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Homocysteine Metabolism in Children with Idiopathic Nephrotic Syndrome
Background Homocysteine metabolism is altered in children with idiopathic nephrotic syndrome. Hyperhomocysteinemia is a risk factor of early atherosclerosis and glomerulosclerosis and may occur at time of first occurrence of idiopathic nephrotic syndrome. Methods Thirty children with first episode o...
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Published in: | Clinical and translational science 2014-04, Vol.7 (2), p.132-136 |
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creator | Kundal, Mohan Saha, Abhijeet Dubey, N.K. Kapoor, Kanika Basak, Trayambak Bhardwaj, Gaurav Tanwar, Vinay Singh Sengupta, Shantanu Batra, Vinita Upadhayay, Ashish Dutt Bhatt, Ajay |
description | Background
Homocysteine metabolism is altered in children with idiopathic nephrotic syndrome. Hyperhomocysteinemia is a risk factor of early atherosclerosis and glomerulosclerosis and may occur at time of first occurrence of idiopathic nephrotic syndrome.
Methods
Thirty children with first episode of idiopathic nephrotic syndrome (FENS) aged 1–16 years along with 30 age‐ and sex‐matched healthy controls were enrolled in this study. Homocysteine and cysteine were measured with HPLC; vitamin B12 and folic acid were measured with electro‐chemilumiscence immunoassay. Primary outcome measure was plasma homocysteine level in children with FENS and in controls. Secondary outcome measures were (1) plasma and urine homocysteine and cysteine levels in children with FENS at 12 weeks and 1 year (remission) and (2) plasma and urine levels of vitamin B12 and folic acid in children with FENS, at 12 weeks and 1 year (remission).
Results
Plasma homocysteine and cysteine levels were comparable to controls in children with FENS, at 12 weeks and 1‐year remission. Plasma levels of vitamin B12 and folic acid were significantly decreased compared to controls in FENS due to increased urinary excretion, which normalize during remission at 12 weeks and 1 year. Urinary homocysteine and cysteine levels were significantly raised in FENS compared to controls and continued to be raised even at 12‐week and 1‐year remission.
Conclusion
Homocysteine metabolism is deranged in children with FENS. Renal effects of long‐term raised urinary homocysteine levels need to be studied. |
doi_str_mv | 10.1111/cts.12145 |
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fullrecord | <record><control><sourceid>proquest_24P</sourceid><recordid>TN_cdi_doaj_primary_oai_doaj_org_article_f11202583034401b8a61ead3bac7ae4d</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><doaj_id>oai_doaj_org_article_f11202583034401b8a61ead3bac7ae4d</doaj_id><sourcerecordid>1520111094</sourcerecordid><originalsourceid>FETCH-LOGICAL-c5375-6206bb52beb13a872e9e8cf854ea929bf5327a0b52da549d7c468614386a54163</originalsourceid><addsrcrecordid>eNp9kktv1DAQgC0EoqX0wB9AkbiUw7Z-x7kgoVVLVypwaHu2_Jg0XiXxYmep9t_jNmVFkcAXj-1Pn8fjQegdwaekjDM35VNCCRcv0CGpBV0oLOnLfSz4AXqT8xpjyaQSr9EB5VxIoepDdHEZh-h2eYIwQvUVJmNjH_JQhbFadqH3CcbqPkxdtfIhbszUBVd9g02X4lSi693oUxzgLXrVmj7D8dN8hG4vzm-Wl4ur719Wy89XCydYLRaSYmmtoBYsYUbVFBpQrlWCg2loY1vBaG1wIbwRvPG141JJwpmSZU0kO0Kr2eujWetNCoNJOx1N0I8bMd1pk0piPeiWEIqpUAwzzjGxykgCxjNrXG2A--L6NLs2WzuAdzBOyfTPpM9PxtDpu_hTCyZwI2gRnDwJUvyxhTzpIWQHfW9GiNusiaC4fA9ueEE__IWu4zaNpVSasgYXriH4fxQRpBQIU_Zw7ceZcinmnKDdp0ywfugHXfpBP_ZDYd__-cY9-bsBCnA2A_ehh92_TXp5cz0rfwE32L1D</addsrcrecordid><sourcetype>Open Website</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1519290232</pqid></control><display><type>article</type><title>Homocysteine Metabolism in Children with Idiopathic Nephrotic Syndrome</title><source>Wiley Online Library Open Access</source><creator>Kundal, Mohan ; Saha, Abhijeet ; Dubey, N.K. ; Kapoor, Kanika ; Basak, Trayambak ; Bhardwaj, Gaurav ; Tanwar, Vinay Singh ; Sengupta, Shantanu ; Batra, Vinita ; Upadhayay, Ashish Dutt ; Bhatt, Ajay</creator><creatorcontrib>Kundal, Mohan ; Saha, Abhijeet ; Dubey, N.K. ; Kapoor, Kanika ; Basak, Trayambak ; Bhardwaj, Gaurav ; Tanwar, Vinay Singh ; Sengupta, Shantanu ; Batra, Vinita ; Upadhayay, Ashish Dutt ; Bhatt, Ajay</creatorcontrib><description>Background
Homocysteine metabolism is altered in children with idiopathic nephrotic syndrome. Hyperhomocysteinemia is a risk factor of early atherosclerosis and glomerulosclerosis and may occur at time of first occurrence of idiopathic nephrotic syndrome.
