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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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characterized by dysfunction of neuroendocrine and immune networks. Trans-resveratrol, a phenolic compound presented in polygonum cuspidatum, was demonstrated previously to exert antidepressant-like effects through regulating monoaminergic system, oxidative\u002Fantioxidant defense and inflammatory response. The present study investigated the synergistic antidepressant-like effect of trans-resveratrol and piperine, a bioavailability enhancer, in mice and explored the possible mechanism. Trans-resveratrol was shown to reduce the immobility time both in the tail suspension and forced swimming tests (TST and FST). But the maximal inhibition was nearly 60 % even if the doses were increased by 160 mg\u002Fkg; while piperine produced weak antidepressant-like effects in these two models. The interaction between trans-resveratrol and piperine was shown a clear-cut synergistic effect as evidenced by an isobolographic analysis. The further study suggested that the anti-immobility response from the subthreshold dose of piperine (2.5 mg\u002Fkg) and low doses of trans-resveratrol (10 and 20 mg\u002Fkg) was abolished by pretreatment with para-chlorophenylalanine (PCPA, 300 mg\u002Fkg, i.p.) in TST and FST, indicating the involvement of serotonergic system. Moreover, treatment with the subthreshold dose of piperine and low doses of trans-resveratrol attenuated reserpine-induced hypothermia and ptosis arguing for the relevance of noradrenaline. Additional evidence from neurochemical (monoamines in the frontal cortex, hippocampus, and hypothalamus) and biochemical (monoamine oxidase, MAO activity) assays corroborated the synergistically elevated monoaminergic system after co-treatment with trans-resveratrol and piperine. The present results indicate the effect of trans-resveratrol combined with piperine on depressive-like behaviors may be partly due to the potentiated activation of monoaminergic system in the brain. Further studies are necessary to elucidate the involvement of the oxidative\u002Fnitrosative stress, inflammatory and neuroprotective pathway in the antidepressant-like effect of this combination. The synergistic effect obtained from the combination may provide innovative clues for designing novel antidepressants with high efficacy and low side effects.",{"EN":962},"Piperine potentiates the antidepressant-like effect of trans-resveratrol: involvement of monoaminergic system",{"VOID":964},"citation_journal_title=Pychoneuroendocrinology; citation_title=Curcumin ameliorates reserpine-induced pain-depression dyad: behavioral, biochemical, neurochemical and molecular evidences; citation_author=V Arora, A Kuhad, V Tiwari, K Chopra; citation_volume=36; citation_publication_date=2011; citation_pages=1570-1581; citation_doi=10.1016\u002Fj.psyneuen.2011.04.012; citation_id=CR1\ncitation_journal_title=Chin Med J; citation_title=Sequence of fat partitioning and its relationship with whole body insulin resistance; citation_author=XP Bai, HL Li, WY Yang, JZ Xiao, B Wang, DJ Lou, RQ Du; citation_volume=36; citation_publication_date=2011; citation_pages=3605-3611; 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West Virginia University, Morgantown, USA",[],{},{"title":1153},{"VI":1154},"Xu, Ying",{"id":1156,"sortIndex":47,"researcher":28,"roles":1157,"affiliations":1158,"properties":1165,"displayName":1167,"givenName":28,"familyName":28},"21f6c76a-17db-4363-8871-84a22fe7de0c",[974],[1159],{"id":977,"sortIndex":32,"affiliation":1160,"properties":28},{"id":977,"createTime":28,"updateTime":28,"relativeEntities":1161,"slug":28,"properties":1162,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1164,"statistic":28},[],{"title":1163},{"VI":982},[],{"title":1166},{"VI":1167},"Pan, 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management and clinical trials of patients with overt hepatic encephalopathy (OHE) are compromised by lack of standardized and reproducible tools for its clinical diagnosis or for caregiver (CG) identification of OHE manifestations which merit medical evaluation. Using an iterative Delphi method, Steering Committee and international hepatologist panel, the West Haven (WH) scale was modified to develop and operationalize a clinician tool for OHE identification and grading (HE Grading Instrument, HEGI™). Major diagnostic criteria included disorientation to time, place, and person, asterixis, lethargy, and coma. Minimum HEGI requirements for OHE diagnosis included: (1) disorientation, or (2) presence of both lethargy and asterixis, or (3) coma. Inter- and intra-rater HEGI reproducibility were 97 % and 98 %, respectively. When applied to a phase II clinical trial population of 178 patients with 388 OHE episodes, HEGI demonstrated excellent concordance with investigator judgement. Additionally, a multi-stage study was conducted to develop a daily CG e-diary, based on OHE manifestations recognizable by CG including speech difficulties, unusual behavior, forgetfulness, confusion, disorientation and level of consciousness. The e-diary was designed for use on smart phone, laptop or desktop, utilized branching logic and skip patterns, incorporated automatic daily completion reminders and real time alerts to clinical sites to facilitate daily standardized CG input and was found to be user friendly and understandable. The HEGI and e-diary, which were developed using methodology accepted by regulatory authorities, are designed to facilitate the design and interpretation of clinical trials for OHE and improve outcomes for OHE patients in clinical practice.","Quản lý lâm sàng và thử nghiệm lâm sàng đối với bệnh nhân bị rối loạn tâm thần gan rõ ràng (OHE) bị ảnh hưởng bởi việc thiếu các công cụ chuẩn hóa và tái hiện được để chẩn đoán lâm sàng hoặc giúp người chăm sóc (CG) nhận diện các biểu hiện của OHE mà cần được đánh giá y tế. Sử dụng phương pháp Delphi lặp đi lặp lại, Ủy ban điều hành và ban bác sĩ gan quốc tế đã điều chỉnh thang đo West Haven (WH) nhằm phát triển và hiện thực hóa một công cụ cho bác sĩ để nhận diện và phân loại OHE (Công cụ phân loại rối loạn tâm thần gan, HE Grading Instrument hoặc HEGI™). Các tiêu chuẩn chẩn đoán chính bao gồm mất phương hướng về thời gian, địa điểm và nhân thân, dấu hiệu asterixis, tình trạng uể oải và hôn mê. Các yêu cầu tối thiểu của HEGI để chẩn đoán OHE bao gồm: (1) mất phương hướng, hoặc (2) sự hiện diện của cả tình trạng uể oải và asterixis, hoặc (3) hôn mê. Độ tái lặp đo HEGI giữa các người đánh giá và trong cùng một người lần lượt là 97% và 98%. Khi áp dụng cho một nhóm thử nghiệm lâm sàng giai đoạn II với 178 bệnh nhân có 388 lần xuất hiện OHE, HEGI cho thấy sự đồng thuận xuất sắc với sự đánh giá của nhà nghiên cứu. Thêm vào đó, một nghiên cứu đa giai đoạn đã được thực hiện để phát triển một nhật ký điện tử hàng ngày cho người chăm sóc, dựa trên các biểu hiện OHE mà người chăm sóc có thể nhận diện như khó khăn trong việc nói, hành vi không bình thường, hay quên, nhầm lẫn, mất phương hướng và mức độ ý thức. Nhật ký điện tử được thiết kế để sử dụng trên điện thoại thông minh, máy tính xách tay hoặc máy tính để bàn, ứng dụng logic phân nhánh và các mẫu bỏ qua, tích hợp nhắc nhở hoàn thành hàng ngày tự động và cảnh báo thời gian thực đến các cơ sở lâm sàng nhằm hỗ trợ sự nhập liệu chuẩn hóa hàng ngày của người chăm sóc và đã được tìm thấy dễ sử dụng và dễ hiểu. HEGI và nhật ký điện tử, được phát triển bằng phương pháp được các cơ quan quản lý chấp nhận, được thiết kế để thúc đẩy việc thiết kế và giải thích các thử nghiệm lâm sàng về OHE và cải thiện kết quả cho bệnh nhân OHE trong thực hành lâm sàng.",{"EN":1237,"VI":1238},"Overt hepatic encephalopathy: development of a novel clinician reported outcome tool and electronic caregiver diary","Rối loạn tâm thần gan rõ ràng: phát triển công cụ đo lường kết quả báo cáo bởi bác sĩ mới và nhật ký điện tử cho người chăm sóc",{"VI":1240},"Rối loạn tâm thần gan rõ ràng, công cụ đo lường kết quả, nhật ký điện tử, người chăm sóc, thang đo HEGI",{"VOID":1242},"Amodio P, Montagnese S, Gatta A, Morgan MY (2004) Characteristics of minimal hepatic encephalopathy. Metab Brain Dis 19:253–267\nBajaj JS, Cordoba J, Mullen KD, et al. Review article: the design of clinical trials in hepatic encephalopathy – an International Society for Hepatic Encephalopathy and Nitrogen Metabolism (ISHEN). consensus statement (2011) Aliment Pharm Ther 33:739–747\nBajaj JS, Bass NM, Frederick RT, Coyne K, Margolis MK, Coakley