amerio, B., Amidei, S., Anastassov, D., Annovi, A., Antos, A., Apollinari, J., Appel, G., J. A., Arisawa, Artikov, T., Asaadi, A., Ashmanskas, J., Auerbach, W., Aurisano, B., Azfar, A., Badgett, F., Bae, W., Barbaro, Galtieri, Barnes, A., V. E., Barnett, B. A., Barria, Bartos, P., Bauce, P., Bedeschi, M., Behari, F., Bellettini, S., Bellinger, G., Benjamin, J., Beretvas, D., Bhatti, A., Bisello, A., Bizjak, D., Bland, I., K. R., Blumenfeld, Bocci, B., Bodek, A., Bortoletto, A., Boudreau, D., Boveia, J., Brigliadori, A., Bromberg, L., Brucken, C., Budagov, E., Budd, J., H. S., Burkett, Busetto, K., Bussey, G., Buzatu, P., Calamba, A., Calancha, A., Camarda, C., Campanelli, S., Campbell, M., Canelli, M., Carls, F., Carlsmith, B., Carosi, D., Carrillo, R., Carron, S., Casal, S., Casarsa, B., Castro, M., Catastini, A., Cauz, P., Cavaliere, D., Cavalli, Sforza, Cerri, M., Cerrito, A., Chen, L., Y. C., Chertok, Chiarelli, M., Chlachidze, G., Chlebana, G., Cho, F., Chokheli, K., Chung, D., W. H., Chung, Y. S., Ciocci, M. A., Clark, Clarke, A., Compostella, C., Convery, G., M. E., Conway, Corbo, J., Cordelli, M., Cox, M., C. A., Cox, D. J., Crescioli, Cuevas, F., Culbertson, J., Dagenhart, R., D'Ascenzo, D., Datta, N., Barbaro, De, Dell'Orso, Mauro, Demortier, M., Deninno, L., Devoto, M., D'Errico, F., Canto, Di, Ruzza, Di, Dittmann, B., J. R., D'Onofrio, Donati, Simone, Dong, P., Dorigo, M., Dorigo, T., Ebina, K., Elagin, A., Eppig, A., Erbacher, R., Errede, S., Ershaidat, N., Eusebi, R., Farrington, S., Feindt, M., Fernandez, J. P., Field, R., Flanagan, G., Forrest, R., Frank, M. J., Franklin, M., Freeman, J. C., Funakoshi, Y., Furic, I., Gallinaro, M., Garcia, J. E., Garfinkel, A. F., Garosi, P., Gerberich, H., Gerchtein, E., Giagu, S., Giakoumopoulou, V., Giannetti, P., Gibson, K., Ginsburg, C. 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N., Moon, C. S., Moore, Morello, R., M. J., Morlock, Movilla, Fernandez, Mukherjee, P., Muller, A., Murat, T., Mussini, P., Nachtman, M., Nagai, J., Naganoma, Y., Nakano, J., Napier, I., Nett, A., Neu, J., Neubauer, C., M. S., Nielsen, Nodulman, J., Noh, L., S. Y., Norniella, Oakes, O., Oh, L., S. H., Oh, Y. D., Oksuzian, Okusawa, I., Orava, T., Ortolan, R., Pagan, Griso, Pagliarone, S., Palencia, C., Papadimitriou, E., Paramonov, V., A. A., Patrick, Pauletta, J., Paulini, G., Paus, M., Pellett, C., D. E., Penzo, Phillips, A., T. J., Piacentino, Pianori, G., Pilot, E., Pitts, J., Plager, K., Pondrom, C., Poprocki, L., Potamianos, S., Prokoshin, K., Pranko, F., Ptohos, A., Punzi, Giovanni, Rahaman, G., Ramakrishnan, A., Ranjan, V., Redondo, N., Renton, I., Rescigno, P., Riddick, M., Rimondi, T., Ristori, F., Robson, L., Rodrigo, A., Rodriguez, T., Rogers, T., Rolli, E., Roser, S., Ruffini, R., Ruiz, F., Russ, A., Rusu, J., Safonov, V., Sakumoto, A., W. 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M., Warburton, Waters, A., Wester, D., W. C., Whiteson, Wicklund, D., A. B., Wicklund, Wilbur, E., Wick, S., Williams, F., H. H., Wilson, J. S., Wilson, Winer, P., B. L., Wittich, Wolbers, P., Wolfe, S., Wright, H., Wu, T., Wu, X., Yamamoto, Z., Yamato, K., Yang, D., Yang, T., U. K., Yang, Y. C., Yao, W. M., Yeh, G. P., Yi, Yoh, K., Yorita, J., Yoshida, K., Yu, T., G. B., Yu, Yu, I., S. S., Yun, J. 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Velev, C. Vellidi, M. Vidal, I. Vila, R. Vilar, J. Vizán, M. Vogel, G. Volpi, P. Wagner, R. Wagner, T. Wakisaka, R. Wallny, S. Wang, A. Warburton, D. Water, W. Wester, D. Whiteson, A. Wicklund, E. Wicklund, S. Wilbur, F. Wick, H. William, J. Wilson, P. Wilson, B. Winer, P. Wittich, S. Wolber, H. Wolfe, T. Wright, X. Wu, Z. Wu, K. Yamamoto, D. Yamato, T. Yang, U. Yang, Y. Yang, W.-M. Yao, G. Yeh, K. Yi, J. Yoh, K. Yorita, T. Yoshida, G. Yu, I. Yu, S. Yu, J. Yun, A. Zanetti, Y. Zeng, C. Zhou, S. Zucchelli, and Universidad de Cantabria

