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2. Effect of the variational symmetries of the Lagrangian on the propagator and associated conserved operators

Author

del Castillo, G. F. Torres and Lechuga-Solís, R. L.

Subjects
Quantum Physics
Abstract

Making use of the expression for the propagator in terms of path integrals, we study the effect of certain variational symmetries of a Lagrangian on the corresponding propagator. We also show that by considering a point transformation that relates two different Lagrangians one can obtain a relation between the corresponding propagators.

Published
2017

3. Genome wide conditional mouse knockout resources

Author

Kaloff, C, Anastassiadis, K, Ayadi, A, Baldock, R, Beig, J, Birling, M-C, Bradley, A, Brown, SDM, Bürger, A, Bushell, W, Chiani, F, Collins, FS, Doe, B, Eppig, JT, Finnell, RH, Fletcher, C, Flicek, P, Fray, M, Friedel, RH, Gambadoro, A, Gates, H, Hansen, J, Herault, Y, Hicks, GG, Hörlein, A, de Angelis, M Hrabé, Iyer, V, de Jong, PJ, Koscielny, G, Kühn, R, Liu, P, Lloyd, KCK, Lopez, RG, Marschall, S, Martínez, S, McKerlie, C, Meehan, T, von Melchner, H, Moore, M, Murray, SA, Nagy, A, Nutter, LMJ, Pavlovic, G, Pombero, A, Prosser, H, Ramirez-Solis, R, Ringwald, M, Rosen, B, Rosenthal, N, Rossant, J, Noppinger, P Ruiz, Ryder, E, Skarnes, WC, Schick, J, Schnütgen, F, Schofield, P, Seisenberger, C, Selloum, M, Smedley, D, Simpson, EM, Stewart, AF, Teboul, L, Valentini, GP Tocchini, Valenzuela, D, West, AP, and Wurst, W

Subjects
Pharmacology and Pharmaceutical Sciences, Biomedical and Clinical Sciences, Genetics, Biotechnology, Stem Cell Research, Stem Cell Research - Embryonic - Non-Human, Human Genome, 2.6 Resources and infrastructure (aetiology), Generic health relevance, Neurosciences, Neurology & Neurosurgery, Pharmacology and pharmaceutical sciences
Abstract

The International Knockout Mouse Consortium (IKMC) developed high throughput gene trapping and gene targeting pipelines that produced mostly conditional mutations of more than 18,500 genes in C57BL/6N mouse embryonic stem (ES) cells which have been archived and are freely available to the research community as a frozen resource. From this unprecedented resource more than 6,000 mutant mouse strains have been produced by the IKMC and mostly the International Mouse Phenotyping Consortium (IMPC). In addition, a cre-driver resource was established including 250 inducible cre-driver mouse strains in a C57BL/6 background. Complementing the cre-driver resource, a collection of comprising 27 cre-driver rAAVs has also been produced. The resources can be easily accessed at the IKMC/IMPC web portal (www.mousephenotype.org). The IKMC/IMPC resource is a standardized reference library of mouse models with defined genetic backgrounds that enables the analysis of gene-disease associations in mice of different genetic makeup and should therefore have a major impact on biomedical research.

Published
2016

4. Coupling circadian rhythms of metabolism and chromatin remodelling

Author

Masri, S, Orozco-Solis, R, Aguilar-Arnal, L, Cervantes, M, and Sassone-Corsi, P

Subjects
Aging, Sleep Research, Genetics, Biotechnology, 1.1 Normal biological development and functioning, Underpinning research, Animals, CLOCK Proteins, Cells, Chromatin Assembly and Disassembly, Circadian Rhythm, Epigenomics, Gene Expression, Humans, Mammals, NAD, Nutritional Physiological Phenomena, Sirtuin 1, Sirtuins, Transcription, Genetic, chromatin remodelling, epigenetics, NAD(+), nutrition, sirtuins, NAD+, Clinical Sciences, Endocrinology & Metabolism
Abstract

The circadian clock controls a large variety of neuronal, endocrine, behavioural and physiological responses in mammals. This control is exerted in large part at the transcriptional level on genes expressed in a cyclic manner. A highly specialized transcriptional machinery based on clock regulatory factors organized in feedback autoregulatory loops governs a significant portion of the genome. These oscillations in gene expression are paralleled by critical events of chromatin remodelling that appear to provide plasticity to circadian regulation. Specifically, the nicotinamide adenine dinucleotide (NAD)(+) -dependent deacetylases SIRT1 and SIRT6 have been linked to circadian control of gene expression. This, and additional accumulating evidence, shows that the circadian epigenome appears to share intimate links with cellular metabolic processes and has remarkable plasticity showing reprogramming in response to nutritional challenges. In addition to SIRT1 and SIRT6, a number of chromatin remodellers have been implicated in clock control, including the histone H3K4 tri-methyltransferase MLL1. Deciphering the molecular mechanisms that link metabolism, epigenetic control and circadian responses will provide valuable insights towards innovative strategies of therapeutic intervention.

