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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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10.1373\u002Fclinchem.2005.057638\nD'Souza, 2004, paracrine actions of natriuretic peptides in the heart, Pharmacol Ther, 101, 113, 10.1016\u002Fj.pharmthera.2003.11.001\nDi Lisa, 2006, Mitochondria and ischemia-reperfusion injury of the heart: fixing a hole, Cardiovasc Res, 70, 191, 10.1016\u002Fj.cardiores.2006.01.016\nSauve, 2010, Genetic deletion or pharmacological inhibition of dipeptidyl peptidase-4 improves cardiovascular outcomes after myocardial infarction in mice, Diabetes, 59, 1063, 10.2337\u002Fdb09-0955\nPost, 2010, Impaired recruitment of HHT-1 mononuclear cells to the ischaemic heart is due to an altered CXCR4\u002FCD26 balance, Cardiovasc Res, 85, 494, 10.1093\u002Fcvr\u002Fcvp313\nMatheeussen, 2012, Dipeptidyl peptidase 4 as a therapeutic target in ischemia\u002Freperfusion injury, Pharmacol Ther, 136, 267, 10.1016\u002Fj.pharmthera.2012.07.012\nYe, 2010, The myocardial infarct size-limiting effect of sitagliptin is PKA-dependent, whereas the protective effect of pioglitazone is partially dependent on PKA, Am J Physiol Heart Circ Physiol, 298, H1454, 10.1152\u002Fajpheart.00867.2009\nScheen, 2013, Cardiovascular effects of dipeptidyl peptidase-4 inhibitors: from risk factors to clinical outcomes, Postgrad Med, 125, 7, 10.3810\u002Fpgm.2013.05.2659\nHocher, 2013, The novel DPP-4 inhibitors linagliptin and BI 14361 reduce infarct size after myocardial ischemia\u002Freperfusion in rats, Int J Cardiol, 167, 87, 10.1016\u002Fj.ijcard.2011.12.007\nJanssen, 2004, Effects of anesthetics on systemic hemodynamics in mice, Am J Physiol Heart Circ Physiol, 287, H1618, 10.1152\u002Fajpheart.01192.2003\nChau, 2011, Mitigation of the progression of heart failure with sildenafil involves inhibition of RhoA\u002FRho-kinase pathway, Am J Physiol Heart Circ Physiol, 300, H2272, 10.1152\u002Fajpheart.00654.2010\nVajda, 2007, Selective cardiac plasma-membrane K(ATP) channel inhibition is defibrillatory and improves survival during acute myocardial ischemia and reperfusion, Eur J Pharmacol, 577, 115, 10.1016\u002Fj.ejphar.2007.08.016\nKanlop, 2011, Granulocyte colony-stimulating factor stabilizes cardiac electrophysiology and decreases infarct size during cardiac ischaemic\u002Freperfusion in swine, Acta Physiol, 202, 11, 10.1111\u002Fj.1748-1716.2011.02259.x\nVillhauer, 2003, 1-[[(3-hydroxy-1-adamantyl)amino]acetyl]-2-cyano-(S)-pyrrolidine: a potent, selective, and orally bioavailable dipeptidyl peptidase IV inhibitor with antihyperglycemic properties, J Med Chem, 46, 2774, 10.1021\u002Fjm030091l\nLivak, 2001, Analysis of relative gene expression data using real-time quantitative PCR and the 2(-Delta C(T)) Method, Methods, 25, 402, 10.1006\u002Fmeth.2001.1262\nSutherland, 2003, Mouse isolated perfused heart: characteristics and cautions, Clin Exp Pharmacol Physiol, 30, 867, 10.1046\u002Fj.1440-1681.2003.03925.x\nSchmidt, 2014, Novel adjunctive treatments of myocardial infarction, World J Cardiol, 6, 434, 10.4330\u002Fwjc.v6.i6.434\nFuentes-Antrás, 2015, Targeting metabolic disturbance in the diabetic heart, Cardiovasc Diabetol, 14\nYin, 2011, Early and late effects of the DPP-4 inhibitor vildagliptin in a rat model of post-myocardial infarction heart failure, Cardiovasc Diabetol, 10, 85, 10.1186\u002F1475-2840-10-85\nRamos, 2009, Ischemia\u002Freperfusion is an independent trigger for increasing myocardial content of mRNA B-type natriuretic peptide, Heart Vessels, 24, 454, 10.1007\u002Fs00380-009-1148-z\ndos Santos, 2013, Circulating dipeptidyl peptidase IV activity correlates with cardiac dysfunction in human and experimental heart failure, Circ Heart Fail, 6, 1029, 10.1161\u002FCIRCHEARTFAILURE.112.000057\nBurley, 2007, GMP and protein kinase-G in myocardial ischaemia-reperfusion: opportunities and obstacles for survival signaling, Br J Pharmacol, 152, 855, 10.1038\u002Fsj.bjp.0707409\nBurley, 2007, B-type natriuretic peptide at early reperfusion limits infarct size in the rat isolated heart, Basic Res Cardiol, 102, 529, 10.1007\u002Fs00395-007-0672-1\nRen, 2010, B-type natriuretic peptide pretreatment attenuates heart ischemia-reperfusion injury in rats, Transplant Proc, 42, 4496, 10.1016\u002Fj.transproceed.2010.09.163\nFadini, 2011, Cardiovascular effects of DPP-4 inhibition: beyond GLP-1, Vascul Pharmacol, 55, 10, 10.1016\u002Fj.vph.2011.05.001\nChaykovska, 2011, Effects of DPP-4 inhibitors on the heart in a rat model of uremic cardiomyopathy, PLoS One, 6, e27861, 10.1371\u002Fjournal.pone.0027861\nSergeeva, 2013, Regulation of expression of atrial and brain natriuretic peptide, biomarkers for heart development and disease, Biochim Biophys Acta, 1832, 2403, 10.1016\u002Fj.bbadis.2013.07.003\nHu, 2017, DPP-4 (CD26) inhibitor sitagliptin exerts anti-inflammatory effects on rat insulinoma (RINm) cells via suppressing NF-(B activation, Endocrine, 55, 754, 10.1007\u002Fs12020-016-1073-8\nZeng, 2014, The DPP-4 inhibitor sitagliptin attenuates the progress of atherosclerosis in apolipoprotein-E-knockout mice via AMPK- and MAPK-dependent mechanisms, Cardiovasc Diabetol, 4, 32, 10.1186\u002F1475-2840-13-32\nPotter, 2006, Natriuretic peptides, their receptors, and cyclic guanosine monophosphate-dependent signaling functions, Endocr Rev, 27, 47, 10.1210\u002Fer.2005-0014\nGerassimou, 2007, Regulation of the expression of soluble guanylyl cyclase by reactive oxygen species, Br J Pharmacol, 150, 1084, 10.1038\u002Fsj.bjp.0707179\nKristian, 1998, Calcium in ischemic cell death, Stroke, 