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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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This review deals with the present day state-of-the-art preventative treatments of portal hypertension in cirrhosis according  to disease stage. Two main disease stages are considered, compensated and decompensated cirrhosis, the first having good prognosis and being mostly asymptomatic, and the second being heralded by the appearance of bleeding or non-bleeding complications of portal hypertension. The aim of treatment in compensated cirrhosis is preventing clinical decompensation, the more frequent event being ascites, followed by variceal bleeding and hepatic encephalopathy. Complications are mainly driven by an increase of hepatic vein pressure gradient (HVPG) to values ≥10 mmHg (defining the presence of Clinically Significant Portal Hypertension, CSPH). Before CSPH, the treatment is limited to etiologic treatment of cirrhosis and healthy life style (abstain from alcohol, avoid\u002Fcorrect obesity…). When CSPH is present, association of a non-selective beta-blocker (NSBB), including carvedilol should be considered. NSBBs are mandatory if moderate\u002Flarge varices are present. Patients should also enter a screening program for hepatocellular carcinoma. In decompensated patients, the goal is to prevent further bleeding if the only manifestation of decompensation was a bleeding episode, but to prevent liver transplantation and death in the common scenario where patients have manifested first non-bleeding complications. Treatment is based on the same principles (healthy life style..) associated with administration of NSBBs in combination if possible with endoscopic band ligation if there has been variceal bleeding, and complemented with simvastatin administration (20-40 mg per day in Child–Pugh A\u002FB, 10–20 mg in Child C). Recurrence shall be treated with TIPS. TIPS might be indicated earlier in patients with: 1) Difficult\u002Frefractory ascites, who are not the best candidates for NSBBs, 2) patients having bleed under NSBBs or showing no HVPG response (decrease in HVPG of at least 20% of baseline or to values equal or below 12 mmHg). Decompensated patients shall all be considered as potential candidates for liver transplantation. Treatment of portal hypertension has markedly improved in recent years. The present day therapy is based on accurate risk stratification according to disease stage.",{"EN":990},"The portal hypertension syndrome: etiology, classification, relevance, and animal models",{"VOID":992},"Tsochatzis EA, Bosch J, Burroughs AK. Liver cirrhosis. Lancet 2014;383:1749–1761\nBlachier M, Leleu H, Peck-Radosavljevic M, Valla DC, Roudot-Thoraval F. The burden of liver disease in Europe: a review of available epidemiological data. J Hepatol 2013;58:593–608\nGarcia-Tsao G, Bosch J. 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Mesenteric vasoconstriction triggers nitric oxide overproduction in the superior mesenteric artery of portal hypertensive rats. Gastroenterology 2003;125:1452–1461\nAbraldes JG, Iwakiri Y, Loureiro-Silva M, Haq O, Sessa WC, Groszmann RJ. Mild increases in portal pressure upregulate vascular endothelial growth factor and endothelial nitric oxide synthase in the intestinal microcirculatory bed, leading to a hyperdynamic state. Am J Physiol Gastrointest Liver Physiol 2006;290:G980–G987\nIwakiri Y, Tsai MH, McCabe TJ, Gratton JP, Fulton D, Groszmann RJ, et al. Phosphorylation of eNOS initiates excessive NO production in early phases of portal hypertension. Am J Physiol Heart Circ Physiol 2002;282:H2084–H2090\nIwakiri Y, Cadelina G, Sessa WC, Groszmann RJ. Mice with targeted deletion of eNOS develop hyperdynamic circulation associated with portal hypertension. Am J Physiol Gastrointest Liver Physiol 2002;283:G1074–G1081\nSikuler E, Kravetz D, Groszmann RJ. 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Adenosine reverses a preestablished CCl4-induced micronodular cirrhosis through enhancing collagenolytic activity and stimulating hepatocyte cell proliferation in rats. Hepatology 2001;34:677–687\nConstandinou C, Henderson N, Iredale JP. Modeling liver fibrosis in rodents. Methods Mol Med 2005;117:237–250\nSieber CC, Lopez-Talavera JC, Groszmann RJ. Role of nitric oxide in the in vitro splanchnic vascular hyporeactivity in ascitic cirrhotic rats. Gastroenterology 1993;104:1750–1754\nGraupera M, Garcia-Pagan JC, Titos E, Claria J, Massaguer A, Bosch J, et al. 5-Lipoxygenase inhibition reduces intrahepatic vascular resistance of cirrhotic rat livers: a possible role of cysteinyl-leukotrienes. Gastroenterology 2002;122:387–393\nLoureiro-Silva MR, Cadelina GW, Groszmann RJ. Deficit in nitric oxide production in cirrhotic rat livers is located in the sinusoidal and postsinusoidal areas. Am J Physiol Gastrointest Liver Physiol 2003;284:G567–G574\nVorobioff J, Bredfeldt JE, Groszmann RJ. Increased blood flow through the portal system in cirrhotic rats. Gastroenterology 1984;87:1120–1126\nCastaneda B, Debernardi-Venon W, Bandi JC, Andreu V, Perez-del-Pulgar S, Moitinho E, et al. The role of portal pressure in the severity of bleeding in portal hypertensive rats. Hepatology 2000;31:581–586\nLee SS, Girod C, Braillon A, Hadengue A, Lebrec D. Hemodynamic characterization of chronic bile duct-ligated rats: effect of pentobarbital sodium. Am J Physiol 1986;251:G176–G180\nHeller J, Shiozawa T, Trebicka J, Hennenberg M, Schepke M, Neef M, et al. Acute haemodynamic effects of losartan in anaesthetized cirrhotic rats. Eur J Clin Investig 2003;33:1006–1012\nSikuler E, Buchs AE, Yaari A, Keynan A. Hemodynamic characterization of conscious and ketamine-anesthetized bile duct-ligated rats. Am J Physiol 1991;260:G161–G166\nLi X, Benjamin IS, Alexander B. Reproducible production of thioacetamide-induced macronodular cirrhosis in the rat with no mortality. J Hepatol 2002;36:488–493\nLuo B, Liu L, Tang L, Zhang J, Ling Y, Fallon MB. ET-1 and TNF-alpha in HPS: analysis in prehepatic portal hypertension and biliary and nonbiliary cirrhosis in rats. Am J Physiol Gastrointest Liver Physiol 2004;286:G294–G303\nPopov Y, Patsenker E, Bauer M, Niedobitek E, Schulze-Krebs A, Schuppan D. Halofuginone induces matrix metalloproteinases in rat hepatic stellate cells via activation of p38 and NFκB. J Biol Chem 2006;281:15090–15098\nLaleman W, Vander Elst I, Zeegers M, Servaes R, Libbrecht L, Roskams T, et al. A stable model of cirrhotic portal hypertension in the rat: thioacetamide revisited. Eur J Clin Investig 2006;36:242–249\nSarin SK, Groszmann RJ, Mosca PG, Rojkind M, Stadecker MJ, Bhatnagar R, et al. Propranolol ameliorates the development of portal-systemic shunting in a chronic murine schistosomiasis model of portal hypertension. J Clin Investig 1991;87:1032–1036\nSarin SK, Mosca P, Sabba C, Groszmann RJ. Hyperdynamic circulation in a chronic murine schistosomiasis model of portal hypertension. Hepatology 1991;13:581–584",{"VOID":994},"10.1007\u002Fs12072-017-9827-9","PUBLICATION","2024-12-14T05:53:58.174+00:00","Auto Verify","https:\u002F\u002Flink.springer.com\u002Farticle\u002F10.1007\u002Fs12072-017-9827-9",[1000,1034],{"id":1001,"sortIndex":32,"researcher":28,"roles":1002,"affiliations":1004,"properties":1031,"displayName":1033,"givenName":28,"familyName":28},"d8812507-0460-407a-8bb9-a33cba278bd6",[1003],"AUTHOR",[1005,1013,1022],{"id":1006,"sortIndex":32,"affiliation":1007,"properties":28},"b4b6794b-ccf9-407e-b158-750ee40cd7b8",{"id":1006,"createTime":28,"updateTime":28,"relativeEntities":1008,"slug":28,"properties":1009,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1012,"statistic":28},[],{"title":1010},{"VI":1011},"Hepatic Hemodynamic Laboratory, Liver Unit, Hospital Clínic-IDIBAPS, University of Barcelona, Barcelona, 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University of Bern, Bern, Switzerland",[],{},{"title":1032},{"VI":1033},"Jaime Bosch",{"id":1035,"sortIndex":40,"researcher":28,"roles":1036,"affiliations":1037,"properties":1046,"displayName":1048,"givenName":28,"familyName":28},"1bd39f38-7e1b-4393-81e4-758625f65da3",[1003],[1038],{"id":1039,"sortIndex":32,"affiliation":1040,"properties":28},"48a8db6f-a62f-4627-892c-bbbb6b4fdcc8",{"id":1039,"createTime":28,"updateTime":28,"relativeEntities":1041,"slug":28,"properties":1042,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1045,"statistic":28},[],{"title":1043},{"VI":1044},"Section of Digestive Diseases, Department of Internal Medicine, Yale University School of Medicine, New Haven, USA",[],{"title":1047},{"VI":1048},"Yasuko Iwakiri","ARTICLE",{"url":998,"publisher":1051,"properties":1093},{"id":868,"createTime":869,"updateTime":870,"relativeEntities":1052,"slug":872,"properties":1053,"entityType":25,"verifyStatus":880,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":32,"subjectFields":1057,"manageAffiliations":1062,"indexDatabases":1073,"url":932,"thumbnailPath":28,"statistic":1088,"gsStatistic":28,"type":55,"analyzePriority":28},[],{"issn":1054,"title":1055,"eissn":1056},{"VOID":875},{"EN":877},{"VOID":879},[1058],{"id":883,"createTime":28,"updateTime":28,"relativeEntities":1059,"label":1060,"description":1061,"parentId":28,"standard":28,"scholarHubFieldId":28},[],{"EN":886},{},[1063,1068],{"id":890,"createTime":28,"updateTime":28,"relativeEntities":1064,"slug":28,"properties":1065,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1067,"statistic":28},[],{"title":1066},{"EN":894},[],{"id":897,"createTime":28,"updateTime":28,"relativeEntities":1069,"slug":28,"properties":1070,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1072,"statistic":28},[],{"title":1071},{"EN":901},[903],[1074,1081],{"id":906,"indexDatabase":1075,"url":912,"indexYears":913,"academicFieldIds":1080,"indexDatabaseRanking":788},{"id":775,"createTime":28,"updateTime":28,"relativeEntities":1076,"label":1077,"description":1078,"key":781,"publicationTags":1079,"standard":28},[],{"EN":778,"VI":778},{"EN":778,"VI":780},[783],[915],{"id":917,"indexDatabase":1082,"url":929,"indexYears":28,"academicFieldIds":1087,"indexDatabaseRanking":28},{"id":919,"createTime":28,"updateTime":28,"relativeEntities":1083,"label":1084,"description":1085,"