Subjects
FERMILAB TEVATRON COLLIDER, Particle physics, CP-violating asymmetries, Meson, B physic, General Physics and Astronomy, FOS: Physical sciences, B physics, Angle distribution, Branching ratio, CDF experiments, CP violations, CP-violating asymmetries, Data sample, Fermilab Tevatron collider, Integrated luminosity, Longitudinal polarization, Vector meson, Longitudinal polarization, 7. Clean energy, 01 natural sciences, High Energy Physics - Experiment, Vector meson, Physics and Astronomy (all), High Energy Physics - Experiment (hep-ex), High Energy Physics - Phenomenology (hep-ph), Mixing (mathematics), Strange b mesons, Phase (matter), 0103 physical sciences, STRANGE QUARK, mixing, Bottom-Strange Meson Mixing Phase, proton antiproton collisions, 010306 general physics, TEVATRON, Nuclear Experiment, BOTTOM QUARK, Physics, Integrated luminosity, 010308 nuclear & particles physics, Branching ratio, High Energy Physics - Phenomenology, CDF experiments, CP violations, Full data, Content (measure theory), Angle distribution, CDF, Production (computer science), High Energy Physics::Experiment, Data sample
Abstract

We report a measurement of the bottom-strange meson mixing phase βs using the time evolution of Bs0→J/ψ(→μ+μ-)ϕ(→K+K-) decays in which the quark-flavor content of the bottom-strange meson is identified at production. This measurement uses the full data set of proton-antiproton collisions at s=1.96 TeV collected by the Collider Detector experiment at the Fermilab Tevatron, corresponding to 9.6 fb-1 of integrated luminosity. We report confidence regions in the two-dimensional space of βs and the Bs0 decay-width difference ΔΓs and measure βs∈[-π/2,-1.51]∪[-0.06,0.30]∪[1.26,π/2] at the 68% confidence level, in agreement with the standard model expectation. Assuming the standard model value of βs, we also determine ΔΓs=0.068±0.026(stat)±0.009(syst) ps-1 and the mean Bs0 lifetime τs=1.528±0.019(stat)±0.009(syst) ps, which are consistent and competitive with determinations by other experiments., This work was supported by the U.S. Department of Energy and National Science Foundation; the Italian Istituto Nazionale di Fisica Nucleare; the Ministry of Education, Culture, Sports, Science and Technology of Japan; the Natural Sciences and Engineering Research Council of Canada; the National Science Council of the Republic of China; the Swiss National Science Foundation; the A. P. Sloan Foundation; the Bundesministerium für Bildung und Forschung, Germany; the Korean World Class University Program, the National Research Foundation of Korea; the Science and Technology Facilities Council and the Royal Society, UK; the Russian Foundation for Basic Research; the Ministerio de Ciencia e Innovación, and Programa Consolider-Ingenio 2010, Spain; the Slovak R&D Agency; the Academy of Finland; and the Australian Research Council (ARC).