29, 705, 10.1161\u002F01.STR.29.3.705\nGupta, 2012, Sitagliptin: anti-platelet effect in diabetes and healthy volunteers, Platelets, 23, 565, 10.3109\u002F09537104.2012.721907\nDai, 2014, DPP-4 inhibitors repress foam cell formation by inhibiting scavenger receptors through protein kinase C pathway, Acta Diabetol, 51, 471, 10.1007\u002Fs00592-013-0541-3\nFerreira, 2010, Effects of sitagliptin treatment on dysmetabolism, inflammation, and oxidative stress in an animal model of type 2 diabetes (ZDF rat), Mediators Inflamm, 2010, 592760, 10.1155\u002F2010\u002F592760\nAndreadou, 2006, Acute administration of vitamin E triggers preconditioning via K(ATP) channels and cyclic-GMP without inhibiting lipid peroxidation, Free Radic Biol Med, 41, 1092, 10.1016\u002Fj.freeradbiomed.2006.06.021\nInserte, 2013, Activation of cGMP\u002Fprotein kinase G pathway in postconditioned myocardium depends on reduced oxidative stress and preserved endothelial nitric oxide synthase coupling, J Am Heart Assoc, 2, e005975, 10.1161\u002FJAHA.112.005975\nGourine, 2005, Endothelin-1 exerts a preconditioning-like cardioprotective effect against ischaemia\u002Freperfusion injury via the ET(A) receptor and the mitochondrial K(ATP) channel in the rat in vivo, Br J Pharmacol, 144, 331, 10.1038\u002Fsj.bjp.0706050\nCavalheiro, 2010, Potent cardioprotective effect of the 4-anilinoquinazoline derivative PD153035: involvement of mitochondrial K(ATP) channel activation, PLoS One, 5, e10666, 10.1371\u002Fjournal.pone.0010666\nOerlemans, 2013, Targeting cell death in the reperfused heart: pharmacological approaches for cardioprotection, Int J Cardiol, 165, 410, 10.1016\u002Fj.ijcard.2012.03.055\nHalestrap, 2009, What is the mitochondrial permeability transition pore?, J Mol Cell Cardiol, 46, 821, 10.1016\u002Fj.yjmcc.2009.02.021\nFliss, 1996, Apoptosis in ischemic and reperfused rat myocardium, Circ Res, 79, 949, 10.1161\u002F01.RES.79.5.949\nWhelan, 2010, Cell death in the pathogenesis of heart disease: mechanisms and significance, Annu Rev Physiol, 72, 19, 10.1146\u002Fannurev.physiol.010908.163111\nKung, 2011, Programmed necrosis, not apoptosis, in the heart, Circ Res, 108, 1017, 10.1161\u002FCIRCRESAHA.110.225730\nNakagawa, 2005, Cyclophilin D-dependent mitochondrial permeability transition regulates some necrotic but not apoptotic cell death, Nature, 434, 652, 10.1038\u002Fnature03317\nMarques, 2014, Sitagliptin prevents inflammation and apoptotic cell death in the kidney of type 2 diabetic animals, Mediators Inflamm, 2014, 538737, 10.1155\u002F2014\u002F538737\nMega, 2014, Sitagliptin prevents aggravation of endocrine and exocrine pancreatic damage in the Zucker Diabetic Fatty rat – focus on amelioration of metabolic profile and tissue cytoprotective properties, Diabetol Metab Syndr, 6, 42, 10.1186\u002F1758-5996-6-42\nKim, 2014, The nonglycemic actions of dipeptidyl peptidase-4 inhibitors, BioMed Res Int, 2014, 368703, 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of lithium on bone mechanical properties in the presence and deficiency of estrogens in rats",{"VOID":1288},"10.1016\u002FS1734-1140(10)71184-1","https:\u002F\u002Flinkinghub.elsevier.com\u002Fretrieve\u002Fpii\u002FS1734114010711841",[1291,1306],{"id":1292,"sortIndex":32,"researcher":28,"roles":1293,"affiliations":1294,"properties":1303},"361412ab-4a46-4d7e-9a80-13ddfdcf7284",[1011],[1295],{"id":1296,"sortIndex":32,"affiliation":1297,"properties":28},"331391b2-15cb-4fbe-8b8f-e8fe1d33fca2",{"id":1296,"createTime":28,"updateTime":28,"relativeEntities":1298,"slug":28,"properties":1299,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1302,"statistic":28},[],{"title":1300},{"VI":1301},"Department of Pharmacology, Medical University of Silesia, Sosnowiec, Poland",[],{"title":1304},{"VI":1305},"Dorota 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ultraviolet B (UVB) from solar radiation increases the generation of reactive oxygen species (ROS), which mediate the production of matrix metalloproteinases (MMPs), and acts mainly on the epidermis layer of the skin. This study was aimed at assessing the anti-photoaging effects of dehydroglyasperin C isolated from Glycyrrhiza uralensis Fisch on MMPs levels in HaCaT human keratinocytes and to elucidate the underlying mechanism. The cell viability was measured by MTT assay. Expression, phosphorylation and enzymatic activity of the protein were examined using ELISA, Western blot or gelatin zymography. Intracellular ROS measurement was evaluated by fluorescent ELISA and 2′,7′-dichlorodihydrofluorescein diacetate (H2 DCF-DA) assay. In the present study, we found that dehydroglyasperin C markedly inhibited UVB-mediated expression of collagenase (MMP-1) and gelatinase (MMP-9) by inhibiting ROS generation. Dehydroglyasperin C treatment also decreased the UVB irradiation-mediated activation of mitogen-activated protein kinase (MAPK), c-Jun phosphorylation, and c-Fos expression. In addition, the down-regulation of UVB-induced c-Jun phosphorylation caused by dehydroglyasperin C treatment was more than the down-regulation of c-Fos expression in the HaCaT human keratinocytes. Our results indicated that dehydroglyasperin C may function as a potential anti-photoaging agent by inhibiting UVB-mediated MMPs expression via suppression of MAPK and AP-1 signaling.",{"EN":1382},"The effect of dehydroglyasperin C on UVB–mediated MMPs expression in human HaCaT cells",{"VOID":1384},"Rittie L, Fisher GJ. Natural and sun-induced aging of human skin. Cold Spring Harb Perspect Med 2015;5(1):a015370, doi:https:\u002F\u002Fdoi.org\u002F10.1101\u002Fcshperspect.a015370.