DF, Mokhtarani MM, Jurek M, Scharschmidt BF. (2015) Development of a Novel Clinician Reported Outcome Tool for Assessment of Hepatic Encephalopathy. Hepatology1 (suppl): 935 A\nBlei AT, Cordoba J (2001) Hepatic encephalopathy. Am J Gastroenterol 96:1968–1976\nBraun V, Clark V (2006) Using thematic analysis in psychology. Qual Res Psychol 3:77–101\nConn HO, Leevy CM, Vlahcevic ZR, Rodgers JB, Maddrey WC, Seeff L, Levy LL (1977) Comparison of lactulose and neomycin in the treatment of chronic potal-systemic encephalopahty. A double blind controlled trial Gastroenterology 72:573–583\nCrisp J, Pelletier D, Duffield C, Adams A, Nagy S (1977) The Delphi method. Nurs Res 46:116–118\nDalkey N, Helmer O (1963) An experimental application of the Delphi method to the use of experts. Manag Sci 9:458–467\nFDA (2010a) http:\u002F\u002Fwww.fda.gov\u002Fdownloads\u002FAdvisoryCommittees\u002FCommitteesMeetingMaterials\u002FDrugs\u002FGastrointestinalDrugsAdvisoryCommittee\u002FUCM201079.pdf\nFDA (2010b) http:\u002F\u002Fwww.fda.gov\u002Fdownloads\u002FAdvisoryCommittees\u002FCommitteesMeetingMaterials\u002FDrugs\u002FGastrointestinalDrugsAdvisoryCommittee\u002FUCM206728.pdf\nFerenci P, Lockwood A, Mullen K, Tarter R, Weissenborn K, Blei AT (2002) Hepatic encephalopathy–definition, nomenclature, diagnosis, and quantification: final report of the working party at the 11th world congresses of gastroenterology, Vienna, 1998. Hepatology 35:716–721\nFood and Drug Administration (www.fda.gov) Guidance for Industry (2009) Patient-reported outcome measures: use in medical product development to support labeling claims. Fed Regist 74:65132–65133\nFrederick RT, Ghabril M, Coyne K, Margolis MK, Santoro M, Coakley DF, Mokhtarani M, Scharschmidt BF, Jurek M. Development of an Electronic Diary (E-Diary) for Caregivers (CG) of Patients with Overt Hepatic Encephalopathy (OHE). (2015) Hepatology; 1 (suppl): 926 A\nGwet KL (2008) Interrater reliability. Wiley Encyclopedia of Clinical Trials. John Wiley and Sons, Hoboken, In, pp. 1–14\nHassanein TI, Tofteng F, Brown RS Jr, McGuire B, Lynch P, Mehta R, Larsen FS, Gombein J, Stange J, Blei AT (2007) Randomized controlled study of extracorporeal albumin dialysis for hepatic encephalopahty in advanced cirrhosis. Hepatology 46:1853–1862\nHassanein TI, Hilsabeck RC, Perry W (2008) Introduction to the hepatic encephalopathy scoring algorithm (HESA). Dig Dis Sci 53:529–538\nHassanein T, Blei AT, Perry W, Hilsabeck R, Stange J, Larsen FS, Brown RS Jr, Caldwell S, McGuire B, Nevens F, Fontana R (2009) Performance of the hepatic encephalopathy scoring algorithm in a clinical trial of patients with cirrhosis and severe hepatic encephalopathy. Am J Gastroenterol 104:1392–1400\nHsu C-C, Sandford BA (2007) The Delphi technique: making sense of consensus. Practical Assessment, Research Evaluation 12:1–8\nKottner J, Audigé L, Brorson S, Donner A, Gajewski BJ, Hróbjartsson A, Roberts C, Shoukri M, Streiner DL (2011) Guidelines for reporting reliability and agreement studies (GRRAS) were proposed. J Clin Epidemiol 64:96–106\nLiao SC, Hunt EA, Chen W (2010) Comparison between inter-rater reliability and inter-rater agreement in performance assessment. Ann Acad Med 39:613–618\nOrtiz M, Córdoba J, Doval E, Jacas C, Pujadas F, Esteban R, Guardia J (2007) Development of a clinical hepatic encephalopathy staging scale. Aliment Pharmacol Ther 26:859–867\nParson-Smith BG, Summerskill WHJ, Dawson AM, Sherlock S (1957) The electroencephalograph in liver disease. Lancet 2:867–871\nPatrick DL, Burke LB, Gwaltney CJ, Leidy NK, Martin ML, Molsen E, Ring L (2011) Content validity—establishing and reporting the evidence in newly developed patient-reported outcomes (PRO) instruments for medical product evaluation: ISPOR PRO good research practices task force report: part 1—eliciting concepts for a new PRO instrument. Value Health 14:967–997\nRockey DC, Vierling JM, Mantry P, Ghabril M, Brown RS Jr, Alexeeva O, Zupanets I, Grinevich V, Baranovsky A, Dudar L, Fadieienko G, Kharchenko N, Klarytska I, Morozov V, Grewal P, McCashland T, Reddy G, Reddy R, Syplyviy V, Bass NM, Dickinson K, Norris C, Coakley D, Mokhtarani M, Scharschmidt, BF for the HALT-HE Study Group (2014) Randomized, controlled, double blind study of glycerol phenylbutyrate in patients with cirrhosis and episodic hepatic encephalopathy. Hepatology 59:1073–1083\nRowe G, Wright G, Bolger F (1991) Delphi: a reevaluation of research and theory. Technol Forecast Soc Chang 39:235–251\nSalam M, Matherly S, Farooq IS, Stravitz RT, Sterling RK, Sanyal AJ, Gibson DP, Wade JB, Thacker LR, Heuman DM, Fuchs M, Puri P, Luketic V, Bickston SJ, Bajaj JS (2012) Modified-orientation log to assess hepatic encephalopathy. Aliment Pharmacol Ther 35:913–920\nVilstrup H, Amodio P, Bajaj J, Cordoba J, Ferenci P, Mullen KD, Weissenborn K, Wong P (2014) Hepatic encephalopathy in chronic liver disease: 2014 practice guideline by the American Association for the Study of Liver Diseases and the European Association for the Study of the liver. Hepatology 60:715–735\nWoudenberg F (1991) An evaluation of Delphi. Technol Forecast Soc Chang 40:131–150",{"VOID":1244},"10.1007\u002Fs11011-016-9851-9","2025-02-06T00:28:18.040+00:00","Auto Verify",[30],"https:\u002F\u002Flink.springer.com\u002Farticle\u002F10.1007\u002Fs11011-016-9851-9",[1250,1265,1280,1298,1313,1328,1343,1358,1371,1384,1397],{"id":1251,"sortIndex":32,"researcher":28,"roles":1252,"affiliations":1253,"properties":1262,"displayName":1264,"givenName":28,"familyName":28},"f86a4365-0b3b-4302-9d50-32789beda991",[974],[1254],{"id":1255,"sortIndex":32,"affiliation":1256,"properties":28},"d9081b05-e252-4415-8781-d0add2a77c9e",{"id":1255,"createTime":28,"updateTime":28,"relativeEntities":1257,"slug":28,"properties":1258,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1261,"statistic":28},[],{"title":1259},{"VI":1260},"Virginia Commonwealth University and McGuire VA Hospital, Richmond, USA",[],{"title":1263},{"VI":1264},"J. S. 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A double blind, placebo controlled study in 62 patients: visual field threshold values were obtained in a Humphrey Field Analyzer from center (30°) and periphery (30–60°), every 4 months during 3-year follow-up. Data were analyzed by univariate regression, with slopes obtained from the best fit lines. Based on slope values, three groups of patients were identified as those showing negative, positive, or zero slope: ≥-1 to ≤ + 1. In controls (32 patients), at central area, the distribution in negative, zero, or positive slope was, respectively, 16 (50%),11 (35%), and 5 (15%). In the treated group (30 patients) this distribution was 6 (20%) negative, 17 (53%) zero, and 7 (23%) positive slope. In periphery, 16 control patients were distributed as 11 (69%) negative, 4 (25%) zero, and 1 (6%) positive slope. In the treated group (17 patients), the distribution was opposite: 1 (6%) negative, 7 (41%) zero, and 9 (53%) positive slope. Nineteen patients receiving treatment up to 6 years showed similar distribution by slope values. Eight out of 9 patients switched from placebo (2 years) to treatment (2–3 years), showed improving changes in their slope values. A beneficial effect of the treatment decreasing the rate of visual field loss was observed, likely through a protective action from free radical reactions in affected photoreceptors.",{"EN":1474},"Treatment with Taurine, Diltiazem, and Vitamin E Retards the Progressive Visual Field Reduction in Retinitis Pigmentosa: A 3-Year Follow-Up Study",{"VOID":1476},"Al-Dohayan, A.D., and Al-Tuwaijri, A.S. (1996). The potential synergistic effect of calcium channel blockers and alpha-tocopherol on gastric mucosal injury induced by ischaemia-reperfusion. Eur. J. Gastroenterol. Hepatol. 8:1107-1110.\nAonuma, H., Koide, K., Masuda, K., and Watanabe, I. (1997). Retinal light damage: Protective effect of alphatocopherol. Jpn. J. Ophthalmol. 41:160-167.\nBaumgartner, W.A. (2000). Etiology, pathogenesis, and experimental treatment of retinitis pigmentosa. Med. Hyptheses 54:814-824.\nBerson, E.L., Rosner, B., Sandberg, M.A., Hayes, K.C., Nicholson, B.W., Weigel-DiFranco, C., and Willet, W.l. (1993). A randomized trial of vitamin A and vitamin E supplementation for retinitis pigmentosa. Arch. Ophthalmol. 111:761-772.\nBerson, E.L., Sandberg, M.A., Rosner, B., Birch, D.G., and Hanson, A.H. (1985). Natural course of retinitis pigmentosa over a three-year interval. Am. J. Ophthalmol. 99:240-251.\nBhattacharya, R., and Rao, P.V.L. (1997). Cyanide induced DNA fragmentation in mammalian cell cultures. Toxicology 123:207-215.