Published
2012

17. Guidelines for the use and interpretation of assays for monitoring autophagy.

Author

Klionsky, Dj, Abdalla, Fc, Abeliovich, H, Abraham, Rt, Acevedo-Arozena, A, Adeli, K, Agholme, L, Agnello, M, Agostinis, P, Aguirre-Ghiso, Ja, Ahn, Hj, Ait-Mohamed, O, Ait-Si-Ali, S, Akematsu, T, Akira, S, Al-Younes, Hm, Al-Zeer, Ma, Albert, Ml, Albin, Rl, Alegre-Abarrategui, J, Aleo, Mf, Alirezaei, M, Almasan, A, Almonte-Becerril, M, Amano, A, Amaravadi, R, Amarnath, S, Amer, Ao, Andrieu-Abadie, N, Anantharam, V, Ann, Dk, Anoopkumar-Dukie, S, Aoki, H, Apostolova, N, Arancia, G, Aris, Jp, Asanuma, K, Asare, Ny, Ashida, H, Askanas, V, Askew, D, Auberger, P, Baba, M, Backues, Sk, Baehrecke, Eh, Bahr, Ba, Bai, Xy, Bailly, Y, Baiocchi, R, Baldini, G, Balduini, W, Ballabio, A, Bamber, Ba, Bampton, Et, Bánhegyi, G, Bartholomew, Cr, Bassham, Dc, Bast RC, Jr, Batoko, H, Bay, Bh, Beau, I, Béchet, Dm, Begley, Tj, Behl, C, Behrends, C, Bekri, S, Bellaire, B, Bendall, Lj, Benetti, L, Berliocchi, L, Bernardi, H, Bernassola, F, Besteiro, S, Bhatia-Kissova, I, Bi, X, Biard-Piechaczyk, M, Blum, J, 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Zuckerbraun, B., and Viscomi M. T. (ORCID:0000-0002-9096-4967)

Abstract

In 2008 we published the first set of guidelines for standardizing research in autophagy. Since then, research on this topic has continued to accelerate, and many new scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Accordingly, it is important to update these guidelines for monitoring autophagy in different organisms. Various reviews have described the range of assays that have been used for this purpose. Nevertheless, there continues to be confusion regarding acceptable methods to measure autophagy, especially in multicellular eukaryotes. A key point that needs to be emphasized is that there is a difference between measurements that monitor the numbers or volume of autophagic elements (e.g., autophagosomes or autolysosomes) at any stage of the autophagic process vs. those that measure flux through the autophagy pathway (i.e., the complete process); thus, a block in macroautophagy that results in autophagosome accumulation needs to be differentiated from stimuli that result in increased autophagic activity, defined as increased autophagy induction coupled with increased delivery to, and degradation within, lysosomes (in most higher eukaryotes and some protists such as Dictyostelium) or the vacuole (in plants and fungi). In other words, it is especially important that investigators new to the field understand that the appearance of more autophagosomes does not necessarily equate with more autophagy. In fact, in many cases, autophagosomes accumulate because of a block in trafficking to lysosomes without a concomitant change in autophagosome biogenesis, whereas an increase in autolysosomes may reflect a reduction in degradative activity. Here, we present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macroautophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused o