Published
2015

5. Consensus on the prevention, diagnosis, and treatment of Clostridium difficile infection

Author

Abreu y Abreu, A.T., Velarde-Ruiz Velasco, J.A., Zavala-Solares, M.R., Remes-Troche, J.M., Carmona-Sánchez, R.I., Aldana-Ledesma, J.M., Camacho-Ortiz, A., Contreras-Omaña, R., Díaz-Seoane, R., Elizondo-Vázquez, C.T., Garza-González, E., Grajales-Figueroa, G., Gómez-Escudero, O., Jacobo-Karam, J.S., Morales-Arámbula, M., Olivares-Guzmán, L.O., Sifuentes-Osornio, J., Siu-Moguel, A.G., Soto-Solís, R., Valdovinos-García, L.R., Valdovinos-Díaz, M.A., Vázquez-Elizondo, G., and Lazo-de la Vega Jasso, S.A.

Published
2019
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6. Epigenetic control and the circadian clock: Linking metabolism to neuronal responses

Author

Orozco-Solis, R and Sassone-Corsi, P

Subjects
Sleep Research, Genetics, Neurosciences, Behavioral and Social Science, Brain Disorders, Underpinning research, 1.1 Normal biological development and functioning, Metabolic and endocrine, Mental health, Generic health relevance, Good Health and Well Being, Animals, Brain, Circadian Clocks, Epigenesis, Genetic, Humans, Male, Sirtuin 1, Stress, Psychological, epigenetic mechanism, clock, SIRT1, metabolism, social zeitgebers, nutrients, Psychology, Cognitive Sciences, Neurology & Neurosurgery
Abstract

Experimental and epidemiological evidence reveal the profound influence that industrialized modern society has imposed on human social habits and physiology during the past 50 years. This drastic change in life-style is thought to be one of the main causes of modern diseases including obesity, type 2 diabetes, mental illness such as depression, sleep disorders, and certain types of cancer. These disorders have been associated to disruption of the circadian clock, an intrinsic time-keeper molecular system present in virtually all cells and tissues. The circadian clock is a key element in homeostatic regulation by controlling a large array of genes implicated in cellular metabolism. Importantly, intimate links between epigenetic regulation and the circadian clock exist and are likely to prominently contribute to the plasticity of the response to the environment. In this review, we summarize some experimental and epidemiological evidence showing how environmental factors such as stress, drugs of abuse and changes in circadian habits, interact through different brain areas to modulate the endogenous clock. Furthermore we point out the pivotal role of the deacetylase silent mating-type information regulation 2 homolog 1 (SIRT1) as a molecular effector of the environment in shaping the circadian epigenetic landscape.

Published
2014

13. Genome wide conditional mouse knockout resources

Author

Kaloff, C., Anastassiadis, K., Ayadi, A., Baldock, R., Beig, J., Birling, M.-C., Bradley, A., Brown, S.D.M., Bürger, A., Bushell, W., Chiani, F., Collins, F.S., Doe, B., Eppig, J.T., Finnell, R.H., Fletcher, C., Flicek, P., Fray, M., Friedel, R.H., Gambadoro, A., Gates, H., Hansen, J., Herault, Y., Hicks, G.G., Hörlein, A., Hrabé de Angelis, M., Iyer, V., de Jong, P.J., Koscielny, G., Kühn, R., Liu, P., Lloyd, K.C.K, Lopez, R.G., Marschall, S., Martínez, S., McKerlie, C., Meehan, T., von Melchner, H., Moore, M., Murray, S.A., Nagy, A., Nutter, L.M.J., Pavlovic, G., Pombero, A., Prosser, H., Ramirez-Solis, R., Ringwald, M., Rosen, B., Rosenthal, N., Rossant, J., Ruiz Noppinger, P., Ryder, E., Skarnes, W.C., Schick, J., Schnütgen, F., Schofield, P., Seisenberger, C., Selloum, M., Smedley, D., Simpson, E.M., Stewart, A.F., Teboul, L., Tocchini Valentini, G.P., Valenzuela, D., West, A.P., and Wurst, W.