\nBoughman, J.A., Coneally, M., and Nance, W.E. (1980). Population genetic studies of retinitis pigmentosa. Am. J. Hum. Genet. 32:223-235.\nBush, R.A., Kononen, L., Machida, S., and Sieving, P.A. (2000). The effect of calcium channel blocker diltiazem on photoreceptor degeneration in the rhodopsin Pro213His rat. Invest. Ophthalmol. Vis. Sci. 9:2697-2701.\nCarmody, R.J., McGowan, A.J., and Cotter, T.G. (1999). Reactive oxygen species as mediators of photoreceptor apoptosis in vitro. Exp. Cell Res. 248:520-530.\nCommunal, C., Singh, K., Pimentel, D.R., and Colucci,W.S. (1998). Norepinephrine stimulates apoptosis in adult rat ventricular myocytes by activation of the beta-adrenergic pathway. Circulation 98:1329-1334.\nEl Idrissi, A., and Trenkner, E. (1999). Growth factors and taurine protect against excitotoxicity by stabilizing calcium homeostasis and energy metabolism. J. Neurosci. 19:9459-9468.\nFrasson, M., Sahel, J.A., Fapre, M., Simmonuti, M., Dreyfus, H., and Picaud, S. (1999). Retinitis pigmentosa: Rod photoreceptor rescue by a calcium-channel blocker in the rd mouse. Nat. Med. 5:1183-1187.\nGrover, S., Fishman, G.A., Anderson, R.J., Alexander, K.R., and Derlacki, D.J. (1997). Rate of visual field loss in retinitis pigmentosa. Ophthalmology 104:460-465.\nHayes, K., Carey, R., and Schmidt, S. (1975). Retinal degeneration associated with taurine deficiency in the cat. Science 188:945-951.\nHeckenlively, J.R. (1988). Retinitis Pigmentosa, Lippincott, Philadelphia, Pennsylvania.\nHolopigian, K., Greenstein, V., Seiple,W., and Carr, R.E. (1996). Rates of change differ among measures of visual function in patients with retinitis pigmentosa. Ophthalmology 103:398-405.\nHumphries, P., Kenna, P., and Farrar, G.J. (1992). On the molecular genetics of retinitis pigmentosa. Science 256:804-808.\nHuxtable, R.J. (1992). The physiological actions of taurine. Physiol. Rev. 72:101-173.\nKeys, S.A., and Zimmerman, W.F. (1999). Antioxidant activity of retinol, glutathione and taurine in bovine photoreceptor membranes. Exp. Eye Res. 68:693-702.\nMarchiafava, P.L., and Longoni, B. (1999). Melatonin as an antioxidant in retinal photoreceptors. J. Pineal Res. 26:184-189.\nMassof, R.W., and Finkelstein, D. (1987). A two-stage hypothesis for the natural course of retinitis pigmentosa. Adv. Biosci. 52:29-58.\nNewsome, D.A., Micele, M.V., Liles, M.R., Tate, D., and Oliver, P.D. (1991). Antioxidants in the retinal pigment epithelium. Prog. Retinal Eye Res. 13:101-122.\nPagon, R.A. (1988). Retinitis pigmentosa. Surv. Ophthalmol. 33:137-177.\nPasantes-Morales, H., Ademe, R.M., and Quesada, O. (1981). Protective effect of taurine on the light-induced disruption of isolated frog rod outer segments. J. Neurosci. Res. 6:337-348.\nPasantes-Morales, H., and Cruz, C. (1984). Protective effect of taurine and zinc on peroxidation-induced damage in photoreceptor outer segments. J. Neurosci. Res. 11:303-311.\nPasantes-Morales, H., Lopez-Escalera, R., and Diaz-Macedo,M.(1988). Taurine and ionic fluxes in photoreceptors. Neurol. Neurobiol. 49:87-104.\nPasantes-Morales, H., Wright, C.E., and Gaull, G.E. (1985). Taurine protection of lymphoblastoid cells from iron-ascorbate induced damage. Biochem. Pharmacol. 34:205-207.\nPearce-Kelling, S.E., Aleman, T.S., Nickle, A., Laties, A.M., Aguirre, G.D., Jacobson, S.G., and Acland, G.M. (2001). Calcium channel blocker D-cis-diltiazem does not slow retinal degeneration in the PDE6B mutant rcd1 canine model of retinitis pigmentosa. Mol. Vis. 7:42-47.\nRobison, W.G., Kuwabara, T., and Bieri, J.G. (1979). Vitamin E deficiency and the retina: Photoreceptor and pigment epithelial changes. Invest. Ophthalmol. Vis. Sci. 18:683-690.\nSchurr, A., Payne, R.S., and Rigor, B.M. (1995a). Synergism between diltiazem and MK-801 but not APV in protecting hippocampal slices against hypoxic damage. Brain Res. 685:233-236.\nSchurr, A., Payne, R.S., and Rigor, B.M. (1995b). Protection by MK-801 against hypoxia-, excitotoxin-, and depolarization-induced neuronal damage in vitro. Neurochem. Int. 26:19-25.\nTarif, N., and Bakris, G.L. (1997). Preservation of renal function: The spectrum of effects by calcium-channel blockers. Nephrol. Dial. Transplant. 12:2244-2250.\nvan Soest, S., Westerveld, A., de Jong, P.T., Bleeker-Wagemakers, E.M., and Bergen, A.A. (1999). Retinitis pigmentosa: Defined from a molecular point of view. Surv. Ophthalmol. 43:321-334.\nWong, F. (1997). Investigating retinitis pigmentosa: A laboratory scientist's perspective. Prog. Retinal Eye Res. 16:353-373.\nWu, O.D., Wang, J.H., Fenessy, F., Redmons, H.P., and Bouchier-Hayes, D. (1999). Taurine prevents high-glucose induced human vascular endothelial cell apoptosis. Am. J. Physiol. 94:2365-2373.",{"VOID":1478},"10.1023\u002FA:1019926122125","Author affiliation is blank","https:\u002F\u002Flink.springer.com\u002Farticle\u002F10.1023\u002FA:1019926122125",[1482,1489,1496],{"id":1483,"sortIndex":32,"researcher":28,"roles":1484,"affiliations":1485,"properties":1486,"displayName":1488,"givenName":28,"familyName":28},"34dae8db-5f1a-455f-8305-e6af330de95b",[974],[],{"title":1487},{"VI":1488},"Herminia Pasantes-Morales",{"id":1490,"sortIndex":40,"researcher":28,"roles":1491,"affiliations":1492,"properties":1493,"displayName":1495,"givenName":28,"familyName":28},"9d1dcd14-0174-4fb1-98d9-f6738073e86f",[974],[],{"title":1494},{"VI":1495},"Hugo Quiroz",{"id":1497,"sortIndex":123,"researcher":28,"roles":1498,"affiliations":1499,"properties":1500,"displayName":1502,"givenName":28,"familyName":28},"01972da5-887d-48ff-b0fc-bcd9f219a961",[974],[],{"title":1501},{"VI":1502},"Octavio Quesada",{"url":1480,"publisher":1504,"properties":1549},{"id":868,"createTime":869,"updateTime":870,"relativeEntities":1505,"slug":872,"properties":1506,"entityType":25,"verifyStatus":882,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":32,"subjectFields":1510,"manageAffiliations":1523,"indexDatabases":1534,"url":28,"thumbnailPath":28,"statistic":28,"gsStatistic":28,"type":28,"analyzePriority":28},[],{"issn":1507,"title":1508,"eissn":1509},{"VOID":877},{"EN":879},{"VOID":875},[1511,1515,1519],{"id":885,"createTime":28,"updateTime":28,"relativeEntities":1512,"label":1513,"description":1514,"parentId":28,"standard":28,"scholarHubFieldId":28},[],{"EN":888},{},{"id":891,"createTime":28,"updateTime":28,"relativeEntities":1516,"label":1517,"description":1518,"parentId":28,"standard":28,"scholarHubFieldId":28},[],{"EN":894},{},{"id":897,"createTime":28,"updateTime":28,"relativeEntities":1520,"label":1521,"description":1522,"parentId":28,"standard":28,"scholarHubFieldId":28},[],{"EN":900},{},[1524,1529],{"id":904,"createTime":28,"updateTime":28,"relativeEntities":1525,"slug":28,"properties":1526,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1528,"statistic":28},[],{"title":1527},{"EN":908},[910],{"id":912,"createTime":28,"updateTime":28,"relativeEntities":1530,"slug":28,"properties":1531,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1533,"statistic":28},[],{"title":1532},{"EN":916},[910],[1535,1542],{"id":920,"indexDatabase":1536,"url":926,"indexYears":927,"academicFieldIds":1541,"indexDatabaseRanking":932},{"id":775,"createTime":28,"updateTime":28,"relativeEntities":1537,"label":1538,"description":1539,"key":781,"publicationTags":1540,"standard":28},[],{"EN":778,"VI":778},{"EN":778,"VI":780},[783],[929,930,931],{"id":934,"indexDatabase":1543,"url":946,"indexYears":28,"academicFieldIds":1548,"indexDatabaseRanking":28},{"id":936,"createTime":28,"updateTime":28,"relativeEntities":1544,"label":1545,"description":1546,"key":943,"publicationTags":1547,"standard":28},[],{"EN":939,"VI":939},{"EN":941,"VI":942},[945,813],[948,949],{"pages":1550,"volume":1552},{"VOID":1551},"183-197",{"VOID":1553},"17","2002-09-01",2002,[932,945],{"id":1558,"createTime":1559,"updateTime":1560,"relativeEntities":1561,"slug":1562,"properties":1563,"entityType":967,"verifyStatus":26,"verifyTime":1560,"verifyNote":1246,"languages":28,"translateLanguages":28,"viewCount":40,"primaryUrl":1572,"fullTextUrl":28,"authors":1573,"publicationType":1168,"publisherRelationship":1701,"citationCount":28,"citationInfo":28,"publishDate":1752,"publishYear":1462,"citationAnalyzeStatus":882,"lastCitationAnalyze":28,"indexDatabases":1753,"openAccess":28,"references":28,"isForceReanalyzing":1225},"0042a94f-f504-44e9-91f8-a5e57da4b14a","2023-12-07T21:50:25.308+00:00","2024-12-29T20:25:09.565+00:00",[],"Retinoic-acid-pretreated-Wharton-s-jelly-mesenchymal-stem-cells-in-combination-with-triiodothyronine-improve-expression-of-neurotrophic-factors-in-the-subventricular-zone-of-the-rat-ischemic-brain-injury",{"abstract":1564,"title":1566,"references":1568,"doi":1570},{"EN":1565},"Stroke