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Artykuły w czasopismach na temat "Lactic acidosis in ruminants"
Dunlop, Robert H., i Paul B. Hammond. "D-LACTIC ACIDOSIS OF RUMINANTS*†". Annals of the New York Academy of Sciences 119, nr 3 (16.12.2006): 1109–32. http://dx.doi.org/10.1111/j.1749-6632.1965.tb47466.x.
Pełny tekst źródłaLorenz, Ingrid, i Arcangelo Gentile. "d-Lactic Acidosis in Neonatal Ruminants". Veterinary Clinics of North America: Food Animal Practice 30, nr 2 (lipiec 2014): 317–31. http://dx.doi.org/10.1016/j.cvfa.2014.03.004.
Pełny tekst źródłaClayton, E. H., i G. P. D. Jones. "Preliminary observations of tumour necrosis factor-alpha in the faeces of sheep following acute lactic acidosis". Australian Journal of Agricultural Research 52, nr 9 (2001): 869. http://dx.doi.org/10.1071/ar00118.
Pełny tekst źródłaPark, Seon Young, Mingyung Lee, Se Ra Lim, Hyemin Kwon, Ye Seul Lee, Ji Hyung Kim i Seongwon Seo. "Diversity and Antimicrobial Resistance in the Streptococcus bovis/Streptococcus equinus Complex (SBSEC) Isolated from Korean Domestic Ruminants". Microorganisms 9, nr 1 (4.01.2021): 98. http://dx.doi.org/10.3390/microorganisms9010098.
Pełny tekst źródłaValente, Tiago Neves Pereira, Cláudia Batista Sampaio, Erico da Silva Lima, Bruno Borges Deminicis, Andréia Santos Cezário i Wallacy Barbacena Rosa dos Santos. "Aspects of Acidosis in Ruminants with a Focus on Nutrition: A Review". Journal of Agricultural Science 9, nr 3 (13.02.2017): 90. http://dx.doi.org/10.5539/jas.v9n3p90.
Pełny tekst źródłaAbeysekara, Saman, Jonathan M. Naylor, Andrew W. A. Wassef, Ulyana Isak i Gordon A. Zello. "d-Lactic acid-induced neurotoxicity in a calf model". American Journal of Physiology-Endocrinology and Metabolism 293, nr 2 (sierpień 2007): E558—E565. http://dx.doi.org/10.1152/ajpendo.00063.2007.
Pełny tekst źródłaGhali, M. B., P. T. Scott, G. A. Alhadrami i R. A. M. Al Jassim. "Identification and characterisation of the predominant lactic acid-producing and lactic acid-utilising bacteria in the foregut of the feral camel (Camelus dromedarius) in Australia". Animal Production Science 51, nr 7 (2011): 597. http://dx.doi.org/10.1071/an10197.
Pełny tekst źródłaHutton, P., C. L. White, Z. Durmic i P. E. Vercoe. "Eremophila glabra is an Australian plant that reduces lactic acid accumulation in an in vitro glucose challenge designed to simulate lactic acidosis in ruminants". Animal 3, nr 9 (2009): 1254–63. http://dx.doi.org/10.1017/s1751731109004789.
Pełny tekst źródłaBacha, Flávia Barbieri, Rayane Chitolina Pupin, Paula Velozo Leal, Nilton Marques Carvalho, Gumercindo Loriano Franco, Camila Celeste Brandão Ferreira Ítavo, Franklin Riet-Correa i Ricardo Antônio Amaral de Lemos. "Experimental poisoning by Enterolobium contortisiliquum in sheep". Pesquisa Veterinária Brasileira 37, nr 1 (styczeń 2017): 23–30. http://dx.doi.org/10.1590/s0100-736x2017000100004.
Pełny tekst źródłaMcAllister, T. A., K. A. Beauchemin, A. Y. Alazzeh, J. Baah, R. M. Teather i K. Stanford. "Review: The use of direct fed microbials to mitigate pathogens and enhance production in cattle". Canadian Journal of Animal Science 91, nr 2 (czerwiec 2011): 193–211. http://dx.doi.org/10.4141/cjas10047.
Pełny tekst źródłaRozprawy doktorskie na temat "Lactic acidosis in ruminants"
Hutton, Peter. "Antimicrobial plants of Australia have the potential to prevent lactic acidosis in ruminants". University of Western Australia. School of Animal Biology, 2008. http://theses.library.uwa.edu.au/adt-WU2008.0159.