key":926,"publicationTags":1086,"standard":28},[],{"EN":922,"VI":922},{"EN":924,"VI":925},[928,813],[931],{"impactFactor":32,"impactFactorByYear":1089,"i10Index":939,"i10IndexLast5Year":149,"totalPublication":940,"totalPublicationByYear":1090,"totalCitation":943,"totalCitationByYear":1091,"totalCitationPerPublication":959,"totalCitationPerPublicationByYear":1092,"hindexLast5Year":138,"hindex":138},{"2012":462,"2013":40,"2014":821,"2015":121,"2016":168,"2017":709,"2018":173,"2019":935,"2020":936,"2021":937,"2022":191,"2023":938},{"2007":69,"2008":436,"2009":131,"2010":328,"2011":560,"2012":436,"2013":829,"2014":942,"2015":162,"2016":151,"2017":149,"2018":436,"2019":829,"2020":428,"2021":574,"2022":153,"2023":334,"2024":133},{"2007":945,"2008":946,"2009":138,"2010":947,"2011":948,"2012":949,"2013":950,"2014":951,"2015":952,"2016":953,"2017":954,"2018":955,"2019":956,"2020":957,"2021":958,"2022":563,"2023":160,"2024":40},{"2007":961,"2008":962,"2009":963,"2010":964,"2011":965,"2012":966,"2013":628,"2014":967,"2015":190,"2016":968,"2017":969,"2018":970,"2019":971,"2020":972,"2021":973,"2022":974,"2023":975,"2024":421},{"pages":1094,"volume":1096},{"VOID":1095},"1-10",{"VOID":1097},"12","2017-10-24",2017,[783,928],false,{"id":1103,"createTime":1104,"updateTime":1105,"relativeEntities":1106,"slug":1107,"properties":1108,"entityType":995,"verifyStatus":26,"verifyTime":1118,"verifyNote":997,"languages":28,"translateLanguages":1119,"viewCount":32,"primaryUrl":1120,"fullTextUrl":28,"authors":1121,"publicationType":1049,"publisherRelationship":1291,"citationCount":28,"citationInfo":28,"publishDate":1339,"publishYear":1340,"citationAnalyzeStatus":880,"lastCitationAnalyze":28,"indexDatabases":1341,"openAccess":28,"references":28,"isForceReanalyzing":1101},"000a5e1c-bb99-4e63-8425-06ffb5715ee8","2024-01-12T12:05:10.555+00:00","2026-09-07T12:17:31.028+00:00",[],"Serum-ferritin-level-is-associated-with-liver-steatosis-and-fibrosis-in-Korean-general-population",{"abstract":1109,"title":1111,"references":1114,"doi":1116},{"EN":1110},"Elevation of serum ferritin levels is frequently observed in non-alcoholic fatty liver disease (NAFLD) patients. Our study aims to examine the association between serum ferritin levels and NAFLD in Korean population. A total of 25,597 participants were selected from Korean National Health and Nutritional Examination Surveys 2007–2012. The NAFLD liver fat score (NLFS) was used to define NAFLD. Elevation of ALT levels was defined as ALT level > 40 IU\u002FL for male and ALT level > 31 IU\u002FL for female. Multiple logistic regression was used to examine the association of serum ferritin levels and NAFLD by sex. After adjusting for multiple covariates, the ORs (95% CI) of the elevated ALT levels were 1.56 (95% CI: 1.17–2.07), 1.84 (95% CI: 1.39–2.45), and 4.08 (95% CI: 3.08–5.40) for the second, third and fourth serum ferritin quartiles in male (p for trend \u003C 0.01), 1.67 (95% CI: 1.24–2.23), 2.23 (95% CI: 1.68–2.96), and 5.72 (95% CI: 4.32–7.60) for the second, third and fourth serum ferritin quartiles in female (p for trend \u003C 0.01). Serum ferritin levels were also significantly associated with NAFLD and liver fibrosis both in male and female. Elevation of serum ferritin level is significantly associated with NAFLD and blood ALT elevation in Korean general population.",{"EN":1112,"VI":1113},"Serum ferritin level is associated with liver steatosis and fibrosis in Korean general population","Nồng độ ferritin huyết thanh liên quan với tình trạng nhiễm mỡ và xơ hóa gan ở dân số chung Hàn Quốc",{"VOID":1115},"Fan JG, Farrell GC. Epidemiology of non-alcoholic fatty liver disease in China. J Hepatol 2009;50:204–210\nAscha MS, Hanouneh IA, Lopez R, et al. The incidence and risk factors of hepatocellular carcinoma in patients with nonalcoholic steatohepatitis. Hepatology 2010;51:1972–1878\nOng JP, Pitts A, Younossi ZM. Increased overall mortality and liver-related mortality in non-alcoholic fatty liver disease. J Hepatol 2008;49:608–612\nYamada T, Fukatsu M, Suzuki S, et al. Fatty liver predicts impaired fasting glucose and type 2 diabetes mellitus in Japanese undergoing a health checkup. J Gastroenterol Hepatol 2010;25:352–356\nTargher G, Bertolini L, Padovani R, et al. Relations between carotid artery wall thickness and liver histology in subjects with nonalcoholic fatty liver disease. Diabetes Care 2006;29:1325–1330\nTargher G, Bertolini L, Padovani R, et al. Prevalence of nonalcoholic fatty liver disease and its association with cardiovascular disease among type 2 diabetic patients. Diabetes Care 2007;30:1212–1218\nLazo M, Hernaez R, Eberhardt MS, et al. Prevalence of nonalcoholic fatty liver disease in the United States: the Third National Health and Nutrition Examination Survey, 1988–1994. Am J Epidemiol 2013;178:38–45\nPark SH, Jeon WK, Kim SH, et al. Prevalence and risk factors of non-alcoholic fatty liver disease among Korean adults. J Gastroenterol Hepatol 2006;21:138–143\nLoomba R, Sanyal AJ. The global NAFLD epidemic. Nat Rev Gastroenterol Hepatol 2013;10:686–690\nYounossi ZM, Stepanova M, Afendy M, et al. Changes in the prevalence of the most common causes of chronic liver diseases in the United States from 1988 to 2008. Clin Gastroenterol Hepatol 2011;9:524–530\nValenti L, Dongiovanni P, Fracanzani AL, et al. Increased susceptibility to nonalcoholic fatty liver disease in heterozygotes for the mutation responsible for hereditary hemochromatosis. Dig Liver Dis 2003;35:172–178\nNelson JE, Bhattacharya R, Lindor KD, et al. HFE C282Y mutations are associated with advanced hepatic fibrosis in Caucasians with nonalcoholic steatohepatitis. Hepatology 2007;46:723–729\nKim CW, Chang Y, Sung E, et al. Serum ferritin levels predict incident non-alcoholic fatty liver disease in healthy Korean men. Metabolism 2012;61:1182–1188\nKowdley KV, Belt P, Wilson LA, et al. Serum ferritin is an independent predictor of histologic severity and advanced fibrosis in patients with nonalcoholic fatty liver disease. Hepatology 2012;55:77–85\nFracanzani AL, Valenti L, Bugianesi E, et al. Risk of nonalcoholic steatohepatitis and fibrosis in patients with nonalcoholic fatty liver disease and low visceral adiposity. J Hepatol 2011;54:1244–1249\nOh CM, Oh IH, Lee JK, et al. Blood cadmium levels are associated with a decline in lung function in males. Environ Res 2014;132:119–125\nRyu SY, Crespi CM, Maxwell AE. Drinking patterns among Korean adults: results of the 2009 Korean community health survey. J Prev Med Public Health 2013;46:183–191\nHaskell WL, Lee IM, Pate RR, et al. Physical activity and public health: updated recommendation for adults from the American College of Sports Medicine and the American Heart Association. Circulation 2007;116:1081–1093\nFleming RE, Ponka P. Iron overload in human disease. N Engl J Med 2012;366:348–359\nGrundy SM, Cleeman JI, Daniels SR, et al. Diagnosis and management of the metabolic syndrome: an American Heart Association\u002FNational Heart, Lung, and Blood Institute Scientific Statement. Circulation 2005;112:2735–2752\nOh SW. Obesity and metabolic syndrome in Korea. Diabetes Metab J 2011;35:561–566\nKotronen A, Peltonen M, Hakkarainen A, et al. Prediction of non-alcoholic fatty liver disease and liver fat using metabolic and genetic factors. Gastroenterology 2009;137:865–872\nLee JH, Kim D, Kim HJ, et al. Hepatic steatosis index: a simple screening tool reflecting nonalcoholic fatty liver disease. Dig Liver Dis 2010;42:503–508\nSterling RK, Lissen E, Clumeck N, et al. Development of a simple noninvasive index to predict significant fibrosis in patients with HIV\u002FHCV coinfection. Hepatology 2006;43:1317–1325\nEguchi Y, Hyogo H, Ono M, et al. Prevalence and associated metabolic factors of nonalcoholic fatty liver disease in the general population from 2009 to 2010 in Japan: a multicenter large retrospective study. J Gastroenterol 2012;47:586–595\nCleophas TJ, Zwinderman AH. Statistics applied to clinical studies. 5th ed. New York: Springer; 2012. p. 313–318\nPark SK, Ryoo JH, Kim MG, et al. Association of serum ferritin and the development of metabolic syndrome in middle-aged Korean men: a 5-year follow-up study. Diabetes Care 2012;35:2521–2526\nKim CH, Kim HK, Bae SJ, et al. Association of elevated serum ferritin concentration with insulin resistance and impaired glucose metabolism in Korean men and women. Metabolism 2011;60:414–420\nUtzschneider KM, Kahn SE. Review: the role of insulin resistance in nonalcoholic fatty liver disease. J Clin Endocrinol Metab 2006;91:4753–4761\nLing JC, Mohamed MN, Jalaludin MY, et al. Determinants of high fasting insulin and insulin resistance among overweight\u002Fobese adolescents. Sci Rep 2016;6:36270\nO’Malley G, Santoro N, Northrup V, et al. High normal fasting glucose level in obese youth: a marker for insulin resistance and beta cell dysregulation. Diabetologia 2010;53:1199–1209\nAlam F, Memon AS, Fatima SS. Increased body mass index may lead to hyperferritinemia irrespective of body iron stores. Pak J Med Sci 2015;31:1521–1526",{"VOID":1117},"10.1007\u002Fs12072-018-9892-8","2024-12-07T06:46:31.163+00:00",[30],"https:\u002F\u002Flink.springer.com\u002Farticle\u002F10.1007\u002Fs12072-018-9892-8",[1122,1137,1152,1165,1180,1195,1208,1223,1245,1258,1278],{"id":1123,"sortIndex":32,"researcher":28,"roles":1124,"affiliations":1125,"properties":1134,"displayName":1136,"givenName":28,"familyName":28},"ef4f8ecc-12a4-49f9-8331-f1913d4f8b82",[1003],[1126],{"id":1127,"sortIndex":32,"affiliation":1128,"properties":28},"601387ef-8cdd-4b29-b41a-39f64c55cc77",{"id":1127,"createTime":28,"updateTime":28,"relativeEntities":1129,"slug":28,"properties":1130,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1133,"statistic":28},[],{"title":1131},{"VI":1132},"Total Healthcare Center, Kangbuk Samsung Hospital, Sungkyunkwan University School of Medicine, Seoul, Republic of Korea",[],{"title":1135},{"VI":1136},"Ju Young Jung",{"id":1138,"sortIndex":40,"researcher":28,"roles":1139,"affiliations":1140,"properties":1149,"displayName":1151,"givenName":28,"familyName":28},"1e8c7344-eb2c-4828-9c5e-074d354b1342",[1003],[1141],{"id":1142,"sortIndex":32,"affiliation":1143,"properties":28},"cc5e2d3b-f784-4c7f-a25e-3fdec76a4ee6",{"id":1142,"createTime":28,"updateTime":28,"relativeEntities":1144,"slug":28,"properties":1145,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1148,"statistic":28},[],{"title":1146},{"VI":1147},"Departments