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Journal of Medicine and Pharmacy","Tạp chí Y Dược học Cần Thơ",{"EN":487,"VI":488},"\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">04\u002F10\u002F2015 Ministry of Information and Communications allowed Can Tho journal of medicine and pharmacy to operate (102 \u002FGP-BTTTT)\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">07\u002F16\u002F2015 Can Tho journal of medicine and pharmacy is internationally recognized: ISSN 2354-1210\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">In 2016, The journal has been included in the list of medical science journals by The State Council for professorship which is awarded a work score of 0-0.5 points for a published article.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Can Tho Journal of Medicine and Pharmacy welcome original works that haven’t been submitted or published in other medical journals. Posts must contain content related to one of the journal’s categories.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">The content published\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">The journal is divided into 3 categories:\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">- Scientific research article: are valuable scientific works, which have been researched and accepted.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">- Overview of medicine, biology and pharmacy: serving the objective of continuing training in the fields of medicine, biology and pharmacy; to systematize classical and modern knowledge.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">- Update information on new knowledge about medicine, biology, pharmacy in the country and in the world.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Scope\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">- Publication and introduction of scientific research in the fields:\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">+ Medicine (internal medicine, surgery, pediatrics, obstetrics and gynecology, odonto-stomatology, laboratory, oncology, traditional medicine, nursing).\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">+ Biology (genetics, biotechnology).\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">+ Pharmacology (pharmaceutics, drug quality analysis-control, synthetic pharmaceutical chemistry, biochemistry, pharmacognosy, botany, clinical pharmacy).\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">- To enhance the quality of undergraduate, postgraduate education, scientifically researching and meet the necessary treatment in hospital.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">- Introducing the updated domestic and oversea information about science technology to promote scientific research and exchanging technology in local, other universities.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">- Exchanging pharmaceutical and medical information for social health developing in the Mekong Delta and Vietnam.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">The object\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Postgraduate students, student of Can Tho University of Medicine and Pharmacy, scientists from schools, research institutes, hospitals, health centers, pharmaceutical companies of the Mekong Delta; 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. Danh sách bài báo theo số Tạp chí được in ấn và phát hành trong năm định kỳ được công bố chính thức trên website: https:\u002F\u002Ftapchi.ctump.edu.vn\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>",{"VOID":490},"wcQ1uqwAAAAJ","2023-05-30T08:17:21.868+00:00",[],[494],{"id":495,"createTime":28,"updateTime":28,"relativeEntities":496,"slug":28,"properties":497,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":507,"parentIds":508,"statistic":28},"6413896b-eca9-442b-a73f-182a58a0ce40",[],{"title":498,"address":501,"country":504,"abbreviation":505},{"EN":499,"VI":500},"Can Tho University of Medicine and Pharmacy","Trường Đại học Y Dược Cần Thơ",{"EN":502,"VI":503},"No 179, Nguyen Van Cu street, An Khanh ward, Ninh Kieu district, Can Tho city, Vietnam","Số 179, đường Nguyễn Văn Cừ, phường An Khánh, quận Ninh Kiều, thành phố Cần Thơ, Việt Nam",{"VOID":15},{"VOID":506},"ctump","http:\u002F\u002Fwww.ctump.edu.vn\u002F",[],[],"https:\u002F\u002Ftapchi.ctump.edu.vn\u002Findex.php\u002Fctump",{"impactFactor":32,"impactFactorByYear":512,"i10Index":32,"i10IndexLast5Year":32,"totalPublication":514,"totalPublicationByYear":515,"totalCitation":520,"totalCitationByYear":521,"totalCitationPerPublication":108,"totalCitationPerPublicationByYear":523,"hindexLast5Year":45,"hindex":45},{"2022":513,"2023":111,"2024":106},0.01,1556,{"2020":47,"2021":516,"2022":517,"2023":518,"2024":519,"2025":122},57,306,801,358,161,{"2021":146,"2022":280,"2023":522},99,{"2021":524,"2022":318,"2023":104},0.23,{"impactFactor":28,"impactFactorByYear":28,"i10Index":123,"i10IndexLast5Year":123,"totalPublication":526,"totalPublicationByYear":527,"totalCitation":526,"totalCitationByYear":528,"totalCitationPerPublication":40,"totalCitationPerPublicationByYear":531,"hindexLast5Year":49,"hindex":49},476,{"0":205,"2019":123,"2021":139,"2022":459,"2023":451,"2024":357,"2025":49,"2026":48},{"2021":42,"2022":123,"2023":161,"2024":529,"2025":360,"2026":530},136,83,{"2021":105,"2022":513,"2023":532,"2024":127,"2025":533,"2026":534},0.62,25.43,13.83,{"id":536,"createTime":537,"updateTime":382,"relativeEntities":538,"slug":539,"properties":540,"entityType":25,"verifyStatus":26,"verifyTime":28,"verifyNote":28,"languages":552,"translateLanguages":28,"viewCount":133,"subjectFields":553,"manageAffiliations":554,"indexDatabases":555,"url":556,"thumbnailPath":557,"statistic":558,"gsStatistic":594,"type":55,"analyzePriority":28},"6984a56a-db70-403b-9cc4-4013e1ceaffa","2023-05-09T06:47:40.346+00:00",[],"T%E1%BA%A1p%20ch%C3%AD%20Nghi%C3%AAn%20c%E1%BB%A9u%20n%C6%B0%E1%BB%9Bc%20ngo%C3%A0i",{"country":541,"issn":542,"title":544,"introduce":547,"gsId":550},{"VOID":15},{"VOID":543},"25252445",{"EN":545,"VI":546},"VNU Journal of Foreign Studies","Tạp chí Nghiên cứu nước ngoài",{"EN":548,"VI":549},"{\"ops\":[{\"insert\":\"\\n\\nThe \\n\"},{\"attributes\":{\"italic\":true},\"insert\":\"VNU Journal of Science\"},{\"insert\":\"\\n was established in 1985 for the publication of national and international research papers in all fields of natural sciences and technology, social sciences and humanities. 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Preference is given to research that provides significant new mechanistic physiological insights that determine the performance of the normal and abnormal heart and circulation.","PENDING",[886,892,898],{"id":887,"createTime":28,"updateTime":28,"relativeEntities":888,"label":889,"description":891,"parentId":28,"standard":28,"scholarHubFieldId":28},"317b242e-4e36-43ab-821e-f9755e22375e",[],{"EN":890},"Physiology",{},{"id":893,"createTime":28,"updateTime":28,"relativeEntities":894,"label":895,"description":897,"parentId":28,"standard":28,"scholarHubFieldId":28},"2e748c70-3f53-41a9-99c9-1e3e45a3dc6d",[],{"EN":896},"Cardiology and Cardiovascular Medicine",{},{"id":899,"createTime":28,"updateTime":28,"relativeEntities":900,"label":901,"description":903,"parentId":28,"standard":28,"scholarHubFieldId":28},"c3a687ae-b679-4131-bf6c-8a4d1beb2acb",[],{"EN":902},"Physiology (medical)",{},[905,912],{"id":906,"createTime":28,"updateTime":28,"relativeEntities":907,"slug":28,"properties":908,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":911,"statistic":28},"ee372727-4c87-4379-b8a3-771408d03bd0",[],{"title":909},{"EN":910},"AMER PHYSIOLOGICAL SOC",[],{"id":913,"createTime":28,"updateTime":28,"relativeEntities":914,"slug":28,"properties":915,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":918,"statistic":28},"b49c938d-bca1-4d52-9e02-c7bc2ebaea8a",[],{"title":916},{"EN":917},"American Physiological