Published
2016
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14. Selenoprotein deficiency disorder predisposes to aortic aneurysm formation.

Author

Schoenmakers, E., Marelli, F., Jørgensen, H.F., Visser, Wesley J., Moran, C., Groeneweg, S., Avalos, C., Jurgens, S.J., Figg, N., Finigan, A., Wali, N., Agostini, M., Wardle-Jones, H., Lyons, G., Rusk, R., Gopalan, D., Twiss, P., Visser, J.J.C.M., Goddard, M., Nashef, S.A.M., Heijmen, R.H., Clift, P., Sinha, S., Pirruccello, J.P., Ellinor, P.T., Busch-Nentwich, E.M., Ramirez-Solis, R., Murphy, M.P., Persani, L., Bennett, M., Chatterjee, K., Schoenmakers, E., Marelli, F., Jørgensen, H.F., Visser, Wesley J., Moran, C., Groeneweg, S., Avalos, C., Jurgens, S.J., Figg, N., Finigan, A., Wali, N., Agostini, M., Wardle-Jones, H., Lyons, G., Rusk, R., Gopalan, D., Twiss, P., Visser, J.J.C.M., Goddard, M., Nashef, S.A.M., Heijmen, R.H., Clift, P., Sinha, S., Pirruccello, J.P., Ellinor, P.T., Busch-Nentwich, E.M., Ramirez-Solis, R., Murphy, M.P., Persani, L., Bennett, M., and Chatterjee, K.

Abstract

Contains fulltext : 300228.pdf (Publisher’s version ) (Open Access), Aortic aneurysms, which may dissect or rupture acutely and be lethal, can be a part of multisystem disorders that have a heritable basis. We report four patients with deficiency of selenocysteine-containing proteins due to selenocysteine Insertion Sequence Binding Protein 2 (SECISBP2) mutations who show early-onset, progressive, aneurysmal dilatation of the ascending aorta due to cystic medial necrosis. Zebrafish and male mice with global or vascular smooth muscle cell (VSMC)-targeted disruption of Secisbp2 respectively show similar aortopathy. Aortas from patients and animal models exhibit raised cellular reactive oxygen species, oxidative DNA damage and VSMC apoptosis. Antioxidant exposure or chelation of iron prevents oxidative damage in patient's cells and aortopathy in the zebrafish model. Our observations suggest a key role for oxidative stress and cell death, including via ferroptosis, in mediating aortic degeneration.

Published
2023

27. MRNIP interacts with sex body chromatin to support meiotic progression, spermatogenesis, and male fertility in mice

Author

Kazi, S. (Samina), Castañeda, J. M. (Julio M.), Savolainen, A. (Audrey), Xu, Y. (Yiding), Liu, N. (Ning), Qiao, H. (Huanyu), Ramirez-Solis, R. (Ramiro), Nozawa, K. (Kaori), Yu, Z. (Zhifeng), Matzuk, M. M. (Martin M.), Prunskaite-Hyyryläinen, R. (Renata), Kazi, S. (Samina), Castañeda, J. M. (Julio M.), Savolainen, A. (Audrey), Xu, Y. (Yiding), Liu, N. (Ning), Qiao, H. (Huanyu), Ramirez-Solis, R. (Ramiro), Nozawa, K. (Kaori), Yu, Z. (Zhifeng), Matzuk, M. M. (Martin M.), and Prunskaite-Hyyryläinen, R. (Renata)

Abstract

Meiosis has a principal role in sexual reproduction to generate haploid gametes in both sexes. During meiosis, the cell nucleus hosts a dynamic environment where some genes are transcriptionally activated, and some are inactivated at the same time. This becomes possible through subnuclear compartmentalization. The sex body, sequestering X and Y chromosomes during male meiosis and creating an environment for the meiotic sex chromosome inactivation (MSCI) is one of the best known and studied subnuclear compartments. Herein, we show that MRNIP forms droplet-like accumulations that fuse together to create a distinct subnuclear compartment that partially overlaps with the sex body chromatin during diplotene. We demonstrate that Mrnip−/− spermatocytes have impaired DNA double-strand break (DSB) repair, they display reduced sex body formation and defective MSCI. We show that Mrnip−/− undergoes critical meiocyte loss at the diplotene stage. Furthermore, we determine that DNA DSBs (induced by SPO11) and synapsis initiation (facilitated by SYCP1) precede Mrnip expression in testes. Altogether, our findings indicate that in addition to an emerging role in DNA DSB repair, MRNIP has an essential function in spermatogenesis during meiosis I by forming drop-like accumulations interacting with the sex body.

