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Both may present fine elastic fragmentation and a decrease in collagen. We analyzed whether alterations in the three-dimensional structure of these fibers could be involved in the pathogenesis of AscAA\u002FAD. Specimens obtained at surgery for these diseases (n = 4 for each) and on coronary artery bypass surgery (controls, n = 4) were submitted to treatments which either preserve collagen or the elastic structure. These samples were examined by scanning electron microscopy. In all groups most of the collagen fibers were packed, forming laminar structures very similar to the elastic lamellae. In AscAA\u002FAD, the fibers showed signs of degradation and\u002For fragmentation. Elastic tissue was distributed in large sheets with fenestrations, with smaller branches between them. In 1 of the dissection cases and 2 of the aneurysm cases elastic sheet fragmentation, which under light microscopy seems to be located at random, had a pattern of clefts which were irregular but approximately transversal to the main axis of the wall. The recognition of this pattern and the degradation\u002Ffragmentation of collagen and elastic fibrils facilitates understanding of why the wall is weak and affected by aneurysms and dissections.\u003C\u002Fjats:p>",{"EN":1196},"Why Do Aortas Cleave or Dilate? 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Migration of rat aortic SMCs from an upper chamber towards a lower one has been studied in a microchemotaxis (Boyden) chamber. Spontaneous migration of SMCs was practically prevented by the presence of endothelium in the lower chamber and was reduced if endothelial cells were substituted with endothelial cell-conditioned medium. Endothelial cells which had been treated with either the inhibitor of protein synthesis cycloheximide or nitric oxide synthesis N<sup>G<\u002Fsup>-nitro-<i>L<\u002Fi>-arginine showed no inhibitory effect on SMC migration. Addition of a nitric oxide donor S-nitroso-N-acetylpenicillamine to cell-free medium in the lower chamber prevented SMC migration. Addition of native LDL to endothelial cells had no effect on SMC migration, while (UV light) oxidised LDL completely abolished the inhibitory effect of endothelial cells on SMC migration. It is concluded that via nitric oxide, endothelium exerts a powerful inhibitory effect on SMC migration. This effect of intact endothelium is completely abolished by oxidised LDL applied in a concentration, which is relevant to those measured in plasma of patients with severe coronary artery disease. It is suggested that oxidised LDL may contribute to the pathogenesis of atherogenesis by stimulating migration of SMCs from media to the intima via abolishing the physiological inhibitory effect of normal endothelium.\u003C\u002Fjats:p>",{"EN":1398},"Inhibition of Vascular Smooth Muscle Cell Migration by Intact Endothelium Is Nitric Oxide-Mediated: Interference by Oxidised Low Density Lipoproteins",{"VOID":1400},"9647330",{"VOID":1402},"10.1159\u002F000025580",[145],"https:\u002F\u002Fkarger.com\u002FJVR\u002Farticle\u002Fdoi\u002F10.1159\u002F000025580",[1406,1425],{"id":1407,"sortIndex":53,"researcher":24,"roles":1408,"affiliations":1409,"properties":1420},"8b2c9185-f7d7-4207-be91-d85b830ca345",[],[1410],{"id":1411,"sortIndex":25,"affiliation":1412,"properties":24},"ac74b8c4-4c7e-4e32-9068-42f025b509d5",{"id":1413,"createTime":1414,"updateTime":1414,"relativeEntities":1415,"slug":1416,"properties":1417,"entityType":52,"verifyStatus":23,"verifyTime":24,"verifyNote":24,"syncStatus":23,"languages":24,"translateLanguages":24,"viewCount":25},"5acbf5e9-221d-4e27-93da-e78bf1a32c54","2024-07-18T16:30:43.734+00:00",[],"Thrombosis-Unit-St-Bartholomew-s-Hospital-London-UK",{"title":1418},{"EN":1419},"Thrombosis Unit, St. Bartholomew’s Hospital, London, UK",{"openalex":1421,"title":1423},{"VOID":1422},"A5002654204",{"EN":1424},"Iren B. Kovács",{"id":1426,"sortIndex":25,"researcher":24,"roles":1427,"affiliations":1428,"properties":1439},"296bedeb-6000-44fe-95e7-6a7544622c2a",[],[1429],{"id":1430,"sortIndex":25,"affiliation":1431,"properties":24},"e3e77896-1151-4ad8-97ed-ec396a6304e7",{"id":1432,"createTime":1433,"updateTime":1433,"relativeEntities":1434,"slug":1435,"properties":1436,"entityType":52,"verifyStatus":23,"verifyTime":24,"verifyNote":24,"syncStatus":23,"languages":24,"translateLanguages":24,"viewCount":25},"29836fee-c595-4dd6-8559-0863373715aa","2024-07-18T16:30:43.721+00:00",[],"Pathopharmacology-Unit-The-William-Harvey-Research-Institute-and",{"title":1437},{"EN":1438},"Pathopharmacology Unit, The William Harvey Research Institute