Society",[],[920,934],{"id":921,"indexDatabase":922,"url":927,"indexYears":928,"academicFieldIds":929,"indexDatabaseRanking":933},"4e5c0008-8ad6-48df-8874-5ba443e30eb8",{"id":775,"createTime":28,"updateTime":28,"relativeEntities":923,"label":924,"description":925,"key":781,"publicationTags":926,"standard":28},[],{"EN":778,"VI":778},{"EN":778,"VI":780},[783],"https:\u002F\u002Fwww.scopus.com\u002Fsourceid\u002F23311","1977-2025",[930,931,932],"f845e4fe-178d-4593-b013-715b3c1cc81c","6265d46a-80a6-48ce-b79a-f3a34594a0bd","d44e3b1d-4abe-47f2-b4aa-783c24a9f903","SCOPUS__Q1",{"id":935,"indexDatabase":936,"url":947,"indexYears":28,"academicFieldIds":948,"indexDatabaseRanking":28},"a8a124f7-1858-4c27-83c1-b94d7ff8a783",{"id":937,"createTime":28,"updateTime":28,"relativeEntities":938,"label":939,"description":941,"key":944,"publicationTags":945,"standard":28},"a4921856-b128-4d9f-8f1f-e80813d3bbd4",[],{"EN":940,"VI":940},"ISI\u002FSCIE - Science Citation Index Expanded",{"EN":942,"VI":943},"SCIE database","Cơ sở dữ liệu SCIE","scie",[946,813],"SCIE","https:\u002F\u002Fmjl.clarivate.com\u002Fsearch-results?issn=0363-6135",[949,950,951],"08b1efac-a7b2-46c7-9e79-ef24d3d9025d","0ddd214e-2317-43ae-8737-4f5747adc536","22fd6c38-3ec0-41e0-8ae8-a4290171207e","https:\u002F\u002Fjournals.physiology.org\u002Fjournal\u002Fajpheart",{"meta":954,"data":956},{"total":955},"238",[957,1192,1351,1718,2213,2579,3068,3390,3796,3913],{"id":958,"createTime":959,"updateTime":960,"relativeEntities":961,"slug":962,"properties":963,"entityType":980,"verifyStatus":26,"verifyTime":959,"verifyNote":981,"languages":982,"translateLanguages":983,"viewCount":32,"primaryUrl":984,"fullTextUrl":28,"authors":985,"publicationType":1030,"publisherRelationship":1031,"citationCount":1085,"citationInfo":1086,"publishDate":1101,"publishYear":1087,"citationAnalyzeStatus":884,"lastCitationAnalyze":28,"indexDatabases":1102,"openAccess":28,"references":1103,"isForceReanalyzing":1191},"a99d1332-181b-4f3c-a631-02de6daff709","2024-08-30T09:36:42.766+00:00","2025-01-21T11:28:00.337+00:00",[],"Physiological-time-series-analysis-using-approximate-entropy-and-sample-entropy",{"mag":964,"keywords":966,"openalex":968,"abstract":970,"title":973,"pm":976,"doi":978},{"VOID":965},"1862394037",{"VI":967},"Entropy, độ phức tạp hệ thống, tim mạch, nghiên cứu sinh học, chuỗi thời gian.",{"VOID":969},"W1862394037",{"EN":971,"VI":972},"\u003Cjats:p> Entropy, as it relates to dynamical systems, is the rate of information production. Methods for estimation of the entropy of a system represented by a time series are not, however, well suited to analysis of the short and noisy data sets encountered in cardiovascular and other biological studies. Pincus introduced approximate entropy (ApEn), a set of measures of system complexity closely related to entropy, which is easily applied to clinical cardiovascular and other time series. ApEn statistics, however, lead to inconsistent results. We have developed a new and related complexity measure, sample entropy (SampEn), and have compared ApEn and SampEn by using them to analyze sets of random numbers with known probabilistic character. We have also evaluated cross-ApEn and cross-SampEn, which use cardiovascular data sets to measure the similarity of two distinct time series. SampEn agreed with theory much more closely than ApEn over a broad range of conditions. The improved accuracy of SampEn statistics should make them useful in the study of experimental clinical cardiovascular and other biological time series. \u003C\u002Fjats:p>","\u003Cjats:p> Entropy, trong mối quan hệ với các hệ thống động, là tỷ lệ sản xuất thông tin. Các phương pháp ước lượng entropy của một hệ thống được biểu diễn bằng chuỗi thời gian không phù hợp với phân tích các tập dữ liệu ngắn và ồn ào mà gặp phải trong các nghiên cứu về tim mạch và các sinh học khác. Pincus đã giới thiệu entropy xấp xỉ (ApEn), một tập hợp các biện pháp về độ phức tạp của hệ thống rất gần liên quan đến entropy, dễ dàng được áp dụng cho các chuỗi thời gian tim mạch lâm sàng và khác. Tuy nhiên, thống kê của ApEn dẫn đến các kết quả không nhất quán. Chúng tôi đã phát triển một biện pháp phức tạp mới và liên quan, entropy mẫu (SampEn), và đã so sánh ApEn và SampEn bằng cách sử dụng chúng để phân tích các tập hợp số ngẫu nhiên với đặc điểm xác suất đã biết. Chúng tôi cũng đã đánh giá cross-ApEn và cross-SampEn, sử dụng các tập dữ liệu tim mạch để đo sự tương đồng của hai chuỗi thời gian khác nhau. SampEn đồng thuận với lý thuyết gần gũi hơn nhiều so với ApEn qua một dải điều kiện rộng. Độ chính xác cải thiện của thống kê SampEn nên làm cho nó hữu ích trong việc nghiên cứu các chuỗi thời gian sinh lý lâm sàng và các sinh học khác.",{"EN":974,"VI":975},"Physiological time-series analysis  using approximate entropy and sample entropy","Phân tích chuỗi thời gian sinh lý sử dụng entropy xấp xỉ và entropy mẫu",{"VOID":977},"10843903",{"VOID":979},"10.1152\u002Fajpheart.2000.278.6.h2039","PUBLICATION","Auto Verify",[31],[30],"https:\u002F\u002Fwww.physiology.org\u002Fdoi\u002F10.1152\u002Fajpheart.2000.278.6.H2039",[986,1013],{"id":987,"sortIndex":32,"researcher":28,"roles":988,"affiliations":989,"properties":1006,"displayName":1010,"givenName":28,"familyName":28},"63d9f747-3453-4f91-8f0a-51b611f47a3f",[],[990,998],{"id":991,"sortIndex":32,"affiliation":992,"properties":28},"884f8d5e-379b-4638-b44f-13fc59fbcb32",{"id":991,"createTime":28,"updateTime":28,"relativeEntities":993,"slug":28,"properties":994,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":997,"statistic":28},[],{"title":995},{"EN":996},"Cardiovascular Division, Department of Internal Medicine, and Department of Molecular Physiology and Biological Physics, and Cardiovascular Research Center, University of Virginia Health Sciences Center, Charlottesville, Virginia 22908; and",[],{"id":999,"sortIndex":40,"affiliation":1000,"properties":28},"146378cf-1c9f-4da4-baa7-5e8ba53ba8c4",{"id":999,"createTime":28,"updateTime":28,"relativeEntities":1001,"slug":28,"properties":1002,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1005,"statistic":28},[],{"title":1003},{"EN":1004},"Medical Automation Systems, Charlottesville, Virginia 22903",[],{"orcid":1007,"title":1009,"openalex":1011},{"VOID":1008},"https:\u002F\u002Forcid.org\u002F0000-0002-6166-7488",{"EN":1010},"Joshua Richman",{"VOID":1012},"A5003401361",{"id":1014,"sortIndex":40,"researcher":28,"roles":1015,"affiliations":1016,"properties":1023,"displayName":1027,"givenName":28,"familyName":28},"f7d30b58-44be-430a-ab1a-2250d2188b3b",[],[1017],{"id":991,"sortIndex":32,"affiliation":1018,"properties":28},{"id":991,"createTime":28,"updateTime":28,"relativeEntities":1019,"slug":28,"properties":1020,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1022,"statistic":28},[],{"title":1021},{"EN":996},[],{"orcid":1024,"title":1026,"openalex":1028},{"VOID":1025},"https:\u002F\u002Forcid.org\u002F0000-0002-5772-1648",{"EN":1027},"J. 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Therefore, the use of alternative methods such as computer simulations is of great importance. In this article we introduce a mathematical model of the action potential of human ventricular cells that, while including a high level of electrophysiological detail, is computationally cost-effective enough to be applied in large-scale spatial simulations for the study of reentrant arrhythmias. The model is based on recent experimental data on most of the major ionic currents: the fast sodium, L-type calcium, transient outward, rapid and slow delayed rectifier, and inward rectifier currents. The model includes a basic calcium dynamics, allowing for the realistic modeling of calcium transients, calcium current inactivation, and the contraction staircase. We are able to reproduce human epicardial, endocardial, and M cell action potentials and show that differences can be explained by differences in the transient outward and slow delayed rectifier currents. Our model reproduces the experimentally observed data on action potential duration restitution, which is an important characteristic for reentrant arrhythmias. The conduction velocity restitution of our model is broader than in other models and agrees better with available data. Finally, we model the dynamics of spiral wave rotation in a two-dimensional sheet of human ventricular tissue and show that the spiral wave follows a complex meandering pattern and has a period of 265 ms. We conclude that the proposed model reproduces a variety of electrophysiological behaviors and provides a basis for studies of reentrant arrhythmias in human ventricular tissue. \u003C\u002Fjats:p>","\u003Cjats:p> Các khả năng nghiên cứu thực nghiệm và lâm sàng đối với các rối loạn nhịp tim trong mô cơ tim thất người rất hạn chế. Do đó, việc sử dụng các phương pháp thay thế như mô phỏng máy tính trở nên