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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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I., 1975, Phlegmouous gastritis, Gastroenterology, 68, 231, 10.1016\u002FS0016-5085(75)80003-5",{"doi":1186},"10.1016\u002FS0016-5085(75)80003-5",{"id":28,"text":1188,"url":28,"identifiers":1189},"10.1136\u002Fgut.29.7.909",{"doi":1188},{"id":28,"text":1191,"url":28,"identifiers":1192},"Paull G., 1989, Campylobacter pylori in Gastritis and Peptic Ulcer Disease, 73",{},{"id":28,"text":1194,"url":28,"identifiers":1195},"Ramirez‐Ramos A., 1987, Campylobacter pyloridis in a developing country, Gastroenterology, 92, 1588",{},{"id":28,"text":1197,"url":28,"identifiers":1198},"Dwyer B., 1989, Campylobacter pylori and Gastroduodenal Disease, 190",{},{"id":28,"text":1200,"url":28,"identifiers":1201},"10.1128\u002FJCM.27.8.1870-1873.1989",{"doi":1200},false,{"id":1204,"createTime":1205,"updateTime":1205,"relativeEntities":1206,"slug":1207,"properties":1208,"entityType":964,"verifyStatus":26,"verifyTime":1205,"verifyNote":965,"languages":1221,"translateLanguages":28,"viewCount":32,"primaryUrl":1222,"fullTextUrl":28,"authors":1223,"publicationType":986,"publisherRelationship":1387,"citationCount":1437,"citationInfo":1438,"publishDate":1442,"publishYear":1439,"citationAnalyzeStatus":884,"lastCitationAnalyze":28,"indexDatabases":1443,"openAccess":28,"references":1444,"isForceReanalyzing":1202},"ca00d820-f95f-49c3-ab65-1ca09fe55940","2024-09-18T22:37:33.339+00:00",[],"Nonalcoholic-fatty-liver-disease-is-associated-with-an-almost-twofold-increased-risk-of-incident-type-2-diabetes-and-metabolic-syndrome-Evidence-from-a-systematic-review-and-meta-analysis",{"openalex":1209,"mag":1211,"abstract":1213,"title":1215,"pm":1217,"doi":1219},{"VOID":1210},"W2264982161",{"VOID":1212},"2264982161",{"EN":1214},"\u003Cjats:title>Abstract\u003C\u002Fjats:title>\u003Cjats:sec>\u003Cjats:title>Background and Aim:\u003C\u002Fjats:title>\u003Cjats:p>The magnitude of the risk of incident type 2 diabetes (T2D) and metabolic syndrome (MetS) among patients with nonalcoholic fatty liver disease (NAFLD) is poorly known. We gauged the risk of developing T2D and MetS in patients with NAFLD diagnosed by either serum liver enzymes (aminotransferases or gamma‐glutamyltransferase [GGT]) or ultrasonography.\u003C\u002Fjats:p>\u003C\u002Fjats:sec>\u003Cjats:sec>\u003Cjats:title>Methods:\u003C\u002Fjats:title>\u003Cjats:p>Pertinent prospective studies were identified through extensive electronic database research, and studies fulfilling enrolment criteria were included in the meta‐analysis.\u003C\u002Fjats:p>\u003C\u002Fjats:sec>\u003Cjats:sec>\u003Cjats:title>Results\u003C\u002Fjats:title>\u003Cjats:p>Overall, in a pooled population of 117020 patients (from 20 studies), who were followed‐up for a median period of 5 years (range: 3–14.7 years), NAFLD was associated with an increased risk of incident T2D with a pooled relative risk of 1.97 (95% confidence interval [CI], 1.80–2.15) for alanine aminotransferase, 1.58 (95% CI, 1.43–1.74) for aspartate aminotransferase, 1.86 (95% CI, 1.71–2.03) for GGT (last \u003Cjats:italic>vs\u003C\u002Fjats:italic> first quartile or quintile), and 1.86 (95% CI, 1.76–1.95) for ultrasonography, respectively. Overall, in a pooled population of 81411 patients (from eight studies) who were followed‐up for a median period of 4.5 years (range: 3–11 years), NAFLD was associated with an increased risk of incident MetS with a pooled relative risk of 1.80 (95% CI, 1.72–1.89) for alanine aminotransferase (last \u003Cjats:italic>vs\u003C\u002Fjats:italic> first quartile or quintile), 1.98 (95% CI, 1.89–2.07) for GGT, and 3.22 (95% CI, 3.05–3.41) for ultrasonography, respectively.