of Internal Medicine, School of Medicine, Kyung Hee University, Seoul, Republic of Korea",[],{"title":1150},{"VI":1151},"Jae-Jun 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meta-analysis was conducted to evaluate the safety and feasibility of pure laparoscopic left lateral hepatectomy in comparison with open approach for pediatric living donor liver transplantation (LDLT). A systemic literature survey was performed by searching the PubMed, EMBASE and Cochrane Library databases for articles that compared pure laparoscopic left lateral living donor hepatectomy (LLDH) and open left lateral living donor hepatectomy (OLDH) by November 2021. Meta-analysis was performed to assess donors’ and recipients’ perioperative outcomes using RevMan 5.3 software. A total of five studies involving 432 patients were included in the analysis. The results demonstrated that LLDH group had significantly less blood loss (WMD = −99.28 ml, 95%CI −152.68 to −45.88, p = 0.0003) and shorter length of hospital stay (WMD = −2.71d, 95%CI −3.78 to −1.64, p \u003C 0.00001) compared with OLDH group. A reduced donor overall postoperative complication rate was observed in the LLDH group (OR = 0.29, 95%CI 0.13–0.64, p = 0.002). In the subgroup analysis, donor bile leakage, wound infection and pulmonary complications were similar between two groups (bile leakage: OR = 1.31, 95%CI 0.43–4.02, p = 0.63; wound infection: OR = 0.38, 95%CI 0.10–1.41, p = 0.15; pulmonary complications: OR = 0.24, 95%CI 0.04–1.41, p = 0.11). For recipients, there were no significant difference in perioperative outcomes between the LLDH and OLDH group, including mortality, overall complications, hepatic artery thrombosis, portal vein and biliary complications. LLDH is a safe and effective alternative to OLDH for pediatric LDLT, reducing invasiveness and benefiting postoperative recovery. Future large-scale multi-center studies are expected to confirm the advantages of LLDH in pediatric LDLT.",{"EN":1352},"Pure laparoscopic versus open left lateral hepatectomy in pediatric living donor liver transplantation: a review and meta-analysis",{"VOID":1354},"Cuenca AG, Kim HB, Vakili K. Pediatric liver transplantation. Semin Pediatr Surg. 2017;26(4):217–223\nKasahara M, Umeshita K, Sakamoto S, Fukuda A, Furukawa H, Uemoto S. Liver transplantation for biliary atresia: a systematic review. Pediatr Surg Int. 2017;33(12):1289–1295\nPham YH, Miloh T. Liver Transplantation in Children. Clin Liver Dis. 2018;22(4):807–821\nRaia S, Nery JR, Mies S. Liver transplantation from live donors. Lancet. 1989;2(8661):497\nKwon CHD, Choi GS, Kim JM, Cho CW, Rhu J, Soo Kim G, et al. laparoscopic donor hepatectomy for adult living donor liver transplantation recipients. Liver Transpl. 2018;24(11):1545–1553\nHong SK, Suh KS, Kim KA, Lee JM, Cho JH, Yi NJ, et al. Pure laparoscopic versus open left hepatectomy including the middle hepatic vein for living donor liver transplantation. Liver Transpl. 2020;26(3):370–378\nCherqui D, Soubrane O, Husson E, Barshasz E, Vignaux O, Ghimouz M, et al. Laparoscopic living donor hepatectomy for liver transplantation in children. Lancet. 2002;359(9304):392–396\nBriceno J, Ciria R, Lopez P, Luque A, Arjona-Sanchez A, Sanchez-Hidalgo JM, et al. Laparoscopic living donor hepatectomy for pediatric liver transplantation: the first 7 cases in Spain. Transplant Proc. 2019;51(1):56–57\nLi H, Zhu Z, Wei L, Tan Y, Zeng Z, Qu W, et al. Laparoscopic left lateral monosegmentectomy in pediatric living donor liver transplantation using real-time ICG fluorescence in situ reduction. J Gastrointest Surg. 2020;24(9):2185–2186\nSamstein B, Griesemer A, Cherqui D, Mansour T, Pisa J, Yegiants A, et al. Fully laparoscopic left-sided donor hepatectomy is safe and associated with shorter hospital stay and earlier return to work: a comparative study. Liver Transpl. 2015;21(6):768–773\nStang A. Critical evaluation of the Newcastle-Ottawa scale for the assessment of the quality of nonrandomized studies in meta-analyses. Eur J Epidemiol. 2010;25(9):603–605\nHozo SP, Djulbegovic B, Hozo I. Estimating the mean and variance from the median, range, and the size of a sample. BMC Med Res Methodol. 2005;5:13\nSoubrane O, Cherqui D, Scatton O, Stenard F, Bernard D, Branchereau S, et al. Laparoscopic left lateral sectionectomy in living donors: safety and reproducibility of the technique in a single center. Ann Surg. 2006;244(5):815–820\nKim WJ, Kim KH, Cho HD, Namgoong JM, Hwang S, Park JI, et al. Long-term safety and efficacy of pure laparoscopic donor hepatectomy in pediatric living donor liver transplantation. Liver Transpl. 2021;27(4):513–524\nGautier S, Monakhov A, Gallyamov E, Tsirulnikova O, Zagaynov E, Dzhanbekov T, et al. Laparoscopic left lateral section procurement in living liver donors: a single center propensity score-matched study. Clin Transplant. 2018;32(9): e13374\nBroering DC, Elsheikh Y, Shagrani M, Abaalkhail F, Troisi RI. Pure laparoscopic living donor left lateral sectionectomy in pediatric transplantation: a propensity score analysis on 220 consecutive patients. Liver Transpl. 2018;24(8):1019–1030\nVieira V, Pacheco L, Demetrio L, Balbi E, Bellinha T, Toledo R, et al. left hepatic lobectomy in the living donor-comparison between open vs laparoscopic surgery. Transplant Proc. 2019;51(5):1601–1604\nMarubashi S, Nagano H. Laparoscopic living-donor hepatectomy: review of its current status. Ann Gastroenterol Surg. 2021;5(4):484–493\nHong SK, Choi GS, Han J, Cho HD, Kim JM, Han YS, et al. Pure laparoscopic donor hepatectomy: a multicenter experience. Liver Transpl. 2021;27(1):67–76\nCherqui D. Pure laparoscopic living donor liver transplantation: prowess or progress? Am J Transplant. 2022;22(1):5–6\nSuh SW, Lee KW, Lee JM, Choi Y, Yi NJ, Suh KS. Clinical outcomes of and patient satisfaction with different incision methods for donor hepatectomy in living donor liver transplantation. Liver Transpl. 2015;21(1):72–78\nMakki K, Chorasiya VK, Sood G, Srivastava PK, Dargan P, Vij V. Laparoscopy-assisted hepatectomy versus conventional (open) hepatectomy for living donors: when you know better, you do better. Liver Transpl. 2014;20(10):1229–1236\nMarubashi S, Wada H, Kawamoto K, Kobayashi S, Eguchi H, Doki Y, et al. Laparoscopy-assisted hybrid left-side donor hepatectomy. World J Surg. 2013;37(9):2202–2210\nCho JY, Han HS, Kaneko H, Wakabayashi G, Okajima H, Uemoto S, et al. Survey results of the expert meeting on laparoscopic living donor hepatectomy and literature review. Dig Surg. 2018;35(4):289–293\nRhu J, Kim MS, Choi GS, Kim JM, Kwon CHD, Joh JW. laparoscopic living donor right hepatectomy regarding the anatomical variation of the portal vein: a propensity score-matched analysis. Liver Transpl. 2021;27(7):984–996\nIshizawa T, Hasegawa K, Kokudo N. Laparoscopy-assisted hybrid left-side donor hepatectomy: is it truly less invasive for living donors? World J Surg. 2014;38(6):1560–1561\nCheah YL, Simpson MA, Pomposelli JJ, Pomfret EA. Incidence of death and potentially life-threatening near-miss events in living donor hepatic lobectomy: a world-wide survey. Liver Transpl. 2013;19(5):499–506\nZhang W, Xu L, Zhang J, Che X. Safety and feasibility of laparoscopic living donor right hepatectomy for adult liver transplantation: a meta-analysis. HPB. 2021;23(3):344–358\nCherqui D, Ciria R, Kwon CHD, Kim KH, Broering D, Wakabayashi G, et al. Expert consensus guidelines on minimally invasive donor hepatectomy for living donor liver transplantation from innovation to implementation: a joint initiative from the international laparoscopic liver society (ILLS) and the Asian-Pacific hepato-pancreato-biliary association (A-PHPBA). Ann Surg. 2021;273(1):96–108\nWang X, Teh CSC, Ishizawa T, Aoki T, Cavallucci D, Lee SY, et al. Consensus guidelines for the use of fluorescence imaging in hepatobiliary surgery. Ann Surg. 2021;274(1):97–106\nLu L, Wang ZX, Zhu WW, Shen CH, Tao YF, Ma ZY, et al. Left hepatic vein preferential approach based on anatomy is safe and feasible for laparoscopic living donor left lateral sectionectomy. Liver Transpl. 2021;27(1):88–95\nSamstein B, Cherqui D, Rotellar F, Griesemer A, Halazun KJ, Kato T, et al. Totally laparoscopic full left hepatectomy for living donor liver transplantation in adolescents and adults. 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6 phosphate dehydrogenase (G6PD) deficiency (G6PDd) can trigger hemolysis following surgical stress. Differentiating G6PDd-related post-operative hemolytic episodes (PHE) and post-hepatectomy liver failure may be challenging especially in living donors where donor safety is paramount. We analysed outcomes of our cohort of G6PDd liver donors. G6PDd individuals with no evidence of hemolysis were considered as living donors if there was no alternative family donor. Outcomes of G6PDd donors undergoing left lateral\u002Fleft lobe donation (Group LL) and right lobe donation (Group RL) were compared with non-G6PDd donors matched in a 1:3 ratio using propensity score matching. 59 G6PDd donors (5.8% of 1011) underwent living donor hepatectomy (LiDH) during the study period. LL-G6PDd donors (22.37%) had higher post-operative peak bilirubin level compared to matched controls, but no difference in morbidity or need for post-operative blood transfusion.RL-G6PDd donors (37.63%) had higher peak bilirubin level, morbidity (16.2% vs. 3.6%, p = 0.017) and more post-operative blood transfusion (21.6% vs. 6.4%, p = 0.023) as compared to matched non-G6PDd cohort. Four RL-G6PDd donors (10.8%) developed PHE. Low G6PD activity (15% vs. 40%, p = 0.034) and lower future liver remnant (FLR) (34.3% vs. 37.8%, p = 0.05) were identified as risk factors for PHE. We report the largest to-date series of G6PDd individuals undergoing LiDH and confirm the safety of LL donation in G6PDd. Our analysis identifies specific risk factors for PHE and suggests that right lobe LiDH be avoided in individuals with less than 25% G6PD activity when the FLR is less than 36%.",{"EN":1527},"Propensity score matched analysis and risk stratification of donors with G6PD deficiency in living donor liver transplantation",{"VOID":1529},"Rela M, Reddy MS. Living donor liver transplant (LDLT) is the way forward in Asia. Hepatol Int. 2017;11:148–151\nRela M, Rammohan A. Why are there so many liver transplants from living donors in Asia and so few in Europe and the US? J Hepatol. 