rất quan trọng. Trong bài viết này, chúng tôi giới thiệu một mô hình toán học về điện thế hành động của các tế bào thất người mà, mặc dù bao gồm một mức độ chi tiết điện sinh lý cao, nhưng vẫn có hiệu suất tính toán đủ hiệu quả để áp dụng vào các mô phỏng không gian quy mô lớn nhằm nghiên cứu các rối loạn nhịp tái nhập. Mô hình dựa trên dữ liệu thực nghiệm gần đây về hầu hết các dòng ion chính, bao gồm dòng natri nhanh, dòng canxi L-type, dòng ra tạm thời, dòng tái phân cực nhanh và chậm, cũng như dòng tái phân cực vào. Mô hình bao gồm động lực học canxi cơ bản, cho phép mô hình hóa thực tế các trạng thái tạm thời của canxi, sự bất hoạt của dòng canxi và bậc thang co bóp. Chúng tôi có thể tái tạo các điện thế hành động của cơ tim màng ngoài tim, màng trong tim và tế bào M của người, và cho thấy rằng những khác biệt này có thể được giải thích bởi những khác biệt trong dòng ra tạm thời và dòng tái phân cực chậm. Mô hình của chúng tôi tái tạo dữ liệu quan sát thực nghiệm về việc khôi phục độ dài điện thế hành động, đây là một đặc điểm quan trọng đối với các rối loạn nhịp tái nhập. Độ rộng khôi phục tốc độ dẫn truyền của mô hình chúng tôi lớn hơn so với các mô hình khác và đồng ý tốt hơn với dữ liệu có sẵn. Cuối cùng, chúng tôi mô hình hóa động lực của sự quay vòng sóng xoáy trong một tấm mô hai chiều của mô tim thất người và cho thấy rằng sóng xoáy theo một mẫu đường nét phức tạp và có chu kỳ 265 ms. Chúng tôi kết luận rằng mô hình đề xuất tái tạo được một loạt hành vi điện sinh lý và cung cấp cơ sở cho các nghiên cứu về các rối loạn nhịp tái nhập trong mô tim thất người. \u003C\u002Fjats:p>",{"EN":1368,"VI":1369},"A model for human ventricular tissue","Mô hình cho mô tim thất người",{"VOID":1371},"14656705",{"VOID":1373},"10.1152\u002Fajpheart.00794.2003",[31],[30],"https:\u002F\u002Fwww.physiology.org\u002Fdoi\u002F10.1152\u002Fajpheart.00794.2003",[1378,1397,1408,1419],{"id":1379,"sortIndex":32,"researcher":28,"roles":1380,"affiliations":1381,"properties":1390,"displayName":1394,"givenName":28,"familyName":28},"60525ba8-a4fc-4cd2-8f5d-b90f8e3fd7d9",[],[1382],{"id":1383,"sortIndex":32,"affiliation":1384,"properties":28},"949e68e9-951d-4980-bb4a-fefc50e4ef96",{"id":1383,"createTime":28,"updateTime":28,"relativeEntities":1385,"slug":28,"properties":1386,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1389,"statistic":28},[],{"title":1387},{"EN":1388},"Department of Theoretical Biology, Utrecht University, 3584 CH Utrecht, The Netherlands. khwjtuss@hotmail.com",[],{"orcid":1391,"title":1393,"openalex":1395},{"VOID":1392},"https:\u002F\u002Forcid.org\u002F0000-0002-1945-7858",{"EN":1394},"Kirsten ten Tusscher",{"VOID":1396},"A5033233639",{"id":1398,"sortIndex":40,"researcher":28,"roles":1399,"affiliations":1400,"properties":1401,"displayName":1405,"givenName":28,"familyName":28},"3b5a9c02-7d22-4e94-99fa-15015ec439d2",[],[],{"orcid":1402,"title":1404,"openalex":1406},{"VOID":1403},"https:\u002F\u002Forcid.org\u002F0000-0002-3013-3694",{"EN":1405},"Denis Noble",{"VOID":1407},"A5050244394",{"id":1409,"sortIndex":123,"researcher":28,"roles":1410,"affiliations":1411,"properties":1412,"displayName":1416,"givenName":28,"familyName":28},"dc00f194-b553-4ed6-a6d0-a8e78563e3de",[],[],{"orcid":1413,"title":1415,"openalex":1417},{"VOID":1414},"https:\u002F\u002Forcid.org\u002F0000-0002-1029-7683",{"EN":1416},"Penelope J. 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Improved guinea-pig ventricular cell model incorporating a diadic space, IKr and IKs, and length- and tension-dependent processes. Can J Cardiol 14: 123–134, 1998.",{},{"id":28,"text":1630,"url":28,"identifiers":1631},"10.1016\u002FS0008-6363(98)00002-9",{"doi":1630},{"id":28,"text":1633,"url":28,"identifiers":1634},"10.1152\u002Fajpheart.2000.278.6.H1908",{"doi":1633},{"id":28,"text":1636,"url":28,"identifiers":1637},"10.1161\u002F01.RES.85.1.38",{"doi":1636},{"id":28,"text":1639,"url":28,"identifiers":1640},"10.1161\u002F01.CIR.0000023042.50192.F4",{"doi":1639},{"id":28,"text":1642,"url":28,"identifiers":1643},"Plonsey R and Barr RC. Bioelectricity. New York: Plenum, 1989.",{"doi":1644},"10.1007\u002F978-1-4757-9456-4",{"id":28,"text":1646,"url":28,"identifiers":1647},"10.1161\u002F01.RES.82.11.1206",{"doi":1646},{"id":28,"text":1649,"url":28,"identifiers":1650},"10.1152\u002Fajpheart.1999.276.1.H269",{"doi":1649},{"id":28,"text":1652,"url":28,"identifiers":1653},"10.1016\u002FS0006-3495(99)77030-X",{"doi":1652},{"id":28,"text":1655,"url":28,"identifiers":1656},"10.1109\u002FTBME.1978.326270",{"doi":1655},{"id":28,"text":1658,"url":28,"identifiers":1659},"10.1161\u002F01.RES.71.3.535",{"doi":1658},{"id":28,"text":1661,"url":28,"identifiers":1662},"10.1161\u002F01.RES.87.10.910",{"doi":1661},{"id":28,"text":1664,"url":28,"identifiers":1665},"10.1006\u002Fjmcc.1998.0748",{"doi":1664},{"id":28,"text":1667,"url":28,"identifiers":1668},"10.1007\u002FBF00374755",{"doi":1667},{"id":28,"text":1670,"url":28,"identifiers":1671},"10.1085\u002Fjgp.20028534",{"doi":1670},{"id":28,"text":1673,"url":28,"identifiers":1674},"10.1152\u002Fajpheart.1997.272.4.H1625",{"doi":1673},{"id":28,"text":1676,"url":28,"identifiers":1677},"10.1006\u002Fjmcc.2000.1105",{"doi":1676},{"id":28,"text":1679,"url":28,"identifiers":1680},"10.1016\u002FS0008-6363(00)00306-0",{"doi":1679},{"id":28,"text":1682,"url":28,"identifiers":1683},"10.1161\u002Fhc3501.093797",{"doi":1682},{"id":28,"text":1685,"url":28,"identifiers":1686},"10.1152\u002Fajpheart.2001.280.1.H354",{"doi":1685},{"id":28,"text":1688,"url":28,"identifiers":1689},"10.1161\u002F01.RES.87.8.e37",{"doi":1688},{"id":28,"text":1691,"url":28,"identifiers":1692},"10.1093\u002Fcvr\u002F28.10.1540",{"doi":1691},{"id":28,"text":1694,"url":28,"identifiers":1695},"10.1046\u002Fj.1540-8167.2001.00196.x",{"doi":1694},{"id":28,"text":1697,"url":28,"identifiers":1698},"10.1161\u002F01.RES.75.3.473",{"doi":1697},{"id":28,"text":1700,"url":28,"identifiers":1701},"10.1152\u002Fajpheart.2001.280.4.H1667",{"doi":1700},{"id":28,"text":1703,"url":28,"identifiers":1704},"10.1152\u002Fajpheart.1996.270.6.H2157",{"doi":1703},{"id":28,"text":1706,"url":28,"identifiers":1707},"10.1161\u002F01.RES.77.1.140",{"doi":1706},{"id":28,"text":1709,"url":28,"identifiers":1710},"Zhou Z, Gong Q, Ye B, Fan Z, Makielski JC, Robertson GA, and January CT. Properties of HERG channels stably expressed in HEK 293 cells studied at physiological temperatures. Biophys J 74: 230–241, 1973.",{"doi":1711},"10.1016\u002FS0006-3495(98)77782-3",{"id":28,"text":1713,"url":28,"identifiers":1714},"10.1152\u002Fajpheart.2001.281.2.H689",{"doi":1713},{"id":28,"text":1716,"url":28,"identifiers":1717},"10.1152\u002Fajpheart.2000.278.5.H1671",{"doi":1716},{"id":1719,"createTime":1720,"updateTime":1721,"relativeEntities":1722,"slug":1723,"properties":1724,"entityType":980,"verifyStatus":26,"verifyTime":1720,"verifyNote":981,"languages":1740,"translateLanguages":1741,"viewCount":32,"primaryUrl":1742,"fullTextUrl":28,"authors":1743,"publicationType":1030,"publisherRelationship":1797,"citationCount":1850,"citationInfo":1851,"publishDate":1857,"publishYear":1852,"citationAnalyzeStatus":884,"lastCitationAnalyze":28,"indexDatabases":1858,"openAccess":28,"references":1859,"isForceReanalyzing":1191},"fce28acb-8965-4fe2-aa76-7faddd65c395","2024-09-03T06:21:04.910+00:00","2025-02-15T13:05:05.486+00:00",[],"Oxidative-stress-and-heart-failure",{"mag":1725,"keywords":1727,"openalex":1728,"abstract":1730,"title":1733,"pm":1736,"doi":1738},{"VOID":1726},"2147653980",{"VI":1361},{"VOID":1729},"W2147653980",{"EN":1731,"VI":1732},"\u003Cjats:p>Oxidative stress, defined as an excess production of reactive oxygen species (ROS) relative to antioxidant defense, has been shown to play an important role in the pathophysiology of cardiac remodeling and heart failure (HF). It induces subtle changes in intracellular pathways, redox signaling, at lower levels, but causes cellular dysfunction and damage at higher levels. ROS are derived from several intracellular sources, including mitochondria, NAD(P)H oxidase, xanthine oxidase, and uncoupled nitric oxide synthase. The production of ROS is increased within the mitochondria from failing hearts, whereas normal antioxidant enzyme activities are preserved. Chronic increases in ROS production in the mitochondria lead to a catastrophic cycle of mitochondrial DNA (mtDNA) damage as well as functional decline, further ROS generation, and cellular injury. ROS directly impair contractile function by modifying proteins central to excitation-contraction coupling. Moreover, ROS activate a broad variety of hypertrophy signaling kinases and transcription factors and mediate apoptosis. They also stimulate cardiac fibroblast proliferation and activate the matrix metalloproteinases, leading to the extracellular matrix remodeling. These cellular events are involved in the development and progression of maladaptive myocardial remodeling and failure. Oxidative stress is also involved in the skeletal muscle dysfunction, which may be associated with exercise intolerance and insulin resistance in HF. Therefore, oxidative stress is involved in the pathophysiology of HF in the heart as well as in the skeletal muscle. A better understanding of these mechanisms may enable the development of novel and effective therapeutic strategies against HF.