\nLee HJ, Hwang E, Park B, Zhang M, Sun ZW, Lee DG, et al. Methanol extract of bitter melon alleviates UVB-induced MMPs expression via MAP kinase and AP-1 signaling in human dermal fibroblasts in vitro. Phytother Res 2016;30(9):1519–26.\nRittie L, Fisher GJ. UV-light-induced signal cascades and skin aging. Ageing Res Rev 2002;1(4):705–20.\nAfaq F, Adhami VM, Mukhtar H. Photochemoprevention of ultraviolet B signaling and photocarcinogenesis. Mutat Res. 2005;571:153–73.\nKammeyer A, Luiten RM. Oxidation events and skin aging. Ageing Res Rev 2015;21:16–29.\nPark SN, Kim MJ, Ha JH, Lee NH, Park J, Lee J, et al. Protective effects of TES trioleate, an inhibitor of phospholipase A2, on reactive oxygen species and UVA-induced cell damage. J Photochem Photobiol B 2016;164:30–5.\nPittayapruek P, Meephansan J, Prapapan O, Komine M, Ohtsuki M. Role of matrix metalloproteinases in photoaging and photocarcinogenesis. Int J Mol Sci 2016;17(6):868.\nGuo PJ, Sun ZR, Liu WL, Chen L, Du Y, Wei XX. Correlation analysis between the rate of respiration in the root and the active components in licorice (Glycyrrhiza uralensis). Exp Ther Med 2014;7:270–4.\nSong W, Si L, Ji S, Wang H, Fang XM, Yu LY, et al. Uralsaponins M-Y, antiviral triterpenoid saponins from the roots of Glycyrrhiza uralensis. J Nat Prod 2014;77(7):1632–43.\nYang N, Patil S, Zhuge J, Wen MC, Bolleddula J, Doddaga S, et al. Glycyrrhiza uralensis flavonoids present in anti-asthma formula, ASHMI, inhibit memory Th2 responses in vitro and in vivo. Phytother Res 2013;27(9):1381–91.\nAsl MN, Hosseinzadeh H. Review of pharmacological effects of Glycyrrhiza sp. and its bioactive compounds. Phytother Res 2008;22(6):709–24.\nAyeka PA, Bian Y, Mwitari PG, Chu X, Zhang Y, Uzayisenga R, et al. Immunomodulatory and anticancer potential of Gan cao (Glycyrrhiza uralensis Fisch.) polysaccharides by CT-26 colon carcinoma cell growth inhibition and cytokine IL-7 upregulation in vitro. BMC Complement Altern Med 2016;16(1):206.\nKim HJ, Seo JY, Suh HJ, Lim SS, Kim JS. Antioxidant activities of licorice-derived prenylflavonoids. Nutr Res Pract 2012;6(6):491–8.\nLee JH, Kim JE, Jang YJ, Lee CC, Lim TG, Jung SK, et al. Dehydroglyasperin C suppresses TPA-induced cell transformation through direct inhibition of MKK4 and PI3K. Mol Carcinog 2016;55(5):552–62.\nKim HJ, Lim SS, Park IS, Lim JS, Seo JY, Kim JS. Neuroprotective effects of dehydroglyasperin C through activation of heme oxygenase-1 in mouse hippocampal cells. J Agric Food Chem 2012;60(22):5583–9.\nKim J, Shim J, Lee S, Lim SS, Lee KW, Lee HJ. Licorice-derived dehydroglyasperin C increases MKP-1 expression and suppresses inflammation-mediated neurodegeneration. Neurochem Int 2013;63(8):732–40.\nSeo JY, Lee YS, Kim HJ, Lim SS, Lim JS, Lee IA, et al. Dehydroglyasperin C isolated from licorice caused Nrf2-mediated induction of detoxifying enzymes. J Agric Food Chem 2010;58(3):1603–8.\nFrankowski H, Gu YH, Heo JH, Milner R, Del Zoppo GJ. Use of gel zymography to examine matrix metalloproteinase (gelatinase) expression in brain tissue or in primary glial cultures. Methods Mol Biol 2012;814:221–33.\nYoshihisa Y, Rehman MU, Shimizu T. Astaxanthin A xanthophyll carotenoid, inhibits ultraviolet-induced apoptosis in keratinocytes. Exp Dermatol 2014;23(3):178–83.\nKondo S. The roles of cytokines in photoaging. J Dermatol Sci 2000;23(Suppl. 1):S30–6.\nFagot D, Asselineau D, Bernerd F. Direct role of human dermal fibroblasts and indirect participation of epidermal keratinocytes in MMP-1 production after UV-B irradiation. Arch Dermatol Res 2002;293:576–83.\nKim M, Park YG, Lee HJ, Lim SJ, Nho CW. Youngiasides A and C isolated from Youngia denticulatum inhibit UVB-induced MMP expression and promote type I procollagen production via repression of MAPK\u002FAP-1\u002FNF-kappaB and activation of AMPK\u002FNrf2 in HaCaT cells and human dermal fibroblasts. J Agric Food Chem 2015;63(22):5428–38.\nSteinbrenner H, Ramos MC, Stuhlmann D, Sies H, Brenneisen P. UVA-mediated downregulation of MMP-2 and MMP-9 in human epidermal keratinocytes. Biochem Biophys Res Commun 2003;308(3):486–91.\nFisher GJ, Talwar HS, Lin JY, Lin PP, McPhillips F, Wang ZQ, et al. Retinoic acid inhibits induction of c-Jun protein by ultraviolet radiation that occurs subsequent to activation of mitogen-activated protein kinase pathways in human skin in vivo. J Clin Invest 1998;101(6):1432–40.\nHwang YP, Oh KN, Yun HJ, Jeong HG. The flavonoids apigenin and luteolin suppress ultraviolet A-induced matrix metalloproteinase-1 expression via MAPKs and AP-1-dependent signaling in HaCaT cells. J Dermatol Sci 2011;61(1):23–31.\nNatarajan VT, Ganju P, Ramkumar A, Grover R, Gokhale RS. Multifaceted pathways protect human skin from UV radiation. Nat Chem Biol 2014;10:542–51.\nKim HH, Shin CM, Park CH, Kim KH, Cho KH, Eun HC, et al. Eicosapentaenoic acid inhibits UV-induced MMP-1 expression in human dermal fibroblasts. J Lipid Res 2005;46(8):1712–20.\nTobin DJ. Introduction to skin aging. J Tissue Viability 2017;26(1):37–46.\nFisher GJ, Wang ZQ, Datta SC, Varani J, Kang S, Voorhees JJ. Pathophysiology of premature skin aging induced by ultraviolet light. N Engl J Med 1997;337(20):1419–28.\nAmano S, Ogura Y, Akutsu N, Matsunaga Y, Kadoya K, Adachi E, et al. Protective effect of matrix metalloproteinase inhibitors against epidermal basement membrane damage: skin equivalents partially mimic photoageing process. Br J Dermatol 2005;153(Suppl. 2):37–46.\nKim KJ, Xuan SH, Park SN. Licoricidin, an isoflavonoid isolated from Glycyrrhiza uralensis Fisher, prevents UVA-induced photoaging of human dermal fibroblasts. Int J Cosmet Sci 2016, doi:https:\u002F\u002Fdoi.org\u002F10.1111\u002Fics.12357.