2021;75:975–980\nLi Z, Rammohan A, Gunasekaran V, Hong S, Chen C-Y, Kim J, et al. Novel benchmark for adult-to-adult living-donor liver transplantation integrating eastern and western experiences. Ann Surg. 2023. https:\u002F\u002Fdoi.org\u002F10.1097\u002FSLA.0000000000006038\nNarasimhan G, Safwan M, Kota V, Reddy MS, Bharathan A, Dabora A, et al. Donor outcomes in living donor liver transplantation-analysis of 275 donors from a single centre in India. Transplantation. 2016;100:1251–1256\nRammohan A, Reddy MS, Narasimhan G, Rajalingam R, Kaliamoorthy I, Krishnan M, et al. Live liver donors: is right still right? World J Surg. 2020;44:2385–2393\nShenkutie TT, Nega D, Hailu A, Kepple D, Witherspoon L, Lo E, et al. Prevalence of G6PD deficiency and distribution of its genetic variants among malaria-suspected patients visiting Metehara health centre. Eastern Ethiopia Malar J. 2022;21:260\nHowes RE, Battle KE, Satyagraha AW, Baird JK, Hay SI. Chapter Four—G6PD deficiency: global distribution, genetic variants and primaquine therapy. In Hay SI, Price R, Baird JKBT-A, editors., Epidemiol plasmodium vivax. Cambridge: Academic Press; 2013. 133–201\nNkhoma ET, Poole C, Vannappagari V, Hall SA, Beutler E. The global prevalence of glucose-6-phosphate dehydrogenase deficiency: a systematic review and meta-analysis. Blood Cells Mol Dis. 2009;42:267–278\nLee HY, Ithnin A, Azma RZ, Othman A, Salvador A, Cheah FC. Glucose-6-phosphate dehydrogenase deficiency and neonatal hyperbilirubinemia: insights on pathophysiology, diagnosis, and gene variants in disease heterogeneity. Front Pediatr. 2022;10: 875877\nLuzzatto L, Nannelli C, Notaro R. Glucose-6-phosphate dehydrogenase deficiency. Hematol Oncol Clin North Am. 2016;30:373–393\nDogar AW, Ullah K, Ghaffar A, Ud-Din S, Hussain A, Ahmed HB, et al. Safety of glucose-6 phosphate dehydrogenase deficient donors in living right lobe liver donation. Clin Transplant. 2022;36:e14627\nReddy MS, Shrivastav M, Kaliamoorthy I, Kota V, Dabora A, Govil S, et al. Safety of live liver donation by individuals with G6PD deficiency: initial results and comparative study. Transplantation. 2016;100:814–818\nElyassi AR, Rowshan HH. Perioperative management of the glucose-6-phosphate dehydrogenase deficient patient: a review of literature. Anesth Prog. 2009;56:86–91\nGoralczyk AD, Moser C, Scherer MN, Tsui TY, Doenecke A, Lorf T, et al. Glucose-6-phosphate dehydrogenase deficiency: a contraindication for living donor liver transplantation? Transpl Int Off J Eur Soc Organ Transplant Switzerland. 2010;23:e65–e66\nRela M, Rammohan A. Living liver donation in adults. Liver Transplant. 2021. https:\u002F\u002Fdoi.org\u002F10.1002\u002F9781119634010.ch24\nZailani MAH, Raja Sabudin RZA, Ithnin A, Alauddin H, Sulaiman SA, Ismail E, et al. Population screening for glucose-6-phosphate dehydrogenase deficiency using quantitative point-of-care tests: a systematic review. Front Genet Switz. 2023;14:1098828\nPfeffer DA, Ley B, Howes RE, Adu P, Alam MS, Bansil P, et al. Quantification of glucose-6-phosphate dehydrogenase activity by spectrophotometry: a systematic review and meta-analysis. PLoS Med. 2020;17: e1003084\nYang JY, Webster-Clark M, Lund JL, Sandler RS, Dellon ES, Stürmer T. Propensity score methods to control for confounding in observational cohort studies: a statistical primer and application to endoscopy research. Gastrointest Endosc. 2019;90:360–369\nWan F. Matched or unmatched analyses with propensity-score-matched data? Stat Med. 2019;38:289–300\nClavien PA, Barkun J, De Oliveira ML, Vauthey JN, Dindo D, Schulick RD, et al. The clavien-dindo classification of surgical complications: five-year experience. Ann Surg. 2009;250:187–196\nBelfield KD, Tichy EM. Review and drug therapy implications of glucose-6-phosphate dehydrogenase deficiency. Am J Heal Pharm AJHP Off J Am Soc Heal Pharm. 2018;75:97–104\nSamanta S, Kumar P, Kishore SS, Garewal G, Narang A. Donor blood glucose 6-phosphate dehydrogenase deficiency reduces the efficacy of exchange transfusion in neonatal hyperbilirubinemia. Pediatrics. 2009;123:e96-100\nRenzaho AMN, Husser E, Polonsky M. Should blood donors be routinely screened for glucose-6-phosphate dehydrogenase deficiency? A systematic review of clinical studies focusing on patients transfused with glucose-6-phosphate dehydrogenase-deficient red cells. Transfus Med Rev. 2014;28:7–17\nGarcia AA, Koperniku A, Ferreira JCB, Mochly-Rosen D. Treatment strategies for glucose-6-phosphate dehydrogenase deficiency: past and future perspectives. Trends Pharmacol Sci. 2021;42:829–844",{"VOID":1531},"10.1007\u002Fs12072-023-10583-0","2025-01-12T14:50:52.147+00:00","https:\u002F\u002Flink.springer.com\u002Farticle\u002F10.1007\u002Fs12072-023-10583-0",[1535,1550,1563,1576,1589,1602,1615,1628,1641,1654],{"id":1536,"sortIndex":32,"researcher":28,"roles":1537,"affiliations":1538,"properties":1547,"displayName":1549,"givenName":28,"familyName":28},"a11ea614-81e7-4547-a0a8-59227ca12a3a",[1003],[1539],{"id":1540,"sortIndex":32,"affiliation":1541,"properties":28},"a7939ad9-354d-4c31-86ba-326f73ddcb7b",{"id":1540,"createTime":28,"updateTime":28,"relativeEntities":1542,"slug":28,"properties":1543,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1546,"statistic":28},[],{"title":1544},{"VI":1545},"Institute of Liver Disease and Transplantation, Dr. Rela Institute and Medical Centre, Chennai, Bharath Institute of Higher Education and Research, Chennai, India",[],{"title":1548},{"VI":1549},"P. 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PD-Ls over-expression is associated with poor prognosis in hepatocellular carcinoma (HCC). However, little is known about how PD-Ls expression is regulated. Here, we investigated the involvement of lncRNA-microRNA network in the regulation of PD-Ls in HCC. The expression of PD-Ls, PCED1B-AS1 and hsa-miR-194-5p was measured in 45 pairs of HCC samples. The interaction between PCED1B-AS1 and hsa-miR-194-5p was measured by microRNA pull down and in vitro binding assay. The effects of PCED1B-AS1 knockdown and over-expression on hsa-miR-194-5p and PD-Ls expression were investigated in HCC cell lines. Immunosuppression was evaluated in co-culture of HCC cell line and human T cells. Exosomes were isolated from HCC cells and their effects on receipt cells were investigated. Tumor behaviors were evaluated by in vitro and in vivo assays. PD-L1 expression was highly correlated with PD-L2 expression in HCC. PCED1B-AS1 and hsa-miR-194-5p expression was up-regulated in HCC. PCED1B-AS1 was positively correlated with PD-Ls but negatively correlated hsa-miR-194-5p in HCC. These correlations were cross-validated by TCGA-LIHC dataset. PCED1B-AS1 interacted with hsa-mir-194-5p which inhibited PD-Ls expression. PCED1B-AS1 enhanced the expression of PD-Ls via sponging hsa-mir-194-5p. PCED1B-AS1-induced PD-Ls-mediated immunosuppression in co-cultured T cells. HCC cells released PCED1B-AS1 containing exosomes and the exosomal PCED1B-AS1 enhanced PD-Ls expression in receipt HCC cells while inhibited receipt T cells and macrophages. Blood exosomal PCED1B-AS1 was correlated with HCC PD-Ls expression. Finally, PCED1B-AS1 promoted cell proliferation, colony formation and in vivo tumor formation in xenografted nude mice while inhibited apoptosis. PCED1B-AS1 enhances the expression and function of PD-Ls via sponging hsa-miR-194-5p to induce immunosuppression in HCC. \n                  \n                    \n                      \n                    \n                  \n                ",{"EN":1725},"Dual targeting of PD-L1 and PD-L2 by PCED1B-AS1 via sponging hsa-miR-194-5p induces immunosuppression in hepatocellular carcinoma",{"VOID":1727},"Villanueva A. Hepatocellular carcinoma. N Engl J Med 2019;380(15):1450–1462\nAlves RC, Alves D, Guz B, Matos C, Viana M, Harriz M, et al. Advanced hepatocellular carcinoma. Review of targeted molecular drugs. Ann Hepatol 2011;10(1):21–27\nRibas A, Wolchok JD. Cancer immunotherapy using checkpoint blockade. Science 2018;359(6382):1350\nFreeman GJ, Long AJ, Iwai Y, Bourque K, Chernova T, Nishimura H, et al. Engagement of the PD-1 immunoinhibitory receptor by a novel B7 family member leads to negative regulation of lymphocyte activation. J Exp Med 2000;192(7):1027–1034\nLarsen TV, Hussmann D, Niesen AL. PD-L1 and PD-L2 expression correlated genes in non-small-cell lung cancer. Cancer Commun 2019;3:39\nYearley JH, Gibson C, Yu N, Moon C, Murphy E, Juco J, et al. PD-L2 expression in human tumors: relevance to anti-PD-1 therapy in cancer. Clin Cancer Res 2017;23(12):3158–3167\nGao Q, Wang XY, Qiu SJ, Yamato I, Sho M, Nakajima Y, et al. Overexpression of PD-L1 significantly associates with tumor aggressiveness and postoperative recurrence in human hepatocellular carcinoma. Clin Cancer Res 2009;15(3):971–979\nJung HI, Jeong D, Ji S, Ahn TS, Bae SH, Chin S, et al. Overexpression of PD-L1 and PD-L2 Is associated with poor prognosis in patients with hepatocellular carcinoma. Cancer Res Treat 2017;49(1):246–254\nYang HY, Zhou XX, Sun LJ, Mao YL. Correlation between PD-L2 expression and clinical outcome in solid cancer patients: a meta-analysis. Front Oncol 2019;13:9\nQuinn JJ, Chang HY. Unique features of long non-coding RNA biogenesis and function. Nat Rev Genet 2016;17(1):47–62\nCesana M, Cacchiarelli D, Legnini I, Santini T, Sthandier O, Chinappi M, et al. A long noncoding RNA controls muscle differentiation by functioning as a competing endogenous RNA. Cell 2011;147(2):358–369\nZhou X, Gao Q, Wang J, Zhang X, Liu K, Duan Z. Linc-RNA-RoR acts as a “sponge” against mediation of the differentiation of endometrial cancer stem cells by microRNA-145. Gynecol Oncol 2014;133(2):333–339\nWu XS, Wang F, Li HF, Hu YP, Jiang L, Zhang F, et al. LncRNA-PAGBC acts as a microRNA sponge and promotes gallbladder tumorigenesis. EMBO Rep 2017;18(10):1837–1853\nXu S, Wang