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Previously, the apo B,E(LDL) receptor and a unique apo E-binding protein (referred to as the apo E receptor) were isolated from solubilized canine and human livers. In the present study, the apo E-binding fraction was further characterized and found to contain at least three proteins, all of which bind apo E-containing lipoproteins with high affinity. The 56-kDa band was found to contain the alpha- and beta-subunits of F1-ATPase, presumably derived from mitochondrial membranes. In addition, an apo E-binding protein with an apparent Mr approximately equal to 59,000 was identified. The 59-kDa protein displays calcium-independent binding on ligand blots, but displays both calcium-dependent and -independent binding in assays performed with detergent-solubilized protein. The 59-kDa protein recognized lipid-free as well as lipid-bound apo E in ligand blots, and also bound apo E-2, apo E-3, and apo E-4 in a comparable way. Monoclonal antibodies produced against the 59-kDa protein did not react with the 56-kDa proteins. Normal human liver, as well as the liver of a patient lacking the apo B,E(LDL) receptor, possessed the 56-kDa and 59-kDa proteins. These data indicate that liver cells possess at least three proteins, in addition to the apo B,E(LDL) receptor, that bind apo E-containing lipoproteins with high affinity. 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Tính miễn dịch với LDL của hai kháng thể (2D8 và 4G3) đặc biệt nhạy cảm với sự biến đổi của các gốc lysine và arginine trong LDL. Các thí nghiệm đồng nồng độ cho thấy các kháng thể 3A8 và 3A10 có thể phản ứng với cùng một định danh và năm kháng thể (5E11, 3A8, 3A10, 4G3 và 3F5) nhận biết các định danh được nhóm lại trong cùng một khu vực của phân tử. Hai kháng thể còn lại (1D1 và 2D8) phản ứng với các định danh xa rời khu vực này. Khi được thử nghiệm với lượng mol thừa so với LDL, các đoạn Fab của 5E11, 3A8, 3A10, 4G3 và 3F5 (nhưng không phải 1D1 hay 2D8) có khả năng chặn liên kết của 125I-LDL với thụ thể LDL và can thiệp vào việc ức chế LDL đối với sự tổng hợp cholesterol trong các tế bào xơ nhuận nuôi cấy. Việc tăng nồng độ gấp 10 lần không làm thay đổi đáng kể kết quả. Dựa trên các kết quả này, chúng tôi đã đề xuất một bản đồ các định danh như chúng sẽ xuất hiện trong LDL.\u003C\u002Fjats:p>","\u003Cjats:p>Seven monoclonal antibodies against human low density lipoprotein (LDL) have been characterized as to their specificity and ability to interfere with the LDL pathway in cultured human fibroblasts. The immunoreactivity with LDL of two of the antibodies (2D8 and 4G3) was particularly sensitive to modification of lysine and arginine residues in LDL. Cotitration experiments indicated that the antibodies 3A8 and 3A10 may react with the same determinant and that five antibodies (5E11, 3A8, 3A10, 4G3 and 3F5) recognized determinants that were grouped in the same region of the molecule. The two other antibodies (1D1 and 2D8) reacted with determinants distant from this region. When tested in molar excess relative to LDL, Fab fragments of 5E11, 3A8, 3A10, 4G3 and 3F5 (but not 1D1 or 2D8) were capable of blocking the binding of 125I-LDL to the LDL receptor and interfering with LDL suppression of cholesterol synthesis in cultured fibroblasts. Increasing the concentration 10-fold did not change the results significantly. Based on these results we have proposed a map of the determinants as they would appear in LDL.\u003C\u002Fjats:p>",{"VI":272,"EN":273},"Đặc điểm của các kháng thể đơn dòng chống lại lipoprotein mật độ thấp ở người.","Characterization of monoclonal antibodies against human low density lipoprotein.",{"VOID":275},"6186232",{"VOID":277},"10.1161\u002F01.atv.3.1.23",[67],[280],"VI","https:\u002F\u002Fwww.ahajournals.org\u002Fdoi\u002F10.1161\u002F01.ATV.3.1.23",[283,303,322,341],{"id":284,"sortIndex":128,"researcher":18,"roles":285,"affiliations":286,"properties":298},"c1c8efd6-9390-4cf6-a392-f49e51fa970b",[],[287],{"id":288,"sortIndex":19,"affiliation":289,"properties":18},"b12ac4de-08ae-4556-a2bc-694b6da15c1c",{"id":290,"createTime":291,"updateTime":292,"relativeEntities":293,"slug":294,"properties":295,"entityType":85,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19},"c5557907-df54-43d1-8d71-29e7b191b08e","2024-11-26T14:57:39.135+00:00","2024-11-28T01:21:41.149+00:00",[],"Y-L-Marcel",{"title":296},{"EN":297},"Y L Marcel",{"openalex":299,"title":301},{"VOID":300},"A5108107008",{"EN":302},"Yves L. 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Mật độ thể tích của myofilament trong tế bào chất của các khu vực có tế bào cơ trơn đã được đo ở các khu vực có tế bào cơ trơn (có thể thấm tự do màu xanh Evans và do đó nhuộm màu xanh) và ở các khu vực được tái nội mạc hoá (vẫn giữ màu trắng sau khi tiêm màu xanh Evans) của động mạch cảnh thỏ. Hai tuần sau chấn thương, mật độ thể tích của myofilament trong các tế bào cơ trơn của lớp nội mạc ở cả hai khu vực màu trắng và màu xanh đều ít hơn đáng kể so với tế bào cơ trơn lớp giữa (67.9% +\u002F- 3.6%; trung bình +\u002F- SE), với giá trị tương ứng là 38.8% +\u002F- 1.0% và 35.9 +\u002F- 3.3%. Đến 6 tuần sau chấn thương, mật độ thể tích đã tăng đáng kể ở cả khu vực màu trắng (55.1% +\u002F- 3.4%) và khu vực màu xanh (53.5% +\u002F- 3.0%), và các giá trị này không thay đổi đáng kể sau 18 tuần. Mật độ thể tích của myofilament trong các tế bào cơ trơn ở lớp lòng trong các khu vực màu xanh thấp hơn đáng kể so với tế bào lớp giữa đối chứng và vẫn duy trì ở mức thấp (26.7% +\u002F- 2.1%) cho đến 18 tuần sau chấn thương. Chấn thương ban đầu do bóng catheter gây ra đã gây ra tổn thương đáng kể cho các tế bào cơ trơn trong lớp giữa, và các tế bào còn lại trong lớp giữa trải qua những thay đổi tương tự về cấu trúc siêu vi so với các tế bào trong lớp nội mạc mới. Tại thời điểm 2 tuần, các tế bào có mật độ thể tích myofilament thấp (44.9% +\u002F- 2.4%), quay trở lại mức không khác biệt đáng kể so với động mạch đối chứng vào 6 tuần sau chấn thương. Không có sự khác biệt nào trong ước lượng mật độ thể tích của myofilament giữa lớp trong và ngoài của các động mạch bị thương. Những phát hiện này cho thấy, sau khi chấn thương do bóng catheter gây ra, các tế bào cơ trơn ở cả lớp giữa và sự dày lên nội mạc kết quả đều trải qua một sự thay đổi có thể đảo ngược trong cấu trúc siêu vi.