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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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the human fetus and placenta are considered to be primarily dependent on glucose oxidation for energy metabolism, the cause of the remarkable association between severe maternal pregnancy complications and the carriage of a fetus with an inborn error of mitochondrial long-chain fatty acid oxidation (FAO) has remained obscure. We analysed human term placenta and chorionic villus samples for the activities of a variety of enzymes involved in FAO, and compared the results with those obtained in human liver. All enzymes were found to be expressed, with a very high activity of two enzymes involved in the metabolism of long-chain fatty acids (CPT2 and VLCAD), whereas the activity of medium-chain acyl-CoA dehydrogenase (MCAD) was found to be low, when compared to liver. These results suggest that fatty acid oxidation may play an important role in energy generation in human placenta, and that a deficiency in the placental oxidation of long-chain FAO may result in placental dysfunction, thus causing gestational complications.",{"EN":1107},"High activity of fatty acid oxidation enzymes in human placenta: Implications for fetal-maternal disease",{"VOID":1109},"Braida L, Crovella S, Boniotto M, et al (2001) A rapid and quantitative mass spectrometry method for determining the concentration of acylcarnitines and aminoacids in amniotic fluid. Prenat Diagn 21: 543-546.\nCarter AM (2000) Placental oxygen consumption. Part I: in vivo studies a review. Placenta 21(supplement A): S31-S37.\nChakrapani A, Olpin S, Cleary M, Walter JH, Wraith JE, Besley GT (2000) Trifunctional protein deficiency: three families with significant maternal hepatic dysfunction in pregnancy not associated with E474Q mutation. J Inherit Metab Dis 23: 826-834.\nden Boer MEJ, Wanders RJA, Morris AAM, IJlst L, Heymans HSA, Wijburg FA (2002a) Long-chain 3-hydroxyacyl-CoA dehydrogenase deficiency: clinical presentation and follow-up of 50 patients. Pediatrics 109: 99-104.\nden Boer MEJ, Dionisi Vici C, Besley GTN, van Thuijl AOJ, Wanders RJA, Wijburg FA (2002b) MTP deficiency: a fatty acid oxidation disorder with a severe phenotype with prominent cardiac involvement. J Inherit Metab Dis 25(supplement 1): 75.\nGranger JP, Alexander BT, Llinas MT, Bennett WA, Khalil RA (2002) Pathophysiology of preeclampsia: linking placental ischemia\u002Fhypoxia with microvascular dysfunction. Microcirculation 9: 147-160.\nHarris RA, Farmer B, Ozawa T (1972) Inhibition of the mitochondrial adenine nucleotide transport system by oleyl-CoA. Arch Biochem Biophys 150: 199-209.\nHerrera E, Gomez Coronado D, Lasunci6n MA (1987) Lipid metabolism in pregnancy. Biol Neonate 51: 70-77.\nHerrmann U Jr, Degiampietro P, Metzger E, Bachmann C, Peheim E (1985) Activities in the placenta and fetal membranes of enzymes involved in energy metabolism. Arch Gynecol 236: 249-254.\nIbdah JA, Benett MJ, Rinaldo P, et al (1999a) A fetal fatty-acid oxidation disorder as a cause of liver disease in pregnant women. N Engl J Med 340: 1723-1731.\nIbdah JA, Dasouki MJ, Strauss AW, et al (1999b) Long-chain 3-hydroxyacyl-CoA dehydrogenase deficiency: variable expressivity of maternal illness during pregnancy and unusual presentation with infantile cholestasis and hypocalcaemia. J Inherit Metab Dis 22: 811-814.\nInnes AM, Seargent LE, Balachandra K, et al (2000) Hepatic carnitine palmitoyltransferase I deficiency presenting as maternal illness in pregnancy. Pediatr Res 47: 43-45.\nJones CT, Rolph TP (1985) Metabolism during fetal life: a functional assessment of metabolic development. Physiol Rev 65: 357-430.\nKnipp GT, Liu B, Audus KL, Fujii H, Ono T, Soares MJ (2000) Fatty acid transport regu-latory proteins in the developing rat placenta and in trophoblast cell culture models. Placenta 21: 367-375.\nKnopp RH, Herrera E, Freinkel N (1970) Carbohydrate metabolism in pregnancy. VIII. Metabolism of adipose tissue isolated from fed and fasted pregnant rats during late gestation. J Clin Invest 49: 1438-1446.