\nPlotnikov A, Zehorai E, Procaccia S, Seger R. The MAPK cascades: signaling components, nuclear roles and mechanisms of nuclear translocation. Biochim Biophys Acta 2011;1813(9):1619–33.\nPark SG, Kim SH, Kim KY, Yu SN, Choi HD, Kim YW, et al. Toyocamycin induces apoptosis via the crosstalk between reactive oxygen species and p38\u002FERK MAPKs signaling pathway in human prostate cancer PC-3 cells. 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Peripheral corticotropin-releasing factor (CRF) induces stimulation of gastric contractions in freely moving conscious rats: role of CRF receptor types 1 and 2, Neurogastroenterol Motil, 25, 190, 10.1111\u002Fnmo.12050\nRivier, 2014, Corticotropin-releasing factor peptide antagonists: design, characterization and potential clinical relevance, Front Neuroendocrinol, 35, 161, 10.1016\u002Fj.yfrne.2013.10.006\nParkes, 2001, Cardiovascular actions of CRH and urocortin: an update, Peptides, 22, 821, 10.1016\u002FS0196-9781(01)00396-5\nRademaker, 2011, Prolonged urocortin 2 administration in experimental heart failure: sustained hemodynamic, endocrine, and rVERl effects, Hypertension, 57, 1136, 10.1161\u002FHYPERTENSIONAHA.111.173203\nLiew, 2012, Therapeutic benefit of urocortin in rats with intracerebral hemorrhage, J Neurosurg, 116, 193, 10.3171\u002F2011.8.JNS101637\nRademaker, 2011, Urocortin 2 sustains haemodynamic and rVERl function during introduction of beta-blockade in experimental heart failure, J Hypertens, 29, 1787, 10.1097\u002FHJH.0b013e3283493776\nKageyama, 2003, Vasodilative effects of urocortin II via protein kinase A and a mitogen-activated protein kinase in rat thoracic aorta, J Cardiovasc Pharmacol, 42, 561, 10.1097\u002F00005344-200310000-00015\nRademaker, 2007, Urocorti administration from onset of rapid left ventricular pacing represses progression to overt heart failure, J Am Phys, 293, H1536\nLiu, 2005, In vivo protective effects of urocortin on ischemia\u002Freperfusion injury in rat heart via free radical mechanisms, Can J Physiol Pharmacol, 83, 459, 10.1139\u002Fy05-033\nCalderón-Sánchez, 2011, Cardioprotective action of urocortin in postconditioning involves recovery of intracellular calcium handling, Cell Calcium, 50, 84, 10.1016\u002Fj.ceca.2011.05.010\nScarabelli, 2002, Urocortin promotes hemodynamic and bioenergetic recovery and improves cell survival in the isolated rat heart exposed to ischemia\u002Freperfusion, J Am Coll Cardiol, 40, 155, 10.1016\u002FS0735-1097(02)01930-7\nWamhoff, 2004, L-type voltage-gated Ca2+ channels modulate expression of smooth muscle differentiation marker genes via a rho kinase\u002Fmyocardin\u002FSRF – dependent mechanism, Circ Res, 95, 406, 10.1161\u002F01.RES.0000138582.36921.9e\nEmeto, 2014, Urocortin 2 is associated with abdominal aortic aneurysm and mediates anti-proliferative effects on vascular smooth muscle cells via corticotrophin releasing factor receptor 2, Clin Sci (Lond), 126, 517, 10.1042\u002FCS20130425\nKageyama, 2012, Regulation and roles of urocortins in the vascular system, Int J Endocrinol, 2012, 873723, 10.1155\u002F2012\u002F873723\nRademaker, 2013, Interactions of enhanced urocortin 2 and mineralocorticoid receptor antagonism in experimental heart failure, Circ Heart Fail, 6, 825, 10.1161\u002FCIRCHEARTFAILURE.112.000205\nWang, 2013, Intravenous injection of urocortin 1 induces a CRF2 mediated increase in circulating ghrelin and glucose levels through distinct mechanisms in rats, Peptides, 39, 164, 10.1016\u002Fj.peptides.2012.11.009\nChitravanshi, 2012, Bradycardic effects of microinjections of urocortin 3 into the nucleus ambiguus of the rat, Am J Physiol Regul Integr Comp Physiol, 303, R1023, 10.1152\u002Fajpregu.00224.2012\nJin, 2011, Different effects of corticotropin-releasing factor and urocortin 2 on apoptosis of prostate cancer cells in vitro, J Mol Endocrinol, 47, 219, 10.1530\u002FJME-11-0048\nLiew, 2012, Systemic administration of urocortin after intracerebral hemorrhage reduces neurological deficits and neuroinflammation in rats, Neuroinflammation, 19, 13, 10.1186\u002F1742-2094-9-13\nNovembri, 2011, Urocortin 2 and urocortin 3 in endometriosis: evidence for a possible role in inflammatory response, Mol Hum Reprod, 17, 587, 10.1093\u002Fmolehr\u002Fgar020\nChen-Scarabelli, 2013, The cardioprotective effects of urocortin are mediated via activation of the Src tyrosine kinase-STAT3 pathway, JAKSTAT, 2, e24812\nLi, 2013, Urocortin 2 autocrine\u002Fparacrine and pharmacologic effects to activate AMP-activated protein kinase in the heart, Proc Natl Acad Sci USA, 110, 16133, 10.1073\u002Fpnas.1312775110",{"VOID":1712},"10.1016\u002Fj.pharep.2014.10.017","https:\u002F\u002Fwww.sciencedirect.com\u002Fscience\u002Farticle\u002Fpii\u002FS1734114014003296",[1715,1730,1745,1758,1771,1784,1797],{"id":1716,"sortIndex":32,"researcher":28,"roles":1717,"affiliations":1718,"properties":1727},"1dac76bf-3827-4bfa-8422-910272c8fac2",[1011],[1719],{"id":1720,"sortIndex":32,"affiliation":1721,"properties":28},"f17f8a12-87f2-496e-8449-3cf05bb660f9",{"id":1720,"createTime":28,"updateTime":28,"relativeEntities":1722,"slug":28,"properties":1723,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1726,"statistic":28},[],{"title":1724},{"VI":1725},"Department of Pharmacology, Liaoning Medical University, JinZhou, 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bowel syndrome (IBS) is a chronic condition with recurring gastrointestinal (GI) symptoms: altered motility and abdominal pain. As endogenous opioid system participates in pain perception