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other provinces and regions in Vietnam and other country.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Address\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Headquarters of Can Tho Journal of Medicine and Pharmacy, located Scientific Research and International Cooperation Office: 179 Nguyen Van Cu Street, An Khanh Ward, Ninh Kieu District, Can Tho City, Vietnam.\u003C\u002Fspan>\u003C\u002Fp>","\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Ngày 16\u002F7\u002F2015, Tạp chí Y Dược học Cần Thơ được cấp chỉ số quốc tế: ISSN 2354-1210.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Từ tháng 4\u002F2016, Tạp chí đã được Hội đồng Giáo sư ngành Y đưa vào danh sách các tạp chí khoa học Y học được tính điểm công trình 0-0,5 điểm cho một bài báo đăng.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Năm 2020 Tạp chí Y Dược học Cần Thơ đã được phê duyệt vào danh mục của các Hội đồng Giáo sư ngành Dược học được tính điểm công trình 0-0,5 điểm cho một bài báo đăng.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Tạp chí Y Dược học Cần Thơ ra 12 số\u002Fnăm, 180-200 trang\u002Fsố.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Từ tháng 12\u002F2022 Tạp chí Y Dược học Cần Thơ là thành viên của hệ thống Crossref và từ tháng 01\u002F2023 tạp chí thực hiện bình duyệt online kín 2 chiều nhằm tăng tính minh bạch, tin cậy của các công trình nghiên cứu khoa học và đảm bảo tốt nhất chất lượng khoa học của bài viết.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Tôn chỉ, mục đích và phạm vi của tạp chí\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Tôn chỉ và mục đích hoạt động của tạp chí: xuất bản nhằm mục đích phổ biến kết quả từ các đề tài nghiên cứu khoa học; giao lưu trao đổi khoa học, chia sẻ kinh nghiệm, học tập, đồng thời cập nhật thông tin khoa học mới trong các lĩnh vực y, sinh, dược học trong và ngoài nước.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Phạm vi của tạp chí: Tạp chí xuất bản được chia thành 3 chuyên mục: (i) Bài báo nghiên cứu khoa học là kết quả công trình nghiên cứu khoa học có giá trị đã được triển khai nghiên cứu, (ii) Bài tổng quan y, sinh, dược học: phục vụ mục tiêu đào tạo liên tục trong lĩnh vực y, sinh, dược học; nhằm hệ thống hóa những kiến thức kinh điển và hiện đại; (iii) Thông tin cập nhật kiến thức mới về y, sinh, dược học trong nước và trên thế giới.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Chính sách truy cập mở\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Tạp chí Y Dược học Cần Thơ áp dụng chính sách truy cập mở đối với các bài báo đã xuất bản đến với độc giả, nhằm mở rộng cơ hội tiếp cận các kết quả nghiên cứu chất lượng cao và tăng cường trao đổi kiến thức. Tạp chí đăng tải trực tuyến (miễn phí) toàn văn các bài báo được công bố trên website của Tạp chí (https:\u002F\u002Ftapchi.ctump.edu.vn).\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Đạo đức xuất bản\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Tạp chí Y Dược học Cần Thơ cam kết tuân thủ đạo đức xuất bản phù hợp với các hướng dẫn và tiêu chuẩn của the Committee on Publication Ethics (COPE), tuân thủ các nguyên tắc của COPE’s Core Practices, Best Practices Guidelines for Journal Editors và Guidelines on Good Publication Practices.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Bản thảo bài báo chỉ được chấp nhận khi được tác giả chịu trách nhiệm chính cam kết các nội dung sau: Các nội dung của bản thảo chưa được đăng tải toàn bộ hoặc một phần ở các tạp chí khác; Tất cả các tác giả đều có đóng góp một cách đáng kể vào quá trình nghiên cứu hoặc chuẩn bị bản thảo và cùng chịu trách nhiệm về các nội dung của bản thảo; Tuân thủ các biện pháp đảm bảo đạo đức nghiên cứu (ví dụ thỏa thuận đồng ý tham gia nghiên cứu).\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Cam kết bảo mật\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Tạp chí cam kết thực hiện và tuân thủ các quy định của luật và các văn bản hướng dẫn liên quan đến bảo mật thông tin cá nhân trên không gian mạng. Các thông tin mà người dùng (tác giả, độc giả, biên tập viên, người phản biện) nhập vào các biểu mẫu trên Hệ thống Quản lý xuất bản trực tuyến của tạp chí chỉ được sử dụng vào các mục đích đã được tuyên bố rõ ràng và sẽ không được cung cấp cho bất kỳ bên thứ ba nào khác, hay dùng vào bất kỳ mục đích nào khác.