\nMatern D, Schehata BM, Shekhawa P, Strauss AW, Bennett MJ, Rinaldo P (2001) Placental floor infarction complicating the pregnancy of a fetus with long-chain 3-hydroxyacyl-CoA dehydrogenase (LCHAD) deficiency. Mol Genet Metab 72: 265-268.\nMeschia G, Battaglia FC, Hay WW, Sparks JW (1980) Utilization of substrates by the ovine placenta in vivo. Fed Proc 39: 245-249.\nMoore KH, Dandurand DM, Kiechle FL (1992) Fasting induced alterations in mitochondrial palmitoyl-CoA metabolism may inhibit adipocyte pyruvate dehydrogenase activity. Int J Biochem 24: 809-814.\nMorel F, Laquin G, Lunardi J, Duszynski J, Vignais PV (1974) An appraisal of the functional significance of the inhibitory effect of long chain acyl-CoAs on mitochondrial transports. FEBS Lett 39: 133-138.\nPrip-Buus C, Pgorier JP, Duee PH, Kohl C, Girard J (1990) Evidence that the sensitivity of carnitine palmitoyl transferase I to inhibition by malonyl-CoA is an important site of regulation of hepatic fatty acid oxidation in the fetal and newborn rabbit. Perinatal devel-opment and effects of pancreatic hormones in cultured rabbit hepatocytes. Biochem J 269: 409 415.\nRakheja D, Bennett MJ, Foster BM, Domiati-Saad R, Rogers BB (2002) Evidence for fatty acid oxidation in human placenta, and the relationship of fatty acid oxidation enzyme activi-ties with gestational age. Placenta 23: 447-450.\nSchoeman MN, Batey RG, Wilcken B (1991) Recurrent acute fatty liver of pregnancy associ-ated with fatty-acid oxidation defect in the offspring. Gastroenterology 100: 544-548.\nSims HF, Bracket JC, Powell CK, et al (1995) The molecular basis of pediatric long chain 3-hydroxyacyl-CoA dehydrogenase deficiency associated with maternal acute fatty liver of pregnancy. Proc Natl Acad Sci USA 92: 841-845.\nSlama A, Brivet M, Boutron A, Legrand A, Saudubray JM, Demaugre F (1996) Complementation analysis of carnitine palmitoyltransferase I and II defects. Pediatr Res 40: 542-546.\nTreem WR, Rinaldo P, Hale DE, et al (1994) Acute fatty liver of pregnancy and long-chain 3-hydroxyacyl-coenzyme A deficiency. Hepatology 19: 339-345.\nTreem WR, Shoup ME, Hale DE, et al (1996) Acute fatty liver of pregnancy, hemolysis, elevated liver enzymes, and low platelets syndrome and long chain 3-hydroxyacyl-coenzyme A dehydrogenase deficiency. Am J Gastroenterol 91: 2293-2300.\nTyni T, Ekholm E, Pihko H (1998) Pregnancy complications are frequent in long-chain 3-hydroxyacyl-coenzyme A dehydrogenase deficiency. Am J Obstet Gynecol 178: 603-608.\nVan Wijk MJ, Nieuwland R, Boer K, van der Post JA, VanBavel E, Sturk A (2002) Microparticle subpopulations are increased in preeclampsia: possible involvement in vascular dysfunction? Am J Obstet Gynecol 187: 450-456.\nVentura FV, Ruiter JPN, IJlst L, de Almeida IT, Wanders RJA (1996) Inhibitory effect of 3-hydroxyacyl-CoAs and other long-chain fatty acid-oxidation intermediates on mitochondrial oxidative phosphorylation. J Inherit Metab Dis 19: 161-164.\nWanders RJ, IJlst L, Poggi F, et al (1992) Human trifunctional protein deficiency: a new disorder of mitochondrial fatty acid beta-oxidation. Biochem Biophys Res Commun 188: 1139-1145.\nWanders RJA, Vreken P, den Boer MEJ, Wijburg FA, van Gennip AH, IJlst L (1999) Dis-orders of mitochondrial fatty acyl-CoA 3-oxidation. J Inherit Metab Dis 22: 442-487.\nYoneyama Y, Sawa R, Suzuki S, et al (2002) Relationship between plasma malondialdehyde levels and adenosine deaminase activities in preeclampsia. 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J Biol Chem 271: 17330–17334.\nGibson KM, Hoffmann G, Nyhan WL, et al (1988) Mevalonate kinase deficiency in a child with cerebellar ataxia, hypotonia and mevalonic aciduria. Eur J Pediatr 148: 250–252.\nGibson KM, Lohr JL, Broock RL, et al (1989) Mevalonate kinase in lysates of cultured human fibroblasts and lymphoblasts: kinetic properties, assay conditions, carrier detection and measurement of residual activity in a patient with mevalonic aciduria. Enzyme 41: 47–55.