\u003C\u002Fjats:p>","\u003Cjats:p>Căng thẳng oxy hóa, được định nghĩa là sự sản xuất quá mức các loài oxy phản ứng (ROS) so với sự bảo vệ của các chất chống oxy hóa, đã được chứng minh là đóng vai trò quan trọng trong bệnh sinh của việc tái cấu trúc tim và suy tim (HF). Nó gây ra những thay đổi tinh vi trong các con đường nội bào, tín hiệu redox, ở mức độ thấp, nhưng gây ra sự suy giảm và tổn thương tế bào ở mức độ cao hơn. ROS được hình thành từ một số nguồn nội bào, bao gồm ty thể, NAD(P)H oxidase, xanthine oxidase, và nitric oxide synthase không liên kết. Sự sản xuất ROS tăng lên trong ty thể từ các trái tim bị suy, trong khi các hoạt động enzyme chống oxy hóa bình thường được bảo tồn. Sự gia tăng mãn tính trong sản xuất ROS trong ty thể dẫn đến một chu kỳ thảm khốc của tổn thương DNA ty thể (mtDNA) cũng như sự suy giảm chức năng, sự tạo ra ROS thêm, và tổn thương tế bào. ROS trực tiếp làm suy yếu chức năng co bóp bằng cách thay đổi các protein trung tâm cho sự kết hợp kích thích-co bóp. Hơn nữa, ROS kích hoạt một loạt các kinase tín hiệu tăng sinh và yếu tố phiên mã và điều hòa quá trình apoptosis. Chúng cũng kích thích sự tăng sinh của nguyên bào sợi tim và hoạt hóa các matrix metalloproteinase, dẫn đến việc tái cấu trúc ma trận ngoại bào. Những sự kiện tế bào này liên quan đến sự phát triển và tiến triển của tái cấu trúc cơ tim không thích nghi và suy tim. Căng thẳng oxy hóa cũng liên quan đến sự suy giảm chức năng cơ vân, mà có thể liên quan đến tình trạng không dung nạp vận động và kháng insulin trong HF. Do đó, căng thẳng oxy hóa có liên quan đến bệnh sinh của HF trong tim cũng như trong cơ vân. Một hiểu biết tốt hơn về những cơ chế này có thể cho phép phát triển các chiến lược điều trị mới và hiệu quả chống lại HF.\u003C\u002Fjats:p>",{"EN":1734,"VI":1735},"Oxidative stress and heart failure","Căng thẳng oxy hóa và suy 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RS, 1986, J Biol Chem, 261, 12390, 10.1016\u002FS0021-9258(18)67252-7",{"doi":2200},"10.1016\u002FS0021-9258(18)67252-7",{"id":28,"text":2202,"url":28,"identifiers":2203},"10.1016\u002Fj.jacc.2004.03.037",{"doi":2202},{"id":28,"text":2205,"url":28,"identifiers":2206},"10.1152\u002Fajpcell.00045.2009",{"doi":2205},{"id":28,"text":2208,"url":28,"identifiers":2209},"10.1111\u002Fj.1742-4658.2007.05914.x",{"doi":2208},{"id":28,"text":2211,"url":28,"identifiers":2212},"10.1016\u002Fj.cardiores.2006.02.019",{"doi":2211},{"id":2214,"createTime":2215,"updateTime":2216,"relativeEntities":2217,"slug":2218,"properties":2219,"entityType":980,"verifyStatus":26,"verifyTime":2235,"verifyNote":981,"languages":2236,"translateLanguages":2237,"viewCount":32,"primaryUrl":2238,"fullTextUrl":28,"authors":2239,"publicationType":1030,"publisherRelationship":2259,"citationCount":2313,"citationInfo":2314,"publishDate":2317,"publishYear":2315,"citationAnalyzeStatus":884,"lastCitationAnalyze":28,"indexDatabases":2318,"openAccess":28,"references":2319,"isForceReanalyzing":1191},"3426ca0a-100f-48ac-8ec9-c391793ce114","2024-10-09T12:39:09.965+00:00","2025-02-15T13:06:03.218+00:00",[],"Mechanotransduction-and-endothelial-cell-homeostasis-the-wisdom-of-the-cell",{"mag":2220,"keywords":2222,"openalex":2223,"abstract":2225,"title":2228,"pm":2231,"doi":2233},{"VOID":2221},"2014171174",{"VI":1361},{"VOID":2224},"W2014171174",{"EN":2226,"VI":2227},"\u003Cjats:p>Vascular endothelial cells (ECs) play significant roles in regulating circulatory functions. Mechanical stimuli, including the stretch and shear stress resulting from circulatory pressure and flow, modulate EC functions by activating mechanosensors, signaling pathways, and gene and protein expressions. Mechanical forces with a clear direction (e.g., the pulsatile shear stress and the uniaxial circumferential stretch existing in the straight part of the arterial tree) cause only transient molecular signaling of pro-inflammatory and proliferative pathways, which become downregulated when such directed mechanical forces are sustained. In contrast, mechanical forces without a definitive direction (e.g., disturbed flow and relatively undirected stretch seen at branch points and other regions of complex geometry) cause sustained molecular signaling of pro-inflammatory and proliferative pathways. The EC responses to directed mechanical stimuli involve the remodeling of EC structure to minimize alterations in intracellular stress\u002Fstrain and elicit adaptive changes in EC signaling in the face of sustained stimuli; these cellular events constitute a feedback control mechanism to maintain vascular homeostasis and are atheroprotective. Such a feedback mechanism does not operate effectively in regions of complex geometry, where the mechanical stimuli do not have clear directions, thus placing these areas at risk for atherogenesis. The mechanotransduction-induced EC adaptive processes in the straight part of the aorta represent a case of the “Wisdom of the Cell,” as a part of the more general concept of the “Wisdom of the Body” promulgated by Cannon, to maintain cellular homeostasis in the face of external perturbations.\u003C\u002Fjats:p>","\u003Cjats:p>Tế bào nội mô (ECs) đóng vai trò quan trọng trong việc điều chỉnh các chức năng tuần hoàn. Các kích thích cơ học, bao gồm sự kéo dãn và áp lực cắt do áp lực và lưu lượng tuần hoàn gây ra, điều chỉnh chức năng của EC bằng cách kích hoạt các cơ chế cảm ứng cơ học, các con đường tín hiệu, cũng như sự biểu hiện gen và protein. Các lực cơ học có hướng rõ ràng (ví dụ: áp lực cắt mạch đập và sự kéo dãn tròn một chiều tồn tại ở phần thẳng của hệ động mạch) chỉ gây ra sự ra tín hiệu phân tử tạm thời đối với các con đường pro-inflammatory và tăng sinh, những con đường này sẽ giảm điều hòa khi các lực cơ học có hướng này được duy trì. Ngược lại, các lực cơ học không có hướng xác định (ví dụ: dòng chảy bị rối loạn và sự kéo dãn tương đối không chỉ định ở các điểm phân nhánh và những khu vực có hình dạng phức tạp khác) gây ra tín hiệu phân tử duy trì các con đường pro-inflammatory và tăng sinh. Phản ứng của EC đối với các kích thích cơ học có hướng liên quan đến việc tái cấu trúc cấu trúc EC để tối thiểu hóa các thay đổi trong ứng suất\u002Fbiến dạng tế bào và kích hoạt những thay đổi thích ứng trong tín hiệu EC đối mặt với các kích thích bền vững; những sự kiện tế bào này tạo thành một cơ chế phản hồi kiểm soát để duy trì cân bằng nội môi của mạch máu và có tác dụng bảo vệ chống lại sự hình thành xơ vữa. Cơ chế phản hồi này không hoạt động hiệu quả ở các vùng có hình dạng phức tạp, nơi mà các kích thích cơ học không có hướng rõ ràng, do đó đặt những khu vực này vào nguy cơ hình thành xơ vữa. Các quá trình thích ứng của EC do cảm ứng cơ học tại phần thẳng của động mạch chủ là một ví dụ cho \"Trí tuệ của Tế bào,\" như một phần của khái niệm tổng quát hơn về \"Trí tuệ của Cơ thể\" được công bố bởi Cannon, nhằm duy trì cân bằng nội môi tế bào trước những rối loạn từ bên ngoài.