Q, Kang Y, Liu J, Yin Y, Liu L, et al. Long noncoding RNAs control the modulation of immune checkpoint molecules in cancer. Cancer Immunol Res 2020;8:937–951\nDing J, Li X, Hu H. TarPmiR: a new approach for microRNA target site prediction. Bioinformatics 2016;32(18):2768–2775\nKruger J, Rehmsmeier M. RNAhybrid: microRNA target prediction easy, fast and flexible. Nucleic Acids Res 2006;34(Web server issue):W451–W454\nPaliard X, de Waal MR, Yssel H, Blanchard D, Chretien I, Abrams J, et al. Simultaneous production of IL-2, IL-4, and IFN-gamma by activated human CD4+ and CD8+ T cell clones. J Immunol 1988;141(3):849–855\nBoyman O, Sprent J. The role of interleukin-2 during homeostasis and activation of the immune system. Nat Rev Immunol 2012;12(3):180–190\nYang JH, Yu D, Liu XSBJ, Changyong E, Yu S. LncRNA PCED1B-AS1 activates the proliferation and restricts the apoptosis of glioma through cooperating with miR-194-5p\u002FPCED1B axis. J Cell Biochem 2020;121:1823–1833\nHou JW, Zhao RC, Xia WY, Chang CW, You Y, Hsu JM, et al. PD-L1-mediated gasdermin C expression switches apoptosis to pyroptosis in cancer cells and facilitates tumour necrosis. Nat Cell Biol 2020;22:1264–1275\nAzuma T, Yao S, Zhu G, Flies AS, Flies SJ, Chen L. B7-H1 is a ubiquitous antiapoptotic receptor on cancer cells. Blood 2008;111(7):3635–3643\nClark CA, Gupta HB, Sareddy G, Pandeswara S, Lao S, Yuan B, et al. Tumor-intrinsic PD-L1 signals regulate cell growth, pathogenesis, and autophagy in ovarian cancer and melanoma. Cancer Res 2016;76(23):6964–6974\nYao Z, Zhang Q, Guo F, Guo S, Yang B, Liu B, et al. Long noncoding RNA PCED1B-AS1 promotes the Warburg effect and tumorigenesis by upregulating HIF-1alpha in glioblastoma. Cell Transplant 2020;29:963689720906777\nYau T, Park JW, Finn RS, Cheng AL, Mathurin P, Edeline J, et al. CheckMate 459: a randomized, multi-center phase III study of nivolumab (NIVO) vs sorafenib (SOR) as first-line (1L) treatment in patients (pts) with advanced hepatocellular carcinoma (aHCC). Ann Oncol 2019;30:874\nKudo M. Immuno-oncology therapy for hepatocellular carcinoma: current status and ongoing trials. Liver Cancer 2019;8(4):221–238\nDorand RD, Nthale J, Myers JT, Barkauskas DS, Avril S, Chirieleison SM, et al. Cdk5 disruption attenuates tumor PD-L1 expression and promotes antitumor immunity. Science 2016;353(6297):399–403\nCasey SC, Tong L, Li YL, Do R, Walz S, Fitzgerald KN, et al. MYC regulates the antitumor immune response through CD47 and PD-L1. Science 2016;352(6282):227–231\nMezzadra R, Sun C, Jae LT, Gomez-Eerland R, de Vries E, Wu W, et al. Identification of CMTM6 and CMTM4 as PD-L1 protein regulators. Nature 2017;549(7670):106\nKataoka K, Shiraishi Y, Takeda Y, Sakata S, Matsumoto M, Nagano S, et al. Aberrant PD-L1 expression through 3′-UTR disruption in multiple cancers. Nature 2016;534(7607):402\nLi M, Cui J, Niu W, Huang J, Feng T, Sun B, et al. Long non-coding PCED1B-AS1 regulates macrophage apoptosis and autophagy by sponging miR-155 in active tuberculosis. Biochem Biophys Res Commun 2019;509(3):803–839\nZhou H, Su J, Hu X, Zhou C, Li H, Chen Z, et al. Glia-to-neuron conversion by CRISPR–CasRx alleviates symptoms of neurological disease in mice. Cell 2020;181(3):590 e16–603 e16\nHerbst RS, Soria JC, Kowanetz M, Fine GD, Hamid O, Gordon MS, et al. Predictive correlates of response to the anti-PD-L1 antibody MPDL3280A in cancer patients. Nature 2014;515(7528):563\nHewson C, Morris KV. Form and function of exosome-associated long non-coding RNAs in cancer. Curr Top Microbiol 2016;394:41–56",{"VOID":1729},"10.1007\u002Fs12072-020-10101-6","2025-01-27T10:37:39.429+00:00","https:\u002F\u002Flink.springer.com\u002Farticle\u002F10.1007\u002Fs12072-020-10101-6",[1733,1748,1761,1774,1787,1802],{"id":1734,"sortIndex":32,"researcher":28,"roles":1735,"affiliations":1736,"properties":1745,"displayName":1747,"givenName":28,"familyName":28},"95b527e8-1879-43c6-bb65-ddf6fcaad7e8",[1003],[1737],{"id":1738,"sortIndex":32,"affiliation":1739,"properties":28},"99a1a36e-b292-430d-bff4-9d93f3b606e5",{"id":1738,"createTime":28,"updateTime":28,"relativeEntities":1740,"slug":28,"properties":1741,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1744,"statistic":28},[],{"title":1742},{"VI":1743},"Department of The Third Ward of Special Treatment, Shanghai Eastern Hepatobiliary Surgery Hospital, Shanghai, China",[],{"title":1746},{"VI":1747},"Fei Fan",{"id":1749,"sortIndex":40,"researcher":28,"roles":1750,"affiliations":1751,"properties":1758,"displayName":1760,"givenName":28,"familyName":28},"7153eddb-8a2e-46df-9d6d-b430d5204821",[1003],[1752],{"id":1738,"sortIndex":32,"affiliation":1753,"properties":28},{"id":1738,"createTime":28,"updateTime":28,"relativeEntities":1754,"slug":28,"properties":1755,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1757,"statistic":28},[],{"title":1756},{"VI":1743},[],{"title":1759},{"VI":1760},"Keji 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Li",{"id":1788,"sortIndex":45,"researcher":28,"roles":1789,"affiliations":1790,"properties":1799,"displayName":1801,"givenName":28,"familyName":28},"d23e4dcd-f4df-4d97-8c7b-37cf1204c5f4",[1003],[1791],{"id":1792,"sortIndex":32,"affiliation":1793,"properties":28},"4ea816f1-2b47-4b8e-bf39-754731f64a93",{"id":1792,"createTime":28,"updateTime":28,"relativeEntities":1794,"slug":28,"properties":1795,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1798,"statistic":28},[],{"title":1796},{"VI":1797},"Department of Hepatic Surgery I, Shanghai Eastern Hepatobiliary Surgery Hospital, Shanghai, China",[],{"title":1800},{"VI":1801},"Caifeng Liu",{"id":1803,"sortIndex":46,"researcher":28,"roles":1804,"affiliations":1805,"properties":1812,"displayName":1814,"givenName":28,"familyName":28},"5d1db426-80d9-4c0e-85cc-926d35b0e975",[1003],[1806],{"id":1738,"sortIndex":32,"affiliation":1807,"properties":28},{"id":1738,"createTime":28,"updateTime":28,"relativeEntities":1808,"slug":28,"properties":1809,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1811,"statistic":28},[],{"title":1810},{"VI":1743},[],{"title":1813},{"VI":1814},"Bin 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kidney injury (AKI) is one of the most severe complications of cirrhosis and is associated with significant morbidity and mortality. Liver fibrosis and liver insufficiency, portal hypertension, systemic vasodilation, and a subsequent hyperdynamic circulation undermine the renal and cardiac function, making cirrhotic patients more susceptible to hemodynamic incidents. In addition, the immune system is impaired in cirrhosis, leading to an exaggerated production of vasoactive mediators, and the adrenal cortisol response is insufficient, which causes further impairment of the vascular tonus, cardiac output, and renal perfusion. Consequently, the cardiovascular and renal dysfunction is aggravated, resulting in a hepatorenal syndrome (HRS). HRS is seen exclusively in patients with liver disease and has been considered an entirely functional prerenal dysfunction, rather than a structural dysfunction, but is not responsive to volume expansion. Recent research indicates that development of hepatic nephropathy represents a continuous spectrum of functional and structural dysfunction and may be precipitated by the inherent immunologic, adrenal, and hemodynamic incompetence in cirrhosis. New research explores several new markers of renal dysfunction that may replace serum creatinine in the future and give new insight on the hepatic nephropathy. Our understanding of the pathophysiological mechanisms causing the immunologic, adrenal, and hemodynamic incompetence, and the impact on renal dysfunction, has improved in recent years, and in this review we aim to highlight recent achievements in this field.",{"EN":1876},"Immunologic, hemodynamic, and adrenal incompetence in cirrhosis: impact on renal dysfunction",{"VOID":1878},"Moller S, Henriksen JH, Bendtsen F. Pathogenetic background for treatment of ascites and hepatorenal syndrome. Hepatol Int. 2008;2(4):416–428\nBelcher JM, Garcia-Tsao G, Sanyal AJ, Bhogal H, Lim JK, Ansari N, et al. Association of AKI with mortality and complications in hospitalized patients with cirrhosis. Hepatology. 2013;57(2):753–762\nAngeli P, Sanyal A, Moller S, Alessandria C, Gadano A, Kim R, et al. Current limits and future challenges in the management of renal dysfunction in patients with cirrhosis: report from the International Club of Ascites. Liver Int. 2013;33(1):16–23\nCardenas A, Gines P. Acute-on-chronic liver failure: the kidneys. Curr Opin Crit Care. 2011;17(2):184–189\nBelcher JM, Parikh CR, Garcia-Tsao G. Acute kidney injury in patients with cirrhosis: perils and promise. Clin Gastroenterol Hepatol. 2013;11(12):1550–1558\nKrag A, Bendtsen F, Burroughs AK, Moller S. The cardiorenal link in advanced cirrhosis. Med Hypotheses. 2012;79(1):53–55\nKakazu E, Kondo Y, Shimosegawa T. The relationship between renal dysfunction and abnormalities of the immune system in patients with decompensated cirrhosis. ISRN Gastroenterol. 2012;2012:123826\nTandon P, Garcia-Tsao G. Bacterial infections, sepsis, and multiorgan failure in cirrhosis. Semin Liver Dis. 2008;28(1):26–42\nKim MY, Baik SK, Lee SS. Hemodynamic alterations in cirrhosis and portal hypertension. Korean J Hepatol. 2010;16(4):347–352\nLiu H, Schuelert N, McDougall JJ, Lee SS. Central neural activation of hyperdynamic circulation in portal hypertensive rats depends on vagal afferent nerves. Gut. 2008;57(7):966–973\nWiese S, Hove JD, Bendtsen F, Moller S. Cirrhotic cardiomyopathy: pathogenesis and clinical relevance. Nat Rev Gastroenterol Hepatol. 2014;11(3):177–186\nIwakiri Y, Groszmann RJ. The hyperdynamic circulation of chronic liver diseases: from the patient to the molecule. Hepatology. 2006;43(2 Suppl 1):S121–S131\nArroyo V, Colmenero J. Ascites and hepatorenal syndrome in cirrhosis: pathophysiological basis of therapy and current management. J Hepatol. 2003;38(Suppl 1):S69–S89\nLaffi G, La VG, Pinzani M, Marra F, Gentilini P. Arachidonic acid derivatives and renal function in liver cirrhosis. Semin Nephrol. 1997;17(6):530–548\nSchrier RW, Arroyo V, Bernardi M, Epstein M, Henriksen JH, Rodes J. Peripheral arterial vasodilation hypothesis: a proposal for the initiation of renal sodium and water retention in cirrhosis. Hepatology. 