\u003C\u002Fjats:p>","\u003Cjats:p>Stereology was used to investigate the changes in ultrastructure of smooth muscle cells during the formation of an experimental intimal thickening induced by injury with an inflated balloon catheter. The volume density of myofilaments in the cell cytoplasm was measured in smooth muscle cell-lined areas (which are freely permeable to Evans blue dye and, hence, stain blue) and in re-endothelialized areas (which remain white after injection of Evans blue) of the rabbit carotid artery. Two weeks after injury, the volume densities of myofilaments in the intimal smooth muscle cells in both white and blue areas were significantly less than that for control medial smooth muscle (67.9% +\u002F- 3.6%; mean +\u002F- SE), being 38.8% +\u002F- 1.0% and 35.9 +\u002F- 3.3%, respectively. By 6 weeks after injury, the volume density had increased significantly in both white (55.1% +\u002F- 3.4%) and blue areas (53.5% +\u002F- 3.0%), and these values did not change significantly by 18 weeks. The volume density of myofilaments in the luminal (lining) smooth muscle cells in the blue areas was significantly less than that of control medial cells and remained low (26.7% +\u002F- 2.1%) up to 18 weeks after injury. The initial balloon-induced injury caused considerable damage to the smooth muscle cells in the media, and the remaining medial cells underwent similar changes in ultrastructure to the cells in the neointima. At 2 weeks, the cells had a low volume density of myofilaments (44.9% +\u002F- 2.4%), which returned to a level not significantly different from the control artery by 6 weeks after injury. There were no differences in the estimates of the volume density of myofilaments between the inner and outer media of the injured arteries. These findings suggest that, after injury produced by a balloon catheter, the smooth muscle cells in both the media and the resultant intimal thickening undergo a reversible change in ultrastructure.\u003C\u002Fjats:p>",{"VI":402,"EN":403},"Tổn thương động mạch cảnh thỏ do bóng catheter. I. Những thay đổi trong kiểu hình cơ trơn.","Balloon catheter injury to rabbit carotid artery. I. Changes in smooth muscle phenotype.",{"VOID":405},"2719591",{"VOID":407},"10.1161\u002F01.atv.9.3.289",[67],[280],"https:\u002F\u002Fwww.ahajournals.org\u002Fdoi\u002F10.1161\u002F01.ATV.9.3.289",[412,432,447,462,479],{"id":413,"sortIndex":19,"researcher":18,"roles":414,"affiliations":415,"properties":427},"76b7e659-7d5f-49c3-96d1-3af31fada7cf",[],[416],{"id":417,"sortIndex":19,"affiliation":418,"properties":18},"025e1717-c12d-4069-8920-b458c955887e",{"id":419,"createTime":420,"updateTime":421,"relativeEntities":422,"slug":423,"properties":424,"entityType":85,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19},"01e28b81-65cb-4e27-82f0-45cd8e3566bb","2024-09-03T16:00:17.227+00:00","2025-06-11T15:19:17.165+00:00",[],"Department-of-Anatomy-University-of-Melbourne-Parkville-Victoria-Australia-",{"title":425},{"EN":426},"Department of Anatomy, University of Melbourne, Parkville, Victoria, Australia.",{"openalex":428,"title":430},{"VOID":429},"A5083917247",{"EN":431},"J A Manderson",{"id":433,"sortIndex":27,"researcher":18,"roles":434,"affiliations":435,"properties":442},"c003e234-ed2d-488b-8fc7-aa88497faf59",[],[436],{"id":437,"sortIndex":19,"affiliation":438,"properties":18},"0e389955-7ade-4e8d-ab21-aad148b50e63",{"id":419,"createTime":420,"updateTime":421,"relativeEntities":439,"slug":423,"properties":440,"entityType":85,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19},[],{"title":441},{"EN":426},{"openalex":443,"title":445},{"VOID":444},"A5108220902",{"EN":446},"Peter R.L. Mosse",{"id":448,"sortIndex":161,"researcher":18,"roles":449,"affiliations":450,"properties":457},"d15d21c7-76dd-4351-9810-c278f6394661",[],[451],{"id":452,"sortIndex":19,"affiliation":453,"properties":18},"4ad2bbc4-354c-4ac5-8b2b-602d7030bbcf",{"id":419,"createTime":420,"updateTime":421,"relativeEntities":454,"slug":423,"properties":455,"entityType":85,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19},[],{"title":456},{"EN":426},{"openalex":458,"title":460},{"VOID":459},"A5104055330",{"EN":461},"Gordon Campbell",{"id":463,"sortIndex":128,"researcher":18,"roles":464,"affiliations":465,"properties":472},"79c30cdd-5c80-464e-b3e4-5d84940fdbe5",[],[466],{"id":467,"sortIndex":19,"affiliation":468,"properties":18},"5d30d910-a848-48eb-b533-a213ff4f8220",{"id":419,"createTime":420,"updateTime":421,"relativeEntities":469,"slug":423,"properties":470,"entityType":85,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19},[],{"title":471},{"EN":426},{"openalex":473,"orcid":475,"title":477},{"VOID":474},"A5062507391",{"VOID":476},"https:\u002F\u002Forcid.org\u002F0000-0001-7415-6380",{"EN":478},"Sokphea Young",{"id":480,"sortIndex":197,"researcher":18,"roles":481,"affiliations":482,"properties":489},"8f857247-36f6-4276-a619-61184b8aed89",[],[483],{"id":484,"sortIndex":19,"affiliation":485,"properties":18},"01320546-7c09-47c3-afe3-53da15f7a526",{"id":419,"createTime":420,"updateTime":421,"relativeEntities":486,"slug":423,"properties":487,"entityType":85,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19},[],{"title":488},{"EN":426},{"openalex":490,"title":492},{"VOID":491},"A5061114512",{"EN":493},"J A Safstrom",{"url":18,"publisher":495,"properties":508},{"id":6,"createTime":7,"updateTime":8,"relativeEntities":496,"slug":10,"properties":497,"entityType":16,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19,"subjectFields":500,"manageAffiliations":501,"indexDatabases":502,"url":18,"thumbnailPath":18,"statistic":503,"gsStatistic":18,"type":18,"analyzePriority":18},[],{"issn":498,"title":499},{"VOID":13},{"EN":15},[],[],[],{"impactFactor":19,"impactFactorByYear":504,"i10Index":25,"i10IndexLast5Year":19,"totalPublication":25,"totalPublicationByYear":505,"totalCitation":28,"totalCitationByYear":506,"totalCitationPerPublication":37,"totalCitationPerPublicationByYear":507,"hindexLast5Year":25,"hindex":25},{},{"1981":27,"1983":27,"1984":27,"1985":27,"1988":27,"1989":27,"1990":27},{"1981":30,"1983":31,"1984":32,"1985":33,"1988":34,"1989":35,"1990":36},{"1981":30,"1983":31,"1984":32,"1985":33,"1988":34,"1989":35,"1990":36},{"volume":509,"pages":511,"issue":513},{"VOID":510},"9",{"VOID":512},"289-298",{"VOID":247},131,{"total":514,"publishYear":18,"statisticByYear":516},{"2012":197,"2014":27,"2016":27,"2017":161,"2019":27,"2021":27,"2023":27,"2024":27},"1989-05-01",1989,[],{"id":521,"createTime":522,"updateTime":523,"relativeEntities":524,"slug":525,"properties":526,"entityType":62,"verifyStatus":63,"verifyTime":542,"verifyNote":65,"syncStatus":17,"languages":543,"translateLanguages":544,"viewCount":19,"primaryUrl":545,"fullTextUrl":18,"authors":546,"publicationType":226,"publisherRelationship":582,"citationCount":601,"citationInfo":602,"publishDate":517,"publishYear":518,"citationAnalyzeStatus":17,"lastCitationAnalyze":18,"indexDatabases":18,"openAccess":18,"references":604,"isForceReanalyzing":254},"887f50bc-432e-458f-83f7-050b5cdf4ddf","2024-12-24T06:03:30.920+00:00","2024-12-31T22:23:09.806+00:00",[],"Cholesterol-homeostasis-in-mononuclear-leukocytes-from-patients-with-familial-hypercholesterolemia-treated-with-lovastatin-",{"mag":527,"keywords":529,"openalex":530,"abstract":532,"title":535,"pm":538,"doi":540},{"VOID":528},"1964382916",{"VI":265},{"VOID":531},"W1964382916",{"VI":533,"EN":534},"\u003Cjats:p>Chúng