\nHoffmann GF, Sweetman L, Bremer HJ, et al (1991) Facts and artefacts in mevalonic aciduria: development of a stable isotope dilution GCMS assay for mevalonic acid and its application to physiological fluids, tissue samples, prenatal diagnosis and carrier detection. Clin Chim Acta 198: 209–228.\nHoffmann GF, Charpentier C, Mayatepek E, et al (1993) Clinical and biochemical phenotype in 11 patients with mevalonic aciduria. Pediatrics 91: 915–921.\nSweetman L (1991) Organic acid analysis. In Hommes FA, ed. 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Concentrations of organic acids in the urine of healthy newborn children. Ann. Clin. Biochem. 15 (1978) 245–249\nAnonymous. Sudden infant death and inherited metabolic disease. Lancet 2 (1986) 1073–1075\nBennett, M. J., Allison, F., Pollitt, R. J., Manning, N. J., Gray, R. G. F., Green, A., Hale, D. E. and Coates, P. M. Prenatal diagnosis of medium-chain acyl-CoA dehydrogenase deficiency in a family with sudden infant death. Lancet 1 (1987) 440–441\nBjorkman, L., McLean, C. and Steen, G. Organic acids in urine from human newborns. Clin. Chem. 22 (1976) 49–52\nCoates, P. M., Hale, D. E., Stanley, C. A., Corkey, B. E., Hall, C. L. and Cortner, J. A. Genetic deficiency of MCAD; studies in cultured skin fibroblasts and peripheral mononuclear leukocytes. Pediatr. Res. 19 (1985) 671–676\nGregersen, N., Ingerslev, J. and Rasmussen, K. Low molecular weight organic acids in the urine of the newborn. Acta Paediatr. Scand. 66 (1977) 85–89\nGregersen, N., Kølvraa, S., Rasmussen, K., Mortensen, P. B., Divry, P., David, M. and Hobloth, N. General (medium-chain) acyl-CoA dehydrogenase deficiency (non-ketotic dicarboxylic aciduria): quantitative urinary excretion pattern of 23 biologically significant metabolites in three cases. Clin. Chim. Acta 132 (1983) 181–191\nHowat, A. J., Bennett, M. J., Variend, S., Shaw, L. and Engel, P. C. Defects of metabolism of fatty acids in the sudden infant death syndrome. Br. Med. J. 290 (1985) 1771–1773\nThompson, J. A., Miles, B. S. and Fennessey, P. V. Urinary organic acids quantitated by age groups in a healthy pediatric population. Clin. 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Within the WD cohort, correlations of BMD with WD disease parameters, lab results, type of treatment and known osteoporosis risk factors were analysed. Hip and lumbar spine absolute BMD and T-score were measured by dual-energy X-ray absorptiometry. Osteoporosis and osteopenia were defined as a T-score ≤ −2.5, and between −1 and −2.5, respectively. There were significantly more subjects with abnormal T-scores in the WD population (58.8 %) than in the control population (45.3 %) (χ2 = 6.65, df = 2, p = 0.036), as there were 50.0 % osteopenic and 8.8 % osteoporotic WD patients, vs. 41.2 % and 4.1 %, respectively, in the controls. Especially L2-L4 spine BMD measurements (BMD and T-scores) differed significantly between the WD population and matched controls. L2-L4 spine BMD for WD patients was on average 0.054 g\u002Fcm2 (5.1 %) lower than in matched normal controls (0.995 ± 0.156 vs 1.050 ± 0.135; p = 0.002). We found no significant correlation between BMD values and any of the WD disease parameters (e.g. the severity of liver disease), lab results, type of treatment or known osteoporosis risk factors. Duration of D-penicillamine treatment was negatively correlated with femoral BMD value, but in a clinically irrelevant manner, compared to age and gender. Importantly, BMD remained significantly lower in WD patients (n = 89) vs. controls after excluding WD patients with cirrhosis (p = 0.009). Our study suggests that WD is intrinsically associated with bone demineralisation.",{"EN":1590},"Bone demineralisation in a large cohort of Wilson disease patients",{"VOID":1592},"Arnal N, de Alaniz MJ, Marra CA (2013) Effect of copper overload on the survival of HepG2 and A-549 human-derived cells. Hum Exp Toxicol 32:299–315\nBax BE, Alam AS, Banerji B et al (1992) Stimulation of osteoclastic bone resorption by hydrogen peroxide. Biochem Biophys Res Commun 183:1153–1158\nFerenci P (2006) Regional distribution of mutations of the ATP7B gene in patients with Wilson disease: impct on genetic testing. Hum Genet 120:151–159\nGaetke