Pełny tekst źródłaWiryawan, I. Komang Gede. "Microbial control of lactic acidosis in grain-fed sheep". Title page, contents and summary only, 1994. http://web4.library.adelaide.edu.au/theses/09PH/09phw799.pdf.
Pełny tekst źródłaNordin, Angelica. "Genetic and functional studies of hereditary myopathy with lactic acidosis". Doctoral thesis, Umeå universitet, Medicinsk och klinisk genetik, 2011. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-50592.
Pełny tekst źródłaOsler, Meg. "Associations of severe hyperlactataemia and lactic acidosis in HIV-infected patients receiving antiretroviral theraphy". Master's thesis, University of Cape Town, 2007. http://hdl.handle.net/11427/7438.
Pełny tekst źródłaSevere symptomatic hyperlactataemia and lactic acidosis (SHLA) are life-threatening events that are occurring at increasing incidence levels in South Africa. Globally, the rise in SHLA cases is closely correlated to the increased accessibility of anti retroviral (ARV) medication for human immunodeficiency virus (HIV). Although hyperlactataemia and lactic acidosis were once thought of as rare conditions, they are now being recognized as important concerns when administering antiretroviral therapy. A better understanding of the risk factors for SHLA is important in combating the morbidity and mortality associated with such an adverse event.
Nlooto, Manimbulu. "Effect of stavudine dosage reduction on the incidence of symptomatic hyperlactataemia/lactic acidosis in adults female HIV/AIDS infected patients treated at Dr George Mukhari Hospital". Thesis, University of Limpopo (Medunsa Campus), 2010. http://hdl.handle.net/10386/216.
Pełny tekst źródłaWith the availability of Highly Active Antiretroviral Therapy (HAART), one of the limitations of treatment safety is the occurrence of adverse events associated with antiretroviral agents. The aim of this study was to establish whether stavudine dosage reduction prevents toxicity from developing and minimizes the incidence of symptomatic hyperlactataemia/lactic acidosis (LA) in adults female HIV/AIDS infected patients. This retrospective study covered adult patients treated at the adult ARV clinic, Dr George Mukhari Hospital. The records of 88 patients aged between 27 and 59 years, initiated and treated from August 2004 to January 2006, were analyzed ( 67 females and 21 males). Twenty nine females started their treatment on a regimen containing 40 mg stavudine while 38 females were started on 30 mg stavudine. A group of male patients (n=21) were included for comparison. Seven males started on 40 mg stavudine and 14 were on 30 mg stavudine. Ten out of twenty nine females who started treatment on 40 mg stavudine developed elevated lactate levels while nineteen received 30 mg stavudine as reduced dose. Eight out of nineteen further developed elevated lactate levels when on 30 mg stavudine but eleven out of nineteen remained stable on treatment with 30 mg stavudine as reduced dose. In the group started on 30 mg stavudine, thirteen females out of thirty seven developed elevated lactate levels while twenty four were stable on their treatment. Key words: stavudine, dosage reduction, lactate levels, hyperlactataemia, lactic acidosis.
Maruta, Celso Akio. "Comparação da susceptibilidade de bovinos das raças Jersey e Gir à acidose láctica ruminal, induzida experimentalmente com sacarose". Universidade de São Paulo, 2000. http://www.teses.usp.br/teses/disponiveis/10/10136/tde-24072007-082404/.
Pełny tekst źródłaFour Jersey (J) and four Gir (G) rumen-cannulated steers were used. The steers were fed, for two months before the beginning of the rumen lactic acidosis (RLA) induction, a standard diet of hay and concentrates. The RLA was induced experimentally through the administration of sucrose into the rumen, according to the corrected metabolic weight, after ORTOLANI (1995). Blood, rumen fluid, urine, and fecal samples were collected and clinical examination carried out in the following times after the induction: zero, 14, 16, 18, 20, 22 and 24 hours. The pH, the total lactic acid and its L and D isomers were determined in all samples. The hematocrit, acid-base variables and the creatinine concentration were determined in the blood samples; creatinine was also determined in the urine samples. All the rumen content was evacuated in order to evaluate its volume at the 24th h. A intense rumen acidosis was reached; no differences in the rumen fluid pH and in the concentration of the total lactic acid and its isomers were found in both studied breeds. A moderate level of systemic metabolic acidosis was reached in both breeds, but lower overall mean of bicarbonate and TCO2 (p < 0.0001) as well as blood pH (p < 0.025) were found in the J steers. These steers absorbed higher amounts of total lactic and its D isomer than the G animals; the higher the blood D-lactate concentration, the lower the blood pH (r = - O.78) in the former breed. Better blood pH homeostasis were kept, at the end of induction, by the G steers, probably by their higher efficiency to metabolize L-lactate. However, the G steers exhibited a higher level of dehydration as seen by the greater hematocrit and plasma volume deficit (p < 0.00001). They also presented a lower glomerular filtration as evidenced by the higher creatinine serum levels (p < 0.00001), its lower urinary clearance (p < 0.003) and the lower estimated urinary volume (p < 0.05). There were no differences in the fecal pH values presented by both breeds. There was a negative correlation between the fecal total lactate concentration and the fecal pH (r = - 0.65).