and in the control of GI peristalsis, opioids have been proposed as a promising therapy in IBS. In a previous study, we observed that morphiceptin derivative, P-317 (Dmt-cyclo-(d-Lys-Phe-d-Pro-Asp)-NH2), presents promising features to be applied in IBS. In this project, we tested whether modifications in cyclic morphiceptin-based structure: fluorination (compound 1) or peptide bond reduction (compound 2) improve pharmacological effect. We evaluated tested derivatives in the mouse GI system under physiological (GI transit) and pathophysiological (castor oil diarrhea, stress-induced hypermotility, visceral pain) conditions. Both compounds prolonged GI transit. Compound 1 and P-317 inhibited upper GI transit and motility of the colon; compound 2 remained inactive. Compound 1 and P-317 inhibited hypermotility in stressed mice and delayed the acute diarrhea in comparison to control. Only P-317 exerted antinociceptive effect. None of tested derivatives, similar to P-317, affected locomotor activity. Compound 1 is equally effective as P-317 in the mouse GI tract. The peptide bond reduction decreased the activity of compound 2. Fluorination appears to be an efficient way to increase the effects of morphiceptin analogs in the GI tract.",{"EN":1875},"Cyclic derivatives of morphiceptin possess anti-transit effect in the gastrointestinal tract and alleviate abdominal pain in mice",{"VOID":1877},"Enck P, Aziz Q, Barbara G, Farmer AD, Fukudo S, Mayer EA, et al. Irritable bowel syndrome. Nat Rev Dis Prim. 2016;2:16014. https:\u002F\u002Fwww.ncbi.nlm.nih.gov\u002Fpubmed\u002F27159638.\nZeevenhooven J, Koppen IJN, Benninga MA. The new Rome IV criteria for functional gastrointestinal disorders in infants and toddlers. Pediatr Gastroenterol Hepatol Nutr. 2017;20(1):1.\nSobczak M, Sałaga M, Storr MA, Fichna J. Physiology, signaling, and pharmacology of opioid receptors and their ligands in the gastrointestinal tract: current concepts and future perspectives. J Gastroenterol. 2014;49(1):24–45. https:\u002F\u002Fwww.ncbi.nlm.nih.gov\u002Fpubmed\u002F23397116.\nJarmuż A, Banaszek M, Leń K, Storr M, Zielińska M, Fichna J. The role of MOP and DOP receptors in treatment of diarrhea-predominant irritable bowel syndrome. Mini Rev Med Chem. 2016. https:\u002F\u002Fwww.ncbi.nlm.nih.gov\u002Fpubmed\u002F27494159.\nAwouters F, Megens A, Verlinden M, Schuurkes J, Niemegeers C, Janssen PAJ. Loperamide. Dig Dis Sci. 1993;38(6):977–95. https:\u002F\u002Flink.springer.com\u002F10.1007\u002FBF01295711.\nShen K-F, Crain SM. Biphalin, an enkephalin analog with unexpectedly high antinociceptive potency and low dependence liability in vivo, selectively antagonizes excitatory opioid receptor functions of sensory neurons in culture. Brain Res. 1995;701(1–2):158–66. https:\u002F\u002Flinkinghub.elsevier.com\u002Fretrieve\u002Fpii\u002F0006899395009991.\nLi M, Zhou L, Ma G, Dong S. Analgesic properties of chimeric peptide based on morphiceptin and PFRTic-amide. Regul Pept. 2012;179(1–3):23–8. https:\u002F\u002Fwww.ncbi.nlm.nih.gov\u002Fpubmed\u002F22960407.\nLembo AJ, Lacy BE, Zuckerman MJ, Schey R, Dove LS, Andrae DA, et al. Eluxadoline for irritable bowel syndrome with diarrhea. N Engl J Med. 2016;374(3):242–53.\nGach K, do-Rego JC, Fichna J, Storr M, Delbro D, Toth G, et al. Synthesis and biological evaluation of novel peripherally active morphiceptin analogs. Peptides. 2010;31(8):1617–24. https:\u002F\u002Fwww.sciencedirect.com\u002Fscience\u002Farticle\u002Fabs\u002Fpii\u002FS0196978110001725?via%3Dihub.\nZielińska M, Chen C, Mokrowiecka A, Cygankiewicz AI, Zakrzewski PK, Sałaga M, et al. Orally administered novel cyclic pentapeptide P-317 alleviates symptoms of diarrhoea-predominant irritable bowel syndrome. J Pharm Pharmacol. 2015;67(2):244–54. https:\u002F\u002Fwww.ncbi.nlm.nih.gov\u002Fpubmed\u002F25515402.\nSobczak M, Cami-Kobeci G, Sałaga M, Husbands SM, Fichna J. Novel mixed NOP\u002FMOP agonist BU08070 alleviates pain and inhibits gastrointestinal motility in mouse models mimicking diarrhea-predominant irritable bowel syndrome symptoms. Eur J Pharmacol. 2014;736:63–9.\nZielińska M, Jarmuż A, Sałaga M, Lipkowski AW, Fichna J. Mixed MOP\u002FDOP agonist biphalin elicits anti-transit effect in mouse models mimicking diarrhea-predominant irritable bowel syndrome symptoms. Pharmacol Rep. 2016;68(1):32–6. https:\u002F\u002Fwww.ncbi.nlm.nih.gov\u002Fpubmed\u002F26721348.\nPels K, Kodadek T. Solid-phase synthesis of diverse peptide tertiary amides by reductive amination. ACS Comb Sci. 2015;17(3):152–5. https:\u002F\u002Fwww.ncbi.nlm.nih.gov\u002Fpubmed\u002F25695359.\nWang J, Sa M, Acen L, del Pozo C, Sorochinsky AE, Fustero S, et al. 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New morphine analogs produce peripheral antinociception within a certain dose range of their systemic administration. J Pharmacol Exp Ther. 2016;359(1):171–81.",{"VOID":1879},"10.1007\u002Fs43440-020-00084-4","http:\u002F\u002Flink.springer.com\u002F10.1007\u002Fs43440-020-00084-4",[1882,1897,1910,1934,1954,1967],{"id":1883,"sortIndex":32,"researcher":28,"roles":1884,"affiliations":1885,"properties":1894},"8726b079-a021-46be-8110-a28f6cf6e837",[1011],[1886],{"id":1887,"sortIndex":32,"affiliation":1888,"properties":28},"4c43be48-a002-4eea-b7ba-6d54862145fd",{"id":1887,"createTime":28,"updateTime":28,"relativeEntities":1889,"slug":28,"properties":1890,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1893,"statistic":28},[],{"title":1891},{"VI":1892},"Department of Biochemistry, Faculty of Medicine, Medical University of Lodz, Lodz, Poland",[],{"title":1895},{"VI":1896},"Agata 