LM, Chow CK (2003) Copper toxicity, oxidative stress, and antioxidant nutrients. Toxicology 189:147–163\nGielen E, Vanderschueren D, Callewaert F et al (2011) Osteoporosis in men. Best Pract Res Clin Endocrinol Metab 25:321–335\nGolding DN, Walshe JM (1977) Arthropathy of Wilson’s disease. Ann Rheum Dis 36:99–111\nGu M, Cooper JM, Butler P et al (2000) Oxidative-phosphorylation defects in liver of patients with Wilson’s disease. Lancet 356:469–474\nGuo Y, Yang TL, Liu YZ et al (2011) Mitochondria-wide association study of common variants in osteoporosis. Ann Hum Genet 75:569–574\nHegedus D, Ferencz V, Lakatos PL et al (2002) Decreased bone density, elevated serum osteoprotegerin, and beta-cross-laps in Wilson disease. J Bone Miner Res 17:1961–1967\nHerman JS, Easterbrook PJ (2001) The metabolic toxicities of antiretroviral therapy. Int J STD AIDS 12:555–562\nHuh YJ, Kim JM, Kim H et al (2006) Regulation of osteoclast differentiation by the redox-dependent modulation of nuclear import of transcription factors. Cell Death Differ 13:1138–1146\nKikuyama A, Fukuda K, Mori S et al (2002) Hydrogen peroxide induces apoptosis of osteocytes: involvement of calcium ion and caspase activity. Calcif Tissue Int 71:243–248\nLang PA, Schenck M, Nicolay JP et al (2007) Liver cell death and anemia in Wilson disease involve acid sphingomyelinase and ceramide. Nat Med 13:164–170\nLi S, Wang M, Chen X, Li SF, Li-Ling J, Xie HQ (2014) Inhibition of osteogenic differentiation of mesenchymal stem cells by copper supplementation. Cell Prolif 47(1):81–90\nLooker AC, Orwoll ES, Johnston CC Jr et al (1997) Prevalence of low femoral bone density in older U.S. adults from NHANES III. J Bone Miner Res 12:1761–1768\nLowette KF, Desmet K, Witters P, Laleman W, Verslype C, Nevens F, Fevery J, Cassiman DM (2010) Wilson’s disease: long-term follow-up of a cohort of 24 patients treated with D-penicillamine. Eur J Gastroenterol Hepatol 22(5):564–571\nMaggio D, Barabani M, Pierandrei M et al (2003) Marked decrease in plasma antioxidants in aged osteoporotic women: results of a cross-sectional study. J Clin Endocrinol Metab 88:1523–1527\nMindelzun R, Elkin M, Scheinberg IH, Sternlieb I (1970) Skeletal changes in Wilson’s disease. A radiology study. Radiol 94(1):127–132\nNakchbandi IA, van der Merwe SW (2009) Current understanding of osteoporosis associated with liver disease. Nat Rev Gastroenterol Hepatol 6:660–670\nPfeiffenberger J, Mogler C, Gotthardt DN, Schulze-Bergkamen H, Litwin T, Reuner U, Hefter H, Huster D, Schemmer P, Członkowska A, Schirmacher P, Stremmel W, Cassiman D, Weiss KH (2014) Hepatobiliary malignancies in Wilson disease. Liver Int. doi:10.1111\u002Fliv.12727\nQuemeneur AS, Trocello JM, Ea HK, Ostertag A, Leyendecker A, Duclos-Vallée JC, de Vernejoul MC, Woimant F, Lioté F (2014) Bone status and fractures in 85 adults with Wilson’s disease. Osteoporos Int 25(11):2573–2580\nRoberts EA, Robinson BH, Yang S (2008) Mitochondrial structure and function in the untreated Jackson toxic milk (tx-j) mouse, a model for Wilson disease. Mol Genet Metab 93:54–65\nRodríguez Nieva N, Febrer Rotger A, Meléndez Plumed M et al (2004) Osteoarthropathy in three siblings with Wilson’s disease. An Pediatr (Barc) 61:181–184\nSelimoglu MA, Ertekin V, Doneray H et al (2008) Bone mineral density of children with Wilson disease: efficacy of penicillamine and zinc therapy. J Clin Gastroenterol 42:194–198\nSeth R, Yang S, Choi S et al (2004) In vitro assessment of copper-induced toxicity in the human hepatoma line, Hep G2. Toxicol In Vitro 18:501–509\nSokol RJ, Twedt D, McKim JM Jr et al (1994) Oxidant injury to hepatic mitochondria in patients with Wilson’s disease and Bedlington terriers with copper toxicosis. Gastroenterology 107:1788–1798\nSözeri E, Feist D, Ruder H et al (1997) Proteinuria and other renal functions in Wilson’s disease. Pediatr Nephrol 11:307–311\nStrand S, Hofmann WJ, Grambihler A et al (1998) Hepatic failure and liver cell damage in acute Wilson’s disease involve CD95 (APO-1\u002FFas) mediated apoptosis. Nat Med 4:588–593\nTrifunovic A, Wredenberg A, Falkenberg M et