Rojas, Jesus Antonio. "Evaluation of the pH-stat modified approach for the treatment of non-respiratory (lactic) acidosis and vascular hyporeactivity caused by hemorrhagic shock in dogs". Columbus, Ohio : Ohio State University, 2003. http://rave.ohiolink.edu/etdc/view?acc%5fnum=osu1063035811.
Pełny tekst źródłaTitle from first page of PDF file. Document formatted into pages; contains xvi, 246 p.; also contains graphics. Includes abstract and vita. Advisor: William W. Muir, Dept. of Veterinary Clinical Sciences. Includes bibliographical references (p. 229-246).
Rojas, Jesus Antonio Sr. "Evaluation of the pH-stat modified approach for the treatment of non-respiratory (lactic) acidosis and vascular hyporeactivity caused by hemorrhagic shock in dogs". The Ohio State University, 2003. http://rave.ohiolink.edu/etdc/view?acc_num=osu1063035811.
Pełny tekst źródłaSarti, Luís Marcelo Nave [UNESP]. "Efeito da suplementação com anticorpos policlonais e/ou monensina sódica sobre a saúde ruminal de bovinos jovens confinados". Universidade Estadual Paulista (UNESP), 2010. http://hdl.handle.net/11449/95211.
Pełny tekst źródłaCoordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)
Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
Universidade Estadual Paulista (UNESP)
O objetivo deste estudo foi avaliar os efeitos dos anticorpos policlonais, preparados contra as bactérias ruminais Streptococcus bovis, Fusobacterium necrophorum, Lactobacillus e endotoxina, ou monensina sódica sobre perfil metabólico sanguíneo e variações na ingestão diária de matéria seca de bovinos jovens confinados com diferentes níveis de concentrado. Foram utilizados 72 animais Brangus, machos, não castrados, desmamados com nove meses de idade, com peso vivo médio inicial de 261,04 ± 34,73 kg divididos em 24 baias (3 animais/baia), com 6 repetições (baias) em cada tratamento. Todos os animais foram submetidos à mesma dieta (ad libitum), tipo de alojamento e manejo. As dietas apenas foram diferentes no tocante aos aditivos alimentares utilizados: controle (sem aditivo), monensina sódica - MON, anticorpos policlonais – PAP ou mistura de monensina sódica com anticorpos policlonais – MIX, estes, na forma de pó. O delineamento experimental foi inteiramente casualizado em arranjo fatorial 2 x 2 com medidas repetidas no tempo, sendo os fatores: inclusão ou não de monensina sódica e inclusão ou não de anticorpos policlonais. Medidas de tempo foram tomadas de acordo com o período: adaptação, crescimento e terminação. Os dados de gasometria foram avaliados após 21 dias do início de cada período. A ingestão e a variação diária de matéria seca (IDMS e VIDMS, respectivamente) foram obtidas nos quatro primeiros dias após mudança do período de adaptação para crescimento e de crescimento para terminação. Não houve efeito (P<0,05) de aditivos para IDMS e VIDMS, apenas interação entre período e os 4 dias para as duas variáveis, com maior IDMS no dia 3 seguido de queda no dia 4 durante o período de crescimento e VIDMS nos quatro dias após mudança de dieta. Durante a terminação houve menor IDMS no dia 2 mas não foi observado VIDMS nos quatro primeiros...