and",{"openalex":1440,"title":1442},{"VOID":1441},"A5060516072",{"EN":1443},"P. Görög",{"url":24,"publisher":1445,"properties":1475},{"id":6,"createTime":7,"updateTime":8,"relativeEntities":1446,"slug":10,"properties":1447,"entityType":22,"verifyStatus":23,"verifyTime":24,"verifyNote":24,"syncStatus":23,"languages":24,"translateLanguages":24,"viewCount":25,"subjectFields":1453,"manageAffiliations":1454,"indexDatabases":1455,"url":106,"thumbnailPath":24,"statistic":1470,"gsStatistic":24,"type":24,"analyzePriority":24},[],{"country":1448,"issn":1449,"introduce":1450,"eissn":1451,"title":1452},{"VOID":13},{"VOID":15},{"EN":17},{"VOID":19},{"EN":21},[],[],[1456,1463],{"id":87,"indexDatabase":1457,"url":100,"indexYears":101,"academicFieldIds":1462,"indexDatabaseRanking":105},{"id":89,"createTime":90,"updateTime":91,"relativeEntities":1458,"label":1459,"description":1460,"key":97,"publicationTags":1461,"standard":24},[],{"EN":94,"VI":94},{"EN":94,"VI":96},[99],[103,104],{"id":67,"indexDatabase":1464,"url":82,"indexYears":24,"academicFieldIds":1469,"indexDatabaseRanking":24},{"id":69,"createTime":70,"updateTime":71,"relativeEntities":1465,"label":1466,"description":1467,"key":78,"publicationTags":1468,"standard":24},[],{"EN":74,"VI":74},{"VI":76,"EN":77},[80,81],[84,85],{"impactFactor":25,"impactFactorByYear":1471,"i10Index":109,"i10IndexLast5Year":25,"totalPublication":110,"totalPublicationByYear":1472,"totalCitation":113,"totalCitationByYear":1473,"totalCitationPerPublication":119,"totalCitationPerPublicationByYear":1474,"hindexLast5Year":109,"hindex":109},{"2015":53},{"1998":53,"1999":53,"2001":112,"2013":53},{"1998":115,"1999":116,"2001":117,"2013":118},{"1998":115,"1999":116,"2001":121,"2013":118},{"volume":1476,"pages":1478,"issue":1480},{"VOID":1477},"35",{"VOID":1479},"165-169",{"VOID":1481},"3",{"total":115,"publishYear":24,"statisticByYear":1483},{"2016":53,"2018":53,"2019":112,"2023":53,"2024":53},"1998-01-01",1998,[1487,1490,1493,1496],{"id":24,"text":1488,"url":24,"identifiers":1489},"10.1016\u002F0008-6363(96)00038-7",{"doi":1488},{"id":24,"text":1491,"url":24,"identifiers":1492},"10.1056\u002FNEJM199303043280903",{"doi":1491},{"id":24,"text":1494,"url":24,"identifiers":1495},"10.1083\u002Fjcb.120.4.1011",{"doi":1494},{"id":24,"text":1497,"url":24,"identifiers":1498},"10.1016\u002F0022-1759(92)90004-D",{"doi":1497},{"id":1500,"createTime":1501,"updateTime":1502,"relativeEntities":1503,"slug":1504,"properties":1505,"entityType":141,"verifyStatus":23,"verifyTime":1501,"verifyNote":942,"syncStatus":23,"languages":1522,"translateLanguages":1523,"viewCount":25,"primaryUrl":1525,"fullTextUrl":24,"authors":1526,"publicationType":242,"publisherRelationship":1570,"citationCount":1606,"citationInfo":1607,"publishDate":1484,"publishYear":1485,"citationAnalyzeStatus":23,"lastCitationAnalyze":24,"indexDatabases":24,"openAccess":24,"references":1609,"isForceReanalyzing":646},"ee1fd225-3c44-4c80-88d2-b7c1fb6e2153","2024-09-24T12:16:09.269+00:00","2025-02-14T16:18:26.321+00:00",[],"Modulation-of-Arterial-Growth-of-the-Rabbit-Carotid-Artery-Associated-with-Experimental-Elevation-of-Blood-Flow",{"mag":1506,"keywords":1508,"openalex":1510,"abstract":1512,"title":1515,"pm":1518,"doi":1520},{"VOID":1507},"1998819332",{"VI":1509},"",{"VOID":1511},"W1998819332",{"EN":1513,"VI":1514},"\u003Cjats:p>We examined the growth of the right common carotid artery of young rabbits after ligating the left common carotid artery at 3 weeks of age, a procedure that approximately doubled right carotid blood flows. Flow increased from 0.065 ± 0.003 to 0.096 ± 0.009 ml\u002Fs within 1 h and, at 15 weeks of age, carotid blood flows in experimental animals (0.747 ± 0.102 ml\u002Fs) were more than double of those of sham-operated control animals (0.334 ± 0.053 ml\u002Fs). Contralateral carotid ligation resulted in more rapid increases in diameter of the artery with growth in the experimental animals. At 15 weeks of age, the vessel was 15% larger than that of sham-operated controls (2.70 ± 0.09 vs. 2.34 ± 0.05 mm). This more rapid growth of diameter resulted in shear stresses that were not different from controls despite the higher blood flow rates. Interestingly, however, shear stresses in control arteries fell from 17.4 ± 3.4 to 9.19 ± 1.16 dyn\u002Fcm<sup>2<\u002Fsup> over the experimental period (p < 0.05). Elastin accumulation in the experimental artery was much more rapid than in controls and elastin contents were 49% more than in controls at 15 weeks of age. DNA and collagen contents were not significantly affected by contralateral carotid ligation. Previously, we found that experimental manipulations that decreased flow in the same artery of weanling rabbits substantially affected elastin and DNA accumulation, but had no effect on collagen contents. We conclude that increased blood flow is associated with arterial growth and specifically with accumulation of elastin, a wall constituent that bears much of the wall tension at resting blood pressure, and therefore is a primary determinant of resting vessel dimensions.