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Phí gửi bài\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Lệ phí gửi đăng bài: 1.000.000đ\u002Fbài báo\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Lệ phí gửi đăng nhanh: 1.500.000đ\u002Fbài báo\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Đối với tác giả là cán bộ viên chức thuộc Trường Đại học Y Dược Cần Thơ thì được hỗ trợ 50% lệ phí gửi đăng bài.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Đối với sinh viên thực hiện đề tài nghiên cứu khoa học cấp trường được hỗ trợ 100% lệ phí đăng bài ( Tác giả gửi đính kèm “ Quyết định về việc giao tổ chức thực hiện đề tài nghiên cứu khoa học cấp Trường của sinh viên”).\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Hình thức nộp lệ phí:\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">1. Tiền mặt:\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Nộp trực tiếp tại Phòng Tài chính - Kế toán, Trường Đại học Y Dược Cần Thơ, số 179 Nguyễn Văn Cừ, P. An Khánh, Q. Ninh Kiều, thành phố Cần Thơ.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">2. Chuyển khoản:\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Tên Tài khoản: Trường ĐHYD Cần Thơ, Số TK: 0111000115668, tại ngân hàng Vietcombank chi nhánh Cần Thơ.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Thời gian: Áp dụng từ ngày 01\u002F02\u002F2023.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">* Phí gửi bài không được hoàn trả khi bài viết bị từ chối hoặc tác giả xin rút bài viết.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Quy trình phản biện bài báo\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Tạp chí Y Dược học Cần Thơ thực hiện quy trình phản biện kín hai chiều nghiêm ngặt. Danh tính của những người phản biện không được tiết lộ cho các tác giả và ngược lại. Quy trình thẩm định bài báo đăng gồm các bước sau:\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Tiếp nhận bản thảo\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Tác giả liên hệ gửi bản thảo đến Tạp chí qua hệ thống trực tuyến tại website: https:\u002F\u002Ftapchi.ctump.edu.vn. Hướng dẫn về cách đăng ký, gửi bài và chuẩn bị bản thảo được cung cấp trên website của Tạp chí.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Sàng lọc sơ bộ\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Sau khi Tòa soạn nhận được bài báo của tác giả, Ban Thư ký sẽ tiến hành kiểm tra sơ bộ bài báo (các yêu cầu về nội dung và hình thức). Những bài báo không đúng quy cách hoặc có nội dung không phù hợp hoặc vi phạm bản quyền sẽ bị từ chối (Ban Thư ký thông báo phản hồi đến tác giả trong vòng 1 tuần). Những bài báo đủ điều kiện, được Ban Thư ký tòa soạn chuyển đến Ban Biên tập có cùng chuyên môn với nội dung bài báo để đề xuất người phản biện. Thời gian kể từ khi Ban Biên tập nhận bài báo đến khi đề xuất người phản biện bài báo chậm nhất là 5 ngày.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Vòng phản biện\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">1. Ban Thư ký gửi bài và yêu cầu phản biện đến 02 phản biện độc lập.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">2. Các phản biện gởi nhận xét cho Ban Thư ký. Thời gian từ khi gửi bài cho phản biện đến khi nhận ý kiến của phản biện tối đa là 20 ngày.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Xử ký kết quả phản biện\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">1. Nếu ý kiến đồng ý cho đăng và không cần chỉnh sửa, Ban Thư ký tiếp tục đăng bài theo qui trình.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">2. Nếu ý kiến đồng ý đăng và cần chỉnh sửa, Ban Thư ký sẽ thông tin đến tác giả chỉnh sửa theo yêu cầu của người phản biện. Thời gian chỉnh sửa và gửi lại kéo dài không quá 2 tuần, từ khi tác giả bài báo nhận được thông tin (Quá trình này có thể lặp lại tối đa 2 lần\u002F1 bài báo). Khi có sự thống nhất, đồng ý của người phản biện; bài báo được tiếp tục đăng theo qui trình.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">3. Những bài báo có chất lượng không đạt yêu cầu, cả 2 phản biện không đồng ý cho đăng sẽ bị Tòa soạn từ chối đăng.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Xuất bản\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">1. Ban Thư ký tổng hợp các bản thảo đã được tác giả hoàn thiện sau thẩm định trình Ban Biên tập xem xét, Tổng Biên tập phê duyệt, quyết định bài đăng theo các tiêu chí: sự phù hợp nội dung với tôn chỉ và mục đích, thể loại bài viết (ưu tiên các bài có bài có nghiên cứu chuyên sâu, hàm lượng khoa học cao), đóng góp mới bài báo, bài báo được ưu tiên đăng trong số gần nhất của Tạp chí theo thứ tự: tính thời sự, chất lượng bài báo và thời gian gửi bài.