1988;8(5):1151–1157\nMoller S, Bernardi M. Interactions of the heart and the liver. Eur Heart J. 2013;34(36):2804–2811\nArroyo V, Gines P, Gerbes AL, Dudley FJ, Gentilini P, Laffi G, et al. Definition and diagnostic criteria of refractory ascites and hepatorenal syndrome in cirrhosis. International Ascites Club. Hepatology. 1996;23(1):164–176\nSalerno F, Gerbes A, Gines P, Wong F, Arroyo V. Diagnosis, prevention and treatment of hepatorenal syndrome in cirrhosis. 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Am J Kidney Dis. 2004;43(3):405–414\nBelcher JM, Sanyal AJ, Peixoto AJ, Perazella MA, Lim J, Thiessen-Philbrook H, et al. Kidney biomarkers and differential diagnosis of patients with cirrhosis and acute kidney injury. Hepatology. 2014;60(2):622–632\nHan WK, Bailly V, Abichandani R, Thadhani R, Bonventre JV. Kidney Injury Molecule-1 (KIM-1): a novel biomarker for human renal proximal tubule injury. Kidney Int. 2002;62(1):237–244\nNickolas TL, O’Rourke MJ, Yang J, Sise ME, Canetta PA, Barasch N, et al. Sensitivity and specificity of a single emergency department measurement of urinary neutrophil gelatinase-associated lipocalin for diagnosing acute kidney injury. Ann Intern Med. 2008;148(11):810–819\nVerna EC, Brown RS, Farrand E, Pichardo EM, Forster CS, Sola-Del Valle DA, et al. Urinary neutrophil gelatinase-associated lipocalin predicts mortality and identifies acute kidney injury in cirrhosis. Dig Dis Sci. 2012; 57(9):2362–2370\nGerbes AL, Benesic A, Vogeser M, Krag A, Bendtsen F, Moller S. Serum neutrophil gelatinase-associated lipocalin—a sensitive novel marker of renal impairment in liver cirrhosis? Digestion. 2011;84(1):82–83\nGungor G, Ataseven H, Demir A, Solak Y, Gaipov A, Biyik M, et al. Neutrophil gelatinase-associated lipocalin in prediction of mortality in patients with hepatorenal syndrome: a prospective observational study. Liver Int. 2014;34(1):49–57\nSinger E, Marko L, Paragas N, Barasch J, Dragun D, Muller DN, et al. Neutrophil gelatinase-associated lipocalin: pathophysiology and clinical applications. Acta Physiol (Oxf). 2013;207(4):663–672\nBarreto R, Elia C, Sola E, Moreira R, Ariza X, Rodriguez E, et al. Urinary neutrophil gelatinase-associated lipocalin predicts kidney outcome and death in patients with cirrhosis and bacterial infections. J Hepatol. 2014;61(1):35–42\nFagundes C, Pepin MN, Guevara M, Barreto R, Casals G, Sola E, et al. 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Small intestinal motility disturbances and bacterial overgrowth in patients with liver cirrhosis and portal hypertension. Am J Gastroenterol. 2003;98(6):1362–1370\nRiordan SM, Williams R. The intestinal flora and bacterial infection in cirrhosis. J Hepatol. 2006;45(5):744–757\nSuch J, Guardiola JV, de JJ, Casellas JA, Pascual S, Aparicio JR, et al. Ultrastructural characteristics of distal duodenum mucosa in patients with cirrhosis. Eur J Gastroenterol Hepatol. 2002; 14(4):371–376\nMisra V, Misra SP, Dwivedi M, Gupta SC. Histomorphometric study of portal hypertensive enteropathy. Am J Clin Pathol. 1997;108(6):652–657\nTilg H, Wilmer A, Vogel W, Herold M, Nolchen B, Judmaier G, et al. Serum levels of cytokines in chronic liver diseases. Gastroenterology. 1992;103(1):264–274\nWiest R, Garcia-Tsao G. Bacterial translocation (BT) in cirrhosis. Hepatology. 2005;41(3):422–433\nAlbillos A, Hera Ad AL, Reyes E, Monserrat J, Munoz L, Nieto M, et al. Tumour necrosis factor-alpha expression by activated monocytes and altered T-cell homeostasis in ascitic alcoholic cirrhosis: amelioration with norfloxacin. J Hepatol. 2004; 40(4):624–631\nHenriksen JH, Moller S, Ring-Larsen H, Christensen NJ. The sympathetic nervous system in liver disease. J Hepatol. 1998;29(2):328–341\nAcevedo J, Fernandez J, Prado V, Silva A, Castro M, Pavesi M, et al. Relative adrenal insufficiency in decompensated cirrhosis: relationship to short-term risk of severe sepsis, hepatorenal syndrome, and death. Hepatology. 2013;58(5):1757–1765\nWong F, Bernardi M, Balk R, Christman B, Moreau R, Garcia-Tsao G, et al. Sepsis in cirrhosis: report on the 7th meeting of the International Ascites Club. Gut. 2005;54(5):718–725\nMoreau R, Hadengue A, Soupison T, Kirstetter P, Mamzer MF, Vanjak D, et al. Septic shock in patients with cirrhosis: hemodynamic and metabolic characteristics and intensive care unit outcome. Crit Care Med. 1992;20(6):746–750\nTrifan A, Chiriac S, Stanciu C. Update on adrenal insufficiency in patients with liver cirrhosis. World J Gastroenterol. 2013;19(4):445–456\nTsai MH, Peng YS, Chen YC, Liu NJ, Ho YP, Fang JT, et al. Adrenal insufficiency in patients with cirrhosis, severe sepsis and septic shock. Hepatology. 2006;43(4):673–681\nFede G, Spadaro L, Tomaselli T, Privitera G, Germani G, Tsochatzis E, et al. Adrenocortical dysfunction in liver disease: a systematic review. Hepatology. 2012;55(4):1282–1291\nBornstein SR. Predisposing factors for adrenal insufficiency. N Engl J Med. 2009;360(22):2328–2339\nGaillard RC, Turnill D, Sappino P, Muller AF. Tumor necrosis factor alpha inhibits the hormonal response of the pituitary gland to hypothalamic releasing factors. Endocrinology. 1990;127(1):101–106\nTheocharidou E, Krag A, Bendtsen F, Moller S, Burroughs AK. Cardiac dysfunction in cirrhosis—does adrenal function play a role? A hypothesis. Liver Int. 2012;32(9):1327–1332\nWong F, Nadim M, Kellum J, Working Party proposal for a revised classification system of renal dysfunction in patients with cirrhosis. 2011;60(5):702–709. doi:10.1136\u002Fgut.2010.236133",{"VOID":1880},"10.1007\u002Fs12072-014-9581-1","http:\u002F\u002Flink.springer.com\u002F10.1007\u002Fs12072-014-9581-1",[1883,1907,1929],{"id":1884,"sortIndex":32,"researcher":28,"roles":1885,"affiliations":1886,"properties":1904,"displayName":1906,"givenName":28,"familyName":28},"4083c85c-9828-4724-a797-fd09ece93c26",[1003],[1887,1895],{"id":1888,"sortIndex":32,"affiliation":1889,"properties":28},"2ca5c8f2-5783-4010-b76e-78d8074bab1c",{"id":1888,"createTime":28,"updateTime":28,"relativeEntities":1890,"slug":28,"properties":1891,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1894,"statistic":28},[],{"title":1892},{"VI":1893},"Department of Clinical Physiology and Nuclear 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objectives of the study were to evaluate the prognostic value of APASL ACLF Research Consortium—Acute-on-chronic liver failure (AARC-ACLF) score against the current prognostic models in pediatric ACLF and to assess the role of pediatric modifications of AARC-ACLF score and chronic liver failure–sequential organ failure assessment (CLIF–SOFA) score. All children between 1 and 18 years of age satisfying the APASL definition of ACLF were included in the study. All the prognostic scores were calculated retrospectively from hospital records. Outcome was assessed at days 28 and 90. Pediatric modifications of AARC-ACLF and CLIF–SOFA scores were evaluated. Acute-on-chronic liver failure was seen in 86 (13.4%) of 640 children with chronic liver disease. Twenty-five (29.8%) children died, 7 (8.3%) underwent liver transplant and the remaining 52 (61.9%) survived with their native liver. Four prognostic models (AARC-ACLF, AARC-ACLF-Pediatric, CLIF–SOFA and CLIF–SOFA-Pediatric) had an AUROC greater than 0.9 for predicting poor outcome in pediatric ACLF. AARC-ACLF and CLIF–SOFA models were superior to other prognostic scores with a cutoff score of 11 or more predicting poor outcome. Pediatric modifications of AARC-ACLF and CLIF–SOFA scores were not superior to their original scores. Children with poor outcome had rising scores at day 4, whereas the scores were falling in those with good outcome. AARC-ACLF and CLIF–SOFA models are superior to other prognostic scores in pediatric ACLF. The scores are dynamic and a patient with either of these scores ≥ 11 at admission and\u002For a rising score at day 4 has high likelihood of death and needs to be urgently listed for liver transplantation.",{"EN":2003},"How to identify the need for liver transplantation in pediatric acute-on-chronic liver failure?",{"VOID":2005},"Lal BB, Alam S, Sood V, et al. Profile, risk factors and outcome of acute kidney injury in paediatric acute-on-chronic liver failure. Liver Int 2018;38(10):1777–1784\nAlam S, Lal BB, Sood V, et al. Pediatric acute-on-chronic liver failure in a specialized liver unit: prevalence, profile, outcome, and predictive factors. J Pediatr Gastroenterol Nutr 2016;63:400–405\nLal J, Thapa BR, Rawal P, et al. Predictors of outcome in acute-on-chronic liver failure in children. Hepatol Int 2011;5:693–697\nWlodzimirow KA, Eslami S, Abu-Hanna A, et al. A systematic review on prognostic indicators of acute on chronic liver failure and their predictive value for mortality. Liver Int 2013;33(1):40–52\nGarg H, Kumar A, Garg V, et al. Clinical profile and predictors of mortality in patients of acute-on-chronic liver failure. Dig Liver Dis 2012;44(2):166–171\nSun QF, Ding JG, Xu DZ, et al. Prediction of the prognosis of patients with acute-on-chronic hepatitis B liver failure using the model for end-stage liver disease scoring system and a novel logistic regression model. J Viral Hepat 2009;16(7):464–470\nMoreau R, Jalan R, Gines P, et al. Acute-on-chronic liver failure is a distinct syndrome that develops in patients with acute decompensation of cirrhosis. Gastroenterology 2013;144:1426–1437\nShalimar, Kumar D, Vadiraja PK, et al. 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Diagnosis, evaluation, and management of acute kidney injury: a KDIGO summary (Part 1). Crit Care 2013;17:204\nChoudhury A, Kumar M, Sharma BC, et al. Systemic inflammatory response syndrome in acute-on-chronic liver failure: Relevance of ‘golden window’: a prospective study. J Gastroenterol Hepatol 2017;32(12):1989–1997\nDellinger RP, Levy MM, Rhodes A, et al. Surviving Sepsis Campaign: international guidelines for management of severe sepsis and septic shock, 2012. Intensive Care Med 2013;39:165–228\nGoldstein B, Giroir B, Randolph A; International Consensus Conference on Pediatric Sepsis. International pediatric sepsis consensus conference: definitions for sepsis and organ dysfunction in pediatrics. Pediatr Crit Care Med 2005;6(1):2–8\nDeLong ER, DeLong DM, Clarke-Pearson DL. Comparing the areas under two or more correlated receiver operating characteristic curves: a nonparametric approach. Biometrics 1988;44:837–845\nJagadisan B, Srivastava A, Yachha SK, et al. Acute-on-chronic liver disease in children from the developing world: recognition and prognosis. J Pediatr Gastroenterol Nutr 2012;54:77–82\nAngeli P, Gines P, Wong F, et al. Diagnosis and management of acute kidney injury in patients with cirrhosis: revised consensus recommendations of the International Club of Ascites. 