\u003C\u002Fjats:p>\u003C\u002Fjats:sec>\u003Cjats:sec>\u003Cjats:title>Conclusions:\u003C\u002Fjats:title>\u003Cjats:p>Nonalcoholic fatty liver disease, as diagnosed by either liver enzymes or ultrasonography, significantly increases the risk of incident T2D and MetS over a median 5‐year follow‐up.\u003C\u002Fjats:p>\u003C\u002Fjats:sec>",{"EN":1216},"Nonalcoholic fatty liver disease is associated with an almost twofold increased risk of incident type 2 diabetes and metabolic syndrome. 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cell death induced by stresses such as ischemia‐reperfusion, cholestasis and drug toxicity can trigger a sterile inflammatory response with activation of innate immune cells through release of damage‐associated molecular patterns (DAMPs). A similar inflammatory response can be induced by pathogen‐associated molecular patterns (PAMPs) such as endotoxin. Both DAMPs and PAMPs activate through toll‐like receptors the resident macrophages (Kupffer cells) and recruit activated neutrophils and monocytes into the liver. Central to this inflammatory response is promotion of reactive oxygen species (ROS) formation by these phagocytes. ROS are the principal toxic mediators by which inflammatory cells kill their targets, e.g. bacteria during host defense but also hepatocytes and other liver cells. The mechanism of ROS‐induced cell killing during inflammation involves the promotion of mitochondrial dysfunction through an intracellular oxidant stress in hepatocytes leading mainly to oncotic necrosis and less apoptosis. The additional release of cell contents amplifies the inflammatory injury. However, an inflammatory oxidant stress insufficient to directly cause cell damage can induce transcription of stress defence genes including antioxidant genes. This preconditioning effect of ROS enhances the resistance against future inflammatory oxidant stress and promotes the initiation of tissue repair processes. Despite the substantial progress in our understanding of mechanisms of inflammatory liver injury during the last decade, more research is necessary to better understand the role of ROS in acute liver inflammation and to develop clinically applicable therapeutic strategies that selectively target the detrimental effects of oxidant stress without compromising the vital function of ROS in host defense.\u003C\u002Fjats:p>",{"EN":1683},"Reactive oxygen and mechanisms of inflammatory liver injury: Present concepts",{"VOID":1685},"21199529",{"VOID":1687},"10.1111\u002Fj.1440-1746.2010.06592.x","2024-09-23T11:42:18.469+00:00",[31],"https:\u002F\u002Fonlinelibrary.wiley.com\u002Fdoi\u002F10.1111\u002Fj.1440-1746.2010.06592.x",[1692],{"id":1693,"sortIndex":32,"researcher":28,"roles":1694,"affiliations":1695,"properties":1704,"displayName":1708,"givenName":28,"familyName":28},"d39e724d-bd2b-4521-b92e-4a406fecc5d7",[],[1696],{"id":1697,"sortIndex":32,"affiliation":1698,"properties":28},"735dbaaf-55bf-454d-938d-cc011655fcba",{"id":1697,"createTime":28,"updateTime":28,"relativeEntities":1699,"slug":28,"properties":1700,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1703,"statistic":28},[],{"title":1701},{"EN":1702},"Department of Pharmacology, Toxicology and Therapeutics, University of Kansas Medical Center, Kansas City, 66160, USA. hjaeschke@kumc.edu",[],{"orcid":1705,"title":1707,"openalex":1709},{"VOID":1706},"https:\u002F\u002Forcid.org\u002F0000-0002-8695-6980",{"EN":1708},"Hartmut