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">2. Ban Biên tập và Ban Thư ký biên tập bản thảo, chế bản, đọc rà soát lỗi. Thời gian hoàn thành từ 10-15 ngày.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">3. Ban Thư ký có trách nhiệm thông báo cho tác giả bài báo (bằng e-mail) về tình hình phê duyệt bài báo, thời gian, số kỳ, tập xuất bản bài báo theo qui định.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">4. 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Gastrointestinal Tumors. 2014;1(3):155–65.",{"doi":2042},"10.1159\u002F000365310",{"id":2044,"createTime":2045,"updateTime":2046,"relativeEntities":2047,"slug":2048,"properties":2049,"entityType":835,"verifyStatus":25,"verifyTime":2046,"verifyNote":837,"syncStatus":28,"languages":2068,"translateLanguages":2069,"viewCount":36,"primaryUrl":2070,"fullTextUrl":26,"authors":2071,"publicationType":955,"publisherRelationship":2122,"citationCount":787,"citationInfo":2157,"publishDate":2159,"publishYear":2160,"citationAnalyzeStatus":28,"lastCitationAnalyze":26,"indexDatabases":26,"openAccess":26,"references":2161,"isForceReanalyzing":1107},"02a31c7f-ed8b-499b-aae5-cf8c1d0e8de0","2024-04-22T04:38:54.095+00:00","2025-02-09T19:06:27.169+00:00",[],"Epigenetic-targets-of-bioactive-dietary-components-for-cancer-prevention-and-therapy",{"mag":2050,"keywords":2052,"pmc":2054,"openalex":2056,"abstract":2058,"title":2061,"pm":2064,"doi":2066},{"VOID":2051},"2100257850",{"VI":2053},"",{"VOID":2055},"3024548",{"VOID":2057},"W2100257850",{"VI":2059,"EN":2060},"\u003Cjats:title>Tóm tắt\u003C\u002Fjats:title>\n          \u003Cjats:p>Sự quan tâm ngày càng tăng về di truyền biểu sinh trong ung thư xuất phát từ việc các biến đổi biểu sinh có liên quan đến hầu hết mọi bước trong quá trình hình thành khối u. Thú vị hơn, các thay đổi biểu sinh là những thay đổi di truyền có thể đảo ngược, không do sự thay đổi trongchuỗi DNA mà có khả năng làm thay đổi biểu hiện gen. Các tác nhân từ chế độ ăn uống gồm nhiều thành phần sinh học có hoạt tính thường xuyên điều chỉnh các mục tiêu phân tử khác nhau liên quan đến hình thành khối u. Chúng tôi trình bày những bằng chứng cho thấy nhiều thành phần dinh dưỡng sinh học có thể can thiệp vào các mục tiêu biểu sinh khác nhau trong việc phòng ngừa và điều trị ung thư. Các tác nhân này bao gồm curcumin (nghệ), genistein (đậu nành), polyphenol trà (trà xanh), resveratrol (nho) và sulforaphane (rau cải). Những thành phần sinh học này làm thay đổi quá trình methyl hóa DNA và các biến đổi histone cần thiết cho việc kích hoạt hoặc tắt gen trong phòng ngừa và điều trị ung thư. Các thành phần sinh học điều hòa các biến đổi biểu sinh liên quan đến sự kích thích các gen ức chế khối u như \u003Cjats:italic>p21\u003C\u002Fjats:italic>\n            \u003Cjats:sup>\n              \u003Cjats:italic>WAF1\u002FCIP1\u003C\u002Fjats:italic>\n            \u003C\u002Fjats:sup> và ức chế các gen khuyến khích khối u như enzym nhân bản telomerase ở người trong quá trình hình thành khối u. Tại đây, chúng tôi trình bày những bằng chứng đáng kể cho thấy các thành phần sinh học và các mục tiêu biểu sinh của chúng có liên quan đến phòng ngừa và điều trị ung thư, điều này có thể tạo điều kiện cho việc khám phá và phát triển thuốc mới. Ngoài ra, những tiến bộ đáng kể trong việc hiểu biết về các cơ chế biểu sinh cơ bản cũng như sự phát triển nhanh chóng trong việc phát triển các công nghệ mới mạnh mẽ, chẳng hạn như các công nghệ phát hiện nhạy bén và định lượng các thay đổi biểu sinh và biểu genome trong sinh học ung thư, hứa hẹn những phương pháp biểu sinh mới trong việc phòng ngừa và điều trị ung thư.\u003C\u002Fjats:p>","\u003Cjats:title>Abstract\u003C\u002Fjats:title>\n          \u003Cjats:p>The emergent interest in cancer epigenetics stems from the fact that epigenetic modifications are implicated in virtually every step of tumorigenesis. More interestingly, epigenetic changes are reversible heritable changes that are not due to the alteration in DNA sequence but have potential to alter gene expression. Dietary agents consist of many bioactive ingredients which actively regulate various molecular targets involved in tumorigenesis. We present evidence that numerous bioactive dietary components can interfere with various epigenetic targets in cancer prevention and therapy. These agents include curcumin (turmeric), genistein (soybean), tea polyphenols (green tea), resveratrol (grapes), and sulforaphane (cruciferous vegetables). These bioactive components alter the DNA methylation and histone modifications required for gene activation or