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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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tắt\u003C\u002Fjats:title>\n          \u003Cjats:sec>\n            \u003Cjats:title>Đặt vấn đề\u003C\u002Fjats:title>\n            \u003Cjats:p>Tăng lipid máu đóng vai trò quan trọng trong sự phát triển và tiến triển của bệnh động mạch vành (CAD). Các nghiên cứu gần đây đã xác định rằng microRNA (miRNA) là những yếu tố điều hòa chính của chuyển hóa lipid, nhưng còn ít thông tin về các mức độ miRNA liên quan đến chuyển hóa lipid trong huyết thanh và mối quan hệ của chúng với sự hiện diện của CAD ở bệnh nhân tăng lipid máu.\u003C\u002Fjats:p>\n          \u003C\u002Fjats:sec>\n          \u003Cjats:sec>\n            \u003Cjats:title>Phương pháp\u003C\u002Fjats:title>\n            \u003Cjats:p>Trong nghiên cứu này, chúng tôi đã thu nhận tổng cộng 255 bệnh nhân tăng lipid máu có hoặc không có CAD và 100 đối chứng có lipid máu bình thường. Mức độ huyết tương của bốn miRNA liên quan đến chuyển hóa lipid đã biết, miR-122, miR-370, miR-33a và miR-33b được định lượng bằng phương pháp PCR định lượng theo thời gian thực. Mức độ cholesterol toàn phần (TC), triglyceride (TG), cholesterol lipoprotein mật độ thấp (LDL-C) và cholesterol lipoprotein mật độ cao được xác định. Hơn nữa, mức độ nghiêm trọng của CAD được đánh giá bằng hệ thống điểm Gensini dựa trên mức độ thu hẹp lòng mạch và tầm quan trọng về địa lý của nó.\n            \u003C\u002Fjats:p>\n          \u003C\u002Fjats:sec>\n          \u003Cjats:sec>\n            \u003Cjats:title>Kết quả\u003C\u002Fjats:title>\n            \u003Cjats:p> Kết quả của chúng tôi lần đầu tiên cho thấy rằng mức độ huyết tương của miR-122 và miR-370 tăng cao có ý nghĩa ở bệnh nhân tăng lipid máu so với các đối chứng, và mức độ của miR-122 và miR-370 có tương quan dương với các mức TC, TG và LDL-C ở cả bệnh nhân tăng lipid máu và các đối chứng. Phân tích hồi quy logistic đa biến cho thấy rằng mức độ miR-122 và miR-370 tăng cao có liên quan đến sự hiện diện của CAD ngay cả sau khi điều chỉnh cho các yếu tố nguy cơ tim mạch khác. Hơn nữa, mức độ miR-122 và miR-370 cũng có tương quan dương với mức độ nghiêm trọng của CAD được định lượng bằng điểm Gensini. Tuy nhiên, cả miR-33a và miR-33b đều không thể phát hiện được trong huyết tương.\u003C\u002Fjats:p>\n          \u003C\u002Fjats:sec>\n          \u003Cjats:sec>\n            \u003Cjats:title>Kết luận\u003C\u002Fjats:title>\n            \u003Cjats:p>Kết quả của chúng tôi cho rằng mức độ miR-122 và miR-370 trong huyết tương tăng lên có thể liên quan đến sự hiện diện cũng như mức độ nghiêm trọng của CAD ở những bệnh nhân tăng lipid máu.\u003C\u002Fjats:p>\n          \u003C\u002Fjats:sec>","\u003Cjats:title>Abstract\u003C\u002Fjats:title>\n          \u003Cjats:sec>\n            \u003Cjats:title>Background\u003C\u002Fjats:title>\n            \u003Cjats:p>Hyperlipidemia plays a crucial role in the development and progression of coronary artery disease (CAD). Recent studies have identified that microRNAs (miRNAs) are important regulators of lipid metabolism, but little is known about the circulating levels of lipometabolism-related miRNAs and their relationship with the presence of CAD in patients with hyperlipidemia.