\u003C\u002Fjats:p>","\u003Cjats:p>Chúng tôi đã xem xét sự phát triển của động mạch cảnh chung bên phải ở thỏ con sau khi buộc động mạch cảnh chung bên trái ở tuổi 3 tuần, một quy trình đã làm tăng gấp đôi lưu lượng máu ở động mạch cảnh bên phải. Lưu lượng máu đã tăng từ 0.065 ± 0.003 lên 0.096 ± 0.009 ml\u002Fs trong vòng 1 giờ và, khi đến 15 tuần tuổi, lưu lượng máu ở động mạch cảnh của các động vật thí nghiệm (0.747 ± 0.102 ml\u002Fs) gấp hơn 2 lần so với các động vật đối chứng sham-operated (0.334 ± 0.053 ml\u002Fs). Việc buộc động mạch đối diện đã dẫn đến sự gia tăng nhanh hơn về đường kính của động mạch khi các động vật thí nghiệm phát triển. Đến 15 tuần tuổi, mạch máu lớn hơn 15% so với nhóm đối chứng sham-operated (2.70 ± 0.09 so với 2.34 ± 0.05 mm). Sự tăng trưởng nhanh hơn của đường kính này gây ra các ứng suất cắt không khác biệt so với kiểm soát mặc dù lưu lượng máu cao hơn. Tuy nhiên, điều thú vị là các ứng suất cắt trong các động mạch đối chứng đã giảm từ 17.4 ± 3.4 xuống 9.19 ± 1.16 dyn\u002Fcm<sup>2<\u002Fsup> trong suốt giai đoạn thí nghiệm (p < 0.05). Sự tích lũy elastin trong động mạch thí nghiệm nhanh hơn rất nhiều so với các đối chứng và hàm lượng elastin cao hơn 49% so với nhóm đối chứng khi đạt 15 tuần tuổi. DNA và hàm lượng collagen không bị ảnh hưởng đáng kể bởi việc buộc động mạch cảnh đối diện. Trước đó, chúng tôi đã phát hiện rằng các can thiệp thí nghiệm làm giảm lưu lượng máu trong cùng một động mạch ở thỏ vừa cai sữa đã ảnh hưởng đáng kể đến sự tích lũy elastin và DNA, nhưng không có ảnh hưởng đến hàm lượng collagen. Chúng tôi kết luận rằng lưu lượng máu gia tăng có liên quan đến sự phát triển của động mạch và cụ thể là với sự tích lũy của elastin, một thành phần của thành mạch chịu áp lực rất lớn ở huyết áp nghỉ, và do đó là yếu tố chính quyết định kích thước mạch máu nghỉ ngơi.\u003C\u002Fjats:p>",{"EN":1516,"VI":1517},"Modulation of Arterial Growth of the Rabbit Carotid Artery Associated with Experimental Elevation of Blood Flow","Sự điều hòa sự phát triển của động mạch carotid ở thỏ liên quan đến việc tăng cường lưu lượng máu trong thí nghiệm",{"VOID":1519},"9482690",{"VOID":1521},"10.1159\u002F000025559",[145],[1524],"VI","https:\u002F\u002Fkarger.com\u002FJVR\u002Farticle\u002Fdoi\u002F10.1159\u002F000025559",[1527,1546,1561],{"id":1528,"sortIndex":53,"researcher":24,"roles":1529,"affiliations":1530,"properties":1541},"e780db38-71ff-42d6-89b4-34e7b1a5f7a4",[],[1531],{"id":1532,"sortIndex":25,"affiliation":1533,"properties":24},"846056b7-299f-4252-93e6-56874b249f7a",{"id":1534,"createTime":1535,"updateTime":1535,"relativeEntities":1536,"slug":1537,"properties":1538,"entityType":52,"verifyStatus":23,"verifyTime":24,"verifyNote":24,"syncStatus":23,"languages":24,"translateLanguages":24,"viewCount":25},"2f3035cb-bd9a-4cb5-844d-a6085f4c490c","2024-09-24T12:16:09.278+00:00",[],"Toronto-Hospital-Research-Institute-andDepartment-of-Pathology-University-of-Toronto-Canada",{"title":1539},{"EN":1540},"Toronto Hospital Research Institute andDepartment of Pathology, University of Toronto, Canada",{"openalex":1542,"title":1544},{"VOID":1543},"A5025055424",{"EN":1545},"Donna R. Koopmans",{"id":1547,"sortIndex":25,"researcher":24,"roles":1548,"affiliations":1549,"properties":1556},"067f329b-2894-4e19-a310-664eb21aca52",[],[1550],{"id":1551,"sortIndex":25,"affiliation":1552,"properties":24},"9a1e44ea-8951-480a-9fa5-5729ded4096e",{"id":1534,"createTime":1535,"updateTime":1535,"relativeEntities":1553,"slug":1537,"properties":1554,"entityType":52,"verifyStatus":23,"verifyTime":24,"verifyNote":24,"syncStatus":23,"languages":24,"translateLanguages":24,"viewCount":25},[],{"title":1555},{"EN":1540},{"openalex":1557,"title":1559},{"VOID":1558},"A5067967031",{"EN":1560},"Ippazio Stefàno",{"id":1562,"sortIndex":112,"researcher":24,"roles":1563,"affiliations":1564,"properties":1565},"7353d427-ae14-4f45-b1ac-a8c36f6dc838",[],[],{"openalex":1566,"title":1568},{"VOID":1567},"A5033385134",{"EN":1569},"B. Lowell Langille",{"url":24,"publisher":1571,"properties":1601},{"id":6,"createTime":7,"updateTime":8,"relativeEntities":1572,"slug":10,"properties":1573,"entityType":22,"verifyStatus":23,"verifyTime":24,"verifyNote":24,"syncStatus":23,"languages":24,"translateLanguages":24,"viewCount":25,"subjectFields":1579,"manageAffiliations":1580,"indexDatabases":1581,"url":106,"thumbnailPath":24,"statistic":1596,"gsStatistic":24,"type":24,"analyzePriority":24},[],{"country":1574,"issn":1575,"introduce":1576,"eissn":1577,"title":1578},{"VOID":13},{"VOID":15},{"EN":17},{"VOID":19},{"EN":21},[],[],[1582,1589],{"id":87,"indexDatabase":1583,"url":100,"indexYears":101,"academicFieldIds":1588,"indexDatabaseRanking":105},{"id":89,"createTime":90,"updateTime":91,"relativeEntities":1584,"label":1585,"description":1586,"key":97,"publicationTags":1587,"standard":24},[],{"EN":94,"VI":94},{"EN":94,"VI":96},[99],[103,104],{"id":67,"indexDatabase":1590,"url":82,"indexYears":24,"academicFieldIds":1595,"indexDatabaseRanking":24},{"id":69,"createTime":70,"updateTime":71,"relativeEntities":1591,"label":1592,"description":1593,"key":78,"publicationTags":1594,"standard":24},[],{"EN":74,"VI":74},{"VI":76,"EN":77},[80,81],[84,85],{"impactFactor":25,"impactFactorByYear":1597,"i10Index":109,"i10IndexLast5Year":25,"totalPublication":110,"totalPublicationByYear":1598,"totalCitation":113,"totalCitationByYear":1599,"totalCitationPerPublication":119,"totalCitationPerPublicationByYear":1600,"hindexLast5Year":109,"hindex":109},{"2015":53},{"1998":53,"1999":53,"2001":112,"2013":53},{"1998":115,"1999":116,"2001":117,"2013":118},{"1998":115,"1999":116,"2001":121,"2013":118},{"volume":1602,"pages":1603,"issue":1605},{"VOID":1477},{"VOID":1604},"1-7",{"VOID":1319},55,{"total":1606,"publishYear":24,"statisticByYear":1608},{"2012":53,"2014":53,"2015":109,"2016":53,"2017":109,"2018":112,"2020":53},[1610,1613,1616],{"id":24,"text":1611,"url":24,"identifiers":1612},"10.1067\u002Fmva.1987.avs0050413",{"doi":1611},{"id":24,"text":1614,"url":24,"identifiers":1615},"10.1006\u002Fbbrc.1993.2396",{"doi":1614},{"id":24,"text":1617,"url":24,"identifiers":1618},"10.1038\u002F352330a0",{"doi":1617},{"id":1620,"createTime":1621,"updateTime":1622,"relativeEntities":1623,"slug":1624,"properties":1625,"entityType":141,"verifyStatus":142,"verifyTime":1621,"verifyNote":143,"syncStatus":23,"languages":1641,"translateLanguages":1642,"viewCount":25,"primaryUrl":1643,"fullTextUrl":24,"authors":1644,"publicationType":242,"publisherRelationship":1710,"citationCount":1747,"citationInfo":1748,"publishDate":1751,"publishYear":1752,"citationAnalyzeStatus":23,"lastCitationAnalyze":24,"indexDatabases":24,"openAccess":24,"references":1753,"isForceReanalyzing":646},"5c5798b8-cf15-4756-ab9d-6401db66cc51","2024-11-25T23:52:34.309+00:00","2025-02-14T16:17:25.128+00:00",[],"Selective-COX-2-Inhibitors-and-Risk-of-Myocardial-Infarction",{"mag":1626,"keywords":1628,"openalex":1629,"abstract":1631,"title":1634,"pm":1637,"doi":1639},{"VOID":1627},"2155820793",{"VI":1509},{"VOID":1630},"W2155820793",{"EN":1632,"VI":1633},"\u003Cjats:p>Selective inhibitors of cyclooxygenase-2 (COX-2, ‘coxibs’) are highly effective anti-inflammatory and analgesic drugs that exert their action by preventing the formation of prostanoids. Recently some coxibs, which were designed to exploit the advantageous effects of non-steroidal anti-inflammatory drugs while evading their side effects, have been reported to increase the risk of myo cardial infarction and atherothrombotic events. This has led to the withdrawal of rofecoxib from global markets, and warnings have been issued by drug authorities about similar events during the use of celecoxib or valdecoxib\u002Fparecoxib, bringing about questions of an inherent atherothrombotic risk of all coxibs and consequences that should be drawn by health care professionals. These questions need to be addressed in light of the known effects of selective inhibition of COX-2 on the cardiovascular system. Although COX-2, in contrast to the cyclooxygenase-1 (COX-1) isoform, is regarded as an inducible enzyme that only has a role in pathophysiological processes like pain and inflammation, experimental and clinical studies have shown that COX-2 is constitutively expressed in tissues like the kidney or vascular endothelium, where it executes important physiological functions. COX-2-dependent formation of prostanoids not only results in the mediation of pain or inflammatory signals but also in the maintenance of vascular integrity. Especially prostacyclin (PGI<sub>2<\u002Fsub>), which exerts vasodilatory and antiplatelet properties, is formed to a significant extent by COX-2, and its levels are reduced to less than half of normal when COX-2 is inhibited. This review outlines the rationale for the development of selective COX-2 inhibitors and the pathophysiological consequences of selective inhibition of COX-2 with special regard to vasoactive prostaglandins. It describes coxibs that are current ly available, evaluates the current knowledge on the risk of atherothrombotic events associated with their intake and critically discusses the consequences that should be drawn from these insights.