Published
2012

20. Guidelines for the use and interpretation of assays for monitoring autophagy

Author

Klionsky, Daniel J., Abdalla, Fabio C., Abeliovich, Hagai, Abraham, Robert T., Acevedo-Arozena, Abraham, Adeli, Khosrow, Agholme, Lotta, Agnello, Maria, Agostinis, Patrizia, Aguirre-Ghiso, Julio A., Ahn, Hyung Jun, Ait-Mohamed, Ouardia, Ait-Si-Ali, Slimane, Akematsu, Takahiko, Akira, Shizuo, Al-Younes, Hesham M., Al-Zeer, Munir A., Albert, Matthew L., Albin, Roger L., Alegre-Abarrategui, Javier, Aleo, Maria Francesca, Alirezaei, Mehrdad, Almasan, Alexandru, Almonte-Becerril, Maylin, Amano, Atsuo, Amaravadi, Ravi K., Amarnath, Shoba, Amer, Amal O., Andrieu-Abadie, Nathalie, Anantharam, Vellareddy, Ann, David K., Anoopkumar-Dukie, Shailendra, Aoki, Hiroshi, Apostolova, Nadezda, Arancia, Giuseppe, Aris, John P., Asanuma, Katsuhiko, Asare, Nana Y.O., Ashida, Hisashi, Askanas, Valerie, Askew, David S., Auberger, Patrick, Baba, Misuzu, Backues, Steven K., Baehrecke, Eric H., Bahr, Ben A., Bai, Xue-Yuan, Bailly, Yannick, Baiocchi, Robert, Baldini, Giulia, Balduini, Walter, Ballabio, Andrea, Bamber, Bruce A., Bampton, Edward T.W., Juhász, Gábor, Bartholomew, Clinton R., Bassham, Diane C., Bast, Robert C., Batoko, Henri, Bay, Boon-Huat, Beau, Isabelle, Béchet, Daniel M., Begley, Thomas J., Behl, Christian, Behrends, Christian, Bekri, Soumeya, Bellaire, Bryan, Bendall, Linda J., Benetti, Luca, Berliocchi, Laura, Bernardi, Henri, Bernassola, Francesca, Besteiro, Sébastien, Bhatia-Kissova, Ingrid, Bi, Xiaoning, Biard-Piechaczyk, Martine, Blum, Janice S., Boise, Lawrence H., Bonaldo, Paolo, Boone, David L., Bornhauser, Beat C., Bortoluci, Karina R., Bossis, Ioannis, Bost, Frédéric, Bourquin, Jean-Pierre, Boya, Patricia, Boyer-Guittaut, Michaël, Bozhkov, Peter V., Brady, Nathan R, Brancolini, Claudio, Brech, Andreas, Brenman, Jay E., Brennand, Ana, Bresnick, Emery H., Brest, Patrick, Bridges, Dave, Bristol, Molly L., Brookes, Paul S., Brown, Eric J., Brumell, John H., Brunetti-Pierri, Nicola, Brunk, Ulf T., Bulman, Dennis E., Bultman, Scott J., Bultynck, Geert, Burbulla, Lena F., Bursch, Wilfried, Butchar, Jonathan P., Buzgariu, Wanda, Bydlowski, Sergio P., Cadwell, Ken, Cahová, Monika, Cai, Dongsheng, Cai, Jiyang, Cai, Qian, Calabretta, Bruno, Calvo-Garrido, Javier, Camougrand, Nadine, Campanella, Michelangelo, Campos-Salinas, Jenny, Candi, Eleonora, Cao, Lizhi, Caplan, Allan B., Carding, Simon R., Cardoso, Sandra M., Carew, Jennifer S., Carlin, Cathleen R., Carmignac, Virginie, Carneiro, Leticia A.M., Carra, Serena, Caruso, Rosario A., Casari, Giorgio, Casas, Caty, Castino, Roberta, Cebollero, Eduardo, Cecconi, Francesco, Celli, Jean, Chaachouay, Hassan, Chae, Han-Jung, Chai, Chee-Yin, Chan, David C., Chan, Edmond Y., Chang, Raymond Chuen-Chung, Che, Chi-Ming, Chen, Ching-Chow, Chen, Guang-Chao, Chen, Guo-Qiang, Chen, Min, Chen, Quan, Chen, Steve S.-L., Chen, WenLi, Chen, Xi, Chen, Xiangmei, Chen, Xiequn, Chen, Ye-Guang, Chen, Yingyu, Chen, Yongqiang, Chen, Yu-Jen, Chen, Zhixiang, Cheng, Alan, Cheng, Christopher H.K., Cheng, Yan, Cheong, Heesun, Cheong, Jae-Ho, Cherry, Sara, Chess-Williams, Russ, Cheung, Zelda H., Chevet, Eric, Chiang, Hui-Ling, Chiarelli, Roberto, Chiba, Tomoki, Chin, Lih-Shen, Chiou, Shih-Hwa, Chisari, Francis V., Cho, Chi Hin, Cho, Dong-Hyung, Choi, Augustine M.K., Choi, DooSeok, Choi, Kyeong Sook, Choi, Mary E., Chouaib, Salem, Choubey, Divaker, Choubey, Vinay, Chu, Charleen T., Chuang, Tsung-Hsien, Chueh, Sheau-Huei, Chun, Taehoon, Chwae, Yong-Joon, Chye, Mee-Len, Ciarcia, Roberto, Ciriolo, Maria R., Clague, Michael J., Clark, Robert S.B., Clarke, Peter G.H., Clarke, Robert, Codogno, Patrice, Coller, Hilary A., Colombo, María I., Comincini, Sergio, Condello, Maria, Condorelli, Fabrizio, Cookson, Mark R., Coombs, Graham H., Coppens, Isabelle, Corbalan, Ramon, Cossart, Pascale, Costelli, Paola, Costes, Safia, Coto-Montes, Ana, Couve, Eduardo, Coxon, Fraser P., Cregg, James M., Crespo, José L., Cronjé, Marianne J., Cuervo, Ana Maria, Cullen, Joseph J., Czaja, Mark J., D'Amelio, Marcello, Darfeuille-Michaud, Arlette, Davids, Lester M., Davies, Faith E., De Felici, Massimo, de Groot, John F., de Haan, Cornelis A.M., De Martino, Luisa, De Milito, Angelo, De Tata, Vincenzo, Debnath, Jayanta, Degterev, Alexei, Dehay, Benjamin, Delbridge, Lea M.D., Demarchi, Francesca, Deng, Yi Zhen, Dengjel, Jörn, Dent, Paul, Denton, Donna, Deretic, Vojo, Desai, Shyamal D., Devenish, Rodney J., Di Gioacchino, Mario, Di Paolo, Gilbert, Di Pietro, Chiara, Díaz-Araya, Guillermo, Díaz-Laviada, Inés, Diaz-Meco, Maria T., Diaz-Nido, Javier, Dikic, Ivan, Dinesh-Kumar, Savithramma P., Ding, Wen-Xing, Distelhorst, Clark W., Diwan, Abhinav, Djavaheri-Mergny, Mojgan, Dokudovskaya, Svetlana, Dong, Zheng, Dorsey, Frank C., Dosenko, Victor, Dowling, James J., Doxsey, Stephen, Dreux, Marlène, Drew, Mark E., Duan, Qiuhong, Duchosal, Michel A., Duff, Karen E., Dugail, Isabelle, Durbeej, Madeleine, Duszenko, Michael, Edelstein, Charles L., Edinger, Aimee L., Egea, Gustavo, Eichinger, Ludwig, Eissa, N. 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Abstract