\u003C\u002Fjats:p>",{"EN":2229,"VI":2230},"Mechanotransduction and endothelial cell homeostasis: the wisdom of the cell","Cảm ứng cơ học và sự duy trì cân bằng nội môi của tế bào nội mô: trí tuệ của tế bào",{"VOID":2232},"17098825",{"VOID":2234},"10.1152\u002Fajpheart.01047.2006","2024-10-09T12:39:09.964+00:00",[31],[30],"https:\u002F\u002Fwww.physiology.org\u002Fdoi\u002F10.1152\u002Fajpheart.01047.2006",[2240],{"id":2241,"sortIndex":32,"researcher":28,"roles":2242,"affiliations":2243,"properties":2252,"displayName":2256,"givenName":28,"familyName":28},"710142a3-1dcc-4487-bee4-2deb991d6dd5",[],[2244],{"id":2245,"sortIndex":32,"affiliation":2246,"properties":28},"c60bb016-4cac-468f-82df-c5ae5045b4e3",{"id":2245,"createTime":28,"updateTime":28,"relativeEntities":2247,"slug":28,"properties":2248,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":2251,"statistic":28},[],{"title":2249},{"EN":2250},"Dept of Bioengineering, PFBH, Rm 134, Univ of California, San Diego, La Jolla, CA 92093-0412, USA. shuchien@ucsd.edu",[],{"orcid":2253,"title":2255,"openalex":2257},{"VOID":2254},"https:\u002F\u002Forcid.org\u002F0000-0003-0332-285X",{"EN":2256},"Shu 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2003.",{},{"id":28,"text":2436,"url":28,"identifiers":2437},"10.1016\u002Fj.jbiomech.2004.09.030",{"doi":2436},{"id":28,"text":2439,"url":28,"identifiers":2440},"10.1128\u002FMCB.16.11.5947",{"doi":2439},{"id":28,"text":2442,"url":28,"identifiers":2443},"10.1073\u002Fpnas.170282597",{"doi":2442},{"id":28,"text":2445,"url":28,"identifiers":2446},"10.1161\u002F01.ATV.10.5.703",{"doi":2445},{"id":28,"text":2448,"url":28,"identifiers":2449},"10.1016\u002F0021-9150(90)90115-Y",{"doi":2448},{"id":28,"text":2451,"url":28,"identifiers":2452},"10.1161\u002F01.ATV.9.2.230",{"doi":2451},{"id":28,"text":2454,"url":28,"identifiers":2455},"10.1161\u002Fhq0102.101822",{"doi":2454},{"id":28,"text":2457,"url":28,"identifiers":2458},"10.1016\u002F0021-9150(94)05497-7",{"doi":2457},{"id":28,"text":2460,"url":28,"identifiers":2461},"10.1007\u002FBF02066350",{"doi":2460},{"id":28,"text":2463,"url":28,"identifiers":2464},"10.1242\u002Fjcs.02760",{"doi":2463},{"id":28,"text":2466,"url":28,"identifiers":2467},"10.1115\u002F1.2895532",{"doi":2466},{"id":28,"text":2469,"url":28,"identifiers":2470},"Ohashi T, Ishii Y, Ishikawa Y, Matsumoto T, Sato M.Experimental and numerical analyses of local mechanical properties measured by atomic force microscopy for sheared endothelial cells.Biomed Mater Eng12: 319–327, 2002.",{},{"id":28,"text":2472,"url":28,"identifiers":2473},"10.1038\u002F331168a0",{"doi":2472},{"id":28,"text":2475,"url":28,"identifiers":2476},"10.1083\u002Fjcb.200205049",{"doi":2475},{"id":28,"text":2478,"url":28,"identifiers":2479},"10.1016\u002F0092-8674(92)90163-7",{"doi":2478},{"id":28,"text":2481,"url":28,"identifiers":2482},"10.3109\u002F10739689709146808",{"doi":2481},{"id":28,"text":2484,"url":28,"identifiers":2485},"Sato M, Ohashi T.Biorheological views of endothelial cell responses to mechanical stimuli.Biorheology42: 421–441, 2005.",{},{"id":28,"text":2487,"url":28,"identifiers":2488},"10.1016\u002FS0014-5793(00)01746-4",{"doi":2487},{"id":28,"text":2490,"url":28,"identifiers":2491},"10.1074\u002Fjbc.M107026200",{"doi":2490},{"id":28,"text":2493,"url":28,"identifiers":2494},"10.1016\u002F0092-8674(86)90817-2",{"doi":2493},{"id":28,"text":2496,"url":28,"identifiers":2497},"10.1016\u002FS0962-8924(01)02152-3",{"doi":2496},{"id":28,"text":2499,"url":28,"identifiers":2500},"10.1161\u002F01.ATV.9.6.895",{"doi":2499},{"id":28,"text":2502,"url":28,"identifiers":2503},"10.1161\u002F01.RES.62.4.699",{"doi":2502},{"id":28,"text":2505,"url":28,"identifiers":2506},"10.1073\u002Fpnas.92.17.8069",{"doi":2505},{"id":28,"text":2508,"url":28,"identifiers":2509},"10.1073\u002Fpnas.91.11.4678",{"doi":2508},{"id":28,"text":2511,"url":28,"identifiers":2512},"10.1016\u002FS0021-9290(02)00443-8",{"doi":2511},{"id":28,"text":2514,"url":28,"identifiers":2515},"10.1074\u002Fjbc.M300703200",{"doi":2514},{"id":28,"text":2517,"url":28,"identifiers":2518},"10.1114\u002F1.88",{"doi":2517},{"id":28,"text":2520,"url":28,"identifiers":2521},"10.1172\u002FJCI119083",{"doi":2520},{"id":28,"text":2523,"url":28,"identifiers":2524},"10.1016\u002FS0741-5214(99)70249-1",{"doi":2523},{"id":28,"text":2526,"url":28,"identifiers":2527},"10.1007\u002FBF02631337",{"doi":2526},{"id":28,"text":2529,"url":28,"identifiers":2530},"10.1161\u002F01.ATV.8.4.410",{"doi":2529},{"id":28,"text":2532,"url":28,"identifiers":2533},"10.1074\u002Fjbc.274.29.20144",{"doi":2532},{"id":28,"text":2535,"url":28,"identifiers":2536},"10.1161\u002F01.RES.71.4.883",{"doi":2535},{"id":28,"text":2538,"url":28,"identifiers":2539},"10.1038\u002Fnature03952",{"doi":2538},{"id":28,"text":2541,"url":28,"identifiers":2542},"Walpola PL, Gotlieb AI, Langille BL.Monocyte adhesion and changes in endothelial cell number, morphology, and F-actin distribution elicited by low shear stress in vivo.Am J Pathol142: 1392–1400, 1993.",{},{"id":28,"text":2544,"url":28,"identifiers":2545},"10.1016\u002FS0021-9290(01)00150-6",{"doi":2544},{"id":28,"text":2547,"url":28,"identifiers":2548},"10.1016\u002Fj.bbrc.2006.01.089",{"doi":2547},{"id":28,"text":2550,"url":28,"identifiers":2551},"10.1152\u002Fajpcell.00222.2002",{"doi":2550},{"id":28,"text":2553,"url":28,"identifiers":2554},"10.1038\u002F11056",{"doi":2553},{"id":28,"text":2556,"url":28,"identifiers":2557},"10.1152\u002Fajpheart.1985.248.6.H945",{"doi":2556},{"id":28,"text":2559,"url":28,"identifiers":2560},"10.1073\u002Fpnas.1332808100",{"doi":2559},{"id":28,"text":2562,"url":28,"identifiers":2563},"10.1083\u002Fjcb.97.2.416",{"doi":2562},{"id":28,"text":2565,"url":28,"identifiers":2566},"10.1126\u002Fscience.6681677",{"doi":2565},{"id":28,"text":2568,"url":28,"identifiers":2569},"10.1038\u002Fnm1338",{"doi":2568},{"id":28,"text":2571,"url":28,"identifiers":2572},"10.1006\u002Fbbrc.1996.1057",{"doi":2571},{"id":28,"text":2574,"url":28,"identifiers":2575},"10.1161\u002F01.ATV.15.10.1781",{"doi":2574},{"id":28,"text":2577,"url":28,"identifiers":2578},"10.1152\u002Fphysiolgenomics.00024.2002",{"doi":2577},{"id":2580,"createTime":2581,"updateTime":2582,"relativeEntities":2583,"slug":2584,"properties":2585,"entityType":980,"verifyStatus":884,"verifyTime":2581,"verifyNote":1208,"languages":2601,"translateLanguages":2602,"viewCount":32,"primaryUrl":2603,"fullTextUrl":28,"authors":2604,"publicationType":1030,"publisherRelationship":2779,"citationCount":2832,"citationInfo":2833,"publishDate":2836,"publishYear":2834,"citationAnalyzeStatus":884,"lastCitationAnalyze":28,"indexDatabases":2837,"openAccess":28,"references":2838,"isForceReanalyzing":1191},"19af9b0a-d667-4e2e-8311-6363a812a920","2024-10-04T23:03:36.909+00:00","2025-02-15T13:07:00.531+00:00",[],"VEGF-dependent-plasticity-of-fenestrated-capillaries-in-the-normal-adult-microvasculature",{"mag":2586,"keywords":2588,"openalex":2589,"abstract":2591,"title":2594,"pm":2597,"doi":2599},{"VOID":2587},"2132272301",{"VI":1361},{"VOID":2590},"W2132272301",{"EN":2592,"VI":2593},"\u003Cjats:p>Unlike during development, blood vessels in the adult are generally thought not to require VEGF for normal function. However, VEGF is a survival factor for many tumor vessels, and there are clues that some normal blood vessels may also depend on VEGF. In this study, we sought to identify which, if any, vascular beds in adult mice depend on VEGF for survival. Mice were treated with a small-molecule VEGF receptor (VEGFR) tyrosine kinase inhibitor or soluble VEGFRs for 1–3 wk. Blood vessels were assessed using immunohistochemistry or scanning or transmission electron microscopy. In a study of 17 normal organs after VEGF inhibition, we found significant capillary regression in pancreatic islets, thyroid, adrenal cortex, pituitary, choroid plexus, small-intestinal villi, and epididymal adipose tissue. The amount of regression was dose dependent and varied from organ to organ, with a maximum of 68% in thyroid, but was less in normal organs than in tumors in RIP-Tag2-transgenic mice or in Lewis lung carcinoma. VEGF-dependent capillaries were fenestrated, expressed high levels of both VEGFR-2 and VEGFR-3, and had normal pericyte coverage. Surviving capillaries in affected organs had fewer fenestrations and less VEGFR expression. All mice appeared healthy, but distinct physiological changes, including more efficient blood glucose handling, accompanied some regimens of VEGF inhibition. Strikingly, most capillaries in the thyroid grew back within 2 wk after cessation of treatment for 1 wk. Our findings of VEGF dependency of normal fenestrated capillaries and rapid regrowth after regression demonstrate the plasticity of the adult microvasculature.