The aim of this study was to evaluate the effects of polyclonal antibodies preparation (PAP) or monensin (MON) against rumen bacteria (Streptococcus bovis, Fusobacterium necrophorum, Lactobacillus and endotoxin) on blood metabolic profile and variations in daily dry matter intake (DM) of feedlot cattle fed high concentrate diets. Seventy-two 9-mo-old bullocks (261.04 ± 34.73 kg) were housed in 24 pens (3 bullocks/pen) and assigned to a completely randomized with 2 x 2 factorial arrangement with 6 replications per treatment. All animals received the same diet (ad libitum), type of accommodation and management. The diets treatments were different only about feed additives used: control (no additive), MON, PAP or MON + PAP (MIX). Factors were inclusion or not of PAP or MON, at a dose of 300 mg/kg DM or at 30 mg/ kg DM, respectively. Measures over time were taken according to the phase: adaptation, growing and finishing. Blood samples were collected and evaluated after 21 days of the beginning of each phase. The intake and daily variation of dry matter (IDMS and VIDMS, respectively) were obtained in the first four days of each phase. There was no effect (P < 0.05) additive for IDMS and VIDMS, only interaction between phase and four days for both variables, with higher IDMS on day 3 and then decreased on day 4 during the growth phase and VIDMS during four days after changing the diet. During the finishing, IDMS was lower on day 2, but was not observed VIDMS the first four days after change of diet. PAP and MON treatments had higher blood pH compared to MIX, but not different from control. In the finishing phase was observed lower blood pH compared with other phases... (Complete abstract click electronic access below)
Rafael, Arenas-Pinto A. "Studies on clinical and epidemiological factors associated with peripheral neuropathy and severe hyperlactatemia or lactic acidosis in HIV-infected adults exposed to nucleoside analogues reverse transcriptase inhibitors". Thesis, University College London (University of London), 2007. http://discovery.ucl.ac.uk/1444011/.
Pełny tekst źródłaKsiążki na temat "Lactic acidosis in ruminants"
Publications, ICON Health. Lactic Acidosis - A Medical Dictionary, Bibliography, and Annotated Research Guide to Internet References. ICON Health Publications, 2004.
Znajdź pełny tekst źródłaJanssen, Mirian C. H., i Shamima Rahman. Pyruvate Dehydrogenase Complex Deficiency. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0006.
Pełny tekst źródłaNeligan, Patrick J., i Clifford S. Deutschman. Management of metabolic acidosis in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0256.
Pełny tekst źródłaNeligan, Patrick J., i Clifford S. Deutschman. Pathophysiology and causes of metabolic acidosis in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0255.
Pełny tekst źródłaPereira, Luis F., Harold W. Goforth, Esteban Martínez, Joseph Z. Lux, Maria Ferrara i Michael P. Mullen. Cardiovascular Disease, Metabolic Complications and Lipodystrophy in Persons with HIV. Redaktorzy Mary Ann Cohen, Jack M. Gorman, Jeffrey M. Jacobson, Paul Volberding i Scott Letendre. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199392742.003.0046.
Pełny tekst źródłaD’Mello, Ajay. Mitochondrial Disease. Redaktorzy Kirk Lalwani, Ira Todd Cohen, Ellen Y. Choi i Vidya T. Raman. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190685157.003.0047.
Pełny tekst źródłaSedel, Frédéric, i Carla E. M. Hollak. Disorders of Thiamine Metabolism. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0028.
Pełny tekst źródłaTuxen, David V. Pathophysiology and causes of airflow limitation. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0110.
Pełny tekst źródłaBower, Mark, Louise Robinson i Sarah Cox. Endocrine and metabolic complications of advanced cancer. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199656097.003.0142.
Pełny tekst źródłaStaitieh, Bashar S., i Greg S. Martin. Therapeutic goals of fluid resuscitation. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0070.
Pełny tekst źródłaCzęści książek na temat "Lactic acidosis in ruminants"
Hutton, Peter G., T. G. Nagaraja, Colin L. White i Philip E. Vercoe. "Screening Plants for the Antimicrobial Control of Lactic Acidosis in Ruminant Livestock". W In vitro screening of plant resources for extra-nutritional attributes in ruminants: nuclear and related methodologies, 159–89. Dordrecht: Springer Netherlands, 2009. http://dx.doi.org/10.1007/978-90-481-3297-3_9.
Pełny tekst źródłaBacker, Daniel De. "Lactic acidosis". W Applied Physiology in Intensive Care Medicine, 89–92. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-642-01769-8_22.
Pełny tekst źródłaDe Backer, Daniel. "Lactic acidosis". W Applied Physiology in Intensive Care Medicine, 69–72. Berlin, Heidelberg: Springer Berlin Heidelberg, 2006. http://dx.doi.org/10.1007/3-540-37363-2_18.