tôi đã đánh giá tác động của các liều khác nhau của lovastatin, một chất ức chế cạnh tranh của enzym 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMG CoA reductase) - enzym giới hạn tốc độ trong sinh tổng hợp cholesterol, đối với các thông số sự cân bằng cholesterol trong các bạch cầu đơn nhân được lấy từ 19 bệnh nhân có tình trạng tăng cholesterol huyết khối gia đình dị hợp tử. Bệnh nhân được điều trị với các liều lovastatin tăng dần (từ 10 đến 80 mg\u002Fngày theo chế độ uống hai lần\u002Fngày). Hoạt động in vitro của enzym HMG CoA reductase và quá trình tổng hợp cholesterol từ 2-14C-acetate đã được xác định trong các tế bào đơn nhân thu được dưới các điều kiện ổn định sau khi bệnh nhân đã dùng liều 20, 40 hoặc 80 mg\u002Fngày trong 6 tuần. Tổng và độ phân giải cao của 125I-lipoprotein mật độ thấp (LDL) đã được xác định tại thời điểm ban đầu và sau khi dùng lovastatin với liều 80 mg\u002Fngày. Mức cholesterol LDL giảm dần trên nền lovastatin (giảm 38% tại liều 80 mg\u002Fngày, p \u003C 0.005). Những thay đổi này cũng song song với sự tăng 121% trong hoạt động của HMG CoA reductase (p \u003C 0.05) và sự tăng 39% trong tổng hợp cholesterol từ 2-14C-acetate (p \u003C 0.005). Tổng và độ phân giải cao của 125I-LDL tăng từ 27 +\u002F- 3.3 và 12.1 +\u002F- 1.6 ng\u002F4 x 10(6) tế bào\u002F4 giờ chỉ trên chế độ ăn uống lên 69.7 +\u002F- 7.2 và 32.9 +\u002F- 3.6 ng\u002F4 x 10(6) tế bào\u002F4 giờ tương ứng, (trung bình +\u002F- SEM) trong các tế bào đơn nhân lấy từ bệnh nhân dùng 80 mg lovastatin hàng ngày (p \u003C 0.005).(TÓM TẮT BỊ CẮT NGẮN TẠI 250 TỪ)\u003C\u002Fjats:p>","\u003Cjats:p>We evaluated the effects of different doses of lovastatin, a competitive inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMG CoA reductase) and the rate-limiting enzyme in cholesterol biosynthesis, on parameters of cholesterol homeostasis in freshly isolated mononuclear leukocytes from 19 patients with heterozygous familial hypercholesterolemia. Patients were treated with sequentially increasing doses of lovastatin (10 to 80 mg\u002Fday in a twice-daily regimen). The in vitro activity of HMG CoA reductase and cholesterol synthesis from 2-14C-acetate was determined in mononuclear cells obtained under steady-state conditions after patients had spent 6 weeks on doses of 20, 40, or 80 mg\u002Fday. The total and high affinity degradation of 125I-low density lipoprotein (LDL) was determined at baseline and on lovastatin at a dose of 80 mg\u002Fday. LDL cholesterol levels fell progressively on lovastatin (38% reduction on 80 mg daily, p less than 0.005). These changes were paralleled by a 121% increase in the activity of HMG CoA reductase (p less than 0.05) and a 39% increase in cholesterol synthesis from 2-14C-acetate (p less than 0.005). Total and high affinity degradation of 125I-LDL increased from 27 +\u002F- 3.3 and 12.1 +\u002F- 1.6 ng\u002F4 x 10(6) cells\u002F4 hours on the diet only to 69.7 +\u002F- 7.2 and 32.9 +\u002F- 3.6 ng\u002F4 x 10(6) cells\u002F4 hours, respectively, (mean +\u002F- SEM) in mononuclear cells isolated from patients on 80 mg of lovastatin daily (p less than 0.005).(ABSTRACT TRUNCATED AT 250 WORDS)\u003C\u002Fjats:p>",{"VI":536,"EN":537},"Sự cân bằng cholesterol trong tế bào bạch cầu đơn nhân của bệnh nhân mắc bệnh tăng cholesterol di truyền được điều trị bằng lovastatin.","Cholesterol homeostasis in mononuclear leukocytes from patients with familial hypercholesterolemia treated with lovastatin.",{"VOID":539},"2719596",{"VOID":541},"10.1161\u002F01.atv.9.3.355","2024-12-24T06:03:30.917+00:00",[67],[280],"https:\u002F\u002Fwww.ahajournals.org\u002Fdoi\u002F10.1161\u002F01.ATV.9.3.355",[547,567],{"id":548,"sortIndex":27,"researcher":18,"roles":549,"affiliations":550,"properties":562},"3211be4e-8e1f-48e9-b43e-63ba6d3e12b2",[],[551],{"id":552,"sortIndex":19,"affiliation":553,"properties":18},"179d60ca-4c71-4f64-bb73-9606912f1a44",{"id":554,"createTime":555,"updateTime":556,"relativeEntities":557,"slug":558,"properties":559,"entityType":85,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19},"396825e4-62e1-437d-a4c4-db3a39e918d4","2023-12-06T12:30:27.877+00:00","2024-12-24T06:03:30.955+00:00",[],"Department-of-Medicine-Oregon-Health-Sciences-University-Portland-97201-",{"title":560},{"VI":561},"Department of Medicine, Oregon Health Sciences University, Portland 97201.",{"openalex":563,"title":565},{"VOID":564},"A5108780884",{"EN":566},"D. Roger Illingworth",{"id":568,"sortIndex":19,"researcher":18,"roles":569,"affiliations":570,"properties":577},"9574deee-ea6d-4080-b4e5-16edf5371d10",[],[571],{"id":572,"sortIndex":19,"affiliation":573,"properties":18},"133dccaf-d7f2-4728-b899-2e23f9508ca8",{"id":554,"createTime":555,"updateTime":556,"relativeEntities":574,"slug":558,"properties":575,"entityType":85,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19},[],{"title":576},{"VI":561},{"openalex":578,"title":580},{"VOID":579},"A5032583641",{"EN":581},"F. C. 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Cells from available heterozygotes were also analyzed. Good resolution between the normal, heterozygote, and homozygote groups was obtained on the basis of these assays using either cell type. Results obtained with fibroblasts allowed the classification of 13 of these kindreds as being typically receptor-defective, and one kindred with two homozygotes as being receptor-negative. Fibroblasts from homozygotes of the receptor-defective class expressed LDL receptor activities which varied between 3% and 25% of normal. Where two homozygotes from the same family were available for assays (six families), both yielded similar activities. In contrast to fibroblasts, all the lymphoblastoid cells derived from FH homozygotes yielded LDL receptor activities equal to or less than 10% of normal; in a number of cases no significant 125I-LDL binding was detectable. The use of lymphoblastoid cells provides a convenient means for screening for FH at the cellular level. Our results indicate a predominance of a receptor-defective type of abnormality, which is consistent with a founder gene effect in the Afrikaner population.