\u003C\u002Fjats:p>","\u003Cjats:p> Các chất ức chế chọn lọc cyclooxygenase-2 (COX-2, ‘coxibs’) là các loại thuốc chống viêm và giảm đau hiệu quả cao, hoạt động bằng cách ngăn chặn sự hình thành prostanoid. Gần đây, một số coxibs được thiết kế để khai thác các tác động có lợi của thuốc giảm đau chống viêm không steroid trong khi tránh các tác dụng phụ của chúng, đã được báo cáo là làm tăng nguy cơ nhồi máu cơ tim và các sự kiện thuyên tắc động mạch. Điều này đã dẫn đến việc rút rofecoxib khỏi thị trường toàn cầu, và các cơ quan quản lý dược phẩm đã phát đi cảnh báo về các sự kiện tương tự trong quá trình sử dụng celecoxib hoặc valdecoxib\u002Fparecoxib, dấy lên những câu hỏi về nguy cơ thuyên tắc động mạch nội tại của tất cả các coxibs và những hậu quả mà các chuyên gia chăm sóc sức khỏe nên rút ra. Những câu hỏi này cần được giải quyết trong bối cảnh các tác động đã biết của việc ức chế chọn lọc COX-2 đối với hệ thống tim mạch. Mặc dù COX-2, trái ngược với isoform cyclooxygenase-1 (COX-1), được coi là một enzyme có thể kích thích chỉ có vai trò trong các quá trình bệnh lý như đau và viêm, nhưng các nghiên cứu thực nghiệm và lâm sàng đã chỉ ra rằng COX-2 được biểu hiện liên tục ở các mô như thận hoặc nội mạc mạch máu, nơi nó thực hiện các chức năng sinh lý quan trọng. Việc hình thành prostanoid phụ thuộc vào COX-2 không chỉ dẫn đến việc trung gian cho các tín hiệu đau hoặc viêm mà còn giúp duy trì tính toàn vẹn của mạch máu. Đặc biệt, prostacyclin (PGI<sub>2<\u002Fsub>), loại bỏ chất có tác dụng giãn mạch và kháng tiểu cầu, được hình thành trong một mức độ đáng kể bởi COX-2, và nồng độ của nó giảm xuống dưới một nửa so với bình thường khi COX-2 bị ức chế. Bài tổng quan này phác thảo lý do phát triển các chất ức chế COX-2 chọn lọc và các hậu quả bệnh lý của việc ức chế chọn lọc COX-2 với sự chú ý đặc biệt đối với các prostaglandin có tác dụng trên mạch. Nó mô tả các coxibs hiện có, đánh giá kiến thức hiện có về nguy cơ các sự kiện thuyên tắc động mạch liên quan đến việc sử dụng của chúng và thảo luận một cách phê phán các hậu quả nên được rút ra từ những hiểu biết này.\u003C\u002Fjats:p>",{"EN":1635,"VI":1636},"Selective COX-2 Inhibitors and Risk of Myocardial Infarction","Các chất ức chế chọn lọc COX-2 và nguy cơ nhồi máu cơ tim",{"VOID":1638},"15976506",{"VOID":1640},"10.1159\u002F000086459",[145],[1524],"https:\u002F\u002Fkarger.com\u002FJVR\u002Farticle\u002Fdoi\u002F10.1159\u002F000086459",[1645,1665,1680,1695],{"id":1646,"sortIndex":112,"researcher":24,"roles":1647,"affiliations":1648,"properties":1660},"ae3b5811-3d46-4ed2-919f-0ee48ee30ec5",[],[1649],{"id":1650,"sortIndex":25,"affiliation":1651,"properties":24},"81eb122b-3091-4442-8cf7-0d7ebaa0bdf6",{"id":1652,"createTime":1653,"updateTime":1654,"relativeEntities":1655,"slug":1656,"properties":1657,"entityType":52,"verifyStatus":23,"verifyTime":24,"verifyNote":24,"syncStatus":23,"languages":24,"translateLanguages":24,"viewCount":25},"ae5a895c-0c11-481e-9c0f-9117240577cb","2024-08-31T18:01:26.470+00:00","2024-12-05T21:55:58.499+00:00",[],"Cardiology-and",{"title":1658},{"EN":1659},"Cardiology and",{"openalex":1661,"title":1663},{"VOID":1662},"A5041502706",{"EN":1664},"Volker Klauß",{"id":1666,"sortIndex":53,"researcher":24,"roles":1667,"affiliations":1668,"properties":1675},"3426290b-70f4-4f1c-af27-b3dbbfe828c9",[],[1669],{"id":1670,"sortIndex":25,"affiliation":1671,"properties":24},"b394d82e-1eb1-48e4-ba63-82417d1f3ec6",{"id":1652,"createTime":1653,"updateTime":1654,"relativeEntities":1672,"slug":1656,"properties":1673,"entityType":52,"verifyStatus":23,"verifyTime":24,"verifyNote":24,"syncStatus":23,"languages":24,"translateLanguages":24,"viewCount":25},[],{"title":1674},{"EN":1659},{"openalex":1676,"title":1678},{"VOID":1677},"A5086041475",{"EN":1679},"Thomas M. Schiele",{"id":1681,"sortIndex":25,"researcher":24,"roles":1682,"affiliations":1683,"properties":1690},"534f5e8d-5c3b-4f98-a69b-c2174321c821",[],[1684],{"id":1685,"sortIndex":25,"affiliation":1686,"properties":24},"3e1dbb49-79de-434d-a541-76326c9889af",{"id":1652,"createTime":1653,"updateTime":1654,"relativeEntities":1687,"slug":1656,"properties":1688,"entityType":52,"verifyStatus":23,"verifyTime":24,"verifyNote":24,"syncStatus":23,"languages":24,"translateLanguages":24,"viewCount":25},[],{"title":1689},{"EN":1659},{"openalex":1691,"title":1693},{"VOID":1692},"A5075585589",{"EN":1694},"Florian 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tế bào cơ trơn mạch máu, xơ vữa động mạch, hóa chiều hướng, yếu tố tăng trưởng",{"VOID":2000},"W2093867725",{"EN":2002,"VI":2003},"\u003Cjats:p>Bone morphogenetic proteins (BMPs) and their serine\u002Fthreonine kinase receptors have been identified in atherosclerotic arteries and vascular smooth muscle cells, respectively. Thus, BMPs (the largest subfamily of the TGF-β superfamily) have been implicated in the pathogenesis of atherosclerosis. However, the origins of BMP biosynthesis and the functional roles of BMP in blood vessels are unclear. The present study explored BMP-2 gene expression in various human blood vessels and vascular cell types. Functional in vitro studies were also performed to determine the effects of recombinant human BMP-2 on migration (transwell assay) and proliferation ([<sup>3<\u002Fsup>H]-thymidine incorporation) of human aortic vascular smooth muscle cells (HASMC). RT-PCR experiments revealed BMP-2 gene expression in normal and atherosclerotic human arteries as well as cultured human aortic and coronary vascular smooth muscle cells, human umbilical vein endothelial cells (HUVECs) and human macrophages. In