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cancer is one of the most common malignant neoplasms in men. Because of the increase in the number of cases as well as development of cancers resistant to conventional therapy, identification of the new molecular targets for the treatment and prevention is of great importance. For this purpose, many studies are aimed on revealing of molecular mechanisms of prostate cancer development. In this process, dietary lipids and environmental xenobiotics are largely involved and are considered as risk factors. A wide range of endogenous (cholesterol, polyunsaturated fatty acids, etc.) and exogenous (pollutants, drugs) compounds are metabolized in the human organism by cytochrome P450. From other hand, these compounds may alter cytochrome P450 expression levels, especially in prostate, which, in turn, affects cell metabolism. Cytochrome P450 is a member of signaling pathways, regulating cell cycle, apoptosis, invasion and adhesion. Hence, cytochrome P450 most probably plays the important role in initiation and progression of prostate cancer. Based on that, cytochrome P450 enzymes are considered as potential targets for the targeted therapy and prevention, and might serve as specific markers of malignant growth. © 2019 Maj Institute of Pharmacology, Polish Academy of Sciences. Published by Elsevier B.V. All rights reserved.",{"EN":2045},"Dietary lipids and environmental xenobiotics as risk factors for prostate cancer: The role of cytochrome P450",{"VOID":2047},"Bostwick DG, Burke HB, Djakiew D, Euling S, Ho SM, Landolph J, et al. Human prostate cancer risk factors. Cancer 2004;101(10 Suppl):2371–490.\nBidoli E, Talamini R, Bosetti C, Negri E, Maruzzi D, Montella M, et al. Macronutrients, fatty acids, cholesterol and prostate cancer risk. Ann Oncol 2005;16:152–7.\nNithipatikom K, Campbell WB. Roles of eicosanoids in prostate cancer. Future Lipidol 2008;3:453–67.\nLiu Q, Luo Q, Halim A, Song G. Targeting lipid metabolism of cancer cells: a promising therapeutic strategy for cancer. 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Role of NF-kappaB in the regulation of cytochrome P450 enzymes. Curr Drug Metab 2009;10:164–78.\nLeach DA, Powell SM, Bevan C. Women in cancer thematic review: new roles for nuclear receptors in prostate cancer. Endocr-Relat Cancer. 2016;23:T85–T108.\nKajanne R, Miettinen P, Tenhunen M, Leppä S. Transcription factor AP-1 promotes growth and radioresistance in prostate cancer cells. Int J Oncol 2009;35:1175–82.\nFujii-Kuriyama Y, Mimura J. Molecular mechanisms of AhR functions in the regulation of cytochrome P450 genes. Biochem Biophys Res Commun 2005;338:311–7.\nQin S, Liu D, Kohli M, Wang L, Vedell PT, Hillman DW, et al. TSPYL family regulates CYP17A1 and CYP3A4 expression: potential mechanism contributing to abiraterone response in metastatic castration-resistant prostate cancer. Clin Pharmacol Ther 2018;104:201–10.\nWahlang B, Falkner KC, Cave MC, Prough RA. Role of cytochrome P450 monooxygenase in carcinogen and chemotherapeutic drug metabolism. Adv Pharmacol 2015;74:1–33.\nKumagai J, Fujimura T, Takahashi S, Urano T, Ogushi T, et al. Cytochrome P450 2B6 is a growth-inhibitory and prognostic factor for prostate cancer. Prostate 2007;67:1029–37.\nAgündez JA, Martinez C, Olivera M, Gallardo L, Ladero JM, Rosado C, et al. Expression in human prostate of drug-and carcinogen-metabolizing enzymes: association with prostate cancer risk. Br J Cancer 1998;78:1361–7.\nZeigler-Johnson C. CYP3A4: a potential prostate cancer risk factor for high-risk groups. Clin J Oncol Nurs 2001;5:153–4.\nLeskela S, Honrado E, Montero-Conde C, Landa I, Cascon A, et al. Cytochrome P450 3A5 is highly expressed in normal prostate cells but absent in prostate cancer. Endocr Relat Cancer 2007;14:645–54.",{"VOID":2049},"10.1016\u002Fj.pharep.2019.04.011","https:\u002F\u002Flinkinghub.elsevier.com\u002Fretrieve\u002Fpii\u002FS1734114019300477",[2052,2067],{"id":2053,"sortIndex":32,"researcher":28,"roles":2054,"affiliations":2055,"properties":2064},"d78c944e-166c-46d0-a787-b0075119371a",[1011],[2056],{"id":2057,"sortIndex":32,"affiliation":2058,"properties":28},"14946dcb-54dd-4c87-bf1e-b7085b7dba15",{"id":2057,"createTime":28,"updateTime":28,"relativeEntities":2059,"slug":28,"properties":2060,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":2063,"statistic":28},[],{"title":2061},{"VI":2062},"Department of Molecular Oncogenetics, Institute of Molecular Biology and Genetics NAS Ukraine, Kyiv, Ukraine",[],{"title":2065},{"VI":2066},"Oksana 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the principles of multimodal analgesic therapy is necessary to provide appropriate comfort for the patient after surgery. The main objective of the study was evaluating the influence of perioperative intravenous (i.v.) lidocaine infusion on postoperative morphine requirements during the first 48 h postoperatively in children undergoing major spine surgery. Prospective, randomized, double-blind study: 41 children, qualified to multilevel spine surgery, were randomly divided into two treatment groups: lidocaine and placebo (control). The lidocaine group received lidocaine as a bolus of 1.5 mg\u002Fkg over 30 minutes, followed by a continuous infusion at 1 mg\u002Fkg\u002Fh to 6 hours after surgery. The protocol of perioperative management was identical for all patients. Measurements: morphine demand, intensity of postoperative pain (the Numerical Rating Scale), oral feeding initiation time, first attempts at assuming erect position, postoperative quality of life (the Acute Short-form \u002FSF-12\u002F health