al (2004) Premature ageing in mice expressing defective mitochondrial DNA polymerase. Nature 429:417–423\nvon Herbay A, de Groot H, Hegi U et al (1994) Low vitamin E content in plasma of patients with alcoholic liver disease, hemochromatosis and Wilson’s disease. J Hepatol 20:41–46\nWalshe JM (1969) Management of penicillamine nephropathy in Wilson’s disease: a new chelating agent. Lancet 2:1401\nWeiss KH. Wilson Disease. In: GeneReviews™ 1999 [Internet]. Editors: Pagon RA, Adam MP, Bird TD, Dolan CR, Fong CT, Stephens K. University of Washington, Seattle. [updated 2013 May 16]\nWeiss KH, Gotthardt DN, Klemm D, Merle U, Ferenci-Foerster D, Schaefer M, Ferenci P, Stremmel W (2011) Zinc monotherapy is not as effective as chelating agents in treatment of Wilson disease. Gastroenterology 140(4):1189–1198\nWorld Health Organization Study Group on Assessment of Fracture Risk and Its Application to Screening and Postmenopausal Osteoporosis (1994) Report of a WHO Study Group. Technical Report Series (No. 84)\nXie YZ, Zhang XZ, Xu XH et al (1985) Radiologic study of 42 cases of Wilson disease. Skeletal Radiol 13:114–119\nZischka H, Lichtmannegger J, Schmitt S et al (2011) Liver mitochondrial membrane crosslinking and destruction in a rat model of Wilson disease. 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errors involving enzymes essential for pyrimidine nucleotide metabolism have provided new insights into their fundamental physiological roles as vital constituents of nucleic acids as well as substrates of lipid and carbohydrate metabolism and in oxidative phosphorylation. Genetic aberrations of pyrimidine pathways lead to diverse clinical manifestations including neurological, immunological, haematological, renal impairments, adverse reactions to analogue therapy and association with malignancies. Maintenance of cellular nucleotides depends on the three aspects of metabolism of pyrimidines: de novo synthesis, catabolism and recycling of these metabolites. Of the ten recognised disorders of pyrimidine metabolism treatment is currently restricted to only two disorders: hereditary orotic aciduria (oral uridine therapy) and mitochondrial neurogastrointestinal encephalomyopathy (MNGIE; allogeneic hematopoetic stem cell transplant and enzyme replacement). The ubiquitous role that pyrimidine metabolism plays in human life highlights the importance of improving diagnostic evaluation in suggestive clinical settings, which will contribute to the elucidation of new defects, future development of novel drugs and therapeutic strategies. Limited awareness of the expanding phenotypic spectrum, with relatively recent descriptions of newer disorders, compounded by considerable genetic heterogeneity has often contributed to the delays in the diagnosis of this group of disorders. The lack of an easily recognisable, easily measurable end product, akin to uric acid in purine metabolism, has contributed to the under-recognition of these disorders.This review describes the currently known inborn errors of pyrimidine metabolism, their variable phenotypic presentations, established diagnostic methodology and recognised treatment options.",{"EN":1841},"Inborn errors of pyrimidine metabolism: clinical update and therapy",{"VOID":1843},"Bailey CJ (2009) Orotic aciduria and uridine monophosphate synthase: a reappraisal. J Inherit Metab Dis 32(Suppl 1):S227–S233\nBax BE, Bain MD, Scarpelli M, Filosto M, Tonin P, Moran N (2013) Clinical and biochemical improvements in a patient with MNGIE following enzyme replacement. Neurology 81(14):1269–1271\nBerg M, Tymoczko JL, Stryer L (2002) Biosynthesis of nucleotides. In: Berg M, Tymoczko JL, Stryer L (eds) Biochemistry. Freeman, New York, pp 602–626\nBesley GTN, Walter JH, Fairbanks LD et al (2000) Hereditary orotic aciduria without megaloblastic anaemia. J Inherit Metab Dis 23(Suppl 1):194\nBushdid PB, Brantley DM, Yull FE (1998) Inhibition of NF-κB activity results in disruption of the apical ectodermal ridge and aberrant limb morphogenesis. Nature 392:615–618\nCameron JS, Moro F, Simmonds HA (1993) Gout, uric acid and purine metabolism