Methods
Thirty children with first episode of idiopathic nephrotic syndrome (FENS) aged 1–16 years along with 30 age‐ and sex‐matched healthy controls were enrolled in this study. Homocysteine and cysteine were measured with HPLC; vitamin B12 and folic acid were measured with electro‐chemilumiscence immunoassay. Primary outcome measure was plasma homocysteine level in children with FENS and in controls. Secondary outcome measures were (1) plasma and urine homocysteine and cysteine levels in children with FENS at 12 weeks and 1 year (remission) and (2) plasma and urine levels of vitamin B12 and folic acid in children with FENS, at 12 weeks and 1 year (remission).
Results
Plasma homocysteine and cysteine levels were comparable to controls in children with FENS, at 12 weeks and 1‐year remission. Plasma levels of vitamin B12 and folic acid were significantly decreased compared to controls in FENS due to increased urinary excretion, which normalize during remission at 12 weeks and 1 year. Urinary homocysteine and cysteine levels were significantly raised in FENS compared to controls and continued to be raised even at 12‐week and 1‐year remission.
Conclusion
Homocysteine metabolism is deranged in children with FENS. Renal effects of long‐term raised urinary homocysteine levels need to be studied.</description><identifier>ISSN: 1752-8054</identifier><identifier>EISSN: 1752-8062</identifier><identifier>DOI: 10.1111/cts.12145</identifier><identifier>PMID: 24456587</identifier><language>eng</language><publisher>United States: John Wiley & Sons, Inc</publisher><subject>Acids ; Arteriosclerosis ; Binding sites ; Blood pressure ; Case-Control Studies ; Chemical bonds ; Child ; Children ; Cholesterol - blood ; Communication ; Competition ; Cysteine ; Cysteine - blood ; Cysteine - urine ; Demography ; Female ; Folic acid ; Folic Acid - blood ; Health risk assessment ; High-performance liquid chromatography ; Homocysteine ; Homocysteine - blood ; Homocysteine - metabolism ; Humans ; Hyperhomocysteinemia ; Hypertension ; Kidney diseases ; Male ; Metabolism ; Nephrotic syndrome ; Nephrotic Syndrome - blood ; Nephrotic Syndrome - metabolism ; Nephrotic Syndrome - urine ; Pediatrics ; Plasma levels ; Population ; Potassium ; Proteins ; Proteinuria - blood ; Remission ; Remission Induction ; Risk factors ; Serum Albumin - metabolism ; Standard deviation ; Statistical analysis ; Studies ; Thrombosis ; Urine ; Vitamin B ; Vitamin B 12 - blood ; Vitamin B12</subject><ispartof>Clinical and translational science, 2014-04, Vol.7 (2), p.132-136</ispartof><rights>2014 Wiley Periodicals, Inc.</rights><rights>Copyright John Wiley & Sons, Inc. Apr 2014</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5375-6206bb52beb13a872e9e8cf854ea929bf5327a0b52da549d7c468614386a54163</citedby><cites>FETCH-LOGICAL-c5375-6206bb52beb13a872e9e8cf854ea929bf5327a0b52da549d7c468614386a54163</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5350952/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5350952/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,727,780,784,885,11562,27924,27925,46052,46476,53791,53793</link.rule.ids><linktorsrc>$$Uhttps://onlinelibrary.wiley.com/doi/abs/10.1111%2Fcts.12145$$EView_record_in_Wiley-Blackwell$$FView_record_in_$$GWiley-Blackwell</linktorsrc><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24456587$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kundal, Mohan</creatorcontrib><creatorcontrib>Saha, Abhijeet</creatorcontrib><creatorcontrib>Dubey, N.K.</creatorcontrib><creatorcontrib>Kapoor, Kanika</creatorcontrib><creatorcontrib>Basak, Trayambak</creatorcontrib><creatorcontrib>Bhardwaj, Gaurav</creatorcontrib><creatorcontrib>Tanwar, Vinay Singh</creatorcontrib><creatorcontrib>Sengupta, Shantanu</creatorcontrib><creatorcontrib>Batra, Vinita</creatorcontrib><creatorcontrib>Upadhayay, Ashish Dutt</creatorcontrib><creatorcontrib>Bhatt, Ajay</creatorcontrib><title>Homocysteine Metabolism in Children with Idiopathic Nephrotic Syndrome</title><title>Clinical and translational science</title><addtitle>Clin Transl Sci</addtitle><description>Background