\u003C\u002Fjats:p>\n          \u003C\u002Fjats:sec>\n          \u003Cjats:sec>\n            \u003Cjats:title>Methods\u003C\u002Fjats:title>\n            \u003Cjats:p>In the present study, we enrolled a total of 255 hyperlipidemia patients with or without CAD and 100 controls with normal blood lipids. The plasma levels of four known lipometabolism-related miRNAs, miR-122, miR-370, miR-33a, and miR-33b were quantified by real-time quantitative PCR. Blood levels of total cholesterol (TC), triglyceride (TG), low density lipoprotein cholesterol (LDL-C), and high density lipoprotein cholesterol were determined. Furthermore, the severity of CAD was assessed with the Gensini score system based on the degree of luminal narrowing and its geographic importance.\u003C\u002Fjats:p>\n          \u003C\u002Fjats:sec>\n          \u003Cjats:sec>\n            \u003Cjats:title>Results\u003C\u002Fjats:title>\n            \u003Cjats:p>Our results revealed for the first time that plasma levels of miR-122 and miR-370 were significantly increased in hyperlipidemia patients compared with controls, and the levels of miR-122 and miR-370 were positively correlated with TC, TG, and LDL-C levels in both hyperlipidemia patients and controls. Multiple logistic regression analysis demonstrated that the increased levels of miR-122 and miR-370 were associated with CAD presence, even after adjustment for other cardiovascular risk factors. Furthermore, miR-122 and miR-370 levels were positively correlated with the severity of CAD quantified by the Gensini score. However, both miR-33a and miR-33b were undetectable in plasma.\u003C\u002Fjats:p>\n          \u003C\u002Fjats:sec>\n          \u003Cjats:sec>\n            \u003Cjats:title>Conclusions\u003C\u002Fjats:title>\n            \u003Cjats:p>Our results suggest that increased plasma levels of miR-122 and miR-370 might be associated with the presence as well as the severity of CAD in hyperlipidemia patients.\u003C\u002Fjats:p>\n          \u003C\u002Fjats:sec>",{"VI":2534,"EN":2535},"Mức độ miR-122 và miR-370 liên quan đến chuyển hóa lipid trong huyết tương tăng cao ở bệnh nhân tăng lipid máu và có liên quan đến bệnh động mạch vành","Plasma levels of lipometabolism-related miR-122 and miR-370 are increased in patients with hyperlipidemia and associated with coronary artery 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Consumption of trans fatty acids is related to plasma biomarkers of inflammation and endothelial dysfunction. J Nutr. 2005;135:562–6.",{"doi":3504},"10.1093\u002Fjn\u002F135.3.562",{"id":26,"text":3506,"url":26,"identifiers":3507},"Higgins JPT, Green S. Cochrane handbook for systematic reviews of interventions. Version 5.1.0 [updated March 2011]. The Cochrane Collaboration. 2011. Available from: \n                    http:\u002F\u002Fwww.cochrane-handbook.org",{},{"id":3509,"createTime":3510,"updateTime":3511,"relativeEntities":3512,"slug":3513,"properties":3514,"entityType":846,"verifyStatus":25,"verifyTime":3511,"verifyNote":847,"syncStatus":28,"languages":3532,"translateLanguages":3533,"viewCount":36,"primaryUrl":3534,"fullTextUrl":26,"authors":3535,"publicationType":941,"publisherRelationship":3651,"citationCount":3680,"citationInfo":3681,"publishDate":3683,"publishYear":3684,"citationAnalyzeStatus":976,"lastCitationAnalyze":3685,"indexDatabases":26,"openAccess":26,"references":3686,"isForceReanalyzing":1516},"bb1f9c28-0386-4af1-a793-83790ae01d27","2024-04-12T00:30:44.272+00:00","2025-02-04T09:18:24.774+00:00",[],"Mining-literature-for-a-comprehensive-pathway-analysis-A-case-study-for-retrieval-of-homocysteine-related-genes-for-genetic-and-epigenetic-studies",{"mag":3515,"keywords":3517,"pmc":3518,"openalex":3520,"abstract":3522,"title":3525,"pm":3528,"doi":3530},{"VOID":3516},"1519977277",{"VI":2525},{"VOID":3519},"1395315",{"VOID":3521},"W1519977277",{"VI":3523,"EN":3524},"Homocysteine