Published
2022

38. Understanding the neuroprotective effect of tranexamic acid: an exploratory analysis of the CRASH-3 randomised trial

Author

Brenner, A., Belli, A., Chaudhri, R., Coats, T., Frimley, L., Jamaluddin, S. F., Jooma, R., Mansukhani, R., Sandercock, P., Shakur-Still, H., Shokunbi, T., Roberts, I., Aeron-Thomas, A., Chaudary, M. A., Jamaluddin, S. F. B., Javaid, K., Kayani, A., Leech, C., Mahmood, K., Noor, J. M., Mejia-Mantilla, J., Moss, P., Pott, J., Vallecilla, L., Hartzenberg, H. B., Joshipura, M., Perel, P., Clarke, M. J., Ohaegbulam, S. C., Rodgers, A., Brady, T., Dewan, Y., Edwards, P., Komolafe, E. O., Arribas, M., Austin, E., Balogun, E., Barneston, L., Barrow, C., Beaumont, D., Benyahia, M., Brooks, I., Cargill, M., Carrington, L., Cook, L., Cornu-Hewitt, B., Geer, A., Gilbert, D., Gilliam, C., Gil-Onandia, J., Hetherington, D., Howe, C., Hughes, C., I'Anson, D., Jackson, R., Joshi, M., Kansagra, S., Kawahara, T., Ker, K., Kostrov, S., Mahmood, A., Miah, H., Ndungu, B., Needham, K., Okusi, C., Outtandy, A., Pardinaz-Solis, R., Pearson, D., Pepple, T., Pisani, C., Prieto-Merino, D., Prowse, D., Quashi, N., Quinn, A., Ramos, M., Reid, M., Roukas, C., Scrapa, G., Squires, C., Tanner, J., Thayne, A., Vidaurre, L., Woods, E., Fawole, B., Adetayo, O., Okunade, O., Gogichaishvili, T., de los Angeles Munoz-Sanchez, M., Olldashi, F., Krishnan, S., Djientcheu, V., Castellanos, J. L., Rasulo, F., Hama, Q., Mulla, Y., Florian, I. S., Tobar, J., Khamis, H., Deasy, C., Wellsh, B., Williams-Johnson, J., Chandra, S., Mutiso, V., Butt, R., Nasir, M. H., Ahmad, S., Aslam, F., Ishaque, K., Usmani, F., Rizvi, S., Ali, F., Sajjad, O., Zunair, A., Rehman, L., Rizvi, R., Javeed, F., Ahmed, S., Abbas, A., Afzal, A., Mikdad, A., Bashir, A., Chaudary, A., Salahuddin, T., Ahemed, B., Aziz, A., Ashraf, N., Hussain, S., Ahmad, U., Asif, M., Adil, M., Rauf, A., Khan, R., Ahmad, B., Afzal, U., Raza, H., Ain, Q., Yaqoob, S., Waseem, Q., Nishat, M., Semvel, S., Iqbal, J., Majeed, S., Zulfiqar, S., Iqbal, M., Majeed, N., Ahmed, M., Akhtar, N., Malik, M., Shehzad, Y., Yousaf, M., Wahid, A., Samad, A., Shah, S., Ali, M., Zeb, J., Khan, A. S., Irfan, A., Sharif, S., Memon, R., Bloom, B., Harris, T., Skene, I., Bellhouse, G., Boulton, O., Ward, G., Jarvis, C., Swann, C., Ratnam, S., Carrera, R., Yakoub, K., Davies, D., Fellows, E., Jarman, H., Rounding, S., Johnson, E., Loughran, C., Lecky, F., Clayton, K., Michael, A., Coumbarides, A., Kendall, J., Faulkner, B., Worner, R., Gendall, E., Hopkins, P., Riozzi, P., Cotton, H., Astin-Chamberlain, R., Wilson, M., Bodnar, J., Williams, R., Rigoni, A., Sattout, A., Fletcher, J., Edge, C., Maryanji, N., Boyle, A., Hardwick, S., Nichols, E., Hayhurst, C., Coffey, F., Gough, C., Miller, P., Ryan, L., Darwent, M., Espinosa, A., Beer, S., Norton, J., Maguire, H., Finney, K., Kehoe, A., Squire, R., Jeffery, A., Vorwerk, C., Foord, D., Wilkinson, E., Kuhrt, A., Ramlakhan, S., Reid, S., Curran, A., Mcmullan, S., Hassan, T., Nuttall, S., Haig, S., Al-Nahhas, S., Bulters, D., Zolnourian, A., Ribbons, T., Mew, I., de