\u003C\u002Fjats:p>",{"EN":619},"Low density lipoprotein receptor mutations in South African homozygous familial hypercholesterolemic patients.",{"VOID":621},"6324732",{"VOID":623},"10.1161\u002F01.atv.4.3.238","2025-01-25T22:22:49.404+00:00",[67],"https:\u002F\u002Fwww.ahajournals.org\u002Fdoi\u002F10.1161\u002F01.ATV.4.3.238",[628,649,668,689,707,725,743],{"id":629,"sortIndex":161,"researcher":18,"roles":630,"affiliations":631,"properties":642},"3f21a7dd-2a71-4d96-8655-ddf6fc5eff33",[],[632],{"id":633,"sortIndex":19,"affiliation":634,"properties":18},"913376e8-ffc7-4511-a04c-6cda7eeea96d",{"id":635,"createTime":636,"updateTime":636,"relativeEntities":637,"slug":638,"properties":639,"entityType":85,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19},"f50bffa5-0295-4721-ab47-1792f729e661","2025-01-25T22:22:49.892+00:00",[],"W-Gevers",{"title":640},{"EN":641},"W Gevers",{"openalex":643,"orcid":645,"title":647},{"VOID":644},"A5009709312",{"VOID":646},"https:\u002F\u002Forcid.org\u002F0000-0003-1138-2625",{"EN":648},"Wieland Gevers",{"id":650,"sortIndex":128,"researcher":18,"roles":651,"affiliations":652,"properties":663},"c2ec1239-7cb6-4d6b-adbf-0903ff4c2718",[],[653],{"id":654,"sortIndex":19,"affiliation":655,"properties":18},"cf9f3672-a9ca-4da8-b43a-8b450527ee99",{"id":656,"createTime":657,"updateTime":657,"relativeEntities":658,"slug":659,"properties":660,"entityType":85,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19},"fd53f495-9d6e-4c41-ae97-bc631504dff2","2025-01-25T22:22:49.819+00:00",[],"E-H-Harley",{"title":661},{"EN":662},"E H Harley",{"openalex":664,"title":666},{"VOID":665},"A5005225501",{"EN":667},"Eric H. 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Vì các axit béo không bão hòa cis được đưa vào màng tế bào làm tăng độ lỏng của màng và do đó có thể thay đổi đáng kể các chức năng tế bào phụ thuộc vào màng, chúng tôi đã xem xét tác động của việc đưa linoleate và oleate vào màng tế bào đơn nhân trong máu ngoại vi đối với các tính chất vật lý của màng và đồng thời đối với sự hấp thu và phân hủy lipoprotein có mật độ thấp. Chúng tôi phát hiện rằng sự giàu có membrane với linoleate tăng tốc độ phân hủy lipoprotein có mật độ thấp trong cả tế bào đơn nhân vừa được tách ra và tế bào đơn nhân đã được điều chỉnh lại. Sự giàu có với oleate cũng dẫn đến sự gia tăng tương tự trong phân hủy. Sự hấp thu lipoprotein có mật độ thấp \"cụ thể\" bởi các tế bào đã được điều chỉnh lại cũng được cải thiện bởi việc đưa linoleate và oleate vào. Sự giàu có với cả hai axit béo này tạo ra một sự gia tăng độ lỏng của màng, như được chỉ ra bởi sự giảm độ phân cực huỳnh quang tại trạng thái ổn định của 1,6-diphenyl-1,3,5-hexatriene được đưa vào màng. Ngược lại, sự giàu có với stearate có ít tác động đến sự hấp thu hoặc phân hủy lipoprotein có mật độ thấp, cũng như không ảnh hưởng đến độ lỏng của màng. Những dữ liệu này chỉ ra một cơ chế mới cho sự giảm thiểu lipoprotein có mật độ thấp do các axit béo không bão hòa gây ra liên quan đến các tác động vật lý của chúng lên màng tế bào khi liên quan đến sự trao đổi chất của lipoprotein.\u003C\u002Fjats:p>","\u003Cjats:p>The precise mechanism by which unsaturated fatty acids lower low density lipoprotein cholesterol is not known. Because cis-unsaturated fatty acids incorporated in cell membranes increase membrane fluidity and can thereby dramatically alter membrane-dependent cellular functions, we examined the effect of linoleate and oleate incorporation in peripheral blood mononuclear cell membranes on the physical properties of the membrane and concomitantly on low density lipoprotein uptake and degradation. We found that membrane enrichment with linoleate increased the rate of low density lipoprotein degradation in both freshly isolated and derepressed mononuclear cells. Enrichment with oleate led to similar increases in degradation. \"Specific\" low density lipoprotein uptake by derepressed cells was also enhanced by linoleate and oleate incorporation. Enrichment with both of these fatty acids produced an increase in membrane fluidity, as indicated by a reduction in the steady-state fluorescence polarization of 1,6-diphenyl-1,3,5-hexatriene incorporated in the membrane. In contrast, stearate enrichment had little effect on uptake or degradation of low density lipoprotein, nor did it affect membrane fluidity. These data point to a novel mechanism for the reduction in low density lipoprotein produced by unsaturated fatty acids that involves their physical effects on cell membranes as it relates to metabolism of the lipoprotein.\u003C\u002Fjats:p>",{"VI":803,"EN":804},"Các axit béo không bão hòa làm tăng sự hấp thu và phân hủy lipoprotein có mật độ thấp bởi các tế bào đơn nhân trong máu ngoại vi.","Unsaturated fatty acids enhance low density lipoprotein uptake and degradation by peripheral blood mononuclear cells.",{"VOID":806},"3675304",{"VOID":808},"10.1161\u002F01.atv.7.5.450",[67],[280],"https:\u002F\u002Fwww.ahajournals.org\u002Fdoi\u002F10.1161\u002F01.ATV.7.5.450",[813,833,848,865,882],{"id":814,"sortIndex":128,"researcher":18,"roles":815,"affiliations":816,"properties":828},"0200e931-bb3c-427c-8043-c4480bbee7b6",[],[817],{"id":818,"sortIndex":19,"affiliation":819,"properties":18},"ed8ac705-e8e9-4f8e-ac57-72054345c2dc",{"id":820,"createTime":821,"updateTime":822,"relativeEntities":823,"slug":824,"properties":825,"entityType":85,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19},"966e38e8-ba4e-4de8-92f7-9d765d92c7f3","2023-12-05T08:36:51.284+00:00","2024-12-24T06:03:36.257+00:00",[],"Department-of-Medicine-Brigham-and-Women-s-Hospital-Harvard-Medical-School-Boston-Massachusetts-02115",{"title":826},{"VI":827},"Department of Medicine, Brigham and Women’s Hospital, Harvard Medical School, Boston, Massachusetts 02115",{"openalex":829,"title":831},{"VOID":830},"A5017717069",{"EN":832},"I Barsky-Vasserman",{"id":834,"sortIndex":27,"researcher":18,"roles":835,"affiliations":836,"properties":843},"0f0aaa84-5ca0-47b6-912c-1b6de2c5e95f",[],[837],{"id":838,"sortIndex":19,"affiliation":839,"properties":18},"8981dd3a-cc22-4744-8a1e-f6f9361a5684",{"id":820,"createTime":821,"updateTime":822,"relativeEntities":840,"slug":824,"properties":841,"entityType":85,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19},[],{"title":842},{"VI":827},{"openalex":844,"title":846},{"VOID":845},"A5011976722",{"EN":847},"John Freedman",{"id":849,"sortIndex":19,"researcher":18,"roles":850,"affiliations":851,"properties":858},"2dc4df0b-3632-4cb7-aef7-2417e1cdb8d4",[],[852],{"id":853,"sortIndex":19,"affiliation":854,"properties":18},"36181baf-ce50-4999-afda-24ba9d1da7a1",{"id":820,"createTime":821,"updateTime":822,"relativeEntities":855,"slug":824,"properties":856,"entityType":85,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19},[],{"title":857},{"VI":827},{"openalex":859,"orcid":861,"title":863},{"VOID":860},"A5028396638",{"VOID":862},"https:\u002F\u002Forcid.org\u002F0000-0002-1153-8047",{"EN":864},"Joseph Loscalzo",{"id":866,"sortIndex":197,"researcher":18,"roles":867,"affiliations":868,"properties":875},"03e63f54-7a7e-4007-91b0-9ec5823be6a7",[],[869],{"id":870,"sortIndex":19,"affiliation":871,"properties":18},"267f6c1a-339f-4c72-a04f-8713c4c1ce26",{"id":820,"createTime":821,"updateTime":822,"relativeEntities":872,"slug":824,"properties":873,"entityType":85,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19},[],{"title":874},{"VI":827},{"openalex":876,"orcid":878,"title":880},{"VOID":877},"A5061915607",{"VOID":879},"https:\u002F\u002Forcid.org\u002F0000-0001-9533-5070",{"EN":881},"Murray A. 