Pełny tekst źródłaPerret, Cl. "Lactic Acidosis". W Update in Intensive Care and Emergency Medicine, 287–89. Berlin, Heidelberg: Springer Berlin Heidelberg, 1985. http://dx.doi.org/10.1007/978-3-642-70309-6_60.
Pełny tekst źródłaReddi, Alluru S. "Lactic Acidosis". W Acid-Base Disorders, 63–83. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-28895-2_5.
Pełny tekst źródłaSchmidt, G. A. "Lactic Acidosis". W Anaesthesia, Pain, Intensive Care and Emergency Medicine — A.P.I.C.E., 695–705. Milano: Springer Milan, 2002. http://dx.doi.org/10.1007/978-88-470-2099-3_58.
Pełny tekst źródłaDe Backer, Daniel. "Lactic acidosis". W Applied Physiology in Intensive Care Medicine 1, 111–14. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-642-28270-6_25.
Pełny tekst źródłaLevy, B. "Lactic Acidosis and Hyperlactatemia". W Yearbook of Intensive Care and Emergency Medicine, 88–98. Berlin, Heidelberg: Springer Berlin Heidelberg, 2006. http://dx.doi.org/10.1007/3-540-33396-7_9.
Pełny tekst źródłaLalau, Jean-Daniel. "Metformin and Lactic Acidosis". W Mitochondrial Dysfunction Caused by Drugs and Environmental Toxicants, 559–61. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2018. http://dx.doi.org/10.1002/9781119329725.ch37.
Pełny tekst źródłaTentolouris, Nikolaos, i Nikolaos Katsilambros. "Lactic Acidosis in Diabetes". W Diabetic Emergencies, 133–47. Oxford, UK: Wiley-Blackwell, 2011. http://dx.doi.org/10.1002/9781119971825.ch6.
Pełny tekst źródłaStreszczenia konferencji na temat "Lactic acidosis in ruminants"
Raoof, S. "Metformin Associated Lactic Acidosis". W American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a4805.
Pełny tekst źródłaTsay, Junchieh J., Derrick Raptis i David R. Schwartz. "Lactic Acidosis In Metastatic Melanoma". W American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a4609.
Pełny tekst źródłaGanta, Ashwin, Ratna Priya Gangi, Wilson Gonsalves, Sonica Saini i Tammy Wichman. "Inhalational Beta Agonist Induced Lactic Acidosis". W American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a1343.
Pełny tekst źródłaHamarshi, Majdi. "Severe Lactic Acidosis In A Hemodynamically Stable Patient". W American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a3177.
Pełny tekst źródłaSharma, N., D. C. Kazmierski, S. Li i P. O. Ochieng. "The Occult Culprit: Lactic Acidosis Due to Corticosteroids". W American Thoracic Society 2021 International Conference, May 14-19, 2021 - San Diego, CA. American Thoracic Society, 2021. http://dx.doi.org/10.1164/ajrccm-conference.2021.203.1_meetingabstracts.a2908.
Pełny tekst źródłaAnnan, Dorcas A., Nako Maishi, Tomoyoshi Soga, Randa Dawood, Yasuhiro Hida i Kyoko Hida. "Abstract 2054: Tumor endothelial cells survive under lactic acidosis". W Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-2054.
Pełny tekst źródłaKhan, A. A., F. Chaudhary i S. Sarkar. "Metformin Induced Lactic Acidosis - A Rare but Treatable Entity". W American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a1740.
Pełny tekst źródłaAhmed, R., W. Illyas i Y. Hiltzik. "Profound Lactic Acidosis from Metformin Toxicity Confounded by Septic Shock". W American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a5179.
Pełny tekst źródłaSoni, P., V. Ponnusamy, S. Sharma, A. Sinha, C. Seneviratne i Y. Kupfer. "A Case of Severe Lactic Acidosis Due to Metformin Toxicity". W American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a4849.
Pełny tekst źródłaPrice, J. D., i K. El-Kersh. "Thyroid Storm Presenting with Multiorgan Failure and Severe Lactic Acidosis". W American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a1712.
Pełny tekst źródłaRaporty organizacyjne na temat "Lactic acidosis in ruminants"
Rodriquez, Fernando, Mark A. Rasmussen i Milton J. Allison. Discovery of a Probiotic to Reduce the Risk of Lactic Acidosis in Cattle. Ames (Iowa): Iowa State University, styczeń 2007. http://dx.doi.org/10.31274/ans_air-180814-563.
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