cellular migration studies, incubation with BMP-2 produced efficacious (≤610-fold), concentration- and time-dependent chemotaxis of HASMCs (EC<sub>50<\u002Fsub> = 0.8 μ<i>M<\u002Fi>) with little or no effect on HUVEC chemotaxis. The increased HASMC motility induced by BMP-2 was inhibited by coincubation with an anti-BMP-2 mAb. In addition, subthreshold concentrations of BMP-2 produced a dramatic synergistic effect upon platelet-derived growth factor (PDGF)-induced chemotaxis. In contrast to PDGF, BMP-2 had no significant effet on [<sup>3<\u002Fsup>H]-thymidine incorporation in HASMC at chemotaxic concentrations (≤6.0 μ<i>M<\u002Fi>) nor did it synergize with the mitogenic effects of PDGF. In conclusion, the expression of BMP-2 by numerous cell types in the blood vessel wall may play a chemotactic or cochemotactic role in the smooth muscle cell response to vascular injury.\u003C\u002Fjats:p>","\u003Cjats:p>Các protein hình thành xương (BMPs) và các thụ thể kinase serine\u002Fthreonine của chúng đã được phát hiện trong các động mạch xơ vữa và tế bào cơ trơn mạch máu, tương ứng. Do đó, BMPs (tiểu gia đình lớn nhất của siêu gia đình TGF-β) đã được liên quan đến sinh bệnh học của xơ vữa động mạch. Tuy nhiên, nguồn gốc của quá trình sinh tổng hợp BMP và vai trò chức năng của BMP trong mạch máu vẫn còn chưa rõ ràng. Nghiên cứu hiện tại khám phá biểu hiện gen BMP-2 trong nhiều loại mạch máu và tế bào mạch máu người. Các nghiên cứu chức năng in vitro cũng được thực hiện để xác định tác động của BMP-2 tái tổ hợp của người lên sự di chuyển (thí nghiệm transwell) và sự phát triển ([<sup>3<\u002Fsup>H]-thymidine hợp nhất) của tế bào cơ trơn động mạch chủ người (HASMC). Các thí nghiệm RT-PCR cho thấy biểu hiện gen BMP-2 trong các động mạch người bình thường và xơ vữa cũng như trong các tế bào cơ trơn mạch máu động mạch chủ và động mạch vành nuôi cấy, các tế bào nội mô tĩnh mạch rốn người (HUVECs) và các đại thực bào người. Trong các nghiên cứu di động tế bào, việc ủ với BMP-2 tạo ra sự hóa chiều hướng hiệu quả (≤610 lần), phụ thuộc vào nồng độ và thời gian của HASMCs (EC<sub>50<\u002Fsub> = 0.8 μ<i>M<\u002Fi>) với ít hoặc không có tác động đến hóa chiều hướng của HUVEC. Độ di động của HASMC tăng lên do BMP-2 gây ra đã bị ức chế khi đồng ủ với một kháng thể đơn dòng chống BMP-2. Ngoài ra, các nồng độ dưới ngưỡng của BMP-2 tạo ra hiệu ứng phối hợp mạnh mẽ lên sự hóa chiều hướng do yếu tố tăng trưởng xuất phát từ tiểu cầu (PDGF) gây ra. Ngược lại với PDGF, BMP-2 không có tác động đáng kể nào lên việc hợp nhất [<sup>3<\u002Fsup>H]-thymidine trong HASMC ở các nồng độ hóa chiều hướng (≤6.0 μ<i>M<\u002Fi>) và cũng không phối hợp với các tác động sinh sản của PDGF. Tóm lại, sự biểu hiện của BMP-2 bởi nhiều loại tế bào trong thành mạch máu có thể đóng vai trò hóa chiều hướng hoặc đồng hóa chiều hướng trong phản ứng của tế bào cơ trơn đối với chấn thương mạch.",{"EN":2005,"VI":2006},"BMP-2 Gene Expression and Effects on Human Vascular Smooth Muscle Cells","Biểu hiện gen BMP-2 và tác động lên tế bào cơ trơn mạch máu người",{"VOID":2008},"10213907",{"VOID":2010},"10.1159\u002F000025634",[145],[1524],"https:\u002F\u002Fkarger.com\u002FJVR\u002Farticle\u002Fdoi\u002F10.1159\u002F000025634",[2015,2026,2037,2046,2055,2074],{"id":2016,"sortIndex":110,"researcher":24,"roles":2017,"affiliations":2018,"properties":2019},"c7b9b497-db08-4e56-8120-30b9bcac462e",[],[],{"openalex":2020,"orcid":2022,"title":2024},{"VOID":2021},"A5040091190",{"VOID":2023},"https:\u002F\u002Forcid.org\u002F0000-0002-4768-5831",{"EN":2025},"Tianli Yue",{"id":2027,"sortIndex":118,"researcher":24,"roles":2028,"affiliations":2029,"properties":2030},"1225a56d-ef77-436a-89b9-4db883ab3a83",[],[],{"openalex":2031,"orcid":2033,"title":2035},{"VOID":2032},"A5036416060",{"VOID":2034},"https:\u002F\u002Forcid.org\u002F0000-0002-1352-604X",{"EN":2036},"Karen M. Anderson",{"id":2038,"sortIndex":109,"researcher":24,"roles":2039,"affiliations":2040,"properties":2041},"953cd901-4446-47bf-a10e-ea5a8958e9dd",[],[],{"openalex":2042,"title":2044},{"VOID":2043},"A5019548921",{"EN":2045},"Heather Minehart",{"id":2047,"sortIndex":53,"researcher":24,"roles":2048,"affiliations":2049,"properties":2050},"8d6147b8-b3ab-42c5-b902-56a4ba6f9137",[],[],{"openalex":2051,"title":2053},{"VOID":2052},"A5103417563",{"EN":2054},"J L Gu",{"id":2056,"sortIndex":25,"researcher":24,"roles":2057,"affiliations":2058,"properties":2069},"1c831fad-97f0-4155-a887-ac5040c6d6dd",[],[2059],{"id":2060,"sortIndex":25,"affiliation":2061,"properties":24},"cb8cda48-5723-4ff5-862f-136ac190a221",{"id":2062,"createTime":2063,"updateTime":2063,"relativeEntities":2064,"slug":2065,"properties":2066,"entityType":52,"verifyStatus":23,"verifyTime":24,"verifyNote":24,"syncStatus":23,"languages":24,"translateLanguages":24,"viewCount":25},"fd32ed83-8ebe-4fff-9c33-3e928925dea0","2024-09-03T01:52:09.792+00:00",[],"Department-of-Cardiovascular-Pharmacology-SmithKline-Beecham-Pharmaceutics-King-of-Prussia-PA-USA-robert-n-willette-sbphrd-com",{"title":2067},{"EN":2068},"Department