In 2008 we published the first set of guidelines for standardizing research in autophagy. Since then, research on this topic has continued to accelerate, and many new scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Accordingly, it is important to update these guidelines for monitoring autophagy in different organisms. Various reviews have described the range of assays that have been used for this purpose. Nevertheless, there continues to be confusion regarding acceptable methods to measure autophagy, especially in multicellular eukaryotes. A key point that needs to be emphasized is that there is a difference between measurements that monitor the numbers or volume of autophagic elements (e.g., autophagosomes or autolysosomes) at any stage of the autophagic process vs. those that measure flux through the autophagy pathway (i.e., the complete process); thus, a block in macroautophagy that results in autophagosome accumulation needs to be differentiated from stimuli that result in increased autophagic activity, defined as increased autophagy induction coupled with increased delivery to, and degradation within, lysosomes (in most higher eukaryotes and some protists such as Dictyostelium) or the vacuole (in plants and fungi). In other words, it is especially important that investigators new to the field understand that the appearance of more autophagosomes does not necessarily equate with more autophagy. In fact, in many cases, autophagosomes accumulate because of a block in trafficking to lysosomes without a concomitant change in autophagosome biogenesis, whereas an increase in autolysosomes may reflect a reduction in degradative activity. Here, we present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macroautophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes. These guidelines are not meant to be a formulaic set of rules, because the appropriate assays depend in part on the question being asked and the system being used. In addition, we emphasize that no individual assay is guaranteed to be the most appropriate one in every situation, and we strongly recommend the use of multiple assays to monitor autophagy. In these guidelines, we consider these various methods of assessing autophagy and what information can, or cannot, be obtained from them. Finally, by discussing the merits and limits of particular autophagy assays, we hope to encourage technical innovation in the field.

Published
2012
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21. Truncated Human Cathepsin L, Encoded by a Novel Splice Variant, Exhibits Altered Subcellular Localization and Cytotoxicity

Author

Sansanwal, Poonam, Shukla, Abhay, Das, Taposh, and Chauhan, Shyam

Abstract

Cathepsin L (ctsl), a lysosomal cyteine protease over expressed and secreted by cancer cells, has been implicated in a number of physiological and pathological processes including tumor cell proliferation and metastasis. In the present study we demonstrate that an unknown mRNA of human origin (Gene Bank accession number AF 217997) is a splice variant of human cathepsin L mRNA (hCATL A IV) and encodes a truncated form of cathepsin L (ctsl) containing only 151 C-terminal amino acids. This isoform is cytotoxic to the mammalian cells. Transient transfection studies revealed that unlike ctsl, upon over expression in eukaryotic cells ctsl is not secreted in to the media. Immunogold electron microscopy revealed its localization to nuclear, perinuclear and cytosolic regions. In view of its cytotoxic property, targeted expression of ctsl in tumor cells may prove useful in the management of cancer.