is the consequence of limited blood flow to the brain with no established treatment to reduce the neurological deficits. Focusing on therapeutic protocols in targeting subventricular zone (SVZ) neurogenesis has been investigated recently. This study was designed to evaluate the effects of retinoic acid (RA)-pretreated Wharton’s jelly mesenchymal stem cells (WJ-MSCs) in combination with triiodothyronine (T3) in the ischemia stroke model. Male Wistar rats were used to induce focal cerebral ischemia by middle cerebral artery occlusion (MCAO). There were seven groups of six animals: Sham, Ischemic, WJ-MSCs, RA-pretreated WJ-MSCs, T3, WJ-MSCs +T3, and RA-pretreated WJ-MSCs + T3. The treatment was performed at 24 h after ischemia, and animals were sacrificed one week later for assessments of retinoid X receptor β (RXRβ), brain-derived neurotrophic factor (BDNF), Sox2 and nestin in the SVZ. Pro-inflammatory cytokines in sera were measured at days four and seven after ischemia. RXRβ, BDNF, Sox2 and nestin had the significant expressions in gene and protein levels in the treatment groups, compared with the ischemic group, which were more vivid in the RA-pretreated WJ-MSCs + T3 (p ≤ 0.05). The same trend was also resulted for the levels of TNF-α and IL-6 at four days after ischemia (p ≤ 0.05). In conclusion, application of RA-pretreated WJ-MSCs + T3 could be beneficial in exerting better neurotrophic function probably via modulation of pro-inflammatory cytokines.",{"EN":1567},"Retinoic acid-pretreated Wharton’s jelly mesenchymal stem cells in combination with triiodothyronine improve expression of neurotrophic factors in the subventricular zone of the rat ischemic brain injury",{"VOID":1569},"Casals JB, Pieri NC, Feitosa ML, Ercolin A, Roballo K, Barreto RS, et al. (2011) The use of animal models for stroke research: a review. Commun Med 61:305–313\nDrela K, Lech W, Figiel-Dabrowska A, Zychowicz M, Mikula M, Sarnowska A, Domanska-Janik K (2016) Enhanced neuro-therapeutic potential of Wharton’s jelly–derived mesenchymal stem cells in comparison with bone marrow mesenchymal stem cells culture. Cytotherapy 18:497–509\nDugue R, Barone FC (2016) Ischemic, traumatic and neurodegenerative brain inflammatory changes. Future Neurol 11:77–96\nFerri AL, Cavallaro M, Braida D, Di Cristofano A, Canta A, Vezzani A, et al. (2004) Sox2 deficiency causes neurodegeneration and impaired neurogenesis in the adult mouse brain. Development 131:3805–3819\nFrausin S, Viventi S, Falzacappa LV, Quattromani MJ, Leanza G, Tommasini A, Valencic E (2015) Wharton’s jelly derived mesenchymal stromal cells: Biological properties, induction of neuronal phenotype and current applications in neurodegeneration research. Acta Histochem 117:329–338\nGong M, Bi Y, Jiang W, Zhang Y, Chen L, Hou N, et al. (2013) Retinoic acid receptor beta mediates all-trans retinoic acid facilitation of mesenchymal stem cells neuronal differentiation. Int J Biochem Cell Biol 45:866–875\nKatsuki H, Kurimoto E, Takemori S, Kurauchi Y, Hisatsune A, Isohama Y, et al. (2009) Retinoic acid receptor stimulation protects midbrain dopaminergic neurons from inflammatory degeneration via BDNF-mediated signaling. J Neurochem 110:707–718\nKoh SH, Park HH (2016) Neurogenesis in Stroke Recovery. Translational stroke research. doi:10.1007\u002Fs12975–016-0460-z [Epub ahead of print]\nKönig S, Neto VM (2002) Thyroid hormone actions on neural cells. Cell Mol Neurobiol 22:517–544\nKreżel W, Kastner P, Chambon P (1999) Differential expression of retinoid receptors in the adult mouse central nervous system. Neuroscience 89:1291–1300\nLee C, Hu J, Ralls S, Kitamura T, Loh YP, Yang Y, et al. (2012) The molecular profiles of neural stem cell niche in the adult subventricular zone. PLoS One 7:e50501\nLinnarsson S, Willson CA, Ernfors P (2000) Cell death in regenerating populations of neurons in BDNF mutant mice. Mol Brain Res 75:61–69\nLucassen PJ, Oomen CA, Naninck EF, Fitzsimons CP, van Dam A-M, Czeh B, Korosi A (2015) Regulation of adult neurogenesis and plasticity by (early) stress, glucocorticoids, and inflammation. Cold Spring Harb Perspect Biol 7:a021303\nMano H, Mori R, Ozawa T, Takeyama K-i, Yoshizawa Y, Kojima R, et al. (1994) Positive and negative regulation of retinoid X receptor gene expression by thyroid hormone in the rat. Transcriptional and post-transcriptional controls by thyroid hormone. J Biol Chem 269:1591–1594\nMdzinarishvili A, Sutariya V, Talasila PK, Geldenhuys WJ, Sadana P (2013) Engineering triiodothyronine (T3) nanoparticle for use in ischemic brain stroke. Drug delivery and translational research 3(4):309–317\nMortezaee K, Minaii B, Sabbaghziarani F, Kashani IR, Hassanzadeh G, Pasbakhsh P, et al. (2015) Retinoic acid as the stimulating factor for differentiation of Wharton’s jelly-mesenchymal stem cells into hepatocyte-like cells. Avicenna journal of medical biotechnology 7(3):106–112\nNúñez V, Alameda D, Rico D, Mota R, Gonzalo P, Cedenilla M, et al. (2010) Retinoid X receptor α controls innate inflammatory responses through the up-regulation of chemokine expression. Proc Natl Acad Sci 107:10626–10631\nPires AO, Neves-Carvalho A, Sousa N (2014) Salgado AJ (2014) The secretome of bone marrow and wharton jelly derived mesenchymal stem cells induces differentiation and neurite outgrowth in SH-SY5Y Cells. Stem Cells Int 438352\nStraub RH (2014) Interaction of the endocrine system with inflammation: a function of energy and volume regulation. Arthritis Res Ther 16:203\nSui L, Ren W-W, Li B-M (2010) Administration of thyroid hormone increases reelin and brain-derived neurotrophic factor expression in rat hippocampus in vivo. Brain Res 1313:9–24\nSullivan R, Duncan K, Dailey T, Kaneko Y, Tajiri N, Borlongan CV (2015) A possible new focus for stroke treatment–migrating stem cells. Expert Opin Biol Ther 15:949–958\nTovar-y-Romo LB, Penagos-Puig A, Ramírez-Jarquín JO (2016) Endogenous recovery after brain damage: molecular mechanisms that balance neuronal life\u002Fdeath fate. J Neurochem 136:13–27\nWang T-W, Zhang H, Parent JM (2005) Retinoic acid regulates postnatal neurogenesis in the murine subventricular zone-olfactory bulb pathway. Development 132:2721–2732\nZendedel A, Habib P, Dang J, Lammerding L, Hoffmann S, Beyer C, Slowik A (2015) Omega-3 polyunsaturated fatty acids ameliorate neuroinflammation and mitigate ischemic stroke damage through interactions with astrocytes and microglia. J Neuroimmunol 278:200–211",{"VOID":1571},"10.1007\u002Fs11011-016-9897-8","http:\u002F\u002Flink.springer.com\u002F10.1007\u002Fs11011-016-9897-8",[1574,1589,1604,1617,1630,1645,1660,1673,1688],{"id":1575,"sortIndex":32,"researcher":28,"roles":1576,"affiliations":1577,"properties":1586,"displayName":1588,"givenName":28,"familyName":28},"2a731ad9-af5c-4d3e-97f4-bd8b43d67492",[974],[1578],{"id":1579,"sortIndex":32,"affiliation":1580,"properties":28},"90e5418a-7608-4cd5-9b7a-c3d4cf1ad7f1",{"id":1579,"createTime":28,"updateTime":28,"relativeEntities":1581,"slug":28,"properties":1582,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1585,"statistic":28},[],{"title":1583},{"VI":1584},"Department of Anatomy, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran",[],{"title":1587},{"VI":1588},"Fatemeh 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quả lâm sàng của cả L-ornithine–L-aspartate (OA) dạng uống và dạng tiêm đã được xác nhận qua các nghiên cứu ngẫu nhiên, đối chứng giả dược, mù đôi trên bệnh nhân mắc bệnh não do gan biểu hiện và tăng ammoniac huyết. Thuốc có khả năng giảm mức ammoniac trong máu cao do clorua amoni hoặc tiêu thụ protein gây ra, hoặc tồn tại như một biến chứng lâm sàng của xơ gan. Hơn nữa, OA cải thiện hiệu suất trong Bài Kiểm Tra Kết Nối Số-A cũng như phân loại trạng thái tâm thần. Trái ngược với những tác động tích cực quan sát được ở bệnh nhân mắc bệnh não do gan nặng hơn, OA dạng uống dường như không ảnh hưởng đến bệnh não do gan nhẹ. Trong một thử nghiệm gần đây, OA đã giảm sự phân hủy protein và kích thích tổng hợp protein trong cơ. Phương pháp điều trị này có ít tác dụng phụ, tăng lên khi liều lượng tiêm tĩnh mạch cao hơn, và được dung nạp tốt sau khi sử dụng qua đường uống và tiêm tĩnh mạch.","The clinical efficacy of both oral and parenteral L-ornithine–L-aspartate (OA) was confirmed by randomized, placebo-controlled, double-blind studies in patients with manifest hepatic encephalopathy and hyperammonemia. The drug was able to reduce high blood ammonia levels induced either by ammonium chloride or protein ingestion or existing as a clinical complication of cirrhosis per se. Furthermore, OA improved performance in Number Connection Test-A as well as mental state gradation. In contrast to the positive effects observed in patients with more advanced hepatic encephalopathy, oral OA does not seem to affect minimal hepatic encephalopathy. In a recent trial, OA decreased protein breakdown and stimulated protein synthesis in muscle. The therapy had little side effects, increasing with higher intravenously administered dosages, and was well tolerated after oral and parenteral administration.",{"EN":1765,"VI":1766},"Clinical Efficacy of L-Ornithine–L-Aspartate in the Management of Hepatic Encephalopathy","Hiệu Quả Lâm Sàng của L-Ornithine–L-Aspartate trong Quản Lý Bệnh Não do Gan",{"VI":1768},"L-ornithine, L-aspartate, bệnh não do gan, tăng ammoniac huyết, nghiên cứu ngẫu nhiên",{"VOID":1770},"Conn, H.O. (1994). The theoretic therapy of hepatic encephalopathy. In: Conn, H.O., and Bircher, J., (eds.), Hepatic Encephalopathy: Syndromes and Therapies, Medi-Ed Press, East Lansing, MI, pp. 135-148.