of Cardiovascular Pharmacology, SmithKline-Beecham Pharmaceutics, King of Prussia, PA, USA. robert_n_willette@sbphrd.com",{"openalex":2070,"title":2072},{"VOID":2071},"A5084149275",{"EN":2073},"Robert N. Willette",{"id":2075,"sortIndex":112,"researcher":24,"roles":2076,"affiliations":2077,"properties":2078},"04ce4a75-5c01-49e3-94af-a13def457515",[],[],{"openalex":2079,"title":2081},{"VOID":2080},"A5073759684",{"EN":2082},"P G Lysko",{"url":24,"publisher":2084,"properties":2114},{"id":6,"createTime":7,"updateTime":8,"relativeEntities":2085,"slug":10,"properties":2086,"entityType":22,"verifyStatus":23,"verifyTime":24,"verifyNote":24,"syncStatus":23,"languages":24,"translateLanguages":24,"viewCount":25,"subjectFields":2092,"manageAffiliations":2093,"indexDatabases":2094,"url":106,"thumbnailPath":24,"statistic":2109,"gsStatistic":24,"type":24,"analyzePriority":24},[],{"country":2087,"issn":2088,"introduce":2089,"eissn":2090,"title":2091},{"VOID":13},{"VOID":15},{"EN":17},{"VOID":19},{"EN":21},[],[],[2095,2102],{"id":87,"indexDatabase":2096,"url":100,"indexYears":101,"academicFieldIds":2101,"indexDatabaseRanking":105},{"id":89,"createTime":90,"updateTime":91,"relativeEntities":2097,"label":2098,"description":2099,"key":97,"publicationTags":2100,"standard":24},[],{"EN":94,"VI":94},{"EN":94,"VI":96},[99],[103,104],{"id":67,"indexDatabase":2103,"url":82,"indexYears":24,"academicFieldIds":2108,"indexDatabaseRanking":24},{"id":69,"createTime":70,"updateTime":71,"relativeEntities":2104,"label":2105,"description":2106,"key":78,"publicationTags":2107,"standard":24},[],{"EN":74,"VI":74},{"VI":76,"EN":77},[80,81],[84,85],{"impactFactor":25,"impactFactorByYear":2110,"i10Index":109,"i10IndexLast5Year":25,"totalPublication":110,"totalPublicationByYear":2111,"totalCitation":113,"totalCitationByYear":2112,"totalCitationPerPublication":119,"totalCitationPerPublicationByYear":2113,"hindexLast5Year":109,"hindex":109},{"2015":53},{"1998":53,"1999":53,"2001":112,"2013":53},{"1998":115,"1999":116,"2001":117,"2013":118},{"1998":115,"1999":116,"2001":121,"2013":118},{"volume":2115,"pages":2117,"issue":2119},{"VOID":2116},"36",{"VOID":2118},"120-125",{"VOID":1067},{"total":116,"publishYear":24,"statisticByYear":2121},{"2012":776,"2013":118,"2014":109,"2015":109,"2016":109,"2017":118,"2018":112,"2019":109,"2020":118,"2022":112,"2023":53},"1999-01-01",1999,[2125,2128,2131,2134,2137,2140],{"id":24,"text":2126,"url":24,"identifiers":2127},"10.1006\u002Fbbrc.1994.2898",{"doi":2126},{"id":24,"text":2129,"url":24,"identifiers":2130},"10.1073\u002Fpnas.94.17.9314",{"doi":2129},{"id":24,"text":2132,"url":24,"identifiers":2133},"10.1006\u002Fexcr.1993.1131",{"doi":2132},{"id":24,"text":2135,"url":24,"identifiers":2136},"10.1006\u002Fbbrc.1994.2685",{"doi":2135},{"id":24,"text":2138,"url":24,"identifiers":2139},"10.1006\u002Fabio.1987.9999",{"doi":2138},{"id":24,"text":2141,"url":24,"identifiers":2142},"10.1038\u002F39348",{"doi":2141},{"id":2144,"createTime":2145,"updateTime":2146,"relativeEntities":2147,"slug":2148,"properties":2149,"entityType":141,"verifyStatus":142,"verifyTime":2165,"verifyNote":143,"syncStatus":23,"languages":2166,"translateLanguages":2167,"viewCount":25,"primaryUrl":2168,"fullTextUrl":24,"authors":2169,"publicationType":242,"publisherRelationship":2297,"citationCount":2334,"citationInfo":2335,"publishDate":2343,"publishYear":2344,"citationAnalyzeStatus":23,"lastCitationAnalyze":24,"indexDatabases":24,"openAccess":24,"references":2345,"isForceReanalyzing":646},"187c13ff-fccf-42e7-b6be-189034c9fd93","2025-01-01T07:01:07.804+00:00","2025-02-14T16:15:25.493+00:00",[],"Serum-microRNA-21-and-microRNA-221-as-Potential-Biomarkers-for-Cerebrovascular-Disease",{"mag":2150,"keywords":2152,"openalex":2154,"abstract":2156,"title":2159,"pm":2162,"doi":2164},{"VOID":2151},"2041184531",{"VI":2153},"microRNA, miR-21, miR-221, bệnh mạch máu não, dấu hiệu sinh học, đột quỵ",{"VOID":2155},"W2041184531",{"EN":2157,"VI":2158},"\u003Cjats:p><b><i>Background\u002FAims:<\u002Fi><\u002Fb> MicroRNA miR-21, miR-221 and miR-145 have been implicated in the cardiovascular system. We aimed to compare the serum levels of the three microRNAs (miRNAs) in different severities of cerebrovascular diseases and evaluate the feasibility of using these miRNAs as biomarkers for stroke. <b><i>Methods:<\u002Fi><\u002Fb> We enrolled 167 subjects with ischemic stroke, 66 atherosclerosis subjects with any carotid plaque score and 157 healthy controls. These three types of subjects represent three levels of severity in cerebrovascular diseases. Analysis of covariance was used to evaluate the relationship between miRNAs and disease severity with adjustment for conventional risk factors. To test the prediction for stroke, we built