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HBeAg-negative patients received peginterferon alfa-2a (180 μg\u002Fweek) ± lamivudine (100 mg\u002Fday) for 48 weeks as part of a multicenter, randomized study. The planned 5-year efficacy analysis included patients (n = 230) enrolled in the long-term follow-up study. On-treatment hepatitis B surface antigen (HBsAg) decline kinetics were analyzed retrospectively in a subgroup of patients with HBsAg data available at baseline, weeks 12, 24, and 48 on-treatment, and 6 months post-treatment (n = 120). Receiver operating characteristic analyses identified the on-treatment HBsAg levels associated with response at 1 and 5 years post-treatment. HBV DNA ≤2,000 IU\u002FmL and HBsAg clearance at 5 years post-treatment were achieved by 23 and 12% of patients, respectively. High rates of HBsAg clearance at 5 years post-treatment were achieved by patients with HBV DNA ≤2,000 IU\u002FmL at 1 year post-treatment (28%). Rates of HBV DNA ≤2,000 IU\u002FmL at 1 year post-treatment were 47.2 and 43.4% in patients with ≥10% decline from baseline at weeks 12 and 24, respectively, compared with 16.4% (p = 0.0003) and 13.2% (p \u003C 0.0004) in patients with a \u003C10% decline. Rates of HBsAg clearance at 5 years post-treatment were 22.6 and 22.4% in patients with ≥10% decline at weeks 12 and 24, respectively, compared with 7.5% (p = 0.0161) and 3.8% (p \u003C 0.0001) in patients with \u003C10% decline. Peginterferon alfa-2a results in increasing rates of HBsAg clearance during post-treatment follow-up in HBeAg-negative patients. On-treatment decline in HBsAg is significantly associated with long-term post-treatment response.",{"EN":2325},"Hepatitis B surface antigen levels: association with 5-year response to peginterferon alfa-2a in hepatitis B e-antigen-negative patients",{"VOID":2327},"Lok AS, McMahon BJ. Chronic hepatitis B: update 2009. Hepatology 2009;50:1–36\nEuropean Association for the Study of the Liver. EASL clinical practice guidelines: management of chronic hepatitis B. J Hepatol 2009;50:227–242\nFattovich G, Bortolotti F, Donato F. Natural history of chronic hepatitis B: special emphasis on disease progression and prognostic factors. J Hepatol 2008;48:335–352\nYang HI, Lu SN, Liaw YF, et al. Hepatitis B e antigen and the risk of hepatocellular carcinoma. N Engl J Med 2002;347:168–174\nSimonetti J, Bulkow L, McMahon BJ, et al. Clearance of hepatitis B surface antigen and risk of hepatocellular carcinoma in a cohort chronically infected with hepatitis B virus. Hepatology 2010;51:1531–1537\nManesis EK, Hadziyannis SJ. Interferon alfa treatment and retreatment of hepatitis B e antigen-negative chronic hepatitis B. Gastroenterology 2001;121:101–109\nMarcellin P, Bonino F, Lau GK, et al. Sustained response of hepatitis B e antigen-negative patients 3 years after treatment with peginterferon alfa-2a. Gastroenterology 2009;136:2169–2179\nLiaw Y-F, Chu C-M. Hepatitis B virus infection. Lancet 2009;373:582–592\nChen C-J, Iloeje UJ, Yang HI. Long-term outcomes in hepatitis B: the REVEAL-HBV study. Clin Liver Dis 2007;11:797–816\nChen CJ, Yang HI, Su J, et al. Risk of hepatocellular carcinoma across a biological gradient of serum hepatitis B virus DNA level. JAMA 2006;295:65–73\nLampertico P, Del Ninno E, Viganò M, et al. Long-term suppression of hepatitis B e antigen-negative chronic hepatitis B by 24-month interferon therapy. Hepatology 2003;37:756–763\nBrunetto MR, Oliveri F, Coco B, et al. Outcome of anti-HBe positive chronic hepatitis B in alpha-interferon treated and untreated patients: a long-term cohort study. J Hepatol 2002;36:263–270\nMarcellin P, Lau GK, Bonino F, et al. Peginterferon alfa-2a alone, lamivudine alone, and the two in combination in patients with HBeAg-negative chronic hepatitis B. N Engl J Med 2004;351:1206–1217\nMoucari R, Mackiewicz V, Lada O, et al. Early serum HBsAg drop: a strong predictor of sustained virological response to pegylated interferon alfa-2a in HBeAg-negative patients. Hepatology 2009;49:1151–1157\nManesis EK, Hadziyannis ES, Angelopoulou OP, et al. Prediction of treatment-related HBsAg loss in HBeAg-negative chronic hepatitis B: a clue from serum HBsAg levels. Antivir Ther 2007;12:73–82\nKuhns MC, Kleinman SH, McNamara AL, et al. Lack of correlation between HBsAg and HBV DNA levels in blood donors who test positive for HBsAg and anti-HBc: implications for future HBV screening policy. Transfusion 2004;44:1332–1339\nBrunetto MR, Moriconi F, Bonino F, et al. Hepatitis B virus surface antigen levels: a guide to sustained response to peginterferon alfa-2a in HBeAg-negative chronic hepatitis B. Hepatology 2009;49:1141–1150\nChang TT, Lai CL, Kew Yoon S, et al. Entecavir treatment for up to 5 years in patients with hepatitis B e antigen-positive chronic hepatitis B. Hepatology 2010;51:422–430\nMarcellin P, Heathcote EJ, Buti M, et al. Tenofovir disoproxil fumerate versus adefovir dipivoxil for chronic hepatitis B. N Engl J Med 2008;359:2442–2455\nNguyen T, Thompson AJ, Bowden S, et al. Hepatitis B surface antigen levels during the natural history of chronic hepatitis B: a perspective on Asia. J Hepatol 2010;52:508–513\nJaroszewicz J, Calle Serrano B, Wursthorn K, et al. Hepatitis B surface antigen (HBsAg) levels in the natural history of hepatitis B virus (HBV)-infection: a European perspective. J Hepatol 2010;52:514–522\nBonino F, Marcellin P, Lau GK, et al. Predicting response to peginterferon-alpha-2a, lamivudine and the two combined for HBeAg-negative chronic hepatitis B. Gut 2007;56:699–705\nMoucari R, Martinot-Peignoux M, Mackiewicz V, et al. Influence of genotype of hepatitis B surface antigen kinetics in hepatitis B e antigen-negative patients treated with pegylated interferon-alpha2a. Antivir Ther 2009;14:1183–1188\nRijckborst V, Hansen BE, Cakaloglu Y, et al. Early on-treatment prediction of response to peginterferon alfa-2a for HBeAg-negative chronic hepatitis B using HBsAg and HBV DNA levels. Hepatology 2010;52:454–461\nLampertico P, Vigano M, Di Costanzo G, et al. Extended (2 years) treatment with peginterferon alfa-2a (40KD) improves sustained response rates in genotype D patients with HBeAg negative chronic hepatitis B. J Hepatol 2010;52(Suppl. 1):S45\nBrunetto MR, Marcellin P, Bonino F et al. HBsAg decline in HBeAg-negative patients treated with peginterferon alfa-2a is associated with sustained response up to 5 years post-treatment: patients with continuous HbsAg decline starting before week 24 achieve highest rates of response. Hepatology (2010) 50 Suppl 4:137A (P452)",{"VOID":2329},"10.1007\u002Fs12072-012-9343-x","https:\u002F\u002Flink.springer.com\u002Farticle\u002F10.1007\u002Fs12072-012-9343-x",[2332,2347,2362,2377,2392,2405,2420,2435,2450],{"id":2333,"sortIndex":32,"researcher":28,"roles":2334,"affiliations":2335,"properties":2344,"displayName":2346,"givenName":28,"familyName":28},"f60dccf5-2931-4207-ae42-9b2f1fd507aa",[1003],[2336],{"id":2337,"sortIndex":32,"affiliation":2338,"properties":28},"2127f2f4-f8d7-4abe-affa-4c441e62bd27",{"id":2337,"createTime":28,"updateTime":28,"relativeEntities":2339,"slug":28,"properties":2340,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":2343,"statistic":28},[],{"title":2341},{"VI":2342},"Service d’Hépatologie and INSERM U773-CRB3, Hôpital Beaujon, University of Paris, Clichy, France",[],{"title":2345},{"VI":2346},"Patrick 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Hoffmann-La Roche, Basel, Switzerland",[],{"title":2448},{"VI":2449},"Matei Popescu",{"id":2451,"sortIndex":357,"researcher":28,"roles":2452,"affiliations":2453,"properties":2462,"displayName":2464,"givenName":28,"familyName":28},"a736bb56-1975-4df2-ab4d-d5488e4d893a",[1003],[2454],{"id":2455,"sortIndex":32,"affiliation":2456,"properties":28},"4691ed41-d18d-4003-9965-bf61812ffc49",{"id":2455,"createTime":28,"updateTime":28,"relativeEntities":2457,"slug":28,"properties":2458,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":2461,"statistic":28},[],{"title":2459},{"VI":2460},"Hepatology Unit, University Hospital of Pisa, Pisa, Italy",[],{"title":2463},{"VI":2464},"Maurizia