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Vaughan",{"url":18,"publisher":900,"properties":913},{"id":6,"createTime":7,"updateTime":8,"relativeEntities":901,"slug":10,"properties":902,"entityType":16,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19,"subjectFields":905,"manageAffiliations":906,"indexDatabases":907,"url":18,"thumbnailPath":18,"statistic":908,"gsStatistic":18,"type":18,"analyzePriority":18},[],{"issn":903,"title":904},{"VOID":13},{"EN":15},[],[],[],{"impactFactor":19,"impactFactorByYear":909,"i10Index":25,"i10IndexLast5Year":19,"totalPublication":25,"totalPublicationByYear":910,"totalCitation":28,"totalCitationByYear":911,"totalCitationPerPublication":37,"totalCitationPerPublicationByYear":912,"hindexLast5Year":25,"hindex":25},{},{"1981":27,"1983":27,"1984":27,"1985":27,"1988":27,"1989":27,"1990":27},{"1981":30,"1983":31,"1984":32,"1985":33,"1988":34,"1989":35,"1990":36},{"1981":30,"1983":31,"1984":32,"1985":33,"1988":34,"1989":35,"1990":36},{"volume":914,"pages":916,"issue":918},{"VOID":915},"7",{"VOID":917},"450-455",{"VOID":919},"5",42,{"total":920,"publishYear":18,"statisticByYear":922},{},"1987-09-01",1987,[],{"id":927,"createTime":928,"updateTime":929,"relativeEntities":930,"slug":931,"properties":932,"entityType":62,"verifyStatus":63,"verifyTime":948,"verifyNote":65,"syncStatus":17,"languages":949,"translateLanguages":950,"viewCount":19,"primaryUrl":951,"fullTextUrl":18,"authors":952,"publicationType":226,"publisherRelationship":1067,"citationCount":514,"citationInfo":1087,"publishDate":1089,"publishYear":1090,"citationAnalyzeStatus":17,"lastCitationAnalyze":18,"indexDatabases":18,"openAccess":18,"references":1091,"isForceReanalyzing":254},"a0a4f4d6-be8b-4643-91e3-0695a3d49bbc","2024-12-24T06:03:36.774+00:00","2024-12-31T22:21:16.296+00:00",[],"Effect-of-dietary-fat-saturation-and-cholesterol-on-LDL-composition-and-metabolism-In-vivo-studies-of-receptor-and-nonreceptor-mediated-catabolism-of-LDL-in-cebus-monkeys-",{"mag":933,"keywords":935,"openalex":936,"abstract":938,"title":941,"pm":944,"doi":946},{"VOID":934},"2166544755",{"VI":265},{"VOID":937},"W2166544755",{"VI":939,"EN":940},"\u003Cjats:p>Các cơ chế mà chất béo không bão hòa đa làm giảm cholesterol lipoprotein mật độ thấp (LDL) và apolipoprotein (apo) B đã được nghiên cứu trên 20 con khỉ cebus (Cebus albifrons) được cho ăn với chế độ ăn chứa dầu ngô hoặc dầu dừa như nguồn chất béo (31% năng lượng) có hoặc không có cholesterol trong chế độ ăn (0.1% theo trọng lượng) trong khoảng 3 đến 10 năm. Việc cho ăn dầu dừa so với dầu ngô dẫn đến sự gia tăng đáng kể nồng độ cholesterol toàn phần trong huyết tương (176%), cholesterol LDL-VLDL (236%), cholesterol HDL (148%), apo B (78%) và apo A-I (112%). Việc bổ sung cholesterol trong chế độ ăn vào dầu ngô so với dầu ngô đơn thuần đã dẫn đến sự gia tăng nhỏ nhưng đáng kể về nồng độ cholesterol toàn phần (44%), cholesterol HDL (40%) và apo A-I (33%). Mặc dù sự gia tăng cholesterol LDL-VLDL có độ lớn tương tự (52%), nhưng chúng gần như không đạt được sự đáng kể thống kê (p nhỏ hơn 0.08), trong khi sự thay đổi nồng độ apo B là không đáng kể. Việc bổ sung cholesterol trong chế độ ăn vào dầu dừa, so với dầu dừa đơn thuần, không dẫn đến sự thay đổi đáng kể nào về cholesterol lipoprotein hoặc apoprotein, mặc dù nồng độ cholesterol LDL-VLDL và giá trị apo B đã tăng lần lượt 22% và 16%. Mặc dù nồng độ cholesterol tự do ở gan không bị thay đổi bởi chế độ ăn, nhưng việc cho ăn dầu dừa so với dầu ngô đã dẫn đến sự gia tăng đáng kể các este cholesterol ở gan (236%) và triglycerid (325%), trong đó chất béo triglycerid tăng thêm khi cholesterol trong chế độ ăn được bổ sung vào dầu dừa (563%). Để đánh giá thêm tác động của những thay đổi chế độ ăn này đối với chuyển hóa LDL, các thí nghiệm động học LDL có gắn iod phóng xạ bình thường và glucose đã được thực hiện. Tốc độ sản xuất LDL apo B không bị thay đổi bởi chế độ ăn. Với việc cho ăn dầu ngô, 63% sự chuyển hóa LDL diễn ra qua con đường tiếp nhận. Việc cho ăn dầu dừa so với dầu ngô dẫn đến sự giảm 50% tỷ lệ phân hủy LDL apo B qua con đường tiếp nhận và giảm 27% phân hủy LDL apo B không qua tiếp nhận. Việc bổ sung cholesterol trong chế độ ăn vào dầu ngô so với dầu ngô đơn thuần không có tác động đáng kể nào đến sự chuyển hóa LDL apo B. Việc bổ sung cholesterol trong chế độ ăn vào dầu dừa so với dầu dừa đơn thuần không liên quan đến sự thay đổi đáng kể nào trong phân hủy LDL apo B không qua tiếp nhận nhưng có liên quan với việc giảm 58% trong phân hủy LDL qua con đường tiếp nhận (p nhỏ hơn 0.059). Những thay đổi về chuyển hóa LDL do chế độ ăn gây ra có mối tương quan đáng kể với lipid gan, vốn giàu axit béo bão hòa. (TÓM TẮT BỊ CẮT NGẮT TỪ 400 TỪ)\u003C\u002Fjats:p>","\u003Cjats:p>The mechanism(s) by which polyunsaturated fats reduce low density lipoprotein (LDL) cholesterol and apolipoprotein (apo) B were investigated in 20 cebus monkeys (Cebus albifrons) fed diets containing corn oil or coconut oil as fat (31% of calories) with or without dietary cholesterol (0.1% by weight) for 3 to 10 years. Coconut-oil feeding compared to corn-oil feeding resulted in significant increases in levels of plasma total cholesterol (176%), very low density lipoprotein (VLDL)-LDL cholesterol (236%), high density lipoprotein (HDL) cholesterol (148%), apo B (78%), and apo A-I (112%). The addition of dietary cholesterol to corn oil compared to corn oil alone resulted in smaller, but significant, increases in levels of total cholesterol (44%), HDL cholesterol (40%), and apo A-I (33%). Although the increases in VLDL-LDL cholesterol were of similar magnitude (52%), they barely failed to reach statistical significance (p less than 0.08), while the changes in apo B levels were negligible. The addition of dietary cholesterol to coconut oil, compared to coconut oil alone, resulted in no significant changes in lipoprotein cholesterol or apoproteins, although levels of VLDL-LDL cholesterol and apo B values increased 22% and 16%, respectively. Although hepatic free cholesterol content was not altered by diet, coconut-oil compared to corn-oil feeding resulted in significant increases in hepatic cholesteryl esters (236%) and triglycerides (325%), the latter increasing still further when dietary cholesterol was added to coconut oil (563%). To further assess the effects of these dietary changes on LDL metabolism, radioiodinated normal and glucosylated LDL kinetics were performed. The production rate of LDL apo B was not altered by diet. With corn-oil feeding, 63% of LDL catabolism was via the receptor-mediated pathway. Coconut-oil compared to corn-oil feeding resulted in a 50% decrease in receptor-mediated LDL apo B fractional catabolic rate (FCR) and a 27% reduction in nonreceptor-mediated LDL apo B FCR. The addition of dietary cholesterol to corn oil, compared to corn oil alone, resulted in no significant effect on LDL apo B catabolism. The addition of dietary cholesterol to coconut oil, compared to coconut oil alone, was associated with no significant change in nonreceptor catabolism of LDL apo B but with a 58% decrease in receptor-mediated catabolism of LDL (p less than 0.059). The diet-induced alterations of LDL catabolism were significantly correlated with hepatic lipids, which were enriched in saturated fatty acids.