Jaeschke",{"VOID":1710},"A5087156903",{"url":28,"publisher":1712,"properties":1754},{"id":868,"createTime":869,"updateTime":870,"relativeEntities":1713,"slug":872,"properties":1714,"entityType":25,"verifyStatus":884,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":32,"subjectFields":1719,"manageAffiliations":1728,"indexDatabases":1739,"url":943,"thumbnailPath":28,"statistic":28,"gsStatistic":28,"type":28,"analyzePriority":28},[],{"country":1715,"eissn":1716,"issn":1717,"title":1718},{"VOID":875},{"VOID":877},{"VOID":879},{"EN":881},[1720,1724],{"id":887,"createTime":28,"updateTime":28,"relativeEntities":1721,"label":1722,"description":1723,"parentId":28,"standard":28,"scholarHubFieldId":28},[],{"EN":890},{},{"id":893,"createTime":28,"updateTime":28,"relativeEntities":1725,"label":1726,"description":1727,"parentId":28,"standard":28,"scholarHubFieldId":28},[],{"EN":896},{},[1729,1734],{"id":900,"createTime":28,"updateTime":28,"relativeEntities":1730,"slug":28,"properties":1731,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1733,"statistic":28},[],{"title":1732},{"EN":904},[],{"id":907,"createTime":28,"updateTime":28,"relativeEntities":1735,"slug":28,"properties":1736,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1738,"statistic":28},[],{"title":1737},{"EN":911},[],[1740,1747],{"id":915,"indexDatabase":1741,"url":927,"indexYears":28,"academicFieldIds":1746,"indexDatabaseRanking":28},{"id":917,"createTime":28,"updateTime":28,"relativeEntities":1742,"label":1743,"description":1744,"key":924,"publicationTags":1745,"standard":28},[],{"EN":920,"VI":920},{"EN":922,"VI":923},[926,813],[929],{"id":931,"indexDatabase":1748,"url":937,"indexYears":938,"academicFieldIds":1753,"indexDatabaseRanking":942},{"id":786,"createTime":28,"updateTime":28,"relativeEntities":1749,"label":1750,"description":1751,"key":792,"publicationTags":1752,"standard":28},[],{"EN":789,"VI":789},{"EN":789,"VI":791},[794],[940,941],{"issue":1755,"pages":1757,"volume":1759},{"VOID":1756},"s1",{"VOID":1758},"173-179",{"VOID":1760},"26",537,{"total":1761,"publishYear":1763,"statisticByYear":1764},2011,{"2012":353,"2013":436,"2014":279,"2015":208,"2016":152,"2017":148,"2018":279,"2019":353,"2020":139,"2021":69,"2022":133,"2023":352,"2024":146},"2011-01-01",[942,926],[1768,1771,1774,1777,1780,1783,1786,1789,1792,1795,1798,1801,1804,1807,1810,1813,1816,1819,1822,1825,1828,1831,1834,1837,1840,1843,1846,1849,1852,1856,1859,1862,1865,1868,1871,1874,1877,1880,1883,1886,1889,1892,1896,1899,1902,1905,1908,1911,1914,1917,1920,1923,1926,1929,1932,1935,1938,1941,1944,1947,1950,1953,1956,1959,1962,1965,1968,1971,1974,1977,1980,1983,1986,1989,1992,1995,1998],{"id":28,"text":1769,"url":28,"identifiers":1770},"10.1152\u002Fajpgi.00568.2005",{"doi":1769},{"id":28,"text":1772,"url":28,"identifiers":1773},"10.1096\u002Ffasebj.4.15.2253850",{"doi":1772},{"id":28,"text":1775,"url":28,"identifiers":1776},"10.1002\u002Fhep.1840170523",{"doi":1775},{"id":28,"text":1778,"url":28,"identifiers":1779},"Jaeschke H, 1991, Neutrophil‐induced liver cell injury in endotoxin shock is a CD11b\u002FCD18‐dependent mechanism, Am. 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Invest., 119, 2304",{},{"id":2002,"createTime":2003,"updateTime":2003,"relativeEntities":2004,"slug":2005,"properties":2006,"entityType":964,"verifyStatus":26,"verifyTime":2019,"verifyNote":965,"languages":2020,"translateLanguages":28,"viewCount":32,"primaryUrl":2021,"fullTextUrl":28,"authors":2022,"publicationType":986,"publisherRelationship":2084,"citationCount":2132,"citationInfo":2133,"publishDate":2136,"publishYear":2134,"citationAnalyzeStatus":884,"lastCitationAnalyze":28,"indexDatabases":2137,"openAccess":28,"references":2138,"isForceReanalyzing":1202},"6523596f-32d7-456f-8934-008ede47937d","2024-11-26T17:17:50.629+00:00",[],"Epidemiological-characteristics-and-risk-factors-of-hepatocellular-carcinoma",{"openalex":2007,"mag":2009,"abstract":2011,"title":2013,"pm":2015,"doi":2017},{"VOID":2008},"W2159670669",{"VOID":2010},"2159670669",{"EN":2012},"\u003Cjats:title>ABSTRACT\u003C\u002Fjats:title>\u003Cjats:p>Hepatocellular carcinoma (HCC) is one of the major cancers in the world. There is a striking variation in HCC incidence rates between various countries, with a highest‐to‐lowest