\u003C\u002Fjats:p>","\u003Cjats:p>Khác với giai đoạn phát triển, các mạch máu ở người trưởng thành thường không cần VEGF cho chức năng bình thường. Tuy nhiên, VEGF là yếu tố sống còn cho nhiều mạch máu trong khối u, và có những manh mối cho thấy một số mạch máu bình thường cũng có thể phụ thuộc vào VEGF. Trong nghiên cứu này, chúng tôi đã tìm cách xác định các giường mạch nào, nếu có, ở chuột trưởng thành phụ thuộc vào VEGF để tồn tại. Các con chuột được điều trị bằng một chất ức chế tyrosine kinase thụ thể VEGF (VEGFR) nhỏ hoặc các VEGFR hòa tan trong 1-3 tuần. Các mạch máu được đánh giá thông qua nhuộm miễn dịch histochemistry hoặc kính hiển vi điện tử quét hoặc truyền. Trong một nghiên cứu về 17 cơ quan bình thường sau khi ức chế VEGF, chúng tôi phát hiện sự thoái triển mao mạch đáng kể ở các tiểu đảo tụy, tuyến giáp, vỏ tuyến thượng thận, tuyến yên, đám rối màng mạch, nhung mao ruột non, và mô mỡ mào tinh. Mức độ thoái triển phụ thuộc liều và thay đổi từ cơ quan này sang cơ quan khác, với mức tối đa là 68% ở tuyến giáp, nhưng lại ít hơn ở các cơ quan bình thường so với các khối u ở chuột transgenic RIP-Tag2 hoặc ở ung thư phổi Lewis. Các mao mạch phụ thuộc vào VEGF có lỗ, biểu hiện mức cao của cả VEGFR-2 và VEGFR-3, và có phủ tế bào pericyte bình thường. Các mao mạch tồn tại ở các cơ quan bị ảnh hưởng có ít lỗ hơn và ít biểu hiện VEGFR hơn. Tất cả các con chuột đều có vẻ khỏe mạnh, nhưng nhiều thay đổi sinh lý rõ rệt, bao gồm khả năng xử lý glucose trong máu hiệu quả hơn, đi kèm với một số chế độ ức chế VEGF. Một cách đáng chú ý, hầu hết các mao mạch ở tuyến giáp đã hồi phục trong vòng 2 tuần sau khi dừng điều trị trong 1 tuần. 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The mechanism for SARS-CoV-2 infection is the requisite binding of the virus to the membrane-bound form of angiotensin-converting enzyme 2 (ACE2) and internalization of the complex by the host cell. Recognition that ACE2 is the coreceptor for the coronavirus has prompted new therapeutic approaches to block the enzyme or reduce its expression to prevent the cellular entry and SARS-CoV-2 infection in tissues that express ACE2 including lung, heart, kidney, brain, and gut. ACE2, however, is a key enzymatic component of the renin-angiotensin-aldosterone system (RAAS); ACE2 degrades ANG II, a peptide with multiple actions that promote CVD, and generates Ang-(1–7), which antagonizes the effects of ANG II. Moreover, experimental evidence suggests that RAAS blockade by ACE inhibitors, ANG II type 1 receptor antagonists, and mineralocorticoid antagonists, as well as statins, enhance ACE2 which, in part, contributes to the benefit of these regimens. In lieu of the fact that many older patients with hypertension or other CVDs are routinely treated with RAAS blockers and statins, new clinical concerns have developed regarding whether these patients are at greater risk for SARS-CoV-2 infection, whether RAAS and statin therapy should be discontinued, and the potential consequences of RAAS blockade to COVID-19-related pathologies such as acute and chronic respiratory disease. The current perspective critically examines the evidence for ACE2 regulation by RAAS blockade and statins, the cardiovascular benefits of ACE2, and whether ACE2 blockade is a viable approach to attenuate COVID-19. \u003C\u002Fjats:p>\u003Cjats:p> Listen to this article’s corresponding podcast at: https:\u002F\u002Fajpheart.podbean.com\u002Fe\u002Fcovid-19-ace2-and-the-cardiovascular-consequences\u002F . \u003C\u002Fjats:p>","\u003Cjats:p> Đại dịch coronavirus SARS-CoV-2 mới có thể đặc biệt gây hại cho những bệnh nhân có bệnh lý tim mạch nền (CVD). Cơ chế nhiễm SARS-CoV-2 là sự liên kết cần thiết của virus với dạng enzyme chuyển đổi angiotensin 2 (ACE2) gắn trên màng và sự nội hóa phức hợp này vào tế bào chủ. Nhận thức rằng ACE2 là thụ thể đồng cho coronavirus đã thúc đẩy các phương pháp điều trị mới nhằm chặn enzyme này hoặc giảm sự biểu hiện của nó để ngăn chặn sự xâm nhập vào tế bào và nhiễm SARS-CoV-2 vào các tổ chức biểu hiện ACE2 như phổi, tim, thận, não và ruột. Tuy nhiên, ACE2 là một thành phần enzym quan trọng trong hệ thống renin-angiotensin-aldosterone (RAAS); ACE2 phân hủy ANG II, một peptide có nhiều tác dụng thúc đẩy CVD, và tạo ra Ang-(1–7), có tác dụng đối kháng với hiệu ứng của ANG II. Hơn nữa, các bằng chứng thực nghiệm cho thấy việc chặn RAAS bằng các thuốc ức chế ACE, các thuốc đối kháng thụ thể ANG II loại 1, và các thuốc đối kháng mineralocorticoid, cũng như statin, làm tăng ACE2, là một phần trong những lợi ích của các chế độ điều trị này. Với thực tế rằng nhiều bệnh nhân lớn tuổi mắc tăng huyết áp hoặc các bệnh lý tim mạch khác thường xuyên được điều trị bằng các thuốc chặn RAAS và statin, những lo ngại lâm sàng mới đã phát sinh về việc liệu những bệnh nhân này có nguy cơ cao hơn mắc SARS-CoV-2, liệu liệu pháp RAAS và statin có nên ngừng sử dụng, và các hậu quả tiềm tàng của việc chặn RAAS đối với các bệnh lý liên quan đến COVID-19 như bệnh hô hấp cấp và mãn tính. Quan điểm hiện tại sẽ xem xét một cách nghiêm túc các bằng chứng về việc điều chỉnh ACE2 bởi sự chặn RAAS và statin, những lợi ích tim mạch của ACE2, và liệu việc chặn ACE2 có phải là một phương pháp khả thi để giảm thiểu COVID-19 hay không.\u003C\u002Fjats:p>\u003Cjats:p> Nghe podcast liên quan đến bài viết này tại: https:\u002F\u002Fajpheart.podbean.com\u002Fe\u002Fcovid-19-ace2-and-the-cardiovascular-consequences\u002F . \u003C\u002Fjats:p>",{"EN":3086,"VI":3087},"COVID-19, ACE2, and the cardiovascular consequences","COVID-19, ACE2 và những hậu quả về tim mạch",{"VOID":3089},"32228252",{"VOID":3091},"10.1152\u002Fajpheart.00217.2020",[31],[30],"https:\u002F\u002Fjournals.physiology.org\u002Fdoi\u002F10.1152\u002Fajpheart.00217.2020",[3096,3115,3130],{"id":3097,"sortIndex":32,"researcher":28,"roles":3098,"affiliations":3099,"properties":3108,"displayName":3112,"givenName":28,"familyName":28},"dd38d71d-4e13-4dd5-b5df-a16f8e9dcdb0",[],[3100],{"id":3101,"sortIndex":32,"affiliation":3102,"properties":28},"6bd129c9-3ba3-453d-97f7-7f64096e4256",{"id":3101,"createTime":28,"updateTime":28,"relativeEntities":3103,"slug":28,"properties":3104,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":3107,"statistic":28},[],{"title":3105},{"EN":3106},"Cardiovascular Sciences Center, Wake Forest School of Medicine, Winston-Salem, North Carolina",[],{"orcid":3109,"title":3111,"openalex":3113},{"VOID":3110},"https:\u002F\u002Forcid.org\u002F0000-0002-3204-4142",{"EN":3112},"Andrew M. 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Human-induced pluripotent stem cells (hiPSCs) can differentiate into functional cardiomyocytes; however, the electrophysiological properties of hiPSC-derived cardiomyocytes have yet to be fully characterized. We performed detailed electrophysiological characterization of highly pure hiPSC-derived cardiomyocytes. Action potentials (APs) were recorded from spontaneously beating cardiomyocytes using a perforated patch method and had atrial-, nodal-, and ventricular-like properties. Ventricular-like APs were more common and had maximum diastolic potentials close to those of human cardiac myocytes, AP durations were within the range of the normal human electrocardiographic QT interval, and APs showed expected sensitivity to multiple drugs (tetrodotoxin, nifedipine, and E4031). Early afterdepolarizations (EADs) were induced with E4031 and were bradycardia dependent, and EAD peak voltage varied inversely with the EAD take-off potential. Gating properties of seven ionic currents were studied including sodium ( I\u003Cjats:sub>Na\u003C\u002Fjats:sub>), L-type calcium ( I\u003Cjats:sub>Ca\u003C\u002Fjats:sub>), hyperpolarization-activated pacemaker ( I\u003Cjats:sub>f\u003C\u002Fjats:sub>), transient outward potassium ( I\u003Cjats:sub>to\u003C\u002Fjats:sub>), inward rectifier potassium ( I\u003Cjats:sub>K1\u003C\u002Fjats:sub>), and the rapidly and slowly activating components of delayed rectifier potassium ( I\u003Cjats:sub>Kr\u003C\u002Fjats:sub> and I\u003Cjats:sub>Ks\u003C\u002Fjats:sub>, respectively) current. The high purity and large cell numbers also enabled automated patch-clamp analysis. We conclude that these hiPSC-derived cardiomyocytes have ionic currents and channel gating properties underlying their APs and EADs that are quantitatively similar to those reported for human cardiac myocytes. These hiPSC-derived cardiomyocytes have the added advantage that they can be used in high-throughput assays, and they have the potential to impact multiple areas of cardiovascular research and therapeutic