in paediatric nephrology. Pediatr Nephrol 7:105–118\nCaudle KE, Thorn CF, Klein TE, et al (2013) Clinical pharmacogenetics implementation consortium guidelines for dihydropyrimidine dehydrogenase genotype and fluoropyrimidine dosing. Clin Pharmacol Ther 94:640–645\nChiang C, Litingtung Y, Harris MP et al (2001) Manifestation of the limb prepattern: limb development in the absence of sonic hedgehog function. Dev Biol 236:421–435\nChiarelli LR, Fermo E, Zanella A et al (2006) Hereditary erythrocyte pyrimidine 5′-nucleotidase deficiency: a biochemical, genetic and clinical overview. Hematol 11:67–72\nCorson LB, Yamanaka Y, Lai K, Rossant J (2003) Spatial and temporal patterns of ERK signaling during mouse embryogenesis. Development 130:4527–4537\nDervieux T, Furst D, Lein DO et al (2004) Polyglutamation of methotrexate with common polymorphisms in reduced folate carrier, aminoimidazole carboxamide ribonucleotide transformylase, and thymidylate synthase are associated with methotrexate effects in rheumatoid arthritis. Arthritis Rheum 50:2766–2774\nDiPaolo A, Chu E (2004) The role of thymidylate synthase as a molecular biomarker. Clin Cancer Res 10:411–412\nDuran M, Dorland L, Meuleman EE, Allers P, Berger R (1997) Inherited defects of purine and pyrimidine metabolism: laboratory methods for diagnosis. 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Neurology 67:1458–1460\nHorie N, Aiba H, Oguro K, Hojo H, Takeishi K (1995) Functional analysis and DNA polymorphism of the tandemly repeated sequences in the 5′-terminal regulatory region of the human gene for thymidylate synthase. Cell Struct Funct 20:191–197\nImose M, Nagaki M, Kimura K et al (2004) Lefunomide protects from T-cell–mediated liver injury in mice through inhibition of nuclear factor κB. Hepatology 40:1160–1169\nJankowski V, Tölle M, Vanholder R et al (2005) Uridine adenosine tetraphosphate: a novel endothelium-derived vasoconstrictive factor. Nat Med 11:223–227\nJurecka A, Zikanova M, Tylki-Szymanska A et al (2008) Clinical, biochemical and molecular findings in seven Polish patients with adenylosuccinate lyase deficiency. Mol Genet Metab 94:435–442\nKumagai K, Hiyama K, Oyama T, Maeda H, Kohno N (2003) Polymorphisms in the thymidylate synthase and methylenetetrahydrofolate reductase genes and sensitivity to the low-dose methotrexate therapy in patients with rheumatoid arthritis. Int J Mol Med 11:593–600\nLara MC, Weiss B, Illa I et al (2006) Infusion of platelets transiently reduces nucleoside overload in MNGIE. Neurology 67:1461–1463\nLoeffler M, Zameitat E (2004) Pyrimidine biosynthesis. Encycl Biol Chem 3:600–605\nMahdaviani SA, Hirbod-Mobarakeh A, Wang N et al (2012) Novel mutation of the activation-induced cytidine deaminase gene in a Tajik family: special review on hyper-immunoglobulin M syndrome. Expert Rev Clin Immunol 8(6):539–546\nMancuso M, Salviati L, Sacconi S et al (2002) Mitochondrial DNA depletion: mutations in thymidine kinase gene with myopathy and SMA. Neurology 59:1197–1202\nMarti R, Spinazzola A, Tadesse S, Nishino I, Nishigaki Y, Hirano M (2004) Definitive diagnosis of mitochondrial neurogastrointestinal encephalomyopathy by biochemical assays. Clin Chem 50:120–124\nMillington D (2003) Tandem mass spectrometry in clinical diagnosis. In: Blau N, Duran M, Blaskovics M, Gibson M (eds) Physician’s guide to the laboratory diagnosis of metabolic diseases. Springer-Verlag, Berlin, pp 57–76\nNajarian T, Traut TW (2000) Nifedipine and nimodipine competitively inhibit uridine kinase and orotidine-phosphate decarboxylase: theoretical relevance to poor outcome in stroke. Neurorehabil Neural Repair 14:237–241\nNakajima Y, Meijer J, Dobritzsch D et al (2014) Clinical, biochemical and molecular analysis of 13 Japanese patients with β-ureidopropionase deficiency demonstrates high prevalence of the p.977G>A (p.R326Q) mutation. J Inherit Metab Dis\nNg SB, Buckingham KJ, Lee C et al (2010) Exome sequencing identifies the cause of a mendelian disorder. Nat Genet 42:30–35\nNishino I, Spinazzola A, Papadimitriou A et al (2000) Mitochondrial neurogastrointestinal encephalomyopathy: an autosomal recessive disorder due to thymidine phosphorylase mutations. Ann Neurol 47:792–800\nOskoui M, Davidzon G, Pascual J et al (2006) Clinical spectrum of mitochondrial DNA depletion due to mutations in the thymidine kinase 2 gene. Arch Neurol 63:1122–1126\nPawlik A, Herczynska M, Kurzawski M, Safranow K, Dziedziejko V, Drozdzik M (2009) The effect of exon (19C>A) dihydroorotate dehydrogenase gene polymorphism on rheumatoid arthritis treatment with leflunomide. Pharmacogenomics 10:303–309\nPontarin G, Ferraro P, Valentino ML, Hirano M, Reichard P, Bianchi V (2006) Mitochondrial DNA depletion and thymidine phosphate pool dynamics in a cellular model of mitochondrial neurogastrointestinal encephalomyopathy (MNGIE). J Biol Chem 281:22720–22728\nQuartier P, Bustamante J, Sanal O et al (2004) Clinical, immunologic and genetic analysis of 29 patients with autosomal recessive hyper-IgM syndrome due to activation-induced cytidine deaminase deficiency. Clin Immunol 110(1):22–29\nRainger J, Bengani H, Campbell L et al (2012) Miller syndrome (Genee-Wiedemann syndrome) represents a clinically and biochemically distinct subgroup of postaxial acrofacial dysostosis associated with partial deficiency of DHODH. Hum Mol Genet 21(18):3969–3983\nRees DC, Duley JA, Simmonds HA et al (1996) Interaction of haemoglobin E and pyrimidine 5′-nucleotidase deficiency. Blood 88:2761–2767\nRees DC, Duley JA, Marinaki AM (2003) Pyrimidine 5′ nucleotidase deficiency. Br J Haematol 120(3):375–383\nRevy P, Muto T, Levy Y et al (2000) Activation-induced cytidine deaminase (AID) deficiency causes the autosomal recessive form of the hyper-IgM syndrome (HIGM2). Cell 102:565–575\nSaada A, Shaag A, Mandel H et al (2001) Mutant mitochondrial thymidine kinase in mitochondrial DNA depletion myopathy. Nat Genet 29:342–344\nSchweitzer-Krantz S, van Kuilenburg ABP, van Gennip AH, Lehnert W (2002) Dihydropyrimidine dehydrogenase deficiency and arthrogryposis multiplex congenita: clinical improvement under substitution of β-alanine and β-aminoisobutyric acid. J Inherit Metab Dis 25(Suppl 1):155\nSimmonds HA, van Gennip AH (2003) Purine and pyrimidine disorders. In: Blau N, Duran M, Blaskovics M, Gibron KM (eds) Physician’s guide to the laboratory diagnosis of metabolic diseases. Springer, Berlin, pp 445–465\nSimmonds HA, Duley JA, Fairbanks LD, McBride MB (1997) When to investigate for purine and pyrimidine disorders. Introduction and review of clinical and laboratory indications. J Inherit Metab Dis 20:214–226\nSmith LH Jr, Lotz M (1963) Studies on congenital orotic aciduria: comparison of orotic acid metabolism in micro-organisms. 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Springer, Berlin, pp 500–518\nvan Gennip AH (1999) Defects in metabolism of purines and pyrimidines. Ned Tijdsch Klin Chem 24:171–175\nvan Gennip A, van Kuilenburg AB (2000) Defects of pyrimidine degradation: clinical, molecular and diagnostic aspects. Adv Exp Med Biol 486:233–241\nvan Kuilenburg AB (2004) Dihydropyrimidine dehydrogenase and the efficacy and toxicity of 5-fluorouracil. Eur J Cancer 40(7):939–950\nvan Kuilenburg ABP, Vreken P, Abeling NG et al (1999) Genotype and phenotype in patients with dihydropyrimidine dehydrogenase deficiency. Hum Genet 104(1):1–9\nvan Kuilenburg ABP, Meinsma R, Zonnenberg BA et al (2003) Dihydropyrimidinase deficiency and severe 5-fluorouracil toxicity. Clin Cancer Res 9:4363–4367\nvan Kuilenburg AB, Stroomer AE, van Lenthe H, Abeling NG, Van Gennip AH (2004) New insights in dihydropyrimidine dehydrogenase deficiency: a pivotal role for beta-aminoisobutyric acid? 