Homocysteine metabolism is altered in children with idiopathic nephrotic syndrome. Hyperhomocysteinemia is a risk factor of early atherosclerosis and glomerulosclerosis and may occur at time of first occurrence of idiopathic nephrotic syndrome.
Methods
Thirty children with first episode of idiopathic nephrotic syndrome (FENS) aged 1–16 years along with 30 age‐ and sex‐matched healthy controls were enrolled in this study. Homocysteine and cysteine were measured with HPLC; vitamin B12 and folic acid were measured with electro‐chemilumiscence immunoassay. Primary outcome measure was plasma homocysteine level in children with FENS and in controls. Secondary outcome measures were (1) plasma and urine homocysteine and cysteine levels in children with FENS at 12 weeks and 1 year (remission) and (2) plasma and urine levels of vitamin B12 and folic acid in children with FENS, at 12 weeks and 1 year (remission).
Results
Plasma homocysteine and cysteine levels were comparable to controls in children with FENS, at 12 weeks and 1‐year remission. Plasma levels of vitamin B12 and folic acid were significantly decreased compared to controls in FENS due to increased urinary excretion, which normalize during remission at 12 weeks and 1 year. Urinary homocysteine and cysteine levels were significantly raised in FENS compared to controls and continued to be raised even at 12‐week and 1‐year remission.
Conclusion
Homocysteine metabolism is deranged in children with FENS. Renal effects of long‐term raised urinary homocysteine levels need to be studied.</description><subject>Acids</subject><subject>Arteriosclerosis</subject><subject>Binding sites</subject><subject>Blood pressure</subject><subject>Case-Control Studies</subject><subject>Chemical bonds</subject><subject>Child</subject><subject>Children</subject><subject>Cholesterol - blood</subject><subject>Communication</subject><subject>Competition</subject><subject>Cysteine</subject><subject>Cysteine - blood</subject><subject>Cysteine - urine</subject><subject>Demography</subject><subject>Female</subject><subject>Folic acid</subject><subject>Folic Acid - blood</subject><subject>Health risk assessment</subject><subject>High-performance liquid chromatography</subject><subject>Homocysteine</subject><subject>Homocysteine - blood</subject><subject>Homocysteine - metabolism</subject><subject>Humans</subject><subject>Hyperhomocysteinemia</subject><subject>Hypertension</subject><subject>Kidney diseases</subject><subject>Male</subject><subject>Metabolism</subject><subject>Nephrotic syndrome</subject><subject>Nephrotic Syndrome - blood</subject><subject>Nephrotic Syndrome - metabolism</subject><subject>Nephrotic Syndrome - urine</subject><subject>Pediatrics</subject><subject>Plasma levels</subject><subject>Population</subject><subject>Potassium</subject><subject>Proteins</subject><subject>Proteinuria - blood</subject><subject>Remission</subject><subject>Remission Induction</subject><subject>Risk factors</subject><subject>Serum Albumin - metabolism</subject><subject>Standard deviation</subject><subject>Statistical analysis</subject><subject>Studies</subject><subject>Thrombosis</subject><subject>Urine</subject><subject>Vitamin B</subject><subject>Vitamin B 12 - blood</subject><subject>Vitamin