Published
2010

23. Abnormal mitochondrial autophagy in nephropathic cystinosis

Author

Sansanwal, Poonam and Sarwal, Minnie M.

Abstract

Cystinosis, which is characterized by lysosomal accumulation of cystine in many tissues, was the first known storage disorder caused by defective metabolite export from the lysosome. The molecular and cellular mechanisms underlying nephropathic cystinosis, the most severe form, which exhibits generalized proximal tubular dysfunction and progressive renal failure, remain largely unknown. We used renal proximal tubular epithelial (RPTE) cells and fibroblasts from patients with 3 clinical variants of cystinosis: nephropathic, intermediate, and ocular to explore the specific injury mechanism in nephropathic cystinosis. We demonstrate enhanced autophagy of mitochondria, increase in apoptosis and mitochondrial dysfunction in the nephropathic cystinosis phenotype. Furthermore, specific inhibition of autophagy results in significant attenuation of cell death in nephropathic cystinosis. This study provides ultrastructural and functional evidence of abnormal mitochondrial autophagy in nephropathic cystinosis, which may contribute to the renal Fanconi syndrome and progressive renal injury.

Published
2010
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24. Tuberculosis of spleen presenting with pyrexia of unknown origin in a non-immunocompromised woman

Author

Gupta Prem, Fotedar Sanjay, Agarwal Dipti, and Sansanwal Pradeep

Subjects
Splenic tuberculosis, CT guided splenic biopsy, Non-immunocompromised patient, Diseases of the respiratory system, RC705-779
Abstract

Splenic lesions due to tuberculosis are extremely rare in immunocompetent indi-viduals and delays in diagnosis are frequent. Here, we describe a 49-year-woman presenting with pyrexia-of-unknown origin with no evidence of any immunodefi-ciency. Computed tomography of the abdomen showed an enlarged spleen having multiple small focal hypodense lesions; the later were confirmed to be of tubercu-lous etiology on histopathological examination. She had favorable response with anti-tubercular chemotherapy. We report this case of tuberculosis spleen in an im-munocompetent individual for its rarity and to highlight the fact that these patients can be managed by medical treatment effectively.

Published
2008

26. Inhibition of intracellular clusterin attenuates cell death in nephropathic cystinosis.

Author

Sansanwal P, Li L, and Sarwal MM

Subjects
Adolescent, Apoptosis Inducing Factor metabolism, Autophagy, Blotting, Western, Caspase 3 metabolism, Cell Death, Cells, Cultured, Child, Child, Preschool, Epithelial Cells metabolism, Gene Silencing, Humans, Immunohistochemistry, Microscopy, Confocal, Microtubule-Associated Proteins metabolism, RNA-Binding Proteins metabolism, Clusterin metabolism, Cystinosis metabolism, Kidney Tubules, Proximal metabolism
Abstract

Nephropathic cystinosis, characterized by accumulation of cystine in the lysosomes, is caused by mutations in CTNS. The molecular and cellular mechanisms underlying proximal tubular dysfunction and progressive renal failure in nephropathic cystinosis are largely unclear, and increasing evidence supports the notion that cystine accumulation alone is not responsible for the end organ injury in cystinosis. We previously identified clusterin as potentially involved in nephropathic cystinosis. Here, we studied the expression of clusterin in renal proximal tubular epithelial cells obtained from patients with nephropathic cystinosis. The cytoprotective secretory form of clusterin, as evaluated by Western blot analysis, was low or absent in cystinosis cells compared with normal primary cells. Confocal microscopy revealed elevated levels of intracellular clusterin in cystinosis cells. Clusterin in cystinosis cells localized to the nucleus and cytoplasm and showed a filamentous and punctate aggresome-like pattern compared with diffuse cytoplasmic staining in normal cells. In kidney biopsy samples from patients with nephropathic cystinosis, clusterin protein expression was mainly limited to the proximal tubular cells. Furthermore, expression of clusterin overlapped with the expression of apoptotic proteins (apoptosis-inducing factor and cleaved caspase-3) and autophagy proteins (LC3 II and p62). Silencing of the clusterin gene resulted in a significant increase in cell viability and attenuation of apoptosis in cystinosis cells. Results of this study identify clusterin as a pivotal factor in the cell injury mechanism of nephropathic cystinosis and provide evidence linking cellular stress and injury to Fanconi syndrome and progressive renal injury in nephropathic cystinosis., (Copyright © 2015 by the American Society of Nephrology.)