regression models containing the serum miRNA levels and risk factors. Prediction capabilities were compared by the receiver operating characteristic curves. <b><i>Results:<\u002Fi><\u002Fb> Stroke patients and atherosclerosis subjects had significantly higher miR-21 and lower miR-221 serum levels than healthy controls, while the miR-145 expression was too low to provide useful information in this regard. The best model showed that miR-21 and miR-221 were independent predictors. There was a 6.2-fold increase for stroke risk when miR-21 levels increase by log<sub>10<\u002Fsub>2<sup>-ΔCt<\u002Fsup> = 1, while a 10.4-fold increase was observed as miR-221 decreases by log<sub>10<\u002Fsub>2<sup>-ΔCt<\u002Fsup> = 1. <b><i>Conclusions:<\u002Fi><\u002Fb> Serum miR-145 was not detected in over 50% of the patients and it may not be an ideal marker to predict stroke. MiR-21 and miR-221 are novel biomarkers for atherosclerosis and stroke.\u003C\u002Fjats:p>","\u003Cjats:p><b><i>Đặt vấn đề\u002FMục tiêu:<\u002Fi><\u002Fb> MicroRNA miR-21, miR-221 và miR-145 đã được liên kết với hệ thống tim mạch. Chúng tôi nhằm so sánh nồng độ huyết thanh của ba microRNA (miRNAs) này ở các mức độ nghiêm trọng khác nhau của các bệnh mạch máu não và đánh giá khả năng sử dụng các miRNA này như là dấu hiệu sinh học cho đột quỵ. <b><i>Phương pháp:<\u002Fi><\u002Fb> Chúng tôi đã tuyển chọn 167 đối tượng bị đột quỵ thiếu máu, 66 đối tượng xơ vữa động mạch có bất kỳ chỉ số mảng bám carotid nào và 157 người làm chứng khỏe mạnh. Ba loại đối tượng này đại diện cho ba cấp độ nghiêm trọng trong các bệnh mạch máu não. Phân tích phương sai được sử dụng để đánh giá mối quan hệ giữa các miRNA và mức độ nghiêm trọng của bệnh với điều chỉnh cho các yếu tố rủi ro thông thường. Để kiểm tra dự đoán cho đột quỵ, chúng tôi đã xây dựng các mô hình hồi quy bao gồm nồng độ miRNA trong huyết thanh và các yếu tố rủi ro. Khả năng dự đoán được so sánh qua các đường cong đặc trưng của người nhận. <b><i>Kết quả:<\u002Fi><\u002Fb> Bệnh nhân đột quỵ và các đối tượng xơ vữa động mạch có nồng độ miR-21 trong huyết thanh cao hơn và nồng độ miR-221 thấp hơn đáng kể so với các đối tượng khỏe mạnh, trong khi sự biểu hiện của miR-145 quá thấp để cung cấp thông tin hữu ích trong bối cảnh này. Mô hình tốt nhất cho thấy miR-21 và miR-221 là những yếu tố dự đoán độc lập. Có sự gia tăng 6,2 lần nguy cơ đột quỵ khi nồng độ miR-21 tăng lên theo log<sub>10<\u002Fsub>2<sup>-ΔCt<\u002Fsup> = 1, trong khi sự giảm 10,4 lần được quan sát khi miR-221 giảm theo log<sub>10<\u002Fsub>2<sup>-ΔCt<\u002Fsup> = 1. <b><i>Kết luận:<\u002Fi><\u002Fb> Huyết thanh miR-145 không được phát hiện ở hơn 50% bệnh nhân và có thể không phải là một dấu hiệu lý tưởng để dự đoán đột quỵ. MiR-21 và miR-221 là các dấu hiệu sinh học mới cho xơ vữa động mạch và đột quỵ.\u003C\u002Fjats:p>",{"EN":2160,"VI":2161},"Serum microRNA-21 and microRNA-221 as Potential Biomarkers for Cerebrovascular Disease","MicroRNA-21 và microRNA-221 trong huyết thanh như các dấu hiệu sinh học tiềm năng cho bệnh mạch máu não",{"VOID":2163},"23860376",{"VOID":614},"2025-01-01T07:01:07.803+00:00",[145],[1524],"https:\u002F\u002Fkarger.com\u002FJVR\u002Farticle\u002Fdoi\u002F10.1159\u002F000351767",[2170,2189,2209,2230,2263,2280],{"id":2171,"sortIndex":109,"researcher":24,"roles":2172,"affiliations":2173,"properties":2184},"0af5e818-1731-42ff-a8c4-94f219b6ad71",[],[2174],{"id":2175,"sortIndex":25,"affiliation":2176,"properties":24},"d7487146-ea77-4b3f-9e48-0d605a30b2c8",{"id":2177,"createTime":2178,"updateTime":2178,"relativeEntities":2179,"slug":2180,"properties":2181,"entityType":52,"verifyStatus":23,"verifyTime":24,"verifyNote":24,"syncStatus":23,"languages":24,"translateLanguages":24,"viewCount":25},"4502ea8d-42a8-480a-a5a3-eb1a621c830a","2025-01-01T07:01:07.915+00:00",[],"Department-of-Neurology-Kaohsiung-Medical-University-Hospital-Departments-of",{"title":2182},{"EN":2183},"Department of Neurology, Kaohsiung Medical University Hospital, Departments of",{"openalex":2185,"title":2187},{"VOID":2186},"A5112708429",{"EN":2188},"Ruey‐Tay Lin",{"id":2190,"sortIndex":112,"researcher":24,"roles":2191,"affiliations":2192,"properties":2204},"e7f39c51-75d1-44aa-af20-800863b26ca1",[],[2193],{"id":2194,"sortIndex":25,"affiliation":2195,"properties":24},"6ebac467-9726-4284-90c6-fecb8f7de165",{"id":2196,"createTime":2197,"updateTime":2198,"relativeEntities":2199,"slug":2200,"properties":2201,"entityType":52,"verifyStatus":23,"verifyTime":24,"verifyNote":24,"syncStatus":23,"languages":24,"translateLanguages":24,"viewCount":25},"deb70c10-2400-44b8-bab3-64f203b30530","2023-12-04T14:24:36.558+00:00","2025-01-01T07:01:07.830+00:00",[],"Department-of-Medical-Research",{"title":2202},{"VI":2203},"Department of Medical Research",{"openalex":2205,"title":2207},{"VOID":2206},"A5019621922",{"EN":2208},"Yung-Song 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