survey). Patient data did not differ demographically. Compared to the control group, lidocaine treatment reduced the demand for morphine during the first 24h [95% CI 0.13 (0.11-0.28) mg\u002Fkg, p = 0.0122], 48h [95% CI 0.46 (0.22-0.52) mg\u002Fkg, p = 0.0299] after surgery and entire hospitalization [95% CI 0.58 (0.19-0.78) mg\u002Fkg, p = 0.04]; postoperative pain intensity; nutritional withdrawal period [introduction of liquid diet (p = 0.024) and solid diet (p = 0.012)], and accelerated the adoption of an upright position [sitting (p = 0.048); walking (p = 0.049)]. The SF-12 generic health survey did not differ between groups before operation, 2 months and 4 years after surgery. Perioperative lidocaine administration, as a part of the applied analgesic therapy regimen, may decrease postoperative opioid demand and accelerates convalescence of children undergoing major surgery.",{"EN":2154},"Lidocaine as an element of multimodal analgesic therapy in major spine surgical procedures in children: a prospective, randomized, double-blind study",{"VOID":2156},"Shapiro G, Green DW, Fatica NS, Boachie-Adjei O. Medical complications in scoliosis surgery. Curr Opin Pediatr. 2001;13:36–41.\nRusy LM, Hainsworth KR, Nelson TJ, Czarnecki ML, Tassone JC, Thometz JG, et al. Gabapentin use in pediatric spinal fusion patients: a randomized, double-blind, controlled trial. Anesth Analg. 2010;110(5):1393–8. https:\u002F\u002Fdoi.org\u002F10.1213\u002FANE.0b013e3181d41dc2.\nFarag E, Ghobrial M, Sessler DI, Dalton JE, Liu J, Lee JH, et al. Effect of perioperative intravenous lidocaine administration on pain, opioid consumption, and quality of life after complex spine surgery. Anesthesiology. 2013;119(4):932–40. https:\u002F\u002Fdoi.org\u002F10.1097\u002FALN.0b013e318297d4a5.\nRosero EB, Joshi GP. Preemptive, preventive, multimodal analgesia: what do they really mean? Plast Reconstr Surg. 2014;134(4 Suppl 2):85S–93S. https:\u002F\u002Fdoi.org\u002F10.1097\u002FPRS.0000000000000671.\nMergeay M, Verster A, Van Aken D, Vercauteren M. Regional versus general anesthesia for spine surgery. A comprehensive review. Acta Anaesthesiol Belg. 2015;66(1):1–9.\nChoudhry DK, Brenn BR, Sacks K, Shah S. Evaluation of gabapentin and clonidine use in children following spinal fusion surgery for idiopathic scoliosis: A retrospective review. J Pediatr Orthop. 2017. https:\u002F\u002Fdoi.org\u002F10.1097\u002FBPO.0000000000000989\nJabbour HJ, Naccache NM, Jawish RJ, Abou Zeid HA, Jabbour KB, Rabbaa-Khabbaz LG, et al. Ketamine and magnesium association reduces morphine consumption after scoliosis surgery: prospective randomised double-blind study. Acta Anaesthesiol Scand. 2014;58(5):572–9. https:\u002F\u002Fdoi.org\u002F10.1111\u002Faas.12304.\nChoi YS, Shim JK, Song JW, Kim JC, Yoo YC, Kwak YL. Combination of pregabalin and dexamethasone for postoperative pain and functional outcome in patients undergoing lumbar spinal surgery: a randomized placebo-controlled trial. Clin J Pain. 2013;29(1):9–14. https:\u002F\u002Fdoi.org\u002F10.1097\u002FAJP.0b013e318246d1a9.\nKhan JS, Yousuf M, Victor JC, Sharma A, Siddiqui N. An estimation for an appropriate end time for an intraoperative intravenous lidocaine infusion in bowel surgery: a comparative meta-analysis. J Clin Anesth. 2016;28:95–104. https:\u002F\u002Fdoi.org\u002F10.1016\u002Fj.jclinane.2015.07.007.\nJendoubi A, Naceur IB, Bouzouita A, Trifa M, Ghedira S, Chebil M, et al. A comparison between intravenous lidocaine and ketamine on acute and chronic pain after open nephrectomy: a prospective, double-blind, randomized, placebo-controlled study. Saudi J Anaesth. 2017;11:177–84.\nWeibel S, Jokinen J, Pace NL, Schnabel A, Hollmann MW, Hahnenkamp K, et al. Efficacy and safety of intravenous lidocaine for postoperative analgesia and recovery after surgery: a systematic review with trial sequential analysis. Br J Anaesth. 2016;116(6):770–83. https:\u002F\u002Fdoi.org\u002F10.1093\u002Fbja\u002Faew101.\nGonzález MM, Altermatt F. Is intravenous lidocaine effective for decreasing pain and speeding up recovery after surgery? Medwave. 2017;17(9):e7121. https:\u002F\u002Fdoi.org\u002F10.5867\u002Fmedwave.2017.09.7121.\nYousefshahi F, Predescu O, Francisco AJ. The efficacy of systemic lidocaine in the management of chronic pain: a literature review. Anesth Pain Med. 2017;7(3):e44732. https:\u002F\u002Fdoi.org\u002F10.5812\u002Faapm.44732.\nTauzin-Fin P, Bernard O, Sesay M, Biais M, Richebe P, Quinart A, et al. Benefits of intravenous lidocaine on post-operative pain and acute rehabilitation after laparoscopic nephrectomy. J Anaesthesiol Clin Pharmacol. 2014;30(3):366–72. https:\u002F\u002Fdoi.org\u002F10.4103\u002F0970-9185.137269.\nDe Oliveira GS, Fitzgerald P, Streicher LF, Marcus RJ, McCarthy RJ. Systemic lidocaine to improve postoperative quality of recovery after ambulatory laparoscopic surgery. Anesth Analg. 2012;115(2):262–7. https:\u002F\u002Fdoi.org\u002F10.1213\u002FANE.0b013e318257a380.\nIbrahim A, Aly M, Farrag W. Effect of intravenous lidocaine infusion on long-term postoperative pain after spinal fusion surgery. Medicine (Baltimore). 2018;97(13):e0229. https:\u002F\u002Fdoi.org\u002F10.1097\u002FMD.0000000000010229.\nKranke P, Jokinen J, Pace NL, Schnabel A, Hollmann MW, Hahnenkamp K, et al. Continuous intravenous perioperative lidocaine infusion for postoperative pain and recovery. Cochrane Database Syst Rev. 2015. https:\u002F\u002Fdoi.org\u002F10.1002\u002F14651858.CD009642.pub2.\nGandek B, Ware JE, Aaronson NK, Apolone G, Bjorner JB, Brazier JE, et al. Cross-validation of item selection and scoring for the SF-12 Health Survey in nine countries: Results from the IQOLA Project. International Quality of Life Assessment. J Clin Epidemiol. 