là một yếu tố nguy cơ độc lập đối với các bệnh tim mạch. Nó cũng được biết đến là liên quan đến nhiều rối loạn phức tạp khác nhau. Mặc dù có rất nhiều nghiên cứu độc lập chỉ ra vai trò của homocysteine trong các con đường riêng lẻ, cơ chế gây hại do homocysteine vẫn chưa được làm rõ. Việc điều chỉnh biểu hiện gen do homocysteine thông qua việc thay đổi trạng thái methylation hoặc bằng các cơ chế chưa được biết đến dự đoán sẽ dẫn đến nhiều tình trạng bệnh lý, trực tiếp hoặc gián tiếp. Trong bản thảo hiện tại, bằng cách sử dụng phương pháp khai thác tài liệu, chúng tôi đã xác định các gen bị điều chỉnh trực tiếp hoặc gián tiếp bởi mức homocysteine cao. Các gen này sau đó được đặt vào các con đường phù hợp nhằm hiểu cơ sở phân tử của các rối loạn phức tạp do homocysteine gây ra và cung cấp tài nguyên cho việc chọn lọc các gen để kiểm tra đa hình cũng như phân tích đột biến cũng như các sửa đổi epigenetic liên quan đến hyperhomocysteinemia. Chúng tôi đã xác định được 135 gen trong 1137 bản tóm tắt có thể điều chỉnh mức homocysteine hoặc bị tác động bởi mức homocysteine cao. Việc lập bản đồ các gen đến các con đường tương ứng cho thấy mức homocysteine cao dẫn đến xơ vữa động mạch, có thể là do ảnh hưởng trực tiếp đến chuyển hóa và vận chuyển lipid hoặc thông qua stress oxy hóa và\u002Fhoặc stress Lưới nội đồng (ER). Mức homocysteine cao cũng làm giảm khả năng sinh học của nitric oxide và điều chỉnh mức của các chất chuyển hóa khác bao gồm S-adenosyl methionine và S-adenosyl homocysteine, điều này có thể dẫn đến các rối loạn tim mạch hoặc thần kinh. Stress ER nổi lên như một con đường chung liên quan đến apoptosis, xơ vữa động mạch và các rối loạn thần kinh và bị điều chỉnh bởi mức homocysteine. Mạng lưới tổng hợp đã thu thập cho thấy các gen bị điều chỉnh bởi homocysteine, cho thấy rằng homocysteine tác động không chỉ bằng cách điều chỉnh mức nền tảng cho các quá trình xúc tác khác nhau mà còn thông qua việc điều chỉnh biểu hiện của các gen liên quan đến các bệnh phức tạp.","\u003Cjats:title>Abstract\u003C\u002Fjats:title>\n          \u003Cjats:p>Homocysteine is an independent risk factor for cardiovascular diseases. It is also known to be associated with a variety of complex disorders. While there are a large number of independent studies implicating homocysteine in isolated pathways, the mechanism of homocysteine induced adverse effects are not clear. Homocysteine-induced modulation of gene expression through alteration of methylation status or by hitherto unknown mechanisms is predicted to lead to several pathological conditions either directly or indirectly. In the present manuscript, using literature mining approach, we have identified the genes that are modulated directly or indirectly by an elevated level of homocysteine. These genes were then placed in appropriate pathways in an attempt to understand the molecular basis of homocysteine induced complex disorders and to provide a resource for