(ABSTRACT TRUNCATED AT 400 WORDS)\u003C\u002Fjats:p>",{"VI":942,"EN":943},"Tác động của độ bão hòa chất béo trong chế độ ăn và cholesterol đến thành phần và chuyển hóa LDL. Nghiên cứu trực tiếp về sự phân hủy LDL qua con đường tiếp nhận và không tiếp nhận ở khỉ cebus.","Effect of dietary fat saturation and cholesterol on LDL composition and metabolism. 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Stucchi",{"id":1049,"sortIndex":161,"researcher":18,"roles":1050,"affiliations":1051,"properties":1062},"2711c3e6-e59f-4377-a113-22c9a0b718eb",[],[1052],{"id":1053,"sortIndex":19,"affiliation":1054,"properties":18},"07192ede-4782-46b3-8cb0-0d6247e69e82",{"id":1055,"createTime":1056,"updateTime":1056,"relativeEntities":1057,"slug":1058,"properties":1059,"entityType":85,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19},"69e24a7e-7558-4d8e-9070-5d39b1f4e675","2024-12-24T06:03:36.865+00:00",[],"D-M-Hegsted-Department-of-Clinical-Sciences-University-of-Lowell-Massachusetts-01854-",{"title":1060},{"EN":1061},"D M Hegsted Department of Clinical Sciences, University of Lowell, Massachusetts 01854.",{"openalex":1063,"title":1065},{"VOID":1064},"A5110000677",{"EN":1066},"D.M. Hegsted",{"url":18,"publisher":1068,"properties":1081},{"id":6,"createTime":7,"updateTime":8,"relativeEntities":1069,"slug":10,"properties":1070,"entityType":16,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19,"subjectFields":1073,"manageAffiliations":1074,"indexDatabases":1075,"url":18,"thumbnailPath":18,"statistic":1076,"gsStatistic":18,"type":18,"analyzePriority":18},[],{"issn":1071,"title":1072},{"VOID":13},{"EN":15},[],[],[],{"impactFactor":19,"impactFactorByYear":1077,"i10Index":25,"i10IndexLast5Year":19,"totalPublication":25,"totalPublicationByYear":1078,"totalCitation":28,"totalCitationByYear":1079,"totalCitationPerPublication":37,"totalCitationPerPublicationByYear":1080,"hindexLast5Year":25,"hindex":25},{},{"1981":27,"1983":27,"1984":27,"1985":27,"1988":27,"1989":27,"1990":27},{"1981":30,"1983":31,"1984":32,"1985":33,"1988":34,"1989":35,"1990":36},{"1981":30,"1983":31,"1984":32,"1985":33,"1988":34,"1989":35,"1990":36},{"volume":1082,"pages":1084,"issue":1086},{"VOID":1083},"10",{"VOID":1085},"119-128",{"VOID":379},{"total":514,"publishYear":18,"statisticByYear":1088},{"2012":128,"2013":197,"2015":197,"2016":128,"2017":128,"2018":128,"2020":27,"2021":128,"2023":27,"2024":27},"1990-01-01",1990,[],{"id":1093,"createTime":1094,"updateTime":1095,"relativeEntities":1096,"slug":1097,"properties":1098,"entityType":62,"verifyStatus":63,"verifyTime":1094,"verifyNote":65,"syncStatus":17,"languages":1114,"translateLanguages":1115,"viewCount":19,"primaryUrl":1116,"fullTextUrl":18,"authors":1117,"publicationType":226,"publisherRelationship":1191,"citationCount":1211,"citationInfo":1212,"publishDate":1214,"publishYear":518,"citationAnalyzeStatus":17,"lastCitationAnalyze":18,"indexDatabases":18,"openAccess":18,"references":1215,"isForceReanalyzing":254},"a61c55f8-fe16-43c3-a2a5-9b2c7b161bed","2024-12-24T06:03:36.786+00:00","2024-12-31T22:20:17.664+00:00",[],"Effect-of-dietary-fat-saturation-and-cholesterol-on-low-density-lipoprotein-degradation-by-mononuclear-cells-of-Cebus-monkeys-",{"mag":1099,"keywords":1101,"openalex":1102,"abstract":1104,"title":1107,"pm":1110,"doi":1112},{"VOID":1100},"2166187531",{"VI":265},{"VOID":1103},"W2166187531",{"VI":1105,"EN":1106},"\u003Cjats:p>Cơ chế mà axit béo không bão hòa trong chế độ ăn hạ thấp cholesterol lipoprotein mật độ thấp (LDL) vẫn chưa được hiểu rõ. Axit béo không bão hòa được tích hợp vào màng tế bào có thể làm tăng tính linh hoạt của màng và do đó, thay đổi đáng kể các chức năng tế bào phụ thuộc vào màng. Do đó, chúng tôi đã nghiên cứu tác động của việc tiêu thụ chế độ ăn dầu ngô và dầu dừa, có và không có cholesterol, với lượng tương đương của một chế độ ăn uống điển hình ở phương Tây, đến sự phân hủy LDL của con người bởi các tế bào đơn nhân ngoại vi trong khỉ Cebus albifrons. Sự phân hủy LDL ở tế bào đơn nhân thu được từ những con vật được cho ăn dầu ngô đã được cải thiện một cách đáng kể so với những con vật được cho ăn dầu dừa. Việc bổ sung cholesterol vào chế độ ăn dẫn đến sự suy giảm nhẹ sự phân hủy LDL trong nhóm dầu ngô, trong khi không có ảnh hưởng nào được ghi nhận ở nhóm dầu dừa. Các thí nghiệm kết hợp liên kết và phân hủy LDL với LDL được tách ra từ các con vật ăn chế độ dầu ngô và dầu dừa cho thấy sự tăng cường liên kết và phân hủy LDL trong các tế bào đơn nhân từ những con vật ăn chế độ dầu ngô. Sự phân hủy LDL của tế bào đơn nhân được nâng cao đi đôi với sự gia tăng hàm lượng axit béo cis không bão hòa trong tế bào, tăng cường tính linh hoạt của màng, và giảm cholesterol huyết tương. Sự gia tăng hàm lượng axit béo cis không bão hòa trong tế bào cùng với sự gia tăng tính linh hoạt của màng phản ánh hồ sơ mỡ trong chế độ ăn của động vật chủ. Một mối quan hệ tuyến tính giữa sự phân hủy LDL trong tế bào và cả hàm lượng axit béo cis không bão hòa trong tế bào cũng như tính linh hoạt của màng đã được quan sát thấy. Những quan sát này tương tự với kết quả ghi nhận trong các nghiên cứu phân hủy LDL ở động vật toàn thân với những động vật này đã được mô tả ở nơi khác. Những dữ liệu này gợi ý một cơ chế mới mà qua đó axit béo không bão hòa trong chế độ ăn thực hiện tác dụng hạ LDL của chúng.