R. Brunetto",{"url":2330,"publisher":2466,"properties":2508},{"id":868,"createTime":869,"updateTime":870,"relativeEntities":2467,"slug":872,"properties":2468,"entityType":25,"verifyStatus":880,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":32,"subjectFields":2472,"manageAffiliations":2477,"indexDatabases":2488,"url":932,"thumbnailPath":28,"statistic":2503,"gsStatistic":28,"type":55,"analyzePriority":28},[],{"issn":2469,"title":2470,"eissn":2471},{"VOID":875},{"EN":877},{"VOID":879},[2473],{"id":883,"createTime":28,"updateTime":28,"relativeEntities":2474,"label":2475,"description":2476,"parentId":28,"standard":28,"scholarHubFieldId":28},[],{"EN":886},{},[2478,2483],{"id":890,"createTime":28,"updateTime":28,"relativeEntities":2479,"slug":28,"properties":2480,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":2482,"statistic":28},[],{"title":2481},{"EN":894},[],{"id":897,"createTime":28,"updateTime":28,"relativeEntities":2484,"slug":28,"properties":2485,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":2487,"statistic":28},[],{"title":2486},{"EN":901},[903],[2489,2496],{"id":906,"indexDatabase":2490,"url":912,"indexYears":913,"academicFieldIds":2495,"indexDatabaseRanking":788},{"id":775,"createTime":28,"updateTime":28,"relativeEntities":2491,"label":2492,"description":2493,"key":781,"publicationTags":2494,"standard":28},[],{"EN":778,"VI":778},{"EN":778,"VI":780},[783],[915],{"id":917,"indexDatabase":2497,"url":929,"indexYears":28,"academicFieldIds":2502,"indexDatabaseRanking":28},{"id":919,"createTime":28,"updateTime":28,"relativeEntities":2498,"label":2499,"description":2500,"key":926,"publicationTags":2501,"standard":28},[],{"EN":922,"VI":922},{"EN":924,"VI":925},[928,813],[931],{"impactFactor":32,"impactFactorByYear":2504,"i10Index":939,"i10IndexLast5Year":149,"totalPublication":940,"totalPublicationByYear":2505,"totalCitation":943,"totalCitationByYear":2506,"totalCitationPerPublication":959,"totalCitationPerPublicationByYear":2507,"hindexLast5Year":138,"hindex":138},{"2012":462,"2013":40,"2014":821,"2015":121,"2016":168,"2017":709,"2018":173,"2019":935,"2020":936,"2021":937,"2022":191,"2023":938},{"2007":69,"2008":436,"2009":131,"2010":328,"2011":560,"2012":436,"2013":829,"2014":942,"2015":162,"2016":151,"2017":149,"2018":436,"2019":829,"2020":428,"2021":574,"2022":153,"2023":334,"2024":133},{"2007":945,"2008":946,"2009":138,"2010":947,"2011":948,"2012":949,"2013":950,"2014":951,"2015":952,"2016":953,"2017":954,"2018":955,"2019":956,"2020":957,"2021":958,"2022":563,"2023":160,"2024":40},{"2007":961,"2008":962,"2009":963,"2010":964,"2011":965,"2012":966,"2013":628,"2014":967,"2015":190,"2016":968,"2017":969,"2018":970,"2019":971,"2020":972,"2021":973,"2022":974,"2023":975,"2024":421},{"pages":2509,"volume":2511},{"VOID":2510},"88-97",{"VOID":2512},"7","2012-03-23",2012,[783,928],{"id":2517,"createTime":2518,"updateTime":2519,"relativeEntities":2520,"slug":2521,"properties":2522,"entityType":995,"verifyStatus":26,"verifyTime":2519,"verifyNote":997,"languages":28,"translateLanguages":28,"viewCount":32,"primaryUrl":2531,"fullTextUrl":28,"authors":2532,"publicationType":1049,"publisherRelationship":2710,"citationCount":28,"citationInfo":28,"publishDate":2757,"publishYear":1864,"citationAnalyzeStatus":880,"lastCitationAnalyze":28,"indexDatabases":2758,"openAccess":28,"references":28,"isForceReanalyzing":1101},"02774c75-6eb4-44d8-b0aa-6b9472c51e33","2024-02-02T04:04:05.106+00:00","2025-02-19T07:31:07.315+00:00",[],"Spleen-stiffness-measurement-for-assessing-the-response-to-%CE%B2-blockers-therapy-for-high-risk-esophageal-varices-patients",{"abstract":2523,"title":2525,"references":2527,"doi":2529},{"EN":2524},"Non-selective β-blocker (NSBB) therapy is the treatment of choice for primary prophylaxis of cirrhotic patients with high-bleeding risk esophageal varices (HRV). The hemodynamic response to NSBB is assessed by the measurement of the hepatic venous pressure gradient (HVPG). Recently, liver and spleen stiffness measurements (LSM and SSM) were proposed as non-invasive surrogates of HVPG. We aimed to evaluate LSM and SSM changes for assessing hemodynamic response in these patients. Cirrhotic patients with HRV were prospectively enrolled and evaluated at our Department before starting NSBB and after 3 months. Correlation between changes (delta) of HVPG after NSBB treatment and those of LSM or SSM by transient elastography was performed. From the initial 59 patients considered for the study, 20 were finally included in the analysis. Fifteen (15) patients reached hemodynamic response to NSBB according to HVPG. Changes in LSM did not correlate with changes in HVPG (r = 0.107, p value = 0.655), unlike changes in SSM (r = 0.784, p value \u003C 0.0001). Delta SSM presented excellent accuracy in identifying HVPG responders (AUROC 0.973; 95% CI 0.912–1). The best cut-off for delta SSM to identify responders was -10% (sensitivity 100%, specificity 60%, NPV 100% and PPV 90%). SSM could be a reliable non-invasive test for the assessment of hemodynamic response to NSBB therapy as primary prophylaxis for HRV. Similar to HVPG, SSM reduction ≥ 10% is able to assess hemodynamic response. \n                  \n                    \n                      \n                    \n                  \n                ",{"EN":2526},"Spleen stiffness measurement for assessing the response to β-blockers therapy for high-risk esophageal varices patients",{"VOID":2528},"D’Amico G, Garcia-Tsao G, Pagliaro L. Natural history and prognostic indicators of survival in cirrhosis: a systematic review of 118 studies. J Hepatol 2006;44:217–231\nde Franchis R, Primignani M. Natural history of portal hypertension in patients with cirrhosis. Clin Liver Dis 2001;5:645–663\nBosch J, Abraldes JG, Berzigotti A, García-Pagan JC. The clinical use of HVPG measurements in chronic liver disease. Nat Rev Gastroenterol Hepatol 2009;6:573–582\nde Franchis R, VI Baveno Faculty. Expanding consensus in portal hypertension: report of the Baveno VI consensus workshop: stratifying risk and individualizing care for portal hypertension. J Hepatol 2015;63:743–752\nColecchia A, Marasco G, Taddia M, Montrone L, Eusebi LH, Mandolesi D, et al. Liver and spleen stiffness and other noninvasive methods to assess portal hypertension in cirrhotic patients: a review of the literature. Eur J Gastroenterol Hepatol 2015;27:992–1001\nEASL-ALEH Clinical Practice Guidelines: Non-invasive tests for evaluation of liver disease severity and prognosis\nVizzutti F, Arena U, Romanelli RG, Rega L, Foschi M, Colagrande S, et al. Liver stiffness measurement predicts severe portal hypertension in patients with HCV-related cirrhosis. Hepatology 2007;45:1290–1297\nSingh S, Fujii LL, Murad MH, Wang Z, Asrani SK, Ehman RL, et al. Liver stiffness is associated with risk of decompensation, liver cancer, and death in patients with chronic liver diseases: a systematic review and meta-analysis. Clin Gastroenterol Hepatol 2013;11:1573–1584\nReiberger T, Ferlitsch A, Payer BA, Pinter M, Homoncik M, Peck-Radosavljevic M. Non-selective β-blockers improve the correlation of liver stiffness and portal pressure in advanced cirrhosis. J Gastroenterol 2012;47:561–568\nColecchia A, Montrone L, Scaioli E, Bacchi-Reggiani ML, Colli A, Casazza G, et al. Measurement of spleen stiffness to evaluate portal hypertension and the presence of esophageal varices in patients with HCV-related cirrhosis. Gastroenterology 2012;143:646–654\nColecchia A, Colli A, Casazza G, Mandolesi D, Schiumerini R, Reggiani LB, et al. Spleen stiffness measurement can predict clinical complications in compensated HCV-related cirrhosis: a prospective study. J Hepatol Eur Assoc Study Liver 2014;60:1158–1164\nColecchia A, Ravaioli F, Marasco G, Festi D. Spleen stiffness by ultrasound elastography. Diagnostic Methods Cirrhosis Portal Hypertens 2018\nMarasco G, Colecchia A, Colli A, Ravaioli F, Casazza G, Bacchi Reggiani ML, et al. Role of liver and spleen stiffness in predicting the recurrence of hepatocellular carcinoma after resection. J Hepatol 2019;70:440–448\nKim HY, So YH, Kim W, Ahn DW, Jung YJ, Woo H, et al. Non-invasive response prediction in prophylactic carvedilol therapy for cirrhotic patients with esophageal varices. J Hepatol 2019;70:412–422\nDietrich CF, Bamber J, Berzigotti A, Bota S, Cantisani V, Castera L, et al. EFSUMB guidelines and recommendations on the clinical use of liver ultrasound elastography, update 2017 (long version). Ultraschall der Medizin 2017;38:e16–e47\nMandorfer M, Reiberger T. Beta blockers and cirrhosis, 2016. Dig Liver Dis 2017;3–10\nZacharias AP, Jeyaraj R, Hobolth L, Bendtsen F, Gluud LL, Morgan MY. Carvedilol versus traditional, non-selective beta-blockers for adults with cirrhosis and gastroesophageal varices. Cochrane Database Syst Rev 2018;10:11510\nFeu F, García-Pagán JC, Bosch J, Luca A, Escorsell A, Rodés J, et al. Relation between portal pressure response to pharmacotherapy and risk of recurrent variceal haemorrhage in patients with cirrhosis. Lancet 1995;346:1056–1059\nRavaioli F, Conti F, Brillanti S, Andreone P, Mazzella G, Buonfiglioli F, et al. Hepatocellular carcinoma risk assessment by the measurement of liver stiffness variations in HCV cirrhotics treated with direct acting antivirals. Dig Liver Dis 2018;50:573–579\nColecchia A, Ravaioli F, Marasco G, Colli A, Dajti E, Di Biase AR, et al. A combined model based on spleen stiffness measurement and Baveno VI criteria to rule out high-risk varices in advanced chronic liver disease. J Hepatol 2018;69:308–317\nMandorfer M, Kozbial K, Schwabl P, Chromy D, Semmler G, Stättermayer AF, et al. Changes in hepatic venous pressure gradient predict hepatic decompensation in patients who achieved sustained virologic response to interferon-free therapy. Hepatology 2020;71:1023–1036\nBalakrishnan M, Souza F, Munoz C, Augustin S, Loo N, Deng Y, et al. Liver and spleen stiffness measurements by point shear wave elastography via acoustic radiation force impulse: intraobserver and interobserver variability and predictors of variability in a US population. J Ultrasound Med Engl 2016;35:2373–2380\nLin YH, Yeh ML, Huang CI, Yang JF, Liang PC, Huang CF, et al. The performance of acoustic radiation force impulse imaging in predicting liver fibrosis in chronic liver diseases. Kaohsiung J Med Sci 2016;32:362–366\nHernández-Gea V, Procopet B, Giráldez Á, Amitrano L, Villanueva C, Thabut D, et al. Preemptive-TIPS improves outcome in high-risk variceal bleeding: an observational study. Hepatology 2019;69:282–293\nPiecha F, Paech D, Sollors J, Seitz H-K, Rössle M, Rausch V, et al. Rapid change of liver stiffness after variceal ligation and TIPS implantation. Am J Physiol Liver Physiol 2018;314:G179–G187187\nVillanueva C, Albillos A, Genescà J, Garcia-Pagan JC, Calleja JL, Aracil C, et al. β blockers to prevent decompensation of cirrhosis in patients with clinically significant portal hypertension (PREDESCI): a randomised, double-blind, placebo-controlled, multicentre trial. Lancet (London, England) 2019;393:1597–1608\nTurco L, Villanueva C, La Mura V, García-Pagán JC, Reiberger T, Genescà J, et al. Lowering portal pressure improves outcomes of patients with cirrhosis, with or without ascites: a meta-analysis. Clin Gastroenterol Hepatol 2020;18(313–327):e6\nReiberger T, Ulbrich G, Ferlitsch A, Payer BA, Schwabl P, Pinter M, et al. Carvedilol for primary prophylaxis of variceal bleeding in cirrhotic patients with haemodynamic non-response to propranolol. Gut 2013;62:1634–1641.\nMandorfer M, Hernández-Gea V, Reiberger T, García-Pagán JC. Hepatic venous pressure gradient response in non-selective beta-blocker treatment—is it worth measuring? 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