selection of genes for polymorphism screening and analysis of mutations as well as epigenetic modifications in relation to hyperhomocysteinemia. We have identified 135 genes in 1137 abstracts that either modulate the levels of homocysteine or are modulated by elevated levels of homocysteine. Mapping the genes to their respective pathways revealed that an elevated level of homocysteine leads to the atherosclerosis either by directly affecting lipid metabolism and transport or via oxidative stress and\u002For Endoplasmic Reticulum (ER) stress. Elevated levels of homocysteine also decreases the bioavailability of nitric oxide and modulates the levels of other metabolites including S-adenosyl methionine and S-adenosyl homocysteine which may result in cardiovascular or neurological disorders. The ER stress emerges as the common pathway that relates to apoptosis, atherosclerosis and neurological disorders and is modulated by levels of homocysteine. The comprehensive network collated has lead to the identification of genes that are modulated by homocysteine indicating that homocysteine exerts its effect not only through modulating the substrate levels for various catalytic processes but also through regulation of expression of genes involved in complex diseases.\u003C\u002Fjats:p>",{"VI":3526,"EN":3527},"Khảo sát tài liệu để phân tích con đường tổng quát: Nghiên cứu trường hợp thu thập các gen liên quan đến homocysteine cho các nghiên cứu di truyền và epigenetic","Mining literature for a comprehensive pathway analysis: A case study for retrieval of homocysteine related genes for genetic and epigenetic studies",{"VOID":3529},"16430779",{"VOID":3531},"10.1186\u002F1476-511x-5-1",[102],[101],"https:\u002F\u002Flipidworld.biomedcentral.com\u002Farticles\u002F10.1186\u002F1476-511X-5-1",[3536,3556,3572,3586,3602,3616,3635],{"id":3537,"sortIndex":135,"researcher":26,"roles":3538,"affiliations":3539,"properties":3549},"ec982f20-1160-4120-9227-50839ed5e538",[],[3540],{"id":26,"sortIndex":36,"affiliation":3541,"properties":26},{"id":3542,"createTime":3543,"updateTime":3543,"relativeEntities":3544,"slug":3545,"properties":3546,"entityType":98,"verifyStatus":28,"verifyTime":26,"verifyNote":26,"syncStatus":28,"languages":26,"translateLanguages":26,"viewCount":36},"d777feb5-125a-44b1-9f57-c4373cb4d67c","2024-04-12T00:30:44.280+00:00",[],"Department-of-Proteomics-and-Structural-Biology-Institute-of-Genomics-and-Integrative-Biology-Mall-Road-Delhi-110007-India",{"title":3547},{"EN":3548},"Department of Proteomics and Structural Biology, Institute of Genomics and Integrative Biology, Mall Road, Delhi, 110007, India",{"openalex":3550,"orcid":3552,"title":3554},{"VOID":3551},"A5014047868",{"VOID":3553},"https:\u002F\u002Forcid.org\u002F0000-0001-8461-0735",{"EN":3555},"Shantanu Sengupta",{"id":3557,"sortIndex":162,"researcher":26,"roles":3558,"affiliations":3559,"properties":3565},"d446e268-036c-4abf-aa3a-f93f40c4108d",[],[3560],{"id":26,"sortIndex":36,"affiliation":3561,"properties":26},{"id":3542,"createTime":3543,"updateTime":3543,"relativeEntities":3562,"slug":3545,"properties":3563,"entityType":98,"verifyStatus":28,"verifyTime":26,"verifyNote":26,"syncStatus":28,"languages":26,"translateLanguages":26,"viewCount":36},[],{"title":3564},{"EN":3548},{"openalex":3566,"orcid":3568,"title":3570},{"VOID":3567},"A5048563533",{"VOID":3569},"https:\u002F\u002Forcid.org\u002F0000-0003-0632-4690",{"EN":3571},"Amitabh