applications. \u003C\u002Fjats:p>","\u003Cjats:p> Tế bào gốc đa năng cảm ứng từ con người (hiPSCs) có khả năng phân hóa thành các tế bào cơ tim chức năng; tuy nhiên, các đặc tính sinh điện học của tế bào cơ tim có nguồn gốc từ hiPSC vẫn chưa được đặc trưng đầy đủ. Chúng tôi đã thực hiện phân tích chi tiết các đặc tính sinh điện học của tế bào cơ tim hiPSC có độ tinh khiết cao. Các tiềm năng hành động (APs) được ghi lại từ các tế bào cơ tim tự phát đập bằng phương pháp patch perforated và có các đặc tính giống như nhĩ, nốt và thất. AP giống như thất phổ biến hơn và có tiềm năng tâm trương cực đại gần giống với các tế bào cơ tim người, thời gian AP nằm trong phạm vi của khoảng QT điện tâm đồ bình thường ở người, và AP cho thấy độ nhạy mong đợi với nhiều loại thuốc (tetrodotoxin, nifedipine và E4031). Các hiện tượng khử cực sớm (EADs) được kích thích bằng E4031 và phụ thuộc vào nhịp tim chậm, và điện áp đỉnh của EAD thay đổi tỷ lệ nghịch với tiềm năng khôi phục của EAD. Các đặc tính điều khiển của bảy dòng ion đã được nghiên cứu bao gồm natri ( I\u003Cjats:sub>Na\u003C\u002Fjats:sub>), canxi loại L ( I\u003Cjats:sub>Ca\u003C\u002Fjats:sub>), máy phát nhịp được kích hoạt bởi siêu phân cực ( I\u003Cjats:sub>f\u003C\u002Fjats:sub>), kali thoáng qua ra ngoài ( I\u003Cjats:sub>to\u003C\u002Fjats:sub>), kali chỉnh lưu vào trong ( I\u003Cjats:sub>K1\u003C\u002Fjats:sub>), và các thành phần hoạt động nhanh và chậm của dòng kali điều chỉnh muộn ( I\u003Cjats:sub>Kr\u003C\u002Fjats:sub> và I\u003Cjats:sub>Ks\u003C\u002Fjats:sub>, tương ứng). Độ tinh khiết cao và số lượng tế bào lớn cũng cho phép phân tích patch-clamp tự động. Chúng tôi kết luận rằng các tế bào cơ tim có nguồn gốc từ hiPSC này có các dòng ion và các đặc tính điều khiển kênh nền tảng cho APs và EADs của chúng tương tự về mặt định lượng với những gì đã được báo cáo cho tế bào cơ tim người. 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cống, tưới não tại chỗ, vận chuyển mạch máu não, lưu lượng máu não, hàng rào máu-não",{"VOID":3808},"W2126205988",{"EN":3810,"VI":3811},"\u003Cjats:p> The right cerebral hemisphere of the rat was perfused in situ by retrograde infusion of HCO3 saline or blood into the right external carotid artery. Infusion rate was adjusted to minimize the contribution of systemic blood to flow in the hemisphere. During perfusion with whole or artificial blood, regional cerebral blood flow and blood volume were comparable to respective values in the conscious rat, whereas perfusion with HCO3 saline increased regional flow three- to fourfold due to the low viscosity of the saline perfusate. Perfusion with whole blood for 300 S or with HCO3 saline for 60 S did not alter the permeability of the blood-brain barrier. Cerebrovascular permeability coefficients of eight nonelectrolytes ranged from 10(-8) to 10(-4) cm X S-1 and were directly proportional to the octanol-water partition coefficient of the solute. Thus the in situ brain perfusion technique is a sensitive new method to study cerebrovascular transfer in the rat and permits absolute control of perfusate composition. \u003C\u002Fjats:p>","\u003Cjats:p> Bán cầu não bên phải của chuột cống đã được tưới máu tại chỗ thông qua việc bơm ngược dung dịch HCO3 hoặc máu vào động mạch cảnh ngoài bên phải. Tốc độ bơm đã được điều chỉnh để giảm thiểu sự đóng góp của máu toàn thân vào dòng chảy trong bán cầu. Trong quá trình tưới bằng máu toàn phần hoặc máu nhân tạo, lưu lượng máu não khu vực và thể tích máu tương đương với các giá trị tương ứng ở chuột cống có ý thức, trong khi tưới bằng dung dịch HCO3 đã làm tăng lưu lượng khu vực gấp ba đến bốn lần do độ nhớt thấp của dung dịch tưới máu. Việc tưới bằng máu toàn phần trong 300 giây hoặc bằng dung dịch HCO3 trong 60 giây không làm thay đổi tính thấm của hàng rào máu-não. Hệ số thấm mạch máu não của tám chất không điện ly dao động từ 10(-8) đến 10(-4) cm X giây-1 và tỷ lệ thuận trực tiếp với hệ số phân chia octanol-nước của chất tan. Do đó, kỹ thuật tưới máu não tại chỗ là một phương pháp nhạy cảm mới để nghiên cứu quá trình chuyển giao mạch máu não ở chuột cống và cho phép kiểm soát tuyệt đối thành phần dung dịch tưới.",{"EN":3813,"VI":3814},"An in situ brain perfusion technique to study cerebrovascular transport in the rat","Kỹ thuật tưới máu não tại chỗ để nghiên cứu vận chuyển mạch máu não ở chuột cống",{"VOID":3816},"6476141",{"VOID":3818},"10.1152\u002Fajpheart.1984.247.3.h484","2025-01-25T10:50:04.964+00:00",[31],[30],"https:\u002F\u002Fwww.physiology.org\u002Fdoi\u002F10.1152\u002Fajpheart.1984.247.3.H484",[3824,3833,3844],{"id":3825,"sortIndex":32,"researcher":28,"roles":3826,"affiliations":3827,"properties":3828,"displayName":3830,"givenName":28,"familyName":28},"1093b584-63de-4048-90d0-590f15ca4b8d",[],[],{"title":3829,"openalex":3831},{"EN":3830},"Yoshio Takasato",{"VOID":3832},"A5021983041",{"id":3834,"sortIndex":40,"researcher":28,"roles":3835,"affiliations":3836,"properties":3837,"displayName":3841,"givenName":28,"familyName":28},"d72b47e3-33d2-41d1-bfe4-cb865cdfe437",[],[],{"orcid":3838,"title":3840,"openalex":3842},{"VOID":3839},"https:\u002F\u002Forcid.org\u002F0000-0003-4660-2931",{"EN":3841},"С. И. Рапопорт",{"VOID":3843},"A5103333058",{"id":3845,"sortIndex":123,"researcher":28,"roles":3846,"affiliations":3847,"properties":3848,"displayName":3850,"givenName":28,"familyName":28},"57cc3396-2b04-4afe-aa3e-4946f63d2a33",[],[],{"title":3849,"openalex":3851},{"EN":3850},"Quentin R. Smith",{"VOID":3852},"A5110086509",{"url":28,"publisher":3854,"properties":3900},{"id":868,"createTime":869,"updateTime":870,"relativeEntities":3855,"slug":872,"properties":3856,"entityType":25,"verifyStatus":884,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":32,"subjectFields":3861,"manageAffiliations":3874,"indexDatabases":3885,"url":952,"thumbnailPath":28,"statistic":28,"gsStatistic":28,"type":28,"analyzePriority":28},[],{"country":3857,"eissn":3858,"issn":3859,"title":3860},{"VOID":875},{"VOID":877},{"VOID":879},{"EN":881},[3862,3866,3870],{"id":887,"createTime":28,"updateTime":28,"relativeEntities":3863,"label":3864,"description":3865,"parentId":28,"standard":28,"scholarHubFieldId":28},[],{"EN":890},{},{"id":893,"createTime":28,"updateTime":28,"relativeEntities":3867,"label":3868,"description":3869,"parentId":28,"standard":28,"scholarHubFieldId":28},[],{"EN":896},{},{"id":899,"createTime":28,"updateTime":28,"relativeEntities":3871,"label":3872,"description":3873,"parentId":28,"standard":28,"scholarHubFieldId":28},[],{"EN":902},{},[3875,3880],{"id":906,"createTime":28,"updateTime":28,"relativeEntities":3876,"slug":28,"properties":3877,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":3879,"statistic":28},[],{"title":3878},{"EN":910},[],{"id":913,"createTime":28,"updateTime":28,"relativeEntities":3881,"slug":28,"properties":3882,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":3884,"statistic":28},[],{"title":3883},{"EN":917},[],[3886,3893],{"id":921,"indexDatabase":3887,"url":927,"indexYears":928,"academicFieldIds":3892,"indexDatabaseRanking":933},{"id":775,"createTime":28,"updateTime":28,"relativeEntities":3888,"label":3889,"description":3890,"key":781,"publicationTags":3891,"standard":28},[],{"EN":778,"VI":778},{"EN":778,"VI":780},[783],[930,931,932],{"id":935,"indexDatabase":3894,"url":947,"indexYears":28,"academicFieldIds":3899,"indexDatabaseRanking":28},{"id":937,"createTime":28,"updateTime":28,"relativeEntities":3895,"label":3896,"description":3897,"key":944,"publicationTags":3898,"standard":28},[],{"EN":940,"VI":940},{"EN":942,"VI":943},[946,813],[949,950,951],{"issue":3901,"pages":3902,"volume":3904},{"VOID":2308},{"VOID":3903},"H484-H493",{"VOID":3905},"247",541,{"total":3906,"publishYear":3908,"statisticByYear":3909},1984,{"2012":51,"2013":122,"2014":199,"2015":130,"2016":51,"2017":126,"2018":323,"2019":48,"2020":145,"2021":47,"2022":205,"2023":49,"2024":123},"1984-09-01",[946,933],[],{"id":3914,"createTime":3915,"updateTime":3916,"relativeEntities":3917,"slug":3918,"properties":3919,"entityType":980,"verifyStatus":26,"verifyTime":3915,"verifyNote":981,"languages":3935,"translateLanguages":3936,"viewCount":32,"primaryUrl":3937,"fullTextUrl":28,"authors":3938,"publicationType":1030,"publisherRelationship":4087,"citationCount":4141,"citationInfo":4142,"publishDate":4145,"publishYear":4143,"citationAnalyzeStatus":884,"lastCitationAnalyze":28,"indexDatabases":4146,"openAccess":28,"references":4147,"isForceReanalyzing":1191},"65a4d55d-eadd-4cb1-8fa6-6838836f9dee","2024-09-12T16:25:20.351+00:00","2025-02-15T13:11:01.764+00:00",[],"Tricuspid-annular-plane-systolic-excursion-and-pulmonary-arterial-systolic-pressure-relationship-in-heart-failure-an-index-of-right-ventricular-contractile-function-and-prognosis",{"mag":3920,"keywords":3922,"openalex":3923,"abstract":3925,"title":3928,"pm":3931,"doi":3933},{"VOID":3921},"2079265896",{"VI":1361},{"VOID":3924},"W2079265896",{"EN":3926,"VI":3927},"\u003Cjats:p>Echo-derived