B12</subject><issn>1752-8054</issn><issn>1752-8062</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>DOA</sourceid><recordid>eNp9kktv1DAQgC0EoqX0wB9AkbiUw7Z-x7kgoVVLVypwaHu2_Jg0XiXxYmep9t_jNmVFkcAXj-1Pn8fjQegdwaekjDM35VNCCRcv0CGpBV0oLOnLfSz4AXqT8xpjyaQSr9EB5VxIoepDdHEZh-h2eYIwQvUVJmNjH_JQhbFadqH3CcbqPkxdtfIhbszUBVd9g02X4lSi693oUxzgLXrVmj7D8dN8hG4vzm-Wl4ur719Wy89XCydYLRaSYmmtoBYsYUbVFBpQrlWCg2loY1vBaG1wIbwRvPG141JJwpmSZU0kO0Kr2eujWetNCoNJOx1N0I8bMd1pk0piPeiWEIqpUAwzzjGxykgCxjNrXG2A--L6NLs2WzuAdzBOyfTPpM9PxtDpu_hTCyZwI2gRnDwJUvyxhTzpIWQHfW9GiNusiaC4fA9ueEE__IWu4zaNpVSasgYXriH4fxQRpBQIU_Zw7ceZcinmnKDdp0ywfugHXfpBP_ZDYd__-cY9-bsBCnA2A_ehh92_TXp5cz0rfwE32L1D</recordid><startdate>201404</startdate><enddate>201404</enddate><creator>Kundal, Mohan</creator><creator>Saha, Abhijeet</creator><creator>Dubey, N.K.</creator><creator>Kapoor, Kanika</creator><creator>Basak, Trayambak</creator><creator>Bhardwaj, Gaurav</creator><creator>Tanwar, Vinay Singh</creator><creator>Sengupta, Shantanu</creator><creator>Batra, Vinita</creator><creator>Upadhayay, Ashish Dutt</creator><creator>Bhatt, Ajay</creator><general>John Wiley & Sons, Inc</general><general>John Wiley and Sons Inc</general><general>Wiley</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QP</scope><scope>7T5</scope><scope>7TK</scope><scope>7TM</scope><scope>7U9</scope><scope>8FD</scope><scope>FR3</scope><scope>H94</scope><scope>K9.</scope><scope>M7N</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>201404</creationdate><title>Homocysteine Metabolism in Children with Idiopathic Nephrotic Syndrome</title><author>Kundal, Mohan ; Saha, Abhijeet ; Dubey, N.K. ; Kapoor, Kanika ; Basak, Trayambak ; Bhardwaj, Gaurav ; Tanwar, Vinay Singh ; Sengupta, Shantanu ; Batra, Vinita ; Upadhayay, Ashish Dutt ; Bhatt, Ajay</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5375-6206bb52beb13a872e9e8cf854ea929bf5327a0b52da549d7c468614386a54163</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>Acids</topic><topic>Arteriosclerosis</topic><topic>Binding sites</topic><topic>Blood pressure</topic><topic>Case-Control Studies</topic><topic>Chemical bonds</topic><topic>Child</topic><topic>Children</topic><topic>Cholesterol - blood</topic><topic>Communication</topic><topic>Competition</topic><topic>Cysteine</topic><topic>Cysteine - blood</topic><topic>Cysteine - urine</topic><topic>Demography</topic><topic>Female</topic><topic>Folic acid</topic><topic>Folic Acid - blood</topic><topic>Health risk assessment</topic><topic>High-performance liquid chromatography</topic><topic>Homocysteine</topic><topic>Homocysteine - blood</topic><topic>Homocysteine - metabolism</topic><topic>Humans</topic><topic>Hyperhomocysteinemia</topic><topic>Hypertension</topic><topic>Kidney diseases</topic><topic>Male</topic><topic>Metabolism</topic><topic>Nephrotic syndrome</topic><topic>Nephrotic Syndrome - blood</topic><topic>Nephrotic Syndrome - metabolism</topic><topic>Nephrotic Syndrome - urine</topic><topic>Pediatrics</topic><topic>Plasma levels</topic><topic>Population</topic><topic>Potassium</topic><topic>Proteins</topic><topic>Proteinuria - blood</topic><topic>Remission</topic><topic>Remission Induction</topic><topic>Risk factors</topic><topic>Serum Albumin - metabolism</topic><topic>Standard deviation</topic><topic>Statistical analysis</topic><topic>Studies</topic><topic>Thrombosis</topic><topic>Urine</topic><topic>Vitamin B</topic><topic>Vitamin B 12 - blood</topic><topic>Vitamin B12</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kundal, Mohan</creatorcontrib><creatorcontrib>Saha, Abhijeet</creatorcontrib><creatorcontrib>Dubey, N.K.