Published
2015
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27. Non-HLA antibodies to immunogenic epitopes predict the evolution of chronic renal allograft injury.

Author

Sigdel TK, Li L, Tran TQ, Khatri P, Naesens M, Sansanwal P, Dai H, Hsieh SC, and Sarwal MM

Subjects
Adolescent, Adult, Analysis of Variance, Antibody Formation immunology, Biomarkers blood, Biopsy, Needle, Chronic Disease, Cohort Studies, Female, Follow-Up Studies, HLA Antigens immunology, Humans, Immunohistochemistry, Kidney immunology, Kidney pathology, Kidney Failure, Chronic diagnosis, Kidney Failure, Chronic surgery, Kidney Transplantation immunology, Male, Middle Aged, Predictive Value of Tests, Prospective Studies, Risk Assessment, Transplantation, Homologous adverse effects, Transplantation, Homologous immunology, Young Adult, Epitopes immunology, Graft Rejection immunology, Isoantibodies blood, Kidney Transplantation adverse effects
Abstract

Chronic allograft injury (CAI) results from a humoral response to mismatches in immunogenic epitopes between the donor and recipient. Although alloantibodies against HLA antigens contribute to the pathogenesis of CAI, alloantibodies against non-HLA antigens likely contribute as well. Here, we used high-density protein arrays to identify non-HLA antibodies in CAI and subsequently validated a subset in a cohort of 172 serum samples collected serially post-transplantation. There were 38 de novo non-HLA antibodies that significantly associated with the development of CAI (P<0.01) on protocol post-transplant biopsies, with enrichment of their corresponding antigens in the renal cortex. Baseline levels of preformed antibodies to MIG (also called CXCL9), ITAC (also called CXCL11), IFN-γ, and glial-derived neurotrophic factor positively correlated with histologic injury at 24 months. Measuring levels of these four antibodies could help clinicians predict the development of CAI with >80% sensitivity and 100% specificity. In conclusion, pretransplant serum levels of a defined panel of alloantibodies targeting non-HLA immunogenic antigens associate with histologic CAI in the post-transplant period. Validation in a larger, prospective transplant cohort may lead to a noninvasive method to predict and monitor for CAI.

Published
2012
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28. Mitochondrial autophagy promotes cellular injury in nephropathic cystinosis.

Author

Sansanwal P, Yen B, Gahl WA, Ma Y, Ying L, Wong LJ, and Sarwal MM

Subjects
Adenosine Triphosphate metabolism, Apoptosis Regulatory Proteins metabolism, Beclin-1, Cells, Cultured, Epithelial Cells pathology, Epithelial Cells ultrastructure, Fibroblasts metabolism, Fibroblasts ultrastructure, Humans, Kidney Tubules, Proximal metabolism, Kidney Tubules, Proximal pathology, Kidney Tubules, Proximal ultrastructure, Membrane Proteins metabolism, Microtubule-Associated Proteins metabolism, Mitochondria ultrastructure, Apoptosis physiology, Autophagy physiology, Cystinosis physiopathology, Fibroblasts pathology, Mitochondria pathology
Abstract

The molecular and cellular mechanisms underlying nephropathic cystinosis, which exhibits generalized proximal tubular dysfunction and progressive renal failure, remain largely unknown. Renal biopsies from patients with this disorder can reveal abnormally large mitochondria, but the relevance of this and other ultrastructural abnormalities is unclear. We studied the ultrastructure of fibroblasts and renal proximal tubular epithelial cells from patients with three clinical variants of cystinosis: Nephropathic, intermediate, and ocular. Electron microscopy revealed the presence of morphologically abnormal mitochondria and abnormal patterns of mitochondrial autophagy (mitophagy) with a high number of autophagic vacuoles and fewer mitochondria (P < 0.02) in nephropathic cystinosis. In addition, we observed increased apoptosis in renal proximal tubular epithelial cells, greater expression of LC3-II/LC3-I (microtubule-associated protein 1 light chain 3), and significantly more autophagosomes in the nephropathic variant. The autophagy inhibitor 3-methyl adenine rescued cell death in cystinotic cells. Cystinotic cells had increased levels of beclin-1 and aberrant mitochondrial function with a significant decrease in ATP generation and an increase in reactive oxygen species. This study provides ultrastructural and functional evidence of abnormal mitophagy in nephropathic cystinosis, which may contribute to the renal Fanconi syndrome and progressive renal injury.