silencing in cancer prevention and therapy. Bioactive components mediate epigenetic modifications associated with the induction of tumor suppressor genes such as \u003Cjats:italic>p21\u003C\u002Fjats:italic>\n            \u003Cjats:sup>\n              \u003Cjats:italic>WAF1\u002FCIP1\u003C\u002Fjats:italic>\n            \u003C\u002Fjats:sup> and inhibition of tumor promoting genes such as the human telomerase reverse transcriptase during tumorigenesis processes. Here, we present considerable evidence that bioactive components and their epigenetic targets are associated with cancer prevention and therapy which should facilitate novel drug discovery and development. In addition, remarkable advances in our understanding of basic epigenetic mechanisms as well as the rapid progress that is being made in developing powerful new technologies, such as those for sensitive and quantitative detection of epigenetic and epigenomic changes in cancer biology, hold great promise for novel epigenetic approaches to cancer prevention and therapy.\u003C\u002Fjats:p>",{"VI":2062,"EN":2063},"Các mục tiêu di truyền biểu sinh của các thành phần dinh dưỡng sinh học trong phòng ngừa và điều trị ung thư","Epigenetic targets of bioactive dietary components for cancer prevention and therapy",{"VOID":2065},"21258631",{"VOID":2067},"10.1007\u002Fs13148-010-0011-5",[102],[101],"https:\u002F\u002Fclinicalepigeneticsjournal.biomedcentral.com\u002Farticles\u002F10.1007\u002Fs13148-010-0011-5",[2072,2093,2107],{"id":2073,"sortIndex":36,"researcher":26,"roles":2074,"affiliations":2075,"properties":2086},"5c87e374-a91c-46da-9e25-17eca5e82fd7",[],[2076],{"id":2077,"sortIndex":36,"affiliation":2078,"properties":26},"eef39da5-b4e2-4282-aed5-38f6756caa3e",{"id":2079,"createTime":2080,"updateTime":2080,"relativeEntities":2081,"slug":2082,"properties":2083,"entityType":98,"verifyStatus":28,"verifyTime":26,"verifyNote":26,"syncStatus":28,"languages":26,"translateLanguages":26,"viewCount":36},"2cc3d156-b0b0-47f2-ba78-0712849510c7","2024-04-22T04:38:54.191+00:00",[],"Department-of-Biology-University-of-Alabama-at-Birmingham-1300-University-Boulevard-Campbell-Hall-175-Birmingham-AL-35294-1170-USA",{"title":2084},{"EN":2085},"Department of Biology, University of Alabama at 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Curr Opin Psychiatry. 2011, 24: 226-236.",{"doi":3535},"10.1097\u002FYCO.0b013e328345927e",{"id":3537,"createTime":3538,"updateTime":3539,"relativeEntities":3540,"slug":3541,"properties":3542,"entityType":835,"verifyStatus":25,"verifyTime":3551,"verifyNote":837,"syncStatus":28,"languages":26,"translateLanguages":26,"viewCount":36,"primaryUrl":3552,"fullTextUrl":26,"authors":3553,"publicationType":955,"publisherRelationship":3716,"citationCount":3749,"citationInfo":3750,"publishDate":3752,"publishYear":994,"citationAnalyzeStatus":1338,"lastCitationAnalyze":3753,"indexDatabases":26,"openAccess":26,"references":3754,"isForceReanalyzing":1107},"2588c9ad-53d7-4206-8083-e2e38f029edb","2024-02-08T14:51:31.625+00:00","2026-05-31T06:01:53.851+00:00",[],"TREM2-upregulation-correlates-with-5-hydroxymethycytosine-enrichment-in-Alzheimer-s-disease-hippocampus",{"abstract":3543,"title":3545,"doi":3547,"gsPaper":3549},{"EN":3544},"Recent genome-wide association studies revealed TREM2 rs75932628-T variant to be associated with Alzheimer’s disease (AD) and other neurodegenerative diseases. However, the role that TREM2 plays in sporadic AD is largely unknown. Our aim was to assess messenger RNA (mRNA) expression levels and DNA methylation profiling of TREM2 in human hippocampus in AD brain. We measured TREM2 mRNA levels in the hippocampus in a cohort of neuropathologically confirmed controls and pure AD cases showing no other protein deposits than β-amyloid and phosphorylated tau. We also examined DNA methylation levels in the TREM2 transcription start site (TSS)-associated region by bisulfite cloning sequencing and further extended the study by measuring 5-hydroxymethycytosine (5hmC) enrichment at different regions of TREM2 by 5hmC DNA immunoprecipitation combined with real-time qPCR. A 3.4-fold increase in TREM2 mRNA levels was observed in the hippocampus of AD cases compared to controls (p = 1.1E-05). Interestingly, TREM2 methylation was higher in AD cases compared to controls (76.2 % ± 15.5 versus 57.9 % ± 17.1; p = 0.0016). Moreover, TREM2 mRNA levels in the AD hippocampus correlated with enrichment in 5hmC at the TREM2 gene body (r = 0.771; p = 0.005). \n                           TREM2 mRNA levels are increased in the human hippocampus in AD cases compared to controls. DNA methylation, and particularly 5hmC, may be involved in regulating TREM2 mRNA expression in the AD brain. Further studies are guaranteed to investigate in depth the role of 5hmC in AD and other neurodegenerative disorders.",{"EN":3546},"TREM2 upregulation correlates with 5-hydroxymethycytosine enrichment in Alzheimer’s disease 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CL, Koike M, Spusta SC, Niemi EC, Yenari M, Nakamura MC, et al. A role for TREM2 ligands in the phagocytosis of apoptotic neuronal cells by microglia. J Neurochem. 