Sharma",{"id":3573,"sortIndex":59,"researcher":26,"roles":3574,"affiliations":3575,"properties":3581},"35386b53-2041-4bec-8f71-75d6811626ad",[],[3576],{"id":26,"sortIndex":36,"affiliation":3577,"properties":26},{"id":3542,"createTime":3543,"updateTime":3543,"relativeEntities":3578,"slug":3545,"properties":3579,"entityType":98,"verifyStatus":28,"verifyTime":26,"verifyNote":26,"syncStatus":28,"languages":26,"translateLanguages":26,"viewCount":36},[],{"title":3580},{"EN":3548},{"openalex":3582,"title":3584},{"VOID":3583},"A5021482443",{"EN":3585},"Elayanambi Sundaramoorthy",{"id":3587,"sortIndex":111,"researcher":26,"roles":3588,"affiliations":3589,"properties":3595},"89c038a8-07ae-4708-b28c-75435123d654",[],[3590],{"id":26,"sortIndex":36,"affiliation":3591,"properties":26},{"id":3542,"createTime":3543,"updateTime":3543,"relativeEntities":3592,"slug":3545,"properties":3593,"entityType":98,"verifyStatus":28,"verifyTime":26,"verifyNote":26,"syncStatus":28,"languages":26,"translateLanguages":26,"viewCount":36},[],{"title":3594},{"EN":3548},{"openalex":3596,"orcid":3598,"title":3600},{"VOID":3597},"A5030469052",{"VOID":3599},"https:\u002F\u002Forcid.org\u002F0000-0001-5585-3420",{"EN":3601},"Anubha Mahajan",{"id":3603,"sortIndex":115,"researcher":26,"roles":3604,"affiliations":3605,"properties":3611},"37959ee4-0cd3-4d49-b86d-a9b08ad6c30c",[],[3606],{"id":26,"sortIndex":36,"affiliation":3607,"properties":26},{"id":3542,"createTime":3543,"updateTime":3543,"relativeEntities":3608,"slug":3545,"properties":3609,"entityType":98,"verifyStatus":28,"verifyTime":26,"verifyNote":26,"syncStatus":28,"languages":26,"translateLanguages":26,"viewCount":36},[],{"title":3610},{"EN":3548},{"openalex":3612,"title":3614},{"VOID":3613},"A5079547968",{"EN":3615},"RD Senthilkumar",{"id":3617,"sortIndex":114,"researcher":26,"roles":3618,"affiliations":3619,"properties":3628},"a81d3d9f-2622-4cde-9d98-0f629b7aa193",[],[3620],{"id":26,"sortIndex":36,"affiliation":3621,"properties":26},{"id":3622,"createTime":3623,"updateTime":3623,"relativeEntities":3624,"slug":26,"properties":3625,"entityType":98,"verifyStatus":28,"verifyTime":26,"verifyNote":26,"syncStatus":28,"languages":26,"translateLanguages":26,"viewCount":36},"b2f12401-16ac-49ed-875d-961a737730e4","2024-01-12T21:38:43.331+00:00",[],{"title":3626},{"VI":3627},"Dr. B.R. 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Ann Intern Med. 1999, 131: 363-3.",{"doi":3690},"10.7326\u002F0003-4819-131-5-199909070-00008",{"id":26,"text":3692,"url":26,"identifiers":3693},"McCully KS: Vascular pathology of homocystinemia: Implication for the arteriosclerosis. Am J Pathology. 1969, 56: 111-128.",{},{"id":26,"text":3695,"url":26,"identifiers":3696},"Clarke R, Smith AD, Jobst KA, Refsum H, Sutton L, Ueland PM: Folate, vitamin B12, and serum total homocysteine levels in confirmed Alzheimer disease. Arch Neurol. 1998, 55: 1449-1455. 10.1001\u002Farchneur.55.11.1449",{"doi":3697},"10.1001\u002Farchneur.55.11.1449",{"id":26,"text":3699,"url":26,"identifiers":3700},"Mills JL, McPartlin JM, Kirke PN, Lee YJ, Conley MR, Weir DG, Scott JM: Homocysteine metabolism in pregnancies complicated by neural-tube defects. Lancet. 1995, 345: 149-151. 