\nCooper, A.J.L., Lai, J.C.R., and Gelbard, A.S. (1989). Ammonia in liver and extrahepatic tissues: An overview of metabolism and toxicity in mammals. In: Butterworth, R.F., Pomier-Layrargues, G. (eds.), Hepatic Encephalopathy: Pathophysiology and Treatment, Humana Press, Clifton, pp. 27-48.\nFleig, W.E., Kircheis, G., Spengler, U., Zeuzem, S.T., Görtelmeyer, R., and The German-Austrian-Swiss Multicenter Study Group (1999). Placebo-controlled, double-blind evaluation of L-ornithine-L-aspartate (LOLA) granules in patients with cirrhosis and subclinical (SHE) or mild overt hepatic encephalopathy (HE). J. Hepatol. 30(Suppl. 1):65 (abstract).\nHäussinger, D. (1983). Hepatocyte heterogeneity in glutamine and ammonia metabolism and the role of an intercellular glutamine cycle during ureogenesis in perfused rat liver. Eur. J. Biochem. 133:269-274.\nHäussinger, D., and Gerok,W. (1984). Hepatocyte heterogeneity in ammonia metabolism: Impairment of glutamine synthetase in CCl4-induced liver cell necrosis with no effect on urea synthesis. Chem. Biol. Interact. 48:191-194.\nHenglein-Ottermann, D. (1976). Der Einfluß von Ornithin-Aspartat auf die experimentell erzeugte Hyperammoniämie. Klinisch-experimentelle Studie. Therapie der Gegenwart 115:1504-1518.\nJessy, J., Mans, A.M., DeJoseph, M.R., and Hawkins, R.A. (1990). Hyperammonaemia causes many of the changes found after portacaval shunting. Biochem. J. 272:311-317.\nKaiser, S., Gerok,W., and Häussinger, D. (1988). Ammonia and glutamine metabolism in human liver slices: New aspects of the pathogenesis of hyperammonemia in chronic liver disease. Eur. J. Clin. Invest. 18:535-542.\nKalk, H. (1958). Die Klinik der akuten Leberinsuffizienz. Gastroenterologia 90:271-290.\nKircheis, G., Metz, M., Frey, S., and Seiller, E. (1996). Correlation between pharmacokinetic aspects and clinical efficacy of L-ornithine-L-aspartate (OA): Results of randomized, controlled clinical trials. J. Hepatol. 25(Suppl.1):131 (abstract).\nKircheis, G., Nilius, R., Berndt, H., Buchner, M., Held, C., Hendricks, R., et al. (1997). Therapeutic efficacy of L-ornithine-L-aspartate infusion concentrate in patients with liver cirrhosis and hepatic encephalopathy: A placebo-controlled double-blind study. Hepatology 25:1351-1360.\nLeonhardt, H., and Bungert, H.J. (1972). Therapie der schweren Hyperammoniämie. Med. Klin. 67:1052-1056.\nMolimard, R., Charpentier, C., and Lemonnier, F. (1982). Modifications de l'amino-acidémie des cirrhotiques sous l'influence de sels d'ornithine. Ann. Nutr. Metab. 26:25-36.\nMorrison, W.L., Bouchier, I.A.D., Gibson, J.N.A., and Rennie, M.J. (1990). Skeletal muscle and whole-body turnover in cirrhosis. Clin. Sci. 78:613-619.\nPomier-Layrargues, G., Giguere, J.F., Lavoie, J., and Butterworth, R.F. (1989) Treatment of hepatic encephalopathy. New perspectives on old ideas. In: Pomier-Layrargues, G., and Butterworth, R.F. (eds.), Hepatic Encephalopathy. Pathophysiology and Treatment, Mumana Press, Clifton, New Jersey, pp. 469-481.\nReynolds, N., Downie, S., Smith, K., Kircheis, G., and Rennie, M.J. (1999). Treatment with L-ornithine-L-aspartate infusion restores muscle protein synthesis responsiveness to feeding in patients with cirrhosis. J. Hepatol. 30(Suppl.1):65 (abstract).\nRiordan, S., and Williams, R. (1997). Treatment of Hepatic Encephalopathy. New Engl. J. Med. 337:473-478.\nStaedt, U., Leweling, H., Gladisch, R., Kortsik, C., Hagmüller, E., and Holm, E. (1993). Effects of ornithine aspartate on plasma ammmonia and plasma amino acids in patients with cirrhosis.Adouble-blind, randomized study using a four-fold crossover design. J. Hepatol. 19:424-430.\nStauch, S., Kircheis, G., Adler, G., Beckh, K., Ditschuneit, H., Görtelmeyer, R., et al. (1998). Oral L-ornithine-L-aspartate therapy of chronic hepatic encephalopathy: Results of a placebo-controlled double-blind study. J. Hepatol. 28:856-864.\nStoll, B., and Häussinger, D. (1989). Functional hepatocyte heterogeneity: Vascular oxoglutarate is almost exclusively taken up by perivenous glutamine-synthetase-containing hepatocytes. Eur. J. Biochem. 181:709-716.\nStoll, B., McNelly, S., Buscher, H.P., and Häussinger, D. (1991). Functional hepatocyte heterogeneity in glutamate, aspartate and ?-ketoglutarate uptake: A histoautoradiographical study. Hepatology 13:247-253.\nWeller, M. (1962). Die Ver Wendemyder Berthelotslien Reubtian Auf Anmnaick.",{"VOID":1772},"10.1023\u002FA:1021934607762","2025-01-23T13:56:10.455+00:00",[30],"https:\u002F\u002Flink.springer.com\u002Farticle\u002F10.1023\u002FA:1021934607762",[1777,1784,1791,1798],{"id":1778,"sortIndex":32,"researcher":28,"roles":1779,"affiliations":1780,"properties":1781,"displayName":1783,"givenName":28,"familyName":28},"0ededbf6-47ca-4535-9a15-c49fd1e976f3",[974],[],{"title":1782},{"VI":1783},"G. Kircheis",{"id":1785,"sortIndex":40,"researcher":28,"roles":1786,"affiliations":1787,"properties":1788,"displayName":1790,"givenName":28,"familyName":28},"d9d57900-61bb-447a-b287-bfac6756926c",[974],[],{"title":1789},{"VI":1790},"M. Wettstein",{"id":1792,"sortIndex":123,"researcher":28,"roles":1793,"affiliations":1794,"properties":1795,"displayName":1797,"givenName":28,"familyName":28},"1247b218-e33e-4c41-b850-ca36e988e21a",[974],[],{"title":1796},{"VI":1797},"S. vom Dahl",{"id":1799,"sortIndex":42,"researcher":28,"roles":1800,"affiliations":1801,"properties":1802,"displayName":1804,"givenName":28,"familyName":28},"4c113b37-82f1-410b-9a92-e84391bd4ae8",[974],[],{"title":1803},{"VI":1804},"D. Häussinger",{"url":1775,"publisher":1806,"properties":1851},{"id":868,"createTime":869,"updateTime":870,"relativeEntities":1807,"slug":872,"properties":1808,"entityType":25,"verifyStatus":882,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":32,"subjectFields":1812,"manageAffiliations":1825,"indexDatabases":1836,"url":28,"thumbnailPath":28,"statistic":28,"gsStatistic":28,"type":28,"analyzePriority":28},[],{"issn":1809,"title":1810,"eissn":1811},{"VOID":877},{"EN":879},{"VOID":875},[1813,1817,1821],{"id":885,"createTime":28,"updateTime":28,"relativeEntities":1814,"label":1815,"description":1816,"parentId":28,"standard":28,"scholarHubFieldId":28},[],{"EN":888},{},{"id":891,"createTime":28,"updateTime":28,"relativeEntities":1818,"label":1819,"description":1820,"parentId":28,"standard":28,"scholarHubFieldId":28},[],{"EN":894},{},{"id":897,"createTime":28,"updateTime":28,"relativeEntities":1822,"label":1823,"description":1824,"parentId":28,"standard":28,"scholarHubFieldId":28},[],{"EN":900},{},[1826,1831],{"id":904,"createTime":28,"updateTime":28,"relativeEntities":1827,"slug":28,"properties":1828,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1830,"statistic":28},[],{"title":1829},{"EN":908},[910],{"id":912,"createTime":28,"updateTime":28,"relativeEntities":1832,"slug":28,"properties":1833,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1835,"statistic":28},[],{"title":1834},{"EN":916},[910],[1837,1844],{"id":920,"indexDatabase":1838,"url":926,"indexYears":927,"academicFieldIds":1843,"indexDatabaseRanking":932},{"id":775,"createTime":28,"updateTime":28,"relativeEntities":1839,"label":1840,"description":1841,"key":781,"publicationTags":1842,"standard":28},[],{"EN":778,"VI":778},{"EN":778,"VI":780},[783],[929,930,931],{"id":934,"indexDatabase":1845,"url":946,"indexYears":28,"academicFieldIds":1850,"indexDatabaseRanking":28},{"id":936,"createTime":28,"updateTime":28,"relativeEntities":1846,"label":1847,"description":1848,"key":943,"publicationTags":1849,"standard":28},[],{"EN":939,"VI":939},{"EN":941,"VI":942},[945,813],[948,949],{"pages":1852,"volume":1854},{"VOID":1853},"453-462",{"VOID":1553},"2002-12-01",[932,945],{"id":1858,"createTime":1859,"updateTime":1860,"relativeEntities":1861,"slug":1862,"properties":1863,"entityType":967,"verifyStatus":26,"verifyTime":1860,"verifyNote":1246,"languages":28,"translateLanguages":28,"viewCount":32,"primaryUrl":1872,"fullTextUrl":28,"authors":1873,"publicationType":1168,"publisherRelationship":1915,"citationCount":28,"citationInfo":28,"publishDate":1966,"publishYear":1967,"citationAnalyzeStatus":882,"lastCitationAnalyze":28,"indexDatabases":1968,"openAccess":28,"references":28,"isForceReanalyzing":1225},"00b6d540-5e68-4a6d-9b78-15e831712cb5","2023-12-24T20:34:24.178+00:00","2025-01-14T22:58:56.362+00:00",[],"Possible-involvement-of-NO-sGC-cGMP-signaling-in-the-antidepressant-like-effect-of-pyridoxine-in-mice",{"abstract":1864,"title":1866,"references":1868,"doi":1870},{"EN":1865},"The