\u003C\u002Fjats:p>","\u003Cjats:p>The mechanism by which dietary unsaturated fatty acids lower low density lipoprotein (LDL) cholesterol is unknown. Unsaturated fatty acids incorporated into the cell membrane can increase membrane fluidity and, as a result, dramatically alter membrane-dependent cell functions. Therefore, we examined the effect of long-term dietary consumption of corn oil and coconut oil with and without cholesterol in amounts equivalent to those of a typical Western diet on the degradation of human LDL by peripheral blood mononuclear cells in Cebus albifrons monkeys. Cellular LDL degradation was dramatically enhanced in the mononuclear cells isolated from animals fed corn oil in comparison with those from animals fed coconut oil. The addition of cholesterol to the diets resulted in a slight attenuation of LDL degradation in the corn oil group while no effect was noted in the coconut oil group. Crossover LDL binding and degradation experiments with LDL isolated from animals fed corn oil diets and coconut oil diets demonstrated increased binding and degradation of LDL in mononuclear cells from animals fed corn oil diets. Enhanced mononuclear cell LDL degradation was accompanied by increased cellular cis-unsaturated fatty acyl content, increased membrane fluidity, and decreased plasma cholesterol. Increased cellular cis-unsaturated fatty acyl content with its concomitant increase in membrane fluidity mirrored the dietary lipid profile of the host animal. A linear relationship was observed between cellular LDL degradation and both cellular cis-unsaturated fatty acyl content and membrane fluidity. These observations parallel results noted in whole-animal LDL catabolic studies with these same animals described elsewhere. These data suggest a novel mechanism by which dietary unsaturated fatty acids exert their LDL-lowering effect.\u003C\u002Fjats:p>",{"VI":1108,"EN":1109},"Tác động của độ bão hòa chất béo trong chế độ ăn và cholesterol đến sự phân hủy lipoprotein mật độ thấp bởi các tế bào đơn nhân của khỉ Cebus.","Effect of dietary fat saturation and cholesterol on low density lipoprotein degradation by mononuclear cells of Cebus monkeys.",{"VOID":1111},"2590069",{"VOID":1113},"10.1161\u002F01.atv.9.6.919",[67],[280],"https:\u002F\u002Fwww.ahajournals.org\u002Fdoi\u002F10.1161\u002F01.ATV.9.6.919",[1118,1137,1155,1172],{"id":1119,"sortIndex":19,"researcher":18,"roles":1120,"affiliations":1121,"properties":1132},"5853d04c-c1a6-4712-bf0c-1b0be2013cc6",[],[1122],{"id":1123,"sortIndex":19,"affiliation":1124,"properties":18},"b14d7984-7a8d-465a-a419-8b818a87d4db",{"id":1125,"createTime":1126,"updateTime":1126,"relativeEntities":1127,"slug":1128,"properties":1129,"entityType":85,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19},"b61140bc-7188-4274-99e3-355929d125c0","2024-12-24T06:03:36.808+00:00",[],"P-C-Kuo-Department-of-Medicine-Brigham-and-Women-s-Hospital-Boston-MA-02115-",{"title":1130},{"EN":1131},"P C Kuo Department of Medicine, Brigham and Women's Hospital, Boston, MA 02115.",{"openalex":1133,"title":1135},{"VOID":1134},"A5077124089",{"EN":1136},"P C Kuo",{"id":1138,"sortIndex":128,"researcher":18,"roles":1139,"affiliations":1140,"properties":1151},"111f85c6-e708-4029-98a9-f736e2ecfa8d",[],[1141],{"id":1142,"sortIndex":19,"affiliation":1143,"properties":18},"73db2535-1c42-439e-a990-83c8a8c2ddd7",{"id":1144,"createTime":1145,"updateTime":1145,"relativeEntities":1146,"slug":1147,"properties":1148,"entityType":85,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19},"9d0a62c4-64f8-4b42-a428-4a7fd4a85aa4","2024-12-24T06:03:36.856+00:00",[],"J-Loscalzo-Department-of-Medicine-Brigham-and-Women-s-Hospital-Boston-MA-02115-",{"title":1149},{"EN":1150},"J Loscalzo Department of Medicine, Brigham and Women's Hospital, Boston, MA 02115.",{"openalex":1152,"orcid":1153,"title":1154},{"VOID":860},{"VOID":862},{"EN":864},{"id":1156,"sortIndex":197,"researcher":18,"roles":1157,"affiliations":1158,"properties":1169},"231560db-a3dc-4c47-bfc5-9a87c7be706e",[],[1159],{"id":1160,"sortIndex":19,"affiliation":1161,"properties":18},"1cd7c6f6-9e18-48de-8605-66069a461849",{"id":1162,"createTime":1163,"updateTime":1163,"relativeEntities":1164,"slug":1165,"properties":1166,"entityType":85,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19},"48b9725e-b0f0-42f8-a652-97ec543809ee","2024-12-24T06:03:36.843+00:00",[],"R-Nicolosi-Department-of-Medicine-Brigham-and-Women-s-Hospital-Boston-MA-02115-",{"title":1167},{"EN":1168},"R Nicolosi Department of Medicine, Brigham and Women's Hospital, Boston, MA 02115.",{"openalex":1170,"title":1171},{"VOID":1026},{"EN":1028},{"id":1173,"sortIndex":27,"researcher":18,"roles":1174,"affiliations":1175,"properties":1187},"ee41ba7f-db69-40a3-8cba-2d4a6b4e0a48",[],[1176],{"id":1177,"sortIndex":19,"affiliation":1178,"properties":18},"a7b852c9-ecd2-404b-b529-b0321c1d2916",{"id":1179,"createTime":1180,"updateTime":1181,"relativeEntities":1182,"slug":1183,"properties":1184,"entityType":85,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19},"03dad7b6-c285-42d4-94a4-868449d6fa5e","2024-12-24T06:03:36.829+00:00","2025-06-11T17:10:00.740+00:00",[],"M-A-Rudd-Department-of-Medicine-Brigham-and-Women-s-Hospital-Boston-MA-02115-",{"title":1185},{"EN":1186},"M A Rudd Department of Medicine, Brigham and Women's Hospital, Boston, MA 02115.",{"openalex":1188,"orcid":1189,"title":1190},{"VOID":877},{"VOID":879},{"EN":881},{"url":18,"publisher":1192,"properties":1205},{"id":6,"createTime":7,"updateTime":8,"relativeEntities":1193,"slug":10,"properties":1194,"entityType":16,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19,"subjectFields":1197,"manageAffiliations":1198,"indexDatabases":1199,"url":18,"thumbnailPath":18,"statistic":1200,"gsStatistic":18,"type":18,"analyzePriority":18},[],{"issn":1195,"title":1196},{"VOID":13},{"EN":15},[],[],[],{"impactFactor":19,"impactFactorByYear":1201,"i10Index":25,"i10IndexLast5Year":19,"totalPublication":25,"totalPublicationByYear":1202,"totalCitation":28,"totalCitationByYear":1203,"totalCitationPerPublication":37,"totalCitationPerPublicationByYear":1204,"hindexLast5Year":25,"hindex":25},{},{"1981":27,"1983":27,"1984":27,"1985":27,"1988":27,"1989":27,"1990":27},{"1981":30,"1983":31,"1984":32,"1985":33,"1988":34,"1989":35,"1990":36},{"1981":30,"1983":31,"1984":32,"1985":33,"1988":34,"1989":35,"1990":36},{"volume":1206,"pages":1207,"issue":1209},{"VOID":510},{"VOID":1208},"919-927",{"VOID":1210},"6",29,{"total":1211,"publishYear":18,"statisticByYear":1213},{"2015":27},"1989-11-01",[],{"id":1217,"createTime":1218,"updateTime":1219,"relativeEntities":1220,"slug":1221,"properties":1222,"entityType":62,"verifyStatus":63,"verifyTime":1218,"verifyNote":65,"syncStatus":17,"languages":1238,"translateLanguages":1239,"viewCount":19,"primaryUrl":1240,"fullTextUrl":18,"authors":1241,"publicationType":226,"publisherRelationship":1262,"citationCount":1281,"citationInfo":1282,"publishDate":1284,"publishYear":1285,"citationAnalyzeStatus":17,"lastCitationAnalyze":18,"indexDatabases":18,"openAccess":18,"references":1286,"isForceReanalyzing":254},"2e913e04-2c4c-45b1-b79b-1dc466e3f1ff","2024-12-24T06:03:38.011+00:00","2024-12-31T22:19:20.042+00:00",[],"Declining-mortality-in-coronary-heart-disease-",{"mag":1223,"keywords":1225,"openalex":1226,"abstract":1228,"title":1231,"pm":1234,"doi":1236},{"VOID":1224},"2010974965",{"VI":265},{"VOID":1227},"W2010974965",{"VI":1229,"EN":1230},"\u003Cjats:p>Kể từ năm 1968, tỷ lệ tử vong do bệnh tim mạch tại Hoa Kỳ đã giảm mạnh một cách chưa từng có, đặc biệt là do bệnh tim mạch vành và đột quỵ. Sự giảm sút này đã được xác nhận là có thật và đã được quan sát thấy ở tất cả các nhóm tuổi, giới tính và chủng tộc. Các nguyên nhân có thể dẫn đến sự giảm tỷ lệ tử vong do bệnh tim mạch vành bao gồm sự phát triển của khái niệm chăm sóc tim cấp, các loại thuốc mới, các kỹ thuật phẫu thuật tinh vi như phẫu thuật bắc cầu động mạch vành, các phương pháp chẩn đoán không xâm lấn để phát hiện bệnh sớm hơn, và việc xác định các yếu tố nguy cơ tim mạch cụ thể. Sự giảm sút này có liên quan đến sự nhận thức và điều chỉnh các yếu tố nguy cơ (chấm dứt hút thuốc, kiểm soát huyết áp, thay đổi chế độ ăn uống và giảm cholesterol). Do đó, cả việc phòng ngừa nguyên phát thông qua thay đổi lối sống và các chế độ điều trị cải thiện đều đã đóng góp vào sự giảm này.