2009;109(4):1144–56. doi:10.1111\u002Fj.1471-4159.2009.06042.x.","https:\u002F\u002Fdoi.org\u002F10.1111\u002Fj.1471-4159.2009.06042.x",{"mag":3759,"pmc":3760,"openalex":3761,"doi":3762},"2026279003","3087597","W2026279003","10.1111\u002Fj.1471-4159.2009.06042.x",{"id":3764,"text":3765,"url":3766,"identifiers":3767},"4464077e-cd2b-47a9-bcf7-1f73732a1e29","Stefano L, Racchetti G, Bianco F, Passini N, Gupta RS, Panina Bordignon P, et al. The surface-exposed chaperone, Hsp60, is an agonist of the microglial TREM2 receptor. J Neurochem. 2009;110(1):284–94. doi:10.1111\u002Fj.1471-4159.2009.06130.x.","https:\u002F\u002Fonlinelibrary.wiley.com\u002Fdoi\u002F10.1111\u002Fj.1471-4159.2009.06130.x",{"doi":3768},"10.1111\u002Fj.1471-4159.2009.06130.x",{"id":3770,"text":3771,"url":3772,"identifiers":3773},"73196c93-8ec2-4330-bf7a-b277aaf2c0f6","Takahashi K, Rochford CD, Neumann H. Clearance of apoptotic neurons without inflammation by microglial triggering receptor expressed on myeloid cells-2. J Exp Med. 2005;201(4):647–57. doi:10.1084\u002Fjem.20041611.","https:\u002F\u002Frupress.org\u002Fjem\u002Farticle\u002F201\u002F4\u002F647\u002F52887\u002FClearance-of-apoptotic-neurons-without",{"doi":3774},"10.1084\u002Fjem.20041611",{"id":3776,"text":3777,"url":3778,"identifiers":3779},"986288db-decb-43ce-b58d-6efc4616db5b","Rayaprolu S, Mullen B, Baker M, Lynch T, Finger E, Seeley WW, et al. TREM2 in neurodegeneration: evidence for association of the p.R47H variant with frontotemporal dementia and Parkinson’s disease. Mol Neurodegener. 2013;8:19. doi:10.1186\u002F1750-1326-8-19.","https:\u002F\u002Fmolecularneurodegeneration.biomedcentral.com\u002Farticles\u002F10.1186\u002F1750-1326-8-19",{"doi":3780},"10.1186\u002F1750-1326-8-19",{"id":3782,"text":3783,"url":3784,"identifiers":3785},"3a4fade6-f533-46d6-b7ce-2c8b55f6e083","Cady J, Koval ED, Benitez BA, Zaidman C, Jockel-Balsarotti J, Allred P, et al. TREM2 variant p.R47H as a risk factor for sporadic amyotrophic lateral sclerosis. JAMA Neurol. 2014;71(4):449–53. doi:10.1001\u002Fjamaneurol.2013.6237.","http:\u002F\u002Farchneur.jamanetwork.com\u002Farticle.aspx?doi=10.1001\u002Fjamaneurol.2013.6237",{"doi":3786},"10.1001\u002Fjamaneurol.2013.6237",{"id":26,"text":3788,"url":26,"identifiers":3789},"Guerreiro R, Wojtas A, Bras J, Carrasquillo M, Rogaeva E, Majounie E, et al. TREM2 variants in Alzheimer’s disease. N Engl J Med. 2013;368(2):117–27. doi:10.1056\u002FNEJMoa1211851.",{"doi":3790},"10.1056\u002FNEJMoa1211851",{"id":26,"text":3792,"url":3793,"identifiers":3794},"Jonsson T, Stefansson H, Steinberg S, Jonsdottir I, Jonsson PV, Snaedal J, et al. Variant of TREM2 associated with the risk of Alzheimer’s disease. N Engl J Med. 2013;368(2):107–16. doi:10.1056\u002FNEJMoa1211103.","https:\u002F\u002Fdoi.org\u002F10.1056\u002Fnejmoa1211103",{"doi":3795},"10.1056\u002Fnejmoa1211103",{"id":3797,"text":3798,"url":3799,"identifiers":3800},"2803fcc4-9153-41ac-968e-a774d498ce11","Ulrich JD, Finn MB, Wang Y, Shen A, Mahan TE, Jiang H, et al. Altered microglial response to Abeta plaques in APPPS1-21 mice heterozygous for TREM2. Mol Neurodegener. 2014;9:20. doi:10.1186\u002F1750-1326-9-20.","https:\u002F\u002Fmolecularneurodegeneration.biomedcentral.com\u002Farticles\u002F10.1186\u002F1750-1326-9-20",{"doi":3801},"10.1186\u002F1750-1326-9-20",{"id":3803,"text":3804,"url":3805,"identifiers":3806},"2581ca16-75b3-4b1a-a3d3-2d413b93c4af","Lue LF, Schmitz C, Walker DG. What happens to microglial TREM2 in Alzheimer’s disease: immunoregulatory turned into immunopathogenic? Neuroscience. 2014. doi:10.1016\u002Fj.neuroscience.2014.09.050.","https:\u002F\u002Flinkinghub.elsevier.com\u002Fretrieve\u002Fpii\u002FS030645221400801X",{"doi":3807},"10.1016\u002Fj.neuroscience.2014.09.050",{"id":3809,"text":3810,"url":3811,"identifiers":3812},"552ef368-7722-48e7-a41b-c3df7a717661","Rohn TT. The triggering receptor expressed on myeloid cells 2: “TREM-ming” the inflammatory component associated with Alzheimer’s disease. 