pulmonary arterial systolic pressure (PASP) and right ventricular (RV) tricuspid annular plane systolic excursion (TAPSE; from the end of diastole to end-systole) are of basic relevance in the clinical follow-up of heart failure (HF) patients, carrying two- to threefold increase in cardiac risk when increased and reduced, respectively. We hypothesized that the relationship between TAPSE (longitudinal RV fiber shortening) and PASP (force generated by the RV) provides an index of in vivo RV length-force relationship, with their ratio better disclosing prognosis. Two hundred ninety-three HF patients with reduced (HFrEF, n = 247) or with preserved left ventricular (LV) ejection fraction (HFpEF, n = 46) underwent echo-Doppler studies and N-terminal pro-brain-type natriuretic peptide assessment and were tracked for adverse events. The median follow-up duration was 20.8 mo. TAPSE vs. PASP relationship showed a downward regression line shift in nonsurvivors who were more frequently presenting with higher PASP and lower TAPSE. HFrEF and HFpEF patients exhibited a similar distribution along the regression line. Given the TAPSE, PASP, and TAPSE-to-PASP ratio (TAPSE\u002FPASP) collinearity, separate Cox regression and Kaplan-Meier analyses were performed: one with TAPSE and PASP as individual measures, and the other combining them in ratio form. Hazard ratios for variables retained in the multivariate regression were as follows: TAPSE\u002FPASP <\u002F≥ 0.36 mm\u002FmmHg [hazard ratio (HR): 10.4, P < 0.001]; TAPSE <\u002F≥ 16 mm (HR: 5.1, P < 0.01); New York Heart Association functional class <\u002F≥ 3 (HR: 4.4, P < 0.001); E\u002Fe’ (HR: 4.1, P < 0.001). This study shows that the TAPSE vs. PASP relationship is shifted downward in nonsurvivors with a similar distribution in HFrEF and HFpEF, and their ratio improves prognostic resolution. The TAPSE vs. PASP relationship as a possible index of the length-force relationship may be a step forward for a more efficient RV function evaluation and is not affected by the quality of LV dysfunction.\u003C\u002Fjats:p>","\u003Cjats:p>Huyết áp tâm thu động mạch phổi (PASP) được xác định bằng siêu âm và độ kéo dài của mặt đệm van ba lá (TAPSE; từ cuối tâm trương đến cuối tâm thu) có ý nghĩa cơ bản trong việc theo dõi lâm sàng bệnh nhân suy tim (HF), khi tăng và giảm lần lượt có thể làm gia tăng nguy cơ tim mạch từ hai đến ba lần. Chúng tôi giả thuyết rằng mối quan hệ giữa TAPSE (sự rút ngắn sợi cơ thất phải theo chiều dọc) và PASP (lực do thất phải tạo ra) cung cấp một chỉ số về mối quan hệ giữa chiều dài và lực của thất phải trong cơ thể, với tỷ lệ của chúng sẽ làm rõ hơn được tiên lượng. Hai trăm chín mươi ba bệnh nhân suy tim với phân suất tống máu thất trái giảm (HFrEF, n = 247) hoặc bảo tồn (HFpEF, n = 46) đã tham gia nghiên cứu siêu âm Doppler và đánh giá peptide natri lợi niệu pro-B-type N-terminal và được theo dõi các sự kiện bất lợi. Thời gian theo dõi trung bình là 20.8 tháng. Mối quan hệ giữa TAPSE và PASP cho thấy một sự dịch chuyển đường hồi quy xuống trong nhóm không sống sót, nhóm này thường có PASP cao hơn và TAPSE thấp hơn. Bệnh nhân HFrEF và HFpEF có phân bố tương tự dọc theo đường hồi quy. Do tính đồng nhất của TAPSE, PASP, và tỷ lệ TAPSE\u002FPASP, các phân tích hồi quy Cox và Kaplan-Meier riêng biệt đã được thực hiện: một phân tích với TAPSE và PASP như các biện pháp riêng lẻ, và một phân tích kết hợp chúng ở dạng tỷ lệ. Tỷ lệ nguy cơ cho các biến số giữ lại trong hồi quy đa biến như sau: TAPSE\u002FPASP <\u002F≥ 0.36 mm\u002FmmHg [tỷ lệ nguy cơ (HR): 10.4, P < 0.001]; TAPSE <\u002F≥ 16 mm (HR: 5.1, P < 0.01); lớp chức năng New York Heart Association <\u002F≥ 3 (HR: 4.4, P < 0.001); E\u002Fe’ (HR: 4.1, P < 0.001). Nghiên cứu này cho thấy mối quan hệ giữa TAPSE và PASP dịch chuyển xuống trong nhóm không sống sót với phân bố tương tự ở HFrEF và HFpEF, và tỷ lệ của chúng cải thiện độ chính xác tiên lượng. Mối quan hệ giữa TAPSE và PASP như một chỉ số có thể về mối quan hệ giữa chiều dài và lực có thể là một bước tiến tới đánh giá chức năng thất phải hiệu quả hơn và không bị ảnh hưởng bởi chất lượng của rối loạn chức năng thất trái.\u003C\u002Fjats:p>",{"EN":3929,"VI":3930},"Tricuspid annular plane systolic excursion and pulmonary arterial systolic pressure relationship in heart failure: an index of right ventricular contractile function and prognosis","Mối quan hệ giữa độ kéo dài của mặt đệm van ba lá và huyết áp tâm thu động mạch phổi ở bệnh suy tim: một chỉ số của chức năng co bóp thất phải và tiên lượng",{"VOID":3932},"23997100",{"VOID":3934},"10.1152\u002Fajpheart.00157.2013",[31],[30],"https:\u002F\u002Fwww.physiology.org\u002Fdoi\u002F10.1152\u002Fajpheart.00157.2013",[3939,3958,3977,3994,4011,4030,4049,4068],{"id":3940,"sortIndex":32,"researcher":28,"roles":3941,"affiliations":3942,"properties":3951,"displayName":3955,"givenName":28,"familyName":28},"e933c887-cad6-437c-af2c-2090a0b9475d",[],[3943],{"id":3944,"sortIndex":32,"affiliation":3945,"properties":28},"ba6ea477-bac6-445d-8e48-2ce7364d3559",{"id":3944,"createTime":28,"updateTime":28,"relativeEntities":3946,"slug":28,"properties":3947,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":3950,"statistic":28},[],{"title":3948},{"EN":3949},"Heart Failure Unit, Department of Cardiology, University of Milano, Istituto Di Ricovero e Cura a Carattere Scientifico (IRCCS) Policlinico San Donato, Milano, Italy;",[],{"orcid":3952,"title":3954,"openalex":3956},{"VOID":3953},"https:\u002F\u002Forcid.org\u002F0000-0002-8456-609X",{"EN":3955},"Marco Guazzi",{"VOID":3957},"A5059384612",{"id":3959,"sortIndex":40,"researcher":28,"roles":3960,"affiliations":3961,"properties":3970,"displayName":3974,"givenName":28,"familyName":28},"9be37312-32af-4a11-a763-d1080aa6a869",[],[3962],{"id":3963,"sortIndex":32,"affiliation":3964,"properties":28},"91f049d4-e15f-492f-93da-15169e068175",{"id":3963,"createTime":28,"updateTime":28,"relativeEntities":3965,"slug":28,"properties":3966,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":3969,"statistic":28},[],{"title":3967},{"EN":3968},"1Heart Failure Unit, Department of Cardiology, University of Milano, Istituto Di Ricovero e Cura a Carattere Scientifico (IRCCS) Policlinico San Donato, Milano, Italy;",[],{"orcid":3971,"title":3973,"openalex":3975},{"VOID":3972},"https:\u002F\u002Forcid.org\u002F0000-0002-5821-7371",{"EN":3974},"Francesco Bandera",{"VOID":3976},"A5025986417",{"id":3978,"sortIndex":123,"researcher":28,"roles":3979,"affiliations":3980,"properties":3987,"displayName":3991,"givenName":28,"familyName":28},"805879cc-c825-4132-a146-96423061e789",[],[3981],{"id":3963,"sortIndex":32,"affiliation":3982,"properties":28},{"id":3963,"createTime":28,"updateTime":28,"relativeEntities":3983,"slug":28,"properties":3984,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":3986,"statistic":28},[],{"title":3985},{"EN":3968},[],{"orcid":3988,"title":3990,"openalex":3992},{"VOID":3989},"https:\u002F\u002Forcid.org\u002F0000-0003-3851-9054",{"EN":3991},"Gabriele 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Castelvecchio",{"VOID":4010},"A5070943884",{"id":4012,"sortIndex":45,"researcher":28,"roles":4013,"affiliations":4014,"properties":4023,"displayName":4027,"givenName":28,"familyName":28},"1dbe69c4-3030-4217-8ab2-08e511b3a1eb",[],[4015],{"id":4016,"sortIndex":32,"affiliation":4017,"properties":28},"9e7fd76b-def7-49de-b02d-a1dc82c3b52e",{"id":4016,"createTime":28,"updateTime":28,"relativeEntities":4018,"slug":28,"properties":4019,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":4022,"statistic":28},[],{"title":4020},{"EN":4021},"2Department of Cardiosurgery, IRCCS Policlinico San Donato, Milano, Italy;",[],{"orcid":4024,"title":4026,"openalex":4028},{"VOID":4025},"https:\u002F\u002Forcid.org\u002F0000-0001-8530-6284",{"EN":4027},"Lorenzo 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