present study was designed to determine the antidepressant like effect of pyridoxine in mice. Pyridoxine (12.5, 25 and 50 mg\u002Fkg, i.p.) was administered to the mice and depression related behavioral and neurochemical alterations were determined. It was observed that pyridoxine (50 mg\u002Fkg, i.p.) treatment decreased the immobility period in tail suspension test (TST) and forced swim test (FST) significantly as compared to control. Pyridoxine (50 mg\u002Fkg, i.p.) treatment increased the level of serotonin (5-HT) and decreased the level of nitrite in the brain of mice significantly as compared to control. Pyridoxine thus confer antidepressant like effect by increasing the level of 5-HT and by decreasing the level of nitrite in the brain of mice. Further the influence of nitric oxide (NO)\u002F soluble guanylate cyclase (sGC)\u002F cyclic guanosine monophosphate (cGMP) in antidepressant-like effect of pyridoxine was studied. It was observed that the pretreatment of NO donor (i.e. L-Arginine) and cGMP modulator (i.e. sildenafil) counteracted while the pretreatment of NO\u002FsGC inhibitor (i.e. methylene blue) potentiated the effect of pyridoxine in TST and FST. Pretreatment of NO donor did not influence, pretreatment of NO\u002FsGC inhibitor decreased while the pretreatment of cGMP modulator increased the level of brain nitrite in pyridoxine treated mice. Further the pretreatment of NO donor and cGMP modulator decreased while the pretreatment of NO\u002FsGC inhibitor increased the level of brain serotonin in pyridoxine treated mice. Pyridoxine thus exerted antidepressant like effect and NO-sGC-cGMP signaling modulated the antidepressant like effect of pyridoxine in mice.",{"EN":1867},"Possible involvement of NO-sGC-cGMP signaling in the antidepressant like effect of pyridoxine in mice",{"VOID":1869},"Allen GF, Neergheen V, Oppenheim M, Fitzgerald JC, Footitt E, Hyland K, Heales SJ (2010) Pyridoxal 5′‐phosphate deficiency causes a loss of aromatic l‐amino acid decarboxylase in patients and human neuroblastoma cells, implications for aromatic l‐amino acid decarboxylase and vitamin B6 deficiency states. J Neurochem 114(1):87–96. https:\u002F\u002Fdoi.org\u002F10.1111\u002Fj.1471-4159.2010.06742.x\nAlmeida RC, Felisbino CS, López MG, Rodrigues ALS, Gabilan NH (2006) Evidence for the involvement of L-arginine-nitric oxide-cyclic guanosine monophosphate pathway in the antidepressant-like effect of memantine in mice. 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Pharmacol Biochem Behav 103:408–417. https:\u002F\u002Fdoi.org\u002F10.1016\u002Fj.pbb.2012.09.011",{"VOID":1871},"10.1007\u002Fs11011-021-00858-6","https:\u002F\u002Flink.springer.com\u002Farticle\u002F10.1007\u002Fs11011-021-00858-6",[1874,1889,1902],{"id":1875,"sortIndex":32,"researcher":28,"roles":1876,"affiliations":1877,"properties":1886,"displayName":1888,"givenName":28,"familyName":28},"c2993ec8-5290-45ac-98cf-01da3a3e9e07",[974],[1878],{"id":1879,"sortIndex":32,"affiliation":1880,"properties":28},"4a10b824-0be1-42bf-9167-75d298813680",{"id":1879,"createTime":28,"updateTime":28,"relativeEntities":1881,"slug":28,"properties":1882,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1885,"statistic":28},[],{"title":1883},{"VI":1884},"SGT College of Pharmacy, SGT University, Gurugram, India",[],{"title":1887},{"VI":1888},"Sushma 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growth factor-1 (IGF-1) improves obesity-induced cognitive dysfunction, but its mechanism is not fully clarified. The aim of the study was to reveal whether IGF-1 treated cognitive dysfunction by improving tau pathology and neuronal pyroptosis in high-fat diet mice. During in vitro experiment, C57BL\u002F6J mice were fed with high-fat diet, and were treated with PEG-IGF-1, IGF-1 receptor blocker AXL1717, HO-1 blocker Znpp IX or their combinations. Cognitive function was evaluated using Morris water maze. Expression of Nrf2, HO-1, p-tau, NLRP3, caspase-1 and IL-1β in hippocampus was determined using western blotting. Pyroptosis rate in hippocampus was measured using flow cytometry. During in vivo experiment, HN-h cells were treated with palmitic acid, pyroptosis blocker nonecrosulfonamide or their combinations. The expression of the proteins and rate of pyroptosis were also measured using western blotting and flow cytometry. During in vitro experiment, high-fat diet mice showed cognitive dysfunction, significant hyperphosphorylation of tau protein and neuronal pyroptosis in hippocampus compared with the sham mice. After exogenous IGF-1 treatment, these abnormalities were reversed and Nrf2\u002FHO-1 signaling pathway was activated. Inhibition of the signaling pathway using AXL1717 or Znpp IX re-deteriorated cognitive function, tau pathology and neuronal pyroptosis in hippocampus. During in vivo experiment, inhibition of pyroptosis using nonecrosulfonamide improved tau pathology in palmitic acid-treated HN-h cells. Exogenous IGF-1 improved tau pathology induced by high-fat diet through inhibition of neuronal pyroptosis and activation of Nrf2\u002FHO-1 signaling pathway.",{"EN":1979},"Exogenous IGF-1 improves tau pathology and neuronal pyroptosis in high-fat diet mice with cognitive dysfunction",{"VOID":1981},"Abu-Rumeileh S, Capellari S, Parchi P (2018) Rapidly progressive alzheimer’s disease: contributions to clinical-pathological definition and diagnosis. J Alzheimers Dis 63:887–897\nAl Mamun A, Wu Y, Monalisa I et al (2020) Role of pyroptosis in spinal cord injury and its therapeutic implications. J Adv Res 28:97–109\nAli T, Kim T, Rehman SU et al (2018) Natural dietary supplementation of anthocyanins via PI3K\u002FAkt\u002FNrf2\u002FHO-1 pathways mitigate oxidative stress, neurodegeneration, and memory impairment in a mouse model of Alzheimer’s disease. 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Obes Res Clin Pract 14:119–126\nZhang S, Zhao M, Wang F et al (2020b) Relationship between normal weight obesity and mild cognitive impairment is reflected in cognitive-related genes in human peripheral blood mononuclear cells. Psychogeriatrics 20:35–43\nZhou T, Liu L, Wang Q et al (2020) Naringenin alleviates cognition deficits in high-fat diet-fed SAMP8 mice. J Food Biochem 44:e13375",{"VOID":1983},"10.1007\u002Fs11011-021-00787-4","https:\u002F\u002Flink.springer.com\u002Farticle\u002F10.1007\u002Fs11011-021-00787-4",[1986,2001,2016,2031,2044,2057,2072],{"id":1987,"sortIndex":32,"researcher":28,"roles":1988,"affiliations":1989,"properties":1998,"displayName":2000,"givenName":28,"familyName":28},"bf6440b6-c779-483f-923c-3fe1f3007b83",[974],[1990],{"id":1991,"sortIndex":32,"affiliation":1992,"properties":28},"37c4a15b-7420-4f7f-8ecd-2a09605bb119",{"id":1991,"createTime":28,"updateTime":28,"relativeEntities":1993,"slug":28,"properties":1994,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1997,"statistic":28},[],{"title":1995},{"VI":1996},"Department of Child and Adolescent Psychology, Tianjin Anding Hospital, Tianjin, China",[],{"title":1999},{"VI":2000},"Guanghong 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advances in neuroscience are helping to improve many aspects of human life, inequalities exist in this field between Africa and more scientifically-advanced continents. Many African countries lack the infrastructure and appropriately-trained scientists for neuroscience education and research. Addressing these challenges would require the development of innovative approaches to help improve