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Dựa vào những bằng chứng dịch tễ học cho thấy việc tiếp xúc với ô nhiễm không khí trong thời kỳ mang thai có ảnh hưởng bất lợi đến các kết quả ở trẻ sơ sinh như cân nặng khi sinh và sinh non, cần thiết phải chú ý đến các cơ chế tác động cơ bản để hiểu rõ hơn không chỉ về những tác động sức khỏe sớm do ô nhiễm không khí mà còn về những hậu quả trong cuộc sống sau này. Trong bài tổng quan này, chúng tôi đưa ra cái nhìn tổng quan về những thay đổi phân tử ở nhau thai do ô nhiễm không khí quan sát được trong nhóm nghiên cứu ENVIR\u003Cjats:italic>ON\u003C\u002Fjats:italic>AGE và đánh giá các bằng chứng hiện có. Nhìn chung, chúng tôi chỉ ra rằng việc tiếp xúc trước sinh với ô nhiễm không khí liên quan đến stress nitrosative và những thay đổi biểu sinh ở nhau thai. Các mục tiêu CpG bị ảnh hưởng bất lợi đã tham gia vào các quá trình tế bào bao gồm sửa chữa DNA, nhịp sinh học và chuyển hóa năng lượng. Đối với biểu hiện miRNA, các khoảng thời gian nhất định tiếp xúc với ô nhiễm không khí đã liên quan đến sự thay đổi biểu hiện của miR-20a, miR-21, miR-146a và miR-222. Các dấu hiệu lão hóa ở giai đoạn đầu đời bao gồm chiều dài telomere và nội dung DNA ty thể có liên quan đến việc tiếp xúc với ô nhiễm không khí trong thời kỳ mang thai. Trước đó, chúng tôi đã đề xuất giả thuyết lão hóa telomere-ty thể do ô nhiễm không khí với một liên kết trực tiếp giữa telomere và ty thể. Ở đây, chúng tôi mở rộng quan điểm này với một sự tương tác tiềm năng giữa các cơ chế sinh học khác nhau ở mức độ stress oxy hóa nhau thai, di truyền biểu sinh, lão hóa và chuyển hóa năng lượng. Nghiên cứu về nhau thai là một cơ hội cho các nghiên cứu trong tương lai vì nó có thể giúp hiểu cơ bản sinh học làm nền tảng cho khái niệm DOHaD thông qua các tương tác giữa các cơ chế tác động cơ bản, môi trường trước sinh và rủi ro bệnh tật trong cuộc sống sau này. Để ngăn ngừa những hậu quả lâu dài từ việc tiếp xúc với ô nhiễm không khí trong giai đoạn đầu đời, các nhà hoạch định chính sách nên nắm vững những hậu quả sinh học phân tử và rủi ro truyền sinh.","\u003Cjats:title>Abstract\u003C\u002Fjats:title>\u003Cjats:p>According to the “Developmental Origins of Health and Disease” (DOHaD) concept, the early-life environment is a critical period for fetal programming. Given the epidemiological evidence that air pollution exposure during pregnancy adversely affects newborn outcomes such as birth weight and preterm birth, there is a need to pay attention to underlying modes of action to better understand not only these air pollution-induced early health effects but also its later-life consequences. In this review, we give an overview of air pollution-induced placental molecular alterations observed in the ENVIR\u003Cjats:italic>ON\u003C\u002Fjats:italic>AGE birth cohort and evaluate the existing evidence. In general, we showed that prenatal exposure to air pollution is associated with nitrosative stress and epigenetic alterations in the placenta. Adversely affected CpG targets were involved in cellular processes including DNA repair, circadian rhythm, and energy metabolism. For miRNA expression, specific air pollution exposure windows were associated with altered miR-20a, miR-21, miR-146a, and miR-222 expression. Early-life aging markers including telomere length and mitochondrial DNA content are associated with air pollution exposure during pregnancy. Previously, we proposed the air pollution-induced telomere-mitochondrial aging hypothesis with a direct link between telomeres and mitochondria. Here, we extend this view with a potential co-interaction of different biological mechanisms on the level of placental oxidative stress, epigenetics, aging, and energy metabolism. Investigating the placenta is an opportunity for future research as it may help to understand the fundamental biology underpinning the DOHaD concept through the interactions between the underlying modes of action, prenatal environment, and disease risk in later life. To prevent lasting consequences from early-life exposures of air pollution, policy makers should get a basic understanding of biomolecular consequences and transgenerational risks.