Published
2010
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29. Expression of complement components differs between kidney allografts from living and deceased donors.

Author

Naesens M, Li L, Ying L, Sansanwal P, Sigdel TK, Hsieh SC, Kambham N, Lerut E, Salvatierra O, Butte AJ, and Sarwal MM

Subjects
Adolescent, Adult, Age Factors, Biopsy, Brain Death, Child, Child, Preschool, Cold Ischemia, Female, Gene Expression Profiling, Graft Survival, Humans, Infant, Kidney pathology, Kidney Transplantation, Male, Middle Aged, Oligonucleotide Array Sequence Analysis, Transplantation, Homologous, Young Adult, Complement System Proteins metabolism, Kidney metabolism, Living Donors, Transplants
Abstract

A disparity remains between graft survival of renal allografts from deceased donors and from living donors. A better understanding of the molecular mechanisms that underlie this disparity may allow the development of targeted therapies to enhance graft survival. Here, we used microarrays to examine whole genome expression profiles using tissue from 53 human renal allograft protocol biopsies obtained both at implantation and after transplantation. The gene expression profiles of living-donor kidneys and pristine deceased-donor kidneys (normal histology, young age) were significantly different before reperfusion at implantation. Deceased-donor kidneys exhibited a significant increase in renal expression of complement genes; posttransplantation biopsies from well-functioning, nonrejecting kidneys, regardless of donor source, also demonstrated a significant increase in complement expression. Peritransplantation phenomena, such as donor death and possibly cold ischemia time, contributed to differences in complement pathway gene expression. In addition, complement gene expression at the time of implantation was associated with both early and late graft function. These data suggest that complement-modulating therapy may improve graft outcomes in renal transplantation.

Published
2009
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30. Obstructing mass lesion of epiglottis: it can be tubercular.

Author

Gupta R, Fotedar S, Sansanwal P, Yadav SP, Gupta A, Gupta KB, and Saini K

Subjects
Antitubercular Agents, Diagnosis, Differential, Humans, Laryngeal Neoplasms drug therapy, Laryngeal Neoplasms surgery, Male, Middle Aged, Tracheostomy, Tuberculosis, Miliary drug therapy, Tuberculosis, Miliary surgery, Epiglottis pathology, Laryngeal Neoplasms diagnosis, Tuberculosis, Miliary diagnosis
Abstract

We report a case of 60-year old male who had difficulty in breathing as well as in swallowing. On examination, he was found to be having proliferative growth of epiglottis and right aryepiglottic fold mimicking neoplasm. So emergency tracheostomy was performed and biopsy taken. He was found to be having asymptomatic miliary mottling on routine x-ray chest PA view. Further on HRCT, it turned out to be lesion suggesting tubercular etiology. Histopathology (epiglottic biopsy) report confirmed the whole process as tubercular. The patient recovered promptly in due course with anti-tubercular treatment. Point remains to be seen that if we can avoid tracheostomy and its complications in such cases.

Published
2008

31. Primary tuberculous glossitis in an immunocompetent patient.

Author

Gupta PP, Fotedar S, Agarwal D, and Sansanwal P

Subjects
Adult, Glossitis drug therapy, Humans, Immunocompetence, Male, Tuberculosis, Oral drug therapy, Glossitis diagnosis, Tuberculosis, Oral diagnosis
Abstract

Tuberculous glossitis is a rare entity that has been described sporadically. Primary tuberculous glossitis, as described in this case report, is still exceptional. A 25-year-old male with no known immunosuppressive disorder presented with a tuberculoma at the base of his tongue. This was confirmed by tongue biopsy and a positive polymerase chain reaction response to the mycobacterium. The patient had a favourable response to anti-tubercular treatment. This highlights the importance of considering tuberculosis in the differential diagnosis of chronic tongue lesions, even in the absence of pulmonary tuberculosis.

Published
2007

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