scientific competence for neuroscience across the continent. In recent years, science-based non-profit organisations (NPOs) have been supporting the African neuroscience community to build state-of-the-art scientific capacity for sustainable education and research. Some of these contributions have included: the establishment of training courses and workshops to introduce African scientists to powerful-yet-cost-effective experimental model systems; research infrastructural support and assistance to establish research institutes. Other contributions have come in the form of the promotion of scientific networking, public engagement and advocacy for improved neuroscience funding. Here, we discuss the contributions of NPOs to the development of neuroscience in Africa.",{"EN":2155},"Building sustainable neuroscience capacity in Africa: the role of non-profit organisations",{"VOID":2157},"Adams J, King C, Hook D (2010) Global Research Report: Africa\nAndrewes D (2013) Neuropsychology: from theory to practice. Psychology Press, New York\nBaden T, Chagas AM, Gage G et al (2015) Open Labware: 3-D printing your own lab equipment. PLoS Biol 13, e1002086. doi:10.1371\u002Fjournal.pbio.1002086\nBlakemore S-J (2008) The social brain in adolescence. Nat Rev Neurosci 9:267–277. doi:10.1038\u002Fnrn2353\nCamerer C, Loewenstein G, Prelec D (2005) Neuroeconomics: how neuroscience can inform economics. J Econ Lit XLIII:9–64\nChu KM, Jayaraman S, Kyamanywa P, Ntakiyiruta G (2014) Building research capacity in Africa: equity and global health collaborations. PLoS Med 11, e1001612. doi:10.1371\u002Fjournal.pmed.1001612\nDocquier F, Rapoport H (2011) Globalization, brain drain and development. Institute for the study of labor, Germany, discussion paper number. 5590, http:\u002F\u002Fftp.iza.org\u002Fdp5590.pdf. Accessed 2 Apr 2015\nDua T, Cumbrera MG, Mathers C, Saxena S (2006) Global burden of neurological disorders: estimates and projections. Neurological diseases: public health challenges. World Health Organization\nDunne E (2014) Neurosciences: Bringing the TReND to Africa. http:\u002F\u002Fblog.lindau-nobel.org\u002Fneurosciences-bringing-the-trend-to-africa\u002F. Accessed 2 Apr 2015\nFranks DD, Turner JH (2012) Handbook of Neurosociology. Springer Science & Business Media, Netherlands\nGendelman HE, Anantharam V, Bronich T et al (2015) Nanoneuromedicines for degenerative, inflammatory, and infectious nervous system diseases. Nanomed Nanotechnol Biol Med. doi:10.1016\u002Fj.nano.2014.12.014\nGeorge-Carey R, Adeloye D, Chan KY et al (2012) An estimate of the prevalence of dementia in Africa: a systematic analysis. J Glob Health 2:020401. doi:10.7189\u002Fjogh.02.020401\nHruby GG (2012) Three requirements for justifying an educational neuroscience. Br J Educ Psychol 82:1–23. doi:10.1111\u002Fj.2044-8279.2012.02068.x\nJuliano SL (2012) Report on the African teaching tools workshops. Neurology 78:1797–1799. doi:10.1212\u002FWNL.0b013e3182583113\nKarikari TK (2015a) Bioinformatics in Africa: the Rise of Ghana? PLoS Comput Biol: in press. doi:10.1371\u002Fjournal.pcbi.1004308\nKarikari TK (2015b) Neuroscience for kids: online resources that promote student engagement, teaching and learning about the brain. J Undergrad Neurosci Educ 13(2):R14–R15\nKarikari TK (2015c) Letter to the editor. J Microbiol Biol Educ 16(1):3–4. doi:10.1128\u002Fjmbe.v16i1.801\nKarikari TK, Aleksic J (2015) Neurogenomics: an opportunity to integrate neuroscience, genomics and bioinformatics research in Africa. Appl Transl Genomics: in press\nKarikari TK, Yawson NA, Amankwaa AO (2015) Bridging the gap: introducing neuroscience to Ghana. Biochemist 37(1):46–47 http:\u002F\u002Fwww.biochemist.org\u002Fbio\u002F03701\u002F0046\u002F037010046.pdf. Accessed 10 Mar 2015\nKBNF (2015) Korle Bu Neuroscience Foundation: Projects. http:\u002F\u002Fkbnf.org\u002Fcurrent-projects\u002F. Accessed 2 Feb 2015\nLewis KE (2006) How do genes regulate simple behaviours? Understanding how different neurons in the vertebrate spinal cord are genetically specified. Philos Trans R Soc Lond B Biol Sci 361:45–66. doi:10.1098\u002Frstb.2005.1778\nMarzullo TC, Gage GJ (2012) The SpikerBox: a low cost, open-source bioamplifier for increasing public participation in neuroscience inquiry. PLoS ONE. doi:10.1371\u002Fjournal.pone.0030837\nMenken M, Munsat TL, Toole JF (2000) The global burden of disease study: implications for neurology. Arch Neurol 57:418–420\nMuindi F, Keller J (2015) Developing world: build neuroscience capacity in Africa. Nature 518:35. doi:10.1038\u002F518035e\nOgundele OM, Ajonijebu DC, Adeniyi PA et al (2014) Cerebrovascular changes in the rat brain in two models of ischemia. Pathophysiology 21:199–209. doi:10.1016\u002Fj.pathophys.2014.08.002\nParslow P (2014) Setting TReNDs in African science! http:\u002F\u002Fplanetearthinstitute.org.uk\u002Fsetting-trends-african-science\u002F. Accessed 2 Feb 2015\nRock D, Schwartz J (2006) The Neuroscience of Leadership. Strategy+business Summer 2006:43\nSofola S (2014) Challenges of teaching and researching physiology in Sub-Saharan Africa. Physiol Bethesda Md 29:150–152. doi:10.1152\u002Fphysiol.00068.2013\nSrikanth M, Kessler JA (2012) Nanotechnology-novel therapeutics for CNS disorders. Nat Rev Neurol 8:307–318. doi:10.1038\u002Fnrneurol.2012.76\nTakahashi T (2012) Molecular neuroeconomics of crime and punishment: implications for neurolaw. Neuro Endocrinol Lett 33:667–673\nThe World Bank (2014) A decade of development in sub-Saharan African science, technology, engineering and mathematics research. 91016, http:\u002F\u002Fdocuments.worldbank.org\u002Fcurated\u002Fen\u002F2014\u002F09\u002F20240847\u002Fdecade-development-sub-saharan-african-science-technology-engineering-mathematics-research. Accessed 23 Mar 2015\nUNESCO (2010) UNESCO Science Report 2010: the current status of science around the world. UNESCO Publishing, Paris\nUSB-ED (2012) The science of NeuroLeadership to make debut in SA. http:\u002F\u002Fwww.usb-ed.com\u002Fcontent\u002FPages\u002FThe-science-of-NeuroLeadership-to-make-debut-in-SA.aspx. Accessed 2 Feb 2015\nYusuf S, Baden T, Prieto-Godino LL (2014) Bridging the Gap: establishing the necessary infrastructure and knowledge for teaching and research in neuroscience in Africa. Metab Brain Dis 29:217–220. doi:10.1007\u002Fs11011-013-9443-x\nZagorski N (2011) Providing a way to support a scientific will. ASBMB Today May 2011 Issue. http:\u002F\u002Fwww.asbmb.org\u002Fasbmbtoday\u002Fasbmbtoday_article.aspx?id=12746. Accessed 23 Mar 2015",{"VOID":2159},"10.1007\u002Fs11011-015-9687-8","https:\u002F\u002Flink.springer.com\u002Farticle\u002F10.1007\u002Fs11011-015-9687-8",[2162,2186,2201],{"id":2163,"sortIndex":32,"researcher":28,"roles":2164,"affiliations":2165,"properties":2183,"displayName":2185,"givenName":28,"familyName":28},"5795ebd5-ff66-40e0-8e21-47c1b6e41bdf",[974],[2166,2174],{"id":2167,"sortIndex":32,"affiliation":2168,"properties":28},"1fecc6bd-fb73-435b-b722-bb1ced9c05e2",{"id":2167,"createTime":28,"updateTime":28,"relativeEntities":2169,"slug":28,"properties":2170,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":2173,"statistic":28},[],{"title":2171},{"VI":2172},"Neuroscience, School of Life Sciences, University of Warwick, Coventry, UK",[],{"id":2175,"sortIndex":40,"affiliation":2176,"properties":2182},"3b4206b3-a9cd-4f4b-a460-48a421c7060b",{"id":2175,"createTime":28,"updateTime":28,"relativeEntities":2177,"slug":28,"properties":2178,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":2181,"statistic":28},[],{"title":2179},{"VI":2180},"Midlands Integrative Biosciences Training Partnership (MIBTP), University of Warwick, Coventry, UK",[],{},{"title":2184},{"VI":2185},"Thomas K. 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Cobham",{"id":2202,"sortIndex":123,"researcher":28,"roles":2203,"affiliations":2204,"properties":2213,"displayName":2215,"givenName":28,"familyName":28},"0928af14-e08d-46d2-8d10-b74990760816",[974],[2205],{"id":2206,"sortIndex":32,"affiliation":2207,"properties":28},"3cc42fde-1a92-480b-a2a6-5e3ee2ff5faa",{"id":2206,"createTime":28,"updateTime":28,"relativeEntities":2208,"slug":28,"properties":2209,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":2212,"statistic":28},[],{"title":2210},{"VI":2211},"Department of Biological Sciences, Ahmadu Bello University, Zaria, Nigeria",[],{"title":2214},{"VI":2215},"Iliya S. 