ratio of 112.5 for males and 54.7 for females. The high‐risk populations are clustered in sub‐Saharan Africa and eastern Asia. The male‐to‐female ratio for HCC ranges from &lt; 1 to 6.4 and mostly from 2 to 4. There exist significant variations in the incidence of HCC among different ethnic groups living in the same area and among migrants of the same ethnic groups living in different areas. The age curves of HCC are significantly different in various countries, suggesting variability in exposure to risk factors. Chronic carriers of hepatitis B and C viruses (HBV and HCV, respectively) have an increased risk of HCC. The relative and attributable HCC risk of HBV and HCV carrier status varies in different countries. There exists a synergistic interaction on HCC between the two viruses. Aflatoxin exposure, cigarette smoking, heavy alcohol consumption, low vegetable intake, inorganic arsenic ingestion, radioactive thorium dioxide exposure, iron overload and the use of oral contraceptives and anabolic steroids have been documented as HCC risk factors. Recent molecular epidemiological studies have shown that low serum retinol levels as well as elevated serum levels of testosterone, \u003Cjats:italic>neu\u003C\u002Fjats:italic> oncoprotein and aflatoxin B\u003Cjats:sub>1\u003C\u002Fjats:sub>‐albumin adduct are associated with an increased HCC risk. There is a synergistic interaction on HCC between chronic HBV infection and aflatoxin exposure. Familial aggregation of HCC exists and a major susceptibility gene of HCC has been hypothesized. Patients of some genetic diseases are at an increased risk of HCC. The genetic polymorphisms of cytochrome P450 2E1 and 2D6 and arylamine \u003Cjats:italic>N\u003C\u002Fjats:italic>‐acetyltransferase 2 are associated with the development of HCC. A doseresponse relationship between aflatoxin exposure and HCC has been observed among chronic HBV carriers who have null genotypes of glutathione \u003Cjats:italic>S\u003C\u002Fjats:italic>‐transferase M1 or T1, but not among those who have non‐null genotypes. Human hepatocarcinogenesis is a multistage process with the involvement of a multifactorial aetiology. 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Genet, 49, 88",{},{"id":28,"text":2449,"url":28,"identifiers":2450},"HuangKL.Familial aggregation study of hepatocellular carcinoma in the Penghu Islets.Masters thesis Graduate Institute of Public Health National Taiwan University Taipei Taiwan .1994.",{},{"id":28,"text":2452,"url":28,"identifiers":2453},"10.1016\u002F0016-5085(95)90587-1",{"doi":2452},{"id":28,"text":2455,"url":28,"identifiers":2456},"10.1097\u002F00008571-199612000-00003",{"doi":2455},{"id":28,"text":2458,"url":28,"identifiers":2459},"10.1016\u002F0304-3835(96)04209-7",{"doi":2458},{"id":28,"text":2461,"url":28,"identifiers":2462},"10.1038\u002F350427a0",{"doi":2461},{"id":28,"text":2464,"url":28,"identifiers":2465},"10.1038\u002F350429a0",{"doi":2464},{"id":28,"text":2467,"url":28,"identifiers":2468},"Yu MW, 1994, Correlations of chronic hepatitis B virus infection and cigarette smoking with elevated expression of neu oncoprotein in the development of hepatocellular carcinoma, Cancer Res, 54, 5106",{},{"id":28,"text":2470,"url":28,"identifiers":2471},"10.1111\u002Fj.1440-1746.1993.tb01670.x",{"doi":2470},{"id":28,"text":2473,"url":28,"identifiers":2474},"Simon D, 1991, Chromosome abnormalities in peripheral blood cells of hepatitis B virus chronic carriers, Cancer Res, 51, 6176",{},{"id":28,"text":2476,"url":28,"identifiers":2477},"10.1073\u002Fpnas.86.22.8852",{"doi":2476},{"id":28,"text":2479,"url":28,"identifiers":2480},"10.1111\u002Fj.1349-7006.1990.tb02534.x",{"doi":2479},{"id":28,"text":2482,"url":28,"identifiers":2483},"Fujimori M, 1991, Allelotype study of primary hepatocellular carcinoma, Cancer Res, 51, 