Weymarn, T., Hughes, V., Mcvicar, J., Mckiernan, C., Keating, L., Reschreiter, H., Wright, J., Chan, L., Kataria, H., Ireland, A., Body, R., Corfield, A., Francis, S., Townend, W., Gagg, J., Wilson, S., Cottingham, R., Tucker, S., Sutherland, F., Mitchell, L., Parker, L., Afolabi, O., Hunter, F., Jadav, M., Adeboye, K., Grocutt, M., May, G., Watson, D., Wootten, A., Robertshaw, S., Dorrian, S., Perry, R., Choi, H., Mcgroarty, C., Shone, P., Maritz, D., Jamaluddin, S., Noor, J., Rosli, N., Xian, L. L. S., De Jun, Y., Mohamed, F., Song, C. H., Hawari, A., Chin, L. Y., Hussein, H. M., Lotfi, M., Hamid, H., Udin, N., Lian, P., Choo, S., Wong, K., Gani, F., Jusoh, M., Rajakumar, D., Yang, C. B., Dzulkiflee, N. S. B., W. C., Ky, Azman, M. A. B. M., Osman, A. B., Ahmad, A. H., Ismail, R., Lai, S. Q., Mohidin, M. A. B., Deraman, N. B., Selamat, S. B., Abidin, I., Halim, N., Bakar, Z., Ismail, Z. M., Hisham, B., Kamal, R., Effendy, Z., Ismail, M., Azleen, N., Seng, L. Y., Baharuddin, K. A., Kandasamy, R., Kamalludin, A., Asmee, S., Fadzil, M., Basitz, A., Abdullah, N., Ingorokva, G., Ingorokva, S., Agdgomelashvili, I., Mumladze, K., Maisuradze, I., Kugusheva, I., Shalamberidze, B., Tomadze, G., Fernandez-Ortega, J., Seara-Valero, R., Ibanez-Botella, G., Garcia-Martinez, V., Martul, M. G., Ramos, S. F., Preciado, G. L., Garcia-Alfaro, C., Munoz-Sanchez, A., Bellido-Alba, R., Corcobado, C., Bueno, A., Ambros, A., Jimenez, J. T., Ramirez, J. R., Martin, J., Rodriguez, L. I., Fontanals, J., Jimenez-Moragas, J. M., Berbegal, J. P., Oluwole, O., Mahmud, R., Ukwu, N., Bankole, F., Oseni, A., Adebayo, B., Malomo, A., Tiamiyu, L., Adekanmbi, A., Thanni, L., Olubodun, A., Ojeblenu, F., Uwaezuoke, M., Komolafe, E., Owagbemi, O., Ishola, F., Durodola, A., Udoffa, U., James, A., Tella, A., Dongo, A., Ekpemiro, U., Anyanwu, S., Aigoro, N., Mezue, W., Shilong, D., Azeez, A., Babalola, O., Ibrahim, M., Obande, J., Franco, A. C., Salazar, E. V., Londono, S. B., Cardona, V. M., Morales, C., Naranjo, S., Agudelo, J., Carvajal, S., Fajardo-Gaviria, Y., Roka, Y., Ghising, U., Roka, N., Shrestha, M., Devkota, U., Vaidya, B., Nepal, P., Thapa, A., Kc, B., Shrestha, A., Jha, R., Shrestha, P., Hodaj, I., Spaho, E., Selaj, A., Bendo, N., Shoko, T., Endo, H., Senda, A., Hagihara, Y., Fuse, T., Masunaga, N., Otomo, Y., Egashira, R., Ohnuki, T., Almazmi, A., Saha, S., Suvarov, A., Aung, T. L., Tun, K. M., Khaing, T. T., Maw, T., Ndome, O., Moumi, M., Mbida, A., Fondop, J., Sebastien, M., Azim, A., Adil, J., Amiry, Z., Loria-Castellanos, J., Rubio, N. G., Leon, P. O., Estrada, F., de Oca-Garcia, E. M., Sanchez, H., Soria, A., Bonucci, P., Franchi, F., Girardini, A., Hameed, H., Basim, M., Stock, S., Hourt, E., Ilunga, A., Mulenga, J., Ples, H., Danil, A., Gorgan, M., Florian, I., Vlahovic, D., French, J., East, J., Kurniawan, A., and Kiboi, J.