1998;51(11):1171–8.\nAmerican Society of Anesthesiologists Task Force on Acute Pain Management. Practice guidelines for acute pain management in the perioperative setting: an updated report by the American Society of Anesthesiologists Task Force on Acute Pain Management. Anesthesiology. 2012;116(2):248–73. https:\u002F\u002Fdoi.org\u002F10.1097\u002FALN.0b013e31823c1030.\nSotgiu ML, Biella G, Castagna A, Lacerenza M, Marchettini P. Different time-courses of i.v. lidocaine effect on ganglionic and spinal units in neuropathic rats. NeuroReport. 1994;5(8):873–6.\nvan der Wal SE, van den Heuvel SA, Radema SA, van Berkum BF, Vaneker M, Steegers MA, et al. The in vitro mechanisms and in vivo efficacy of intravenous lidocaine on the neuroinflammatory response in acute and chronic pain. Eur J Pain. 2016;20(5):655–74. https:\u002F\u002Fdoi.org\u002F10.1002\u002Fejp.794.\nCepeda MS, Lau J, Carr DB. Defining the therapeutic role of local anesthetic sympathetic blockade in complex regional pain syndrome: a narrative and systematic review. Clin J Pain. 2002;18(4):216–33.\nTanelian DL, MacIver MB. Analgesic concentrations of lidocaine suppress tonic A-delta and C fiber discharges produced by acute injury. Anesthesiology. 1991;74(5):934–6.\nLahav M, Levite M, Bassani L, Lang A, Fidder H, Tal R, et al. Lidocaine inhibits secretion of IL-8 and IL-1beta and stimulates secretion of IL-1 receptor antagonist by epithelial cells. Clin Exp Immunol. 2002;127(2):226–33.\nDocherty RJ, Ginsberg L, Jadoon S, Orrell RW, Bhattacharjee A. TRPA1 insensitivity of human sural nerve axons after exposure to lidocaine. Pain. 2013;154(9):1569–77.\nGronwald C, Vegh V, Hollmann MW, Hahnenkamp A, Garaj V, Hahnenkamp K. The inhibitory potency of local anesthetics on NMDA receptor signalling depends on their structural features. Eur J Pharmacol. 2012;674(1):13–9.\nWerdehausen R, Kremer D, Brandenburger T, Schlösser L, Jadasz J, Küry P, et al. Lidocaine metabolites inhibit glycine transporter 1: a novel mechanism for the analgesic action of systemic lidocaine? Anesthesiology. 2012;116(6):1404 (Erratum).\nKościelniak-Merak B, Batko I, Fleszar M, Kocot-Kępska M, Gamian A, Kobylarz K, et al. Effect of intravenous, perioperative-administrated lidocaine on serum levels of endocannabinoids and related N-acylethanolamines in children. Miner Anestesiol. 2019. https:\u002F\u002Fdoi.org\u002F10.23736\u002FS0375-9393.19.13703-0.\nKościelniak-Merak B, Batko I, Kobylarz K, Sztefko K, Kocot-Kępska M, Tomasik PJ. Impact of intravenous, perioperative-administrated lidocaine on postoperative serum levels of endogenous opioids in children. Curr Pharm Des. 2019;25(30):3209–15. https:\u002F\u002Fdoi.org\u002F10.2174\u002F1381612825666190718153209.\nVigneault L, Turgeon AF, Côté D, Lauzier F, Zarychanski R, Moore L, et al. Perioperative intravenous lidocaine infusion for postoperative pain control: a meta-analysis of randomized controlled trials. Can J Anaesth. 2011;58(1):22–37. https:\u002F\u002Fdoi.org\u002F10.1007\u002Fs12630-010-9407-0.\nDewinter G, Moens P, Fieuws S, Vanaudenaerde B, Van de Velde M, Rex S. Systemic lidocaine fails to improve postoperative morphine consumption, postoperative recovery and quality of life in patients undergoing posterior spinal arthrodesis. A double-blind, randomized, placebo-controlled trial. Br J Anaesth. 2017;118(4):576–85. https:\u002F\u002Fdoi.org\u002F10.1093\u002Fbja\u002Faex038.\nKim KT, Cho DC, Sung JK, Kim YB, Kang H, Song KS, et al. Intraoperative systemic infusion of lidocaine reduces postoperative pain after lumbar surgery: a double-blinded, randomized, placebo-controlled clinical trial. Spine J. 2014;14(8):1559–666. https:\u002F\u002Fdoi.org\u002F10.1016\u002Fj.spinee.2013.09.031.",{"VOID":2158},"10.1007\u002Fs43440-020-00100-7","2024-12-30T22:31:40.678+00:00","https:\u002F\u002Flink.springer.com\u002F10.1007\u002Fs43440-020-00100-7",[2162,2177,2192,2205,2227],{"id":2163,"sortIndex":32,"researcher":28,"roles":2164,"affiliations":2165,"properties":2174},"a6daa0d6-3681-4563-994e-75b6619faa63",[1011],[2166],{"id":2167,"sortIndex":32,"affiliation":2168,"properties":28},"28449f91-c24a-4011-a867-f050b48a8628",{"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},"Department of Anesthesiology and Intensive Care, University Children’s Hospital, Cracow, Poland",[],{"title":2175},{"VI":2176},"Ilona Batko",{"id":2178,"sortIndex":40,"researcher":28,"roles":2179,"affiliations":2180,"properties":2189},"a9367304-dd42-43ce-a75b-9706327cc6f6",[1011],[2181],{"id":2182,"sortIndex":32,"affiliation":2183,"properties":28},"f1c6fc3f-9640-4f3d-8aa1-51b9ad69f876",{"id":2182,"createTime":28,"updateTime":28,"relativeEntities":2184,"slug":28,"properties":2185,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":2188,"statistic":28},[],{"title":2186},{"VI":2187},"Department of Clinical Biochemistry, University Children’s Hospital, Jagiellonian University Medical College, Cracow, Poland",[],{"title":2190},{"VI":2191},"Barbara Kościelniak-Merak",{"id":2193,"sortIndex":123,"researcher":28,"roles":2194,"affiliations":2195,"properties":2202},"29851636-1379-48bb-b787-5fa84f916729",[1011],[2196],{"id":2182,"sortIndex":32,"affiliation":2197,"properties":28},{"id":2182,"createTime":28,"updateTime":28,"relativeEntities":2198,"slug":28,"properties":2199,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":2201,"statistic":28},[],{"title":2200},{"VI":2187},[],{"title":2203},{"VI":2204},"Przemysław J. 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