89",{},{"id":28,"text":2485,"url":28,"identifiers":2486},"Beasley RP., 1982, Hepatitis B virus as the etiologic agent in hepatocellular carcinoma: Epidemiologic considerations, Hepatology, 2, S21",{},{"id":28,"text":2488,"url":28,"identifiers":2489},"Chen DS., 1980, Neoplasm of the Liver, 71",{},{"id":28,"text":2491,"url":28,"identifiers":2492},"10.1016\u002F0016-5085(86)90919-4",{"doi":2491},{"id":28,"text":2494,"url":28,"identifiers":2495},"10.1056\u002FNEJM199306243282501",{"doi":2494},{"id":2497,"createTime":2498,"updateTime":2498,"relativeEntities":2499,"slug":2500,"properties":2501,"entityType":964,"verifyStatus":26,"verifyTime":2498,"verifyNote":965,"languages":2514,"translateLanguages":28,"viewCount":32,"primaryUrl":2515,"fullTextUrl":28,"authors":2516,"publicationType":986,"publisherRelationship":2589,"citationCount":2638,"citationInfo":2639,"publishDate":2643,"publishYear":2640,"citationAnalyzeStatus":884,"lastCitationAnalyze":28,"indexDatabases":2644,"openAccess":28,"references":2645,"isForceReanalyzing":1202},"20d75ec7-0fae-45eb-b754-43bf9535ca1d","2024-09-25T15:21:46.084+00:00",[],"The-epidemiology-of-inflammatory-bowel-disease-East-meets-west",{"openalex":2502,"mag":2504,"abstract":2506,"title":2508,"pm":2510,"doi":2512},{"VOID":2503},"W2979721632",{"VOID":2505},"2979721632",{"EN":2507},"\u003Cjats:title>Abstract\u003C\u002Fjats:title>\u003Cjats:p>The incidence of inflammatory bowel diseases (IBD) in East has risen over the past decade to become a global disease. The increasing number of studies on the incidence and course of IBD in East has enabled us to explore East versus West differences in the epidemiology of IBD which could enhance our understanding of the heterogeneity of the disease and eventually assist in the discovery of novel therapeutic targets and design of preventive strategies.\u003C\u002Fjats:p>\u003Cjats:p>Comparison of population‐based data in East and West reveals that the incidence of IBD has risen rapidly in East while plateauing in West. Furthermore, the clinical presentation and course of IBD differs between East and West with more patients in East presenting with complicated disease. Considering the scarcity of population‐based data from East and the lack of studies with long durations of follow‐up, it remains to be clarified whether these differences reflect true differences in disease presentation. The effects of genetic and environmental risk factors contributing to IBD also differ between Eastern and Western populations. Considering the differential effects of genetic and environmental risk factors in East and West, future studies should seek to discover novel genetic and environmental risk factors which might specifically apply to eastern populations.\u003C\u002Fjats:p>\u003Cjats:p>In this narrative review, we compare the epidemiology of IBD between eastern and western countries by summarizing evidence from population‐based cohort studies in the last ten years. 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Prevalence of NASH in type 2 DM has not been well studied and there is an epidemic rise in type 2 DM in Asian and Western populations. Its association with chronic liver disease in the form of NASH makes it an important health problem. Hence we have studied its prevalence and correlation of biochemical parameters with histological grades of non‐alcoholic fatty liver disease (NAFLD) in otherwise asymptomatic type 2 DM patients.\u003C\u002Fjats:p>\u003Cjats:p>\u003Cjats:bold>Methods: \u003C\u002Fjats:bold> One hundred and forty‐eight individuals were screened. Forty‐eight individuals were excluded due to history of alcohol intake or liver disease as a result of other causes. One hundred non‐alcoholic individuals with type 2 DM underwent abdominal ultrasonography (US abdomen). Forty‐nine patients had evidence of fatty liver on US abdomen, and 32 of these 49 patients underwent liver biopsy.