Subjects
medicine.medical_specialty, Tranexamic acid, Traumatic brain injury, Epidemiology, Critical Care and Intensive Care Medicine, Placebo, CRASH-3 trial, Neuroprotection, Intracranial haemorrhage, law.invention, Emergence care, 03 medical and health sciences, 0302 clinical medicine, Randomized controlled trial, law, Internal medicine, Medicine, Humans, 030212 general & internal medicine, Randomised controlled trial, business.industry, Multiple Trauma, Research, lcsh:Medical emergencies. Critical care. Intensive care. First aid, 030208 emergency & critical care medicine, lcsh:RC86-88.9, Protective Factors, medicine.disease, Polytrauma, Antifibrinolytic Agents, 3. Good health, Neuroprotective Agents, Relative risk, Brain Injuries, business, medicine.drug
Abstract

Background The CRASH-3 trial hypothesised that timely tranexamic acid (TXA) treatment might reduce deaths from intracranial bleeding after traumatic brain injury (TBI). To explore the mechanism of action of TXA in TBI, we examined the timing of its effect on death. Methods The CRASH-3 trial randomised 9202 patients within 3 h of injury with a GCS score ≤ 12 or intracranial bleeding on CT scan and no significant extracranial bleeding to receive TXA or placebo. We conducted an exploratory analysis of the effects of TXA on all-cause mortality within 24 h of injury and within 28 days, excluding patients with a GCS score of 3 or bilateral unreactive pupils, stratified by severity and country income. We pool data from the CRASH-2 and CRASH-3 trials in a one-step fixed effects individual patient data meta-analysis. Results There were 7637 patients for analysis after excluding patients with a GCS score of 3 or bilateral unreactive pupils. Of 1112 deaths, 23.3% were within 24 h of injury (early deaths). The risk of early death was reduced with TXA (112 (2.9%) TXA group vs 147 (3.9%) placebo group; risk ratio [RR] RR 0.74, 95% CI 0.58–0.94). There was no evidence of heterogeneity by severity (p = 0.64) or country income (p = 0.68). The risk of death beyond 24 h of injury was similar in the TXA and placebo groups (432 (11.5%) TXA group vs 421 (11.7%) placebo group; RR 0.98, 95% CI 0.69–1.12). The risk of death at 28 days was 14.0% in the TXA group versus 15.1% in the placebo group (544 vs 568 events; RR 0.93, 95% CI 0.83–1.03). When the CRASH-2 and CRASH-3 trial data were pooled, TXA reduced early death (RR 0.78, 95% CI 0.70–0.87) and death within 28 days (RR 0.88, 95% CI 0.82–0.94). Conclusions Tranexamic acid reduces early deaths in non-moribund TBI patients regardless of TBI severity or country income. The effect of tranexamic acid in patients with isolated TBI is similar to that in polytrauma. Treatment is safe and even severely injured patients appear to benefit when treated soon after injury. Trial registration ISRCTN15088122, registered on 19 July 2011; NCT01402882, registered on 26 July 2011.

Published
2020
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41. Photocatalytic Activity of Bi2O3/BiOCl Heterojunctions Under UV and Visible Light Illumination for Degradation of Caffeine.

Author

Ruiz-Castillo, A. L., Hinojosa-Reyes, M., Camposeco-Solis, R., and Ruiz, F.