\u003C\u002Fjats:p>",{"VI":4061,"EN":4062},"Những thay đổi ở nhau thai do ô nhiễm không khí: sự tương tác giữa stress oxy hóa, di truyền biểu sinh và đặc điểm lão hóa?","Air pollution-induced placental alterations: an interplay of oxidative stress, epigenetics, and the aging phenotype?",{"VOID":4064},"31530287",{"VOID":4066},"10.1186\u002Fs13148-019-0688-z",[102],[101],"https:\u002F\u002Fclinicalepigeneticsjournal.biomedcentral.com\u002Farticles\u002F10.1186\u002Fs13148-019-0688-z",[4071,4091,4106,4121,4136,4153,4173,4190,4207,4224],{"id":4072,"sortIndex":50,"researcher":26,"roles":4073,"affiliations":4074,"properties":4086},"df53bf8f-b8fd-4519-9a04-776f52182163",[],[4075],{"id":4076,"sortIndex":36,"affiliation":4077,"properties":26},"68cbd6eb-c976-449e-8ac0-ecc63044886c",{"id":4078,"createTime":4079,"updateTime":4080,"relativeEntities":4081,"slug":4082,"properties":4083,"entityType":98,"verifyStatus":28,"verifyTime":26,"verifyNote":26,"syncStatus":28,"languages":26,"translateLanguages":26,"viewCount":36},"1587f5e3-38f8-4b9b-85b2-480da290f6ae","2024-01-20T19:42:55.464+00:00","2024-08-09T08:25:12.534+00:00",[],"Centre-for-Environmental-Sciences-Hasselt-University-Hasselt-Belgium",{"title":4084},{"VI":4085},"Centre for Environmental Sciences, Hasselt University, Hasselt, Belgium",{"openalex":4087,"title":4089},{"VOID":4088},"A5083946645",{"EN":4090},"Karen Vrijens",{"id":4092,"sortIndex":135,"researcher":26,"roles":4093,"affiliations":4094,"properties":4101},"e2caef57-41aa-4f20-b3a9-2dbc1fea6ef7",[],[4095],{"id":4096,"sortIndex":36,"affiliation":4097,"properties":26},"5c5edd76-f3f1-48a3-b09b-f7f6a99ae9d4",{"id":4078,"createTime":4079,"updateTime":4080,"relativeEntities":4098,"slug":4082,"properties":4099,"entityType":98,"verifyStatus":28,"verifyTime":26,"verifyNote":26,"syncStatus":28,"languages":26,"translateLanguages":26,"viewCount":36},[],{"title":4100},{"VI":4085},{"openalex":4102,"title":4104},{"VOID":4103},"A5044495885",{"EN":4105},"Harry Roels",{"id":4107,"sortIndex":162,"researcher":26,"roles":4108,"affiliations":4109,"properties":4116},"d81471c0-10e9-47aa-b954-609a15acd29f",[],[4110],{"id":4111,"sortIndex":36,"affiliation":4112,"properties":26},"13f98f99-802b-4e39-bb69-63b5746d671b",{"id":4078,"createTime":4079,"updateTime":4080,"relativeEntities":4113,"slug":4082,"properties":4114,"entityType":98,"verifyStatus":28,"verifyTime":26,"verifyNote":26,"syncStatus":28,"languages":26,"translateLanguages":26,"viewCount":36},[],{"title":4115},{"VI":4085},{"openalex":4117,"title":4119},{"VOID":4118},"A5027233772",{"EN":4120},"Bram G. 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Environ Epigenet. 2018;4(2):dvy018.",{"doi":4754},"10.1093\u002Feep\u002Fdvy018",{"id":4756,"createTime":4757,"updateTime":4758,"relativeEntities":4759,"slug":4760,"properties":4761,"entityType":835,"verifyStatus":25,"verifyTime":4779,"verifyNote":837,"syncStatus":28,"languages":4780,"translateLanguages":4781,"viewCount":36,"primaryUrl":4782,"fullTextUrl":26,"authors":4783,"publicationType":955,"publisherRelationship":4860,"citationCount":4889,"citationInfo":4890,"publishDate":4892,"publishYear":4893,"citationAnalyzeStatus":1338,"lastCitationAnalyze":4894,"indexDatabases":26,"openAccess":26,"references":4895,"isForceReanalyzing":1107},"5a0cffdb-9313-4f29-8d4d-392a497d23ee","2024-04-11T22:29:18.203+00:00","2025-01-24T13:52:20.463+00:00",[],"Machine-learning-and-clinical-epigenetics-a-review-of-challenges-for-diagnosis-and-classification",{"mag":4762,"keywords":4764,"pmc":4765,"openalex":4767,"abstract":4769,"title":4772,"pm":4775,"doi":4777},{"VOID":4763},"3014921497",{"VI":2053},{"VOID":4766},"7118917",{"VOID":4768},"W3014921497",{"VI":4770,"EN":4771},"\u003Cjats:title>Tóm tắt\u003C\u002Fjats:title>\u003Cjats:sec>\n                \u003Cjats:title>Đặt vấn đề\u003C\u002Fjats:title>\n                \u003Cjats:p>Học máy là một lĩnh vực con của trí tuệ nhân tạo, sử dụng dữ liệu lớn để đưa ra các dự đoán cho các sự kiện trong tương lai. Mặc dù hầu hết các thuật toán được sử dụng trong học máy đã được phát triển từ những năm 1950, song sự xuất hiện của \u003Cjats:italic>dữ liệu lớn\u003C\u002Fjats:italic> cùng với sức mạnh tính toán tăng đáng kể đã kích thích mối quan tâm mới vào công nghệ này trong hai thập kỷ qua.\u003C\u002Fjats:p>\n              \u003C\u002Fjats:sec>\u003Cjats:sec>\n                \u003Cjats:title>Nội dung chính\u003C\u002Fjats:title>\n                \u003Cjats:p>Trong lĩnh vực y tế, học máy hứa hẹn sẽ phát triển các công cụ lâm sàng hỗ trợ cho việc phát hiện ví dụ như ung thư và dự đoán bệnh tật. Những tiến bộ gần đây trong công nghệ học sâu, một phân ngành của học máy yêu cầu ít đầu vào từ người dùng hơn nhưng cần nhiều dữ liệu và sức mạnh xử lý hơn, đã liệu rất nhiều trong việc hỗ trợ bác sĩ đạt được chẩn đoán chính xác.