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Older age, HE history and severe liver failure have all been associated with post-TIPS HE but it remains difficult to identify patients at risk. The aim of the present pathophysiological, pilot study was to assess the role of induced hyperammonaemia and associated neuropsychological and neurophysiological changes as predictors of post-TIPS HE. Eighteen TIPS candidates with no overt HE history (56 ± 8 yrs., MELD 11 ± 3) underwent neurophysiological [Electroencephalography (EEG)], neuropsychological [Psychometric Hepatic Encephalopathy Score (PHES) and Scan tests], ammonia and sleepiness assessment at baseline and after the induction of hyperammonaemia by an oral amino acid challenge (AAC). Pre-AAC, 17% of patients had abnormal EEG, 5% abnormal PHES, and 33% abnormal Scan performance. Post-AAC, 17% had abnormal EEG, 0% abnormal PHES, and 17% abnormal Scan performance. Pre-AAC, ammonia concentrations were 201 ± 73 μg\u002FdL and subjective sleepiness 2.5 ± 1.2 (1–9 scale). Post-AAC, patients exhibited the expected increase in ammonia\u002Fsleepiness. Six months post-TIPS, 3 patients developed an episode of HE requiring hospitalization; these showed significantly lower pre-AAC fasting ammonia concentrations compared to patients who did not develop HE (117 ± 63 vs. 227 ± 57 μg\u002FdL p = 0.015). They also showed worse PHES\u002FScan performance pre-AAC, and worse Scan performance post-AAC. Findings at 12 months follow-up (n = 5 HE episodes) were comparable. In conclusion, baseline ammonia levels and both pre- and post-AAC neuropsychiatric indices hold promise in defining HE risk in TIPS candidates with no HE history.",{"EN":2373},"Predictive value of induced hyperammonaemia and neuropsychiatric profiling in relation to the occurrence of post-TIPS hepatic encephalopathy",{"VOID":2375},"Åkerstedt T, Gillberg M (1990) Subjective and objective sleepiness in the active individual. Int J Neurosci 52:29–37\nAl Mardini H, Douglass H, Record C (2006) Amino acid challenge in patients with cirrhosis and control subjects: Ammonia, plasma amino acid and EEG changes. Metab Brain Dis 21:1–10\nAmodio P, Marchetti P, Del Piccolo F et al (1998) Study on the Sternberg paradigm in cirrhotic patients without overt hepatic encephalopathy. Metab Brain Dis 13:159–172\nAmodio P, Marchetti P, Del Piccolo F et al (1999) Spectral versus visual EEG analysis in mild hepatic encephalopathy. Clin Neurophysiol 110:1334–1344\nAmodio P, Montagnese S, Gatta A et al (2004) Characteristics of minimal hepatic encephalopathy. Metab Brain Dis 19:253–267\nAmodio P, Campagna F, Olianas S et al (2008) Detection of minimal hepatic encephalopathy: normalization and optimization of the psychometric hepatic encephalopathy score. A neuropsychological and quantified EEG study. J Hepatol 49:346–353\nAmodio P, Montagnese S, Spinelli G et al (2017) Cognitive reserve is a resilience factor for cognitive dysfunction in hepatic encephalopathy. Metab Brain Dis 32:1287–1293\nBalata S, Damink SW, Ferguson K et al (2003) Induced hyperammonemia alters neuropsychology, brain MR spectroscopy and magnetization transfer in cirrhosis. Hepatology 37:931–939\nBerlioux P, Robic MA, Poirson H et al (2014) Pre-transjugular intrahepatic portosystemic shunts (TIPS) prediction of post-TIPS overt hepatic encephalopathy: the critical flicker frequency is more accurate than psychometric tests. Hepatology. 59:622–629\nBersagliere A, Raduazzo ID, Nardi M et al (2012) Induced hyperammonemia may compromise the ability to generate restful sleep in patients with cirrhosis. Hepatology 55:869–878\nBersagliere A, Raduazzo ID, Schiff S et al (2013) Ammonia-related changes in cerebral electrogenesis in healthy subjects and patients with cirrhosis. Clin Neurophysiol 124:492–646\nCasado M, Bosch J, García-Pagán JC et al (1998) Clinical events after transjugular intrahepatic portosystemic shunt: correlation with hemodynamic findings. Gastroenterology 114:1296–1303\nCasula EP, Bisiacchi PS, Corrias M et al (2015) Acute hyperammonaemia induces a sustained decrease in vigilance, which is modulated by caffeine. Metab Brain Dis 30:143–149\nDel Piccolo F, Sacerdoti D, Amodio P et al (2002) Central nervous system alterations in liver cirrhosis: the role of portal-systemic shunt and portal hypoperfusion. Metab Brain Dis 17:347–358\nDouglass A, Al Mardini H, Record C (2001) Amino acid challenge in patients with cirrhosis: a model for the assessment of treatments for hepatic encephalopathy. J Hepatol 34:658–664\nGuevara M, Baccaro ME, Ríos J et al (2010) Risk factors for hepatic encephalopathy in patients with cirrhosis and refractory ascites: relevance of serum sodium concentration. 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J Hepatol 54:1154–1160\nMcDermott WV, Adams RD (1954) Episodic stupor associated with an Eck fistula in the human with particular reference to the metabolism of ammonia. J Clin Invest 33:1–9\nMontagnese S, Biancardi A, Schiff S et al (2011) Different biochemical correlates for different neuropsychiatric abnormalities in patients with cirrhosis. Hepatology. 53:558–566\nMontagnese S, Schiff S, Turco M et al (2012) Simple tools for complex syndromes: a three-level difficulty test for hepatic encephalopathy. Dig Liver Dis 44:957–960\nNardelli S, Gioia S, Pasquale C et al (2016) Cognitive impairment predicts the occurrence of hepatic encephalopathy after transjugular intrahepatic portosystemic shunt. Am J Gastroenterol 111:523–528\nNolte W, Wiltfang J, Schindler C et al (1998) Portosystemic hepatic encephalopathy after transjugular intrahepatic portosystemic shunt in patients with cirrhosis: clinical, laboratory, psychometric, and electroencephalographic investigations. Hepatology 28:1215–1225\nOng JP, Aggarwal A, Krieger D et al (2003) Correlation between ammonia levels and the severity of hepatic encephalopathy. Am J Med 114:188–193\nOppong KNW, Al-Mardini H, Thick M et al (1997) Oral glutamine challenge in cirrhotics pre- and post-liver transplantation: a psychometric and analyzed EEG study. Hepatology 26:870–876\nParsons-Smith BG, Summerskill WH, Dawson AM et al (1957) The electroencephalograph in liver disease. Lancet 273:867–871\nPhillips GB, Schwartz R, Gabuzda GJ et al (1952) The syndrome of impending hepatic coma in patients with cirrhosis of the liver given certain nitrogenous substances. N Engl J Med 247:239–246\nRiggio O, Merlli M, Pedretti G et al (1996) Hepatic encephalopathy after transjugular intrahepatic portosystemic shunt. Incidence and risk factors. 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Gastroenterology 75:462–469\nRomero-Gómez M, Grande L, Camacho I et al (2002) Altered response to oral glutamine challenge as prognostic factor for overt episodes in patients with minimal hepatic encephalopathy. J Hepatol 37:781–787\nRossle M, Haag K, Ochs A et al (1994) The transjugular intrahepatic portosystemic stent-shunt procedure for variceal bleeding. N Engl J Med 330:165–171\nRössle M, Deibert P, Haag K et al (1997) Randomised trial of transjugular-intrahepatic-portosystemic shunt versus endoscopy plus propranolol for prevention of variceal rebleeding. Lancet 349:1043–1049\nSanyal AJ, Freedman AM, Shiffman ML et al (1994) Portosystemic encephalopathy after transjugular intrahepatic portosystemic shunt: results of a prospective controlled study. Hepatology 20:46–55\nShawcross DL, Wright G, Olde Damink SWM et al (2007) Role of ammonia and inflammation in minimal hepatic encephalopathy. Metab Brain Dis 22:125–138\nSherlock S, Summerskill WH, White LP et al (1954) Portal- systemic encephalopathy; neurological complications of liver disease. Lancet 267:454–457\nSomberg KA, Riegler JL, LaBerge JM et al (1995) Hepatic encephalopathy after transjugular intrahepatic portosystemic shunts: incidence and risk factors. Am J Gastroenterol 90:549–555\nSternberg S (1969) Memory-scanning: mental processes revealed by reaction-time experiments. Am Sci 57:421–457\nVan der Rijt CC, Schalm SW, De Groot GH et al (1984) Objective measurement of hepatic encephalopathy by means of automated EEG analysis. Electroencephalogr Clin Neurophysiol 57:423–426\nVilstrup H, Amodio P, Bajaj J et al (2014) Hepatic encephalopathy in chronic liver disease: 2014 practice guideline by the American Association for the Study of Liver Diseases and the European Association for the Study of the liver. Hepatology 60:715–735\nWatson H, Guevara M, Vilstrup H, Ginès P (2019) Improvement of hyponatremia in cirrhosis is associated with improved complex information processing. J Gastroenterol Hepatol\nWeissenborn K, Ennen JC, Schomerus H et al (2001) Neuropsychological characterization of hepatic encephalopathy. 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