Subjects
HETEROJUNCTIONS, PHOTOCATALYSTS, VISIBLE spectra, BAND gaps, X-ray photoelectron spectroscopy, PHOTOELECTRON spectroscopy
Abstract

Bismuth oxide (Bi2O3) particles were synthesized by calcination and hydrothermal methods and then were treated in-situ with different amounts of hydrochloric acid (HCl) to construct a series of Bi2O3/BiOCl heterojunctions with different ratios. The physicochemical properties of the materials were characterized by X-ray diffraction, scanning electron microscopy, Raman spectroscopy, UV–Vis diffuse reflectance spectroscopy, N2 physisorption, Fourier-transform infrared spectroscopy and X-ray photoelectron spectroscopy. Their photocatalytic activity was evaluated for the degradation of caffeine under UV radiation and visible light. All the heterojunctions possess an enhanced photocatalytic activity compared to pure Bi2O3 and bismuth oxychloride (BiOCl) due to efficient charge separation and transfer across the interface. The heterojunctions obtained from the hydrothermal Bi2O3 were more efficient than those from the calcined Bi2O3, mainly because of differences in their crystalline phases and band gap values. The hydrothermal Bi2O3 has a β-Bi2O3 phase and band gap of 2.4 eV, compared to the α-Bi2O3 phase and 2.8 eV band gap of the calcined Bi2O3. The heterojunction with a Bi2O3/BiOCl ratio of 10/90 has the highest photocatalytic activity for caffeine degradation in UV and visible light experiments, achieving a caffeine degradation of 92% in 2 h with UV light and 25% in 5 h with visible light. This heterojunction shows excellent photostability and high efficiency for caffeine degradation in a three consecutive cycles photocatalytic experiment. The role of the different radical species involved in the photocatalytic process was evaluated, demonstrating that h+ and ·O2− are the major reactive species responsible for caffeine photodegradation. A possible mechanism for the photocatalytic activity of the heterojunctions was proposed. The Bi2O3/BiOCl heterojunctions reported in this study are promising for the degradation of organic pollutants in real wastewater effluents. [ABSTRACT FROM AUTHOR]

Published
2022
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46. TRANSJEJUNAL ERCP (TJ-ERCP) VIA EUS-GUIDED ENTERO-ANASTOMOSES (EUS-EA) IN ROUX-EN-Y-HEPATICOJEJUNOSTOMY (RYHJ): SHORT AND LONG-TERM OUTCOMES OF A VARIANT EUS-DIRECTED ERCP IN A CHALLENGING PATIENT POPULATION

Author

Chavarria, C, additional, Lopez, AYC, additional, Kunda, R, additional, Benito, M De, additional, Solis, R Soto, additional, Aerts, M, additional, Gallardo, MA, additional, Alonso, FJG, additional, Bazaga, S, additional, Sanchez-Ocaña, R, additional, Tejada, JT, additional, De la Serna, C, additional, and Perez-Miranda, M, additional

Published
2020
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50. An Orphan CpG Island Drives Expression of a let-7 miRNA Precursor with an Important Role in Mouse Development

Author

Jim Selfridge, Joanna Bottomley, Adrian Bird, Ramires-Solis R, Lelliott C, Martha V. Koerner, Skarnes B, Barry Rosen, Mark G. Thomas, David J. Adams, De Sousa D, Shaun Webb, Kashyap Chhatbar, Justyna Cholewa-Waclaw, Lelliott, Christopher [0000-0001-8087-4530], and Apollo - University of Cambridge Repository

Subjects
Health, Toxicology and Mutagenesis, lcsh:Medicine, Biology, medicine.disease_cause, Biochemistry, Genetics and Molecular Biology (miscellaneous), Biochemistry, 03 medical and health sciences, 0302 clinical medicine, microRNA, Genetics, medicine, lcsh:QH301-705.5, 030304 developmental biology, 0303 health sciences, Mutation, lcsh:R, micro-RNA, RNA, Promoter, Let-7 miRNA, Embryonic stem cell, Let-7, mouse genetics, CpG site, lcsh:Biology (General), Human genome, 030217 neurology & neurosurgery
Abstract

Most human genes are associated with promoters embedded in non-methylated, G + C-rich CpG islands (CGIs). Not all CGIs are found at annotated promoters, however, raising the possibility that many serve as promoters for transcripts that do not code for proteins. To test this hypothesis, we searched for novel transcripts in embryonic stem cells (ESCs) that originate within orphan CGIs. Among several candidates, we detected a transcript that included three members of the let-7 micro-RNA family: Let-7a-1, let-7f-1, and let-7d. Deletion of the CGI prevented expression of the precursor RNA and depleted the included miRNAs. Mice homozygous for this mutation were sub-viable and showed growth and other defects. The results suggest that despite the identity of their seed sequences, members of the let-7 miRNA family exert distinct functions that cannot be complemented by other members.

Published
2019
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