</creatorcontrib><creatorcontrib>Kapoor, Kanika</creatorcontrib><creatorcontrib>Basak, Trayambak</creatorcontrib><creatorcontrib>Bhardwaj, Gaurav</creatorcontrib><creatorcontrib>Tanwar, Vinay Singh</creatorcontrib><creatorcontrib>Sengupta, Shantanu</creatorcontrib><creatorcontrib>Batra, Vinita</creatorcontrib><creatorcontrib>Upadhayay, Ashish Dutt</creatorcontrib><creatorcontrib>Bhatt, Ajay</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Immunology Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>Clinical and translational science</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext_linktorsrc</fulltext></delivery><addata><au>Kundal, Mohan</au><au>Saha, Abhijeet</au><au>Dubey, N.K.</au><au>Kapoor, Kanika</au><au>Basak, Trayambak</au><au>Bhardwaj, Gaurav</au><au>Tanwar, Vinay Singh</au><au>Sengupta, Shantanu</au><au>Batra, Vinita</au><au>Upadhayay, Ashish Dutt</au><au>Bhatt, Ajay</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Homocysteine Metabolism in Children with Idiopathic Nephrotic Syndrome</atitle><jtitle>Clinical and translational science</jtitle><addtitle>Clin Transl Sci</addtitle><date>2014-04</date><risdate>2014</risdate><volume>7</volume><issue>2</issue><spage>132</spage><epage>136</epage><pages>132-136</pages><issn>1752-8054</issn><eissn>1752-8062</eissn><abstract>Background
Homocysteine metabolism is altered in children with idiopathic nephrotic syndrome. Hyperhomocysteinemia is a risk factor of early atherosclerosis and glomerulosclerosis and may occur at time of first occurrence of idiopathic nephrotic syndrome.
Methods
Thirty children with first episode of idiopathic nephrotic syndrome (FENS) aged 1–16 years along with 30 age‐ and sex‐matched healthy controls were enrolled in this study. Homocysteine and cysteine were measured with HPLC; vitamin B12 and folic acid were measured with electro‐chemilumiscence immunoassay. Primary outcome measure was plasma homocysteine level in children with FENS and in controls. Secondary outcome measures were (1) plasma and urine homocysteine and cysteine levels in children with FENS at 12 weeks and 1 year (remission) and (2) plasma and urine levels of vitamin B12 and folic acid in children with FENS, at 12 weeks and 1 year (remission).
Results
Plasma homocysteine and cysteine levels were comparable to controls in children with FENS, at 12 weeks and 1‐year remission. Plasma levels of vitamin B12 and folic acid were significantly decreased compared to controls in FENS due to increased urinary excretion, which normalize during remission at 12 weeks and 1 year. Urinary homocysteine and cysteine levels were significantly raised in FENS compared to controls and continued to be raised even at 12‐week and 1‐year remission.
Conclusion
Homocysteine metabolism is deranged in children with FENS. Renal effects of long‐term raised urinary homocysteine levels need to be studied.</abstract><cop>United States</cop><pub>John Wiley & Sons, Inc</pub><pmid>24456587</pmid><doi>10.1111/cts.12145</doi><tpages>5</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Acids Arteriosclerosis Binding sites Blood pressure Case-Control Studies Chemical bonds Child Children Cholesterol - blood Communication Competition Cysteine Cysteine - blood Cysteine - urine Demography Female Folic acid Folic Acid - blood Health risk assessment High-performance liquid chromatography Homocysteine Homocysteine - blood Homocysteine - metabolism Humans Hyperhomocysteinemia Hypertension Kidney diseases Male Metabolism Nephrotic syndrome Nephrotic Syndrome - blood Nephrotic Syndrome - metabolism Nephrotic Syndrome - urine Pediatrics Plasma levels Population Potassium Proteins Proteinuria - blood Remission Remission Induction Risk factors Serum Albumin - metabolism Standard deviation Statistical analysis Studies Thrombosis Urine Vitamin B Vitamin B 12 - blood Vitamin B12 |
title | Homocysteine Metabolism in Children with Idiopathic Nephrotic Syndrome |
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