\u003C\u002Fjats:p>","\u003Cjats:p>Since 1968, there has been a dramatic, unprecedented decline in mortality from cardiovascular disease in the United States, especially from coronary heart disease and stroke. The decline has now been confirmed as real and has been observed in all age, sex, and race groups. Possible causes of the decline in coronary heart disease mortality include the development of the concept of acute coronary care, new drugs, sophisticated surgical techniques such as coronary artery bypass, noninvasive diagnostic methods for earlier disease detection, and the identification of specific cardiovascular risk factors. The decline has been temporally related to risk factor awareness and modification (cigarette smoking cessation, hypertension control, diet change and reduction in cholesterol). Thus, both primary prevention through lifestyle changes and improved treatment regimes have played a role in the decline.\u003C\u002Fjats:p>",{"VI":1232,"EN":1233},"Tỷ lệ tử vong do bệnh tim mạch giảm.","Declining mortality in coronary heart disease.",{"VOID":1235},"7052033",{"VOID":1237},"10.1161\u002F01.atv.1.5.312",[67],[280],"https:\u002F\u002Fwww.ahajournals.org\u002Fdoi\u002F10.1161\u002F01.ATV.1.5.312",[1242],{"id":1243,"sortIndex":19,"researcher":18,"roles":1244,"affiliations":1245,"properties":1257},"65bf056e-8549-4559-a82f-752c3e6d29e8",[],[1246],{"id":1247,"sortIndex":19,"affiliation":1248,"properties":18},"8f214cb1-2805-48b5-b800-66fe495616d0",{"id":1249,"createTime":1250,"updateTime":1251,"relativeEntities":1252,"slug":1253,"properties":1254,"entityType":85,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19},"0932f254-6e34-4326-8433-dab27edd8d21","2024-12-24T06:03:38.020+00:00","2025-06-11T22:09:17.211+00:00",[],"R-I-Levy",{"title":1255},{"EN":1256},"R I Levy",{"openalex":1258,"title":1260},{"VOID":1259},"A5105698451",{"EN":1261},"R. I. Levy",{"url":18,"publisher":1263,"properties":1276},{"id":6,"createTime":7,"updateTime":8,"relativeEntities":1264,"slug":10,"properties":1265,"entityType":16,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19,"subjectFields":1268,"manageAffiliations":1269,"indexDatabases":1270,"url":18,"thumbnailPath":18,"statistic":1271,"gsStatistic":18,"type":18,"analyzePriority":18},[],{"issn":1266,"title":1267},{"VOID":13},{"EN":15},[],[],[],{"impactFactor":19,"impactFactorByYear":1272,"i10Index":25,"i10IndexLast5Year":19,"totalPublication":25,"totalPublicationByYear":1273,"totalCitation":28,"totalCitationByYear":1274,"totalCitationPerPublication":37,"totalCitationPerPublicationByYear":1275,"hindexLast5Year":25,"hindex":25},{},{"1981":27,"1983":27,"1984":27,"1985":27,"1988":27,"1989":27,"1990":27},{"1981":30,"1983":31,"1984":32,"1985":33,"1988":34,"1989":35,"1990":36},{"1981":30,"1983":31,"1984":32,"1985":33,"1988":34,"1989":35,"1990":36},{"volume":1277,"pages":1278,"issue":1280},{"VOID":379},{"VOID":1279},"312-325",{"VOID":919},121,{"total":1281,"publishYear":18,"statisticByYear":1283},{"2012":128,"2014":27},"1981-09-01",1981,[],{"id":1288,"createTime":1289,"updateTime":1289,"relativeEntities":1290,"slug":1291,"properties":1292,"entityType":62,"verifyStatus":17,"verifyTime":1289,"verifyNote":1306,"syncStatus":17,"languages":1307,"translateLanguages":18,"viewCount":19,"primaryUrl":1308,"fullTextUrl":18,"authors":1309,"publicationType":226,"publisherRelationship":1368,"citationCount":33,"citationInfo":1387,"publishDate":1389,"publishYear":1390,"citationAnalyzeStatus":17,"lastCitationAnalyze":18,"indexDatabases":18,"openAccess":18,"references":1391,"isForceReanalyzing":254},"d807f3c0-fb78-4a9d-ad3a-5d880e0a4cb4","2024-09-05T22:13:02.825+00:00",[],"Spontaneous-and-diet-induced-coronary-atherosclerosis-in-normal-swine-and-swine-with-von-Willebrand-disease-",{"mag":1293,"keywords":1295,"openalex":1296,"abstract":1298,"title":1300,"pm":1302,"doi":1304},{"VOID":1294},"2112969867",{},{"VOID":1297},"W2112969867",{"EN":1299},"\u003Cjats:p>We have observed that pigs with impaired platelet function in the form of severe von Willebrand's disease (vWd) are resistant to spontaneous and to diet-induced aortic atherosclerosis. However, it has been reported that vWd pigs are susceptible to coronary atherosclerosis produced by balloon-induced injury of coronary arteries combined with an atherogenic diet. We have evaluated the development of coronary atherosclerosis in normal control (NC) and homozygous vWd pigs in two prospective studies: 1) as a spontaneous process in five NC and vWd pigs receiving a regular diet from the age of 3 months to 4 years; and 2) in nine NC and five vWd receiving a high-fat and high-cholesterol (2%) diet from the age of 3 to 9 months. All of the coronary arteries were analyzed postmortem in 5-mm sections. None of the NC nor the vWd pigs in the spontaneous study showed coronary atherosclerosis or myocardial lesions. In the study of diet-induced atherosclerosis, only one NC and one vWd pig had discrete stenoses; the stenoses affected the three coronary arteries and were significant (50% to 80%) in the NC and mild (greater than 25%) in the vWd pigs; no pigs showed myocardial lesions. Pigs with vWd are resistant to atherosclerosis of the aorta. To assess the resistance or susceptibility to coronary disease in these pigs, a longer follow-up study would be necessary.\u003C\u002Fjats:p>",{"EN":1301},"Spontaneous and diet-induced coronary atherosclerosis in normal swine and swine with von Willebrand disease.",{"VOID":1303},"3871327",{"VOID":1305},"10.1161\u002F01.atv.5.1.67","Author affiliation is blank",[67],"https:\u002F\u002Fwww.ahajournals.org\u002Fdoi\u002F10.1161\u002F01.ATV.5.1.67",[1310,1321,1330,1339,1350,1359],{"id":1311,"sortIndex":19,"researcher":18,"roles":1312,"affiliations":1313,"properties":1314},"c9420d34-02ba-46a9-93ae-8cfb08a91bc5",[],[],{"openalex":1315,"orcid":1317,"title":1319},{"VOID":1316},"A5074727212",{"VOID":1318},"https:\u002F\u002Forcid.org\u002F0000-0002-9043-9986",{"EN":1320},"Valentín Fuster",{"id":1322,"sortIndex":161,"researcher":18,"roles":1323,"affiliations":1324,"properties":1325},"fc271098-11fb-4124-b33a-ce4851d0990a",[],[],{"openalex":1326,"title":1328},{"VOID":1327},"A5091476552",{"EN":1329},"Juan J. 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