10.1016\u002FS0140-6736(95)90165-5",{"doi":3701},"10.1016\u002FS0140-6736(95)90165-5",{"id":26,"text":3703,"url":26,"identifiers":3704},"Applebaum J, Shimon H, Sela BA, Belmaker RH, Levine J: Homocysteine levels in newly admitted schizophrenic patients. J Psychiatr Res. 2004, 38: 413-416. 10.1016\u002Fj.jpsychires.2004.01.003",{"doi":3705},"10.1016\u002Fj.jpsychires.2004.01.003",{"id":26,"text":3707,"url":26,"identifiers":3708},"Van GC, Stehouwer CD: Homocysteine metabolism in renal disease. Clin Chem Lab Med. 2003, 41: 1412-1417. 10.1515\u002FCCLM.2003.217",{"doi":3709},"10.1515\u002FCCLM.2003.217",{"id":26,"text":3711,"url":26,"identifiers":3712},"Villadsen MM, Bunger MH, Carstens M, Stenkjaer L, Langdahl BL: Methylenetetrahydrofolate reductase (MTHFR) C677T polymorphism is associated with osteoporotic vertebral fractures, but is a weak predictor of BMD. Osteoporos Int. 2005, 16: 411-416. 10.1007\u002Fs00198-004-1704-4",{"doi":3713},"10.1007\u002Fs00198-004-1704-4",{"id":26,"text":3715,"url":26,"identifiers":3716},"De Luis DA, Fernandez N, Arranz ML, Aller R, Izaola O, Romero E: Total homocysteine levels relation with chronic complications of diabetes, body composition, and other cardiovascular risk factors in a population of patients with diabetes mellitus type 2. J. Diabetes Compl. 2005, 19: 42-46. 10.1016\u002Fj.jdiacomp.2003.12.003. 10.1016\u002Fj.jdiacomp.2003.12.003",{"doi":3717},"10.1016\u002Fj.jdiacomp.2003.12.003",{"id":26,"text":3719,"url":26,"identifiers":3720},"Rudy A, Kowalska I, Straczkowski M, Kinalska I: Homocysteine concentrations and vascular complications in patients with type 2 diabetes. Diabetes Metab. 2005, 31: 112-117.",{"doi":3721},"10.1016\u002FS1262-3636(07)70176-3",{"id":26,"text":3723,"url":26,"identifiers":3724},"Mansoor MA, Bergmark C, Svardal AM, Lønning PE, Ueland PM: Redox Status and Protein Binding of Plasma Homocysteine and Other Aminothiols in Patients with Early-Onset Peripheral Vascular Disease Homocysteine and Peripheral Vascular Disease. Arterioscl Thromb Vasc Biol. 1995, 15: 232-240.",{"doi":3725},"10.1161\u002F01.ATV.15.2.232",{"id":26,"text":3727,"url":26,"identifiers":3728},"Castro R, Rivera I, Martins C, Struys EA, Jansen EE, Clode N, Graca LM, Blom HJ, Jakobs C, Tavares de Almeida I: Intracellular S-adenosylhomocysteine increased levels are associated with DNA hypomethylation in HUVEC. J Mol Med. 2005",{},{"id":26,"text":3730,"url":26,"identifiers":3731},"Hoffman DR, Marion DW, Cornatzer WE, Duerre JA: S-Adenosylmethionine and S-Adenosylhomocysteine Metabolism in isolated Rat Liver. J Biol Chem. 1980, 255: 10822-10827.",{"doi":3732},"10.1016\u002FS0021-9258(19)70381-0",{"id":26,"text":3734,"url":26,"identifiers":3735},"Yi P, Melnyk S, Pogribna M, Pogribny IP, Hine RJ, James SJ: Increase in Plasma Homocysteine Associated with Paralle Increases in Plasma S-Adenosylhomocysteine and Lymphocyte DNA Hypomethylation. J Biol Chem. 2000, 275: 29318-29323. 10.1074\u002Fjbc.M002725200",{"doi":3736},"10.1074\u002Fjbc.M002725200",{"id":26,"text":3738,"url":26,"identifiers":3739},"Li H, Goligorsky MS: Endothelial Gene Responses to Homocysteine: Relation to Atherosclerosis. Exp Nephrol. 2002, 10: 164-169. 10.1159\u002F000049911",{"doi":3740},"10.1159\u002F000049911",{"id":26,"text":3742,"url":26,"identifiers":3743},"Starkebaum G, Harlan JM: Endothelial Cell Injury Due to Copper-catalyzed Hydrogen Peroxide Generation from Homocysteine. 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