\u003C\u002Fjats:p>\n                \u003Cjats:p>Trong lĩnh vực di truyền học và phân ngành của nó là di truyền học biểu sinh, cả hai là ví dụ điển hình của dữ liệu phức tạp, các phương pháp học máy đang gia tăng, khi mà lĩnh vực y học cá thể đang hướng tới việc điều trị cá nhân dựa trên hồ sơ di truyền và biểu sinh của họ.\u003C\u002Fjats:p>\n              \u003C\u002Fjats:sec>\u003Cjats:sec>\n                \u003Cjats:title>Kết luận\u003C\u002Fjats:title>\n                \u003Cjats:p>Hiện tại, chúng ta đang có một số lượng ngày càng tăng các biến đổi biểu sinh được báo cáo trong bệnh tật, và điều này mở ra cơ hội để tăng độ nhạy và độ đặc hiệu của các chẩn đoán và liệu pháp trong tương lai. Hiện nay, có rất ít nghiên cứu áp dụng học máy vào di truyền học biểu sinh. Chúng liên quan đến một loạt các trạng thái bệnh tật và chủ yếu sử dụng các phương pháp học máy có giám sát.\u003C\u002Fjats:p>\n              \u003C\u002Fjats:sec>","\u003Cjats:title>Abstract\u003C\u002Fjats:title>\u003Cjats:sec>\n                \u003Cjats:title>Background\u003C\u002Fjats:title>\n                \u003Cjats:p>Machine learning is a sub-field of artificial intelligence, which utilises large data sets to make predictions for future events. Although most algorithms used in machine learning were developed as far back as the 1950s, the advent of \u003Cjats:italic>big data\u003C\u002Fjats:italic> in combination with dramatically increased computing power has spurred renewed interest in this technology over the last two decades.\u003C\u002Fjats:p>\n              \u003C\u002Fjats:sec>\u003Cjats:sec>\n                \u003Cjats:title>Main body\u003C\u002Fjats:title>\n                \u003Cjats:p>Within the medical field, machine learning is promising in the development of assistive clinical tools for detection of e.g. cancers and prediction of disease. Recent advances in deep learning technologies, a sub-discipline of machine learning that requires less user input but more data and processing power, has provided even greater promise in assisting physicians to achieve accurate diagnoses.\u003C\u002Fjats:p>\n                \u003Cjats:p>Within the fields of genetics and its sub-field epigenetics, both prime examples of complex data, machine learning methods are on the rise, as the field of personalised medicine is aiming for treatment of the individual based on their genetic and epigenetic profiles.\u003C\u002Fjats:p>\n              \u003C\u002Fjats:sec>\u003Cjats:sec>\n                \u003Cjats:title>Conclusion\u003C\u002Fjats:title>\n                \u003Cjats:p>We now have an ever-growing number of reported epigenetic alterations in disease, and this offers a chance to increase sensitivity and specificity of future diagnostics and therapies. Currently, there are limited studies using machine learning applied to epigenetics. They pertain to a wide variety of disease states and have used mostly supervised machine learning methods.\u003C\u002Fjats:p>\n              \u003C\u002Fjats:sec>",{"VI":4773,"EN":4774},"Học máy và di truyền học biểu sinh lâm sàng: một bài đánh giá về những thách thức trong chẩn đoán và phân loại","Machine learning and clinical epigenetics: a review of challenges for diagnosis and classification",{"VOID":4776},"32245523",{"VOID":4778},"10.1186\u002Fs13148-020-00842-4","2024-12-22T10:30:07.001+00:00",[102],[101],"https:\u002F\u002Fclinicalepigeneticsjournal.biomedcentral.com\u002Farticles\u002F10.1186\u002Fs13148-020-00842-4",[4784,4804,4824,4844],{"id":4785,"sortIndex":114,"researcher":26,"roles":4786,"affiliations":4787,"properties":4797},"329230b1-e1f9-46e3-b735-b46dd1636787",[],[4788],{"id":26,"sortIndex":36,"affiliation":4789,"properties":26},{"id":4790,"createTime":4791,"updateTime":4791,"relativeEntities":4792,"slug":4793,"properties":4794,"entityType":98,"verifyStatus":28,"verifyTime":26,"verifyNote":26,"syncStatus":28,"languages":26,"translateLanguages":26,"viewCount":36},"8bce5871-f9b6-4990-acc3-083026d4ea09","2024-04-11T22:29:18.232+00:00",[],"Centre-for-Genetic-Origins-of-Health-and-Disease-The-University-of-Western-Australia-and-Curtin-University-Perth-Western-Australia",{"title":4795},{"EN":4796},"Centre for Genetic Origins of Health and Disease, The University of Western Australia and Curtin University, Perth, Western Australia",{"openalex":4798,"orcid":4800,"title":4802},{"VOID":4799},"A5065841046",{"VOID":4801},"https:\u002F\u002Forcid.org\u002F0000-0003-4026-2964",{"EN":4803},"Phillip E. 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