\u003C\u002Fjats:p>\u003Cjats:p>\u003Cjats:bold>Results: \u003C\u002Fjats:bold> Four of 32 (12.5%) individuals had steatosis alone. Mild, moderate and severe NASH was present in 21\u002F32 (65.5%), 4\u002F32 (12.5%) and 3\u002F32 (9.35%), respectively. Fibrosis was present in 7\u002F32 (21.8%) patients (four grade 1 and three grade 3). There was no significant difference in body mass index (BMI), transaminase levels, serum cholesterol and triglyceride levels among patients with non‐alcoholic fatty liver disease.\u003C\u002Fjats:p>\u003Cjats:p>\u003Cjats:bold>Conclusion: \u003C\u002Fjats:bold> We conclude that the prevalence of NASH is high in type 2 DM patients and liver biopsy is the only investigation to differentiate between non‐alcoholic fatty liver and steatohepatitis.\u003C\u002Fjats:p>",{"EN":2891},"Non‐alcoholic steatohepatitis in type 2 diabetes 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Adipose tissue mesenchymal stem cells (AT‐MSC), known as adipose‐derived stem cells (ASC) are especially attractive in the context of future clinical applications because of their high accessibility and minimal invasiveness during the procedure to obtain them. The goal of the present study was to induce human ASC into functional hepatocytes \u003Cjats:italic>in vitro\u003C\u002Fjats:italic> within a very short period of time and to check their therapeutic potential \u003Cjats:italic>in vivo\u003C\u002Fjats:italic>.\u003C\u002Fjats:p>\u003Cjats:p>\u003Cjats:bold>Methods: \u003C\u002Fjats:bold>  \u003Cjats:italic>In vitro\u003C\u002Fjats:italic> generated ASC‐derived hepatocytes were checked for hepatocyte‐specific markers and functions. Afterwards, they were transplanted into nude mice with liver injury. Twenty‐four hours after transplantation, biochemical parameters were evaluated in blood serum.\u003C\u002Fjats:p>\u003Cjats:p>\u003Cjats:bold>Results: \u003C\u002Fjats:bold> We have shown here that ASC can be differentiated into hepatocytes within 13 days and can reach the functional properties of primary human hepatocytes. After transplantation into mice with acute liver failure, ASC‐derived hepatocytes can restore such liver functions as ammonia and purine metabolism. Markers of liver injury, alanine aminotransferase, aspartate aminotransferase, as well as ammonia, were decreased after ASC‐derived hepatocyte transplantation.\u003C\u002Fjats:p>\u003Cjats:p>\u003Cjats:bold>Conclusions: \u003C\u002Fjats:bold> Our data highlight the properties of ASC as having a special affinity for hepatocyte differentiation \u003Cjats:italic>in vitro\u003C\u002Fjats:italic> and liver regeneration \u003Cjats:italic>in vivo\u003C\u002Fjats:italic>. 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liver injury of many etiologies produces liver fibrosis and may eventually lead to the formation of cirrhosis. Fibrosis is part of a dynamic process associated with the continuous deposition and resorption of extracellular matrix, mainly fibrillar collagen. Studies of fibrogenesis conducted in many organs including the liver demonstrate that the primary source of the extracellular matrix in fibrosis is the myofibroblast. Hepatic myofibroblasts are not present in the normal liver but transdifferentiate from heterogeneous cell populations in response to a variety of fibrogenic stimuli. Debate still exists regarding the origin of hepatic myofibroblasts. It is considered that hepatic stellate cells and portal fibroblasts have fibrogenic potential and are the major origin of hepatic myofibroblasts. Depending on the primary site of injury the fibrosis may be present in the hepatic parenchyma as seen in chronic hepatitis or may be restricted to the portal areas as in most biliary diseases. 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