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Dev Med Child Neurol 55(11):1060–1064\nWadman SK, Beemer FA, de Bree PK et al (1984) New defects of pyrimidine metabolism. Adv Exp Med Biol 165:109–114\nWebster DR, Becroft DM, van Gennip A, Van Kuilenberg A (2001) Hereditary orotic aciduria and other disorders. In: Scriver CR, Beaudet AL, Sly WS, Valle D, Childs B, Kinzler KW, Vogelstein B (eds) The metabolic and molecular bases of inherited disease, 8th edn. McGraw-Hill, New York, pp 2663–2702\nWeisman MH, Furst DE, Park GS et al (2006) Risk genotypes in folate-dependent enzymes and their association with methotrexate-related side effects in rheumatoid arthritis. Arthritis Rheum 54:607–612",{"VOID":1845},"10.1007\u002Fs10545-014-9742-3","https:\u002F\u002Fonlinelibrary.wiley.com\u002Fdoi\u002F10.1007\u002Fs10545-014-9742-3",[1848,1872,1887],{"id":1849,"sortIndex":32,"researcher":28,"roles":1850,"affiliations":1851,"properties":1869,"displayName":1871,"givenName":28,"familyName":28},"67ef7deb-8fac-4825-9f93-b76f82d68819",[967],[1852,1860],{"id":1853,"sortIndex":32,"affiliation":1854,"properties":28},"17a31bdf-2cbb-4aec-9dc9-a24ecca54f20",{"id":1853,"createTime":28,"updateTime":28,"relativeEntities":1855,"slug":28,"properties":1856,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1859,"statistic":28},[],{"title":1857},{"VI":1858},"Metabolic Unit, Princess Margaret Hospital, Perth, Australia",[],{"id":1861,"sortIndex":40,"affiliation":1862,"properties":1868},"2885a68d-fb9a-4bad-8a31-9ccf09ea6605",{"id":1861,"createTime":28,"updateTime":28,"relativeEntities":1863,"slug":28,"properties":1864,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1867,"statistic":28},[],{"title":1865},{"VI":1866},"School of Paediatrics and Child Health, The University of Western Australia, Perth, Australia",[],{},{"title":1870},{"VI":1871},"Shanti Balasubramaniam",{"id":1873,"sortIndex":40,"researcher":28,"roles":1874,"affiliations":1875,"properties":1884,"displayName":1886,"givenName":28,"familyName":28},"c581658c-ec5b-434a-8063-874f8d2d33cb",[967],[1876],{"id":1877,"sortIndex":32,"affiliation":1878,"properties":28},"48503eaa-81c9-4287-9872-f560a6771963",{"id":1877,"createTime":28,"updateTime":28,"relativeEntities":1879,"slug":28,"properties":1880,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1883,"statistic":28},[],{"title":1881},{"VI":1882},"School of Pharmacy and the Mater Research Institute, The University of Queensland, Brisbane, Australia",[],{"title":1885},{"VI":1886},"John A. Duley",{"id":1888,"sortIndex":123,"researcher":28,"roles":1889,"affiliations":1890,"properties":1908,"displayName":1910,"givenName":28,"familyName":28},"0d8fd5df-51f9-44c2-893f-a9e17dc85672",[967],[1891,1899],{"id":1892,"sortIndex":32,"affiliation":1893,"properties":28},"dc9640b4-7bcf-4a6e-a0db-0b41040e0c21",{"id":1892,"createTime":28,"updateTime":28,"relativeEntities":1894,"slug":28,"properties":1895,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1898,"statistic":28},[],{"title":1896},{"VI":1897},"Western Sydney Genetics Program, Children’s Hospital at Westmead, Sydney, Australia",[],{"id":1900,"sortIndex":40,"affiliation":1901,"properties":1907},"2ceaf12a-6229-4b1c-a76d-9ce645afd3ec",{"id":1900,"createTime":28,"updateTime":28,"relativeEntities":1902,"slug":28,"properties":1903,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1906,"statistic":28},[],{"title":1904},{"VI":1905},"Disciplines of Paediatrics and Child Health and Genetic Medicine, University of Sydney, Sydney, Australia",[],{},{"title":1909},{"VI":1910},"John Christodoulou",{"url":1846,"publisher":1912,"properties":1958},{"id":868,"createTime":869,"updateTime":870,"relativeEntities":1913,"slug":872,"properties":1914,"entityType":25,"verifyStatus":880,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":32,"subjectFields":1918,"manageAffiliations":1927,"indexDatabases":1938,"url":942,"thumbnailPath":28,"statistic":1953,"gsStatistic":28,"type":55,"analyzePriority":28},[],{"issn":1915,"title":1916,"eissn":1917},{"VOID":875},{"EN":877},{"VOID":879},[1919,1923],{"id":883,"createTime":28,"updateTime":28,"relativeEntities":1920,"label":1921,"description":1922,"parentId":28,"standard":28,"scholarHubFieldId":28},[],{"EN":886},{},{"id":889,"createTime":28,"updateTime":28,"relativeEntities":1924,"label":1925,"description":1926,"parentId":28,"standard":28,"scholarHubFieldId":28},[],{"EN":892},{},[1928,1933],{"id":896,"createTime":28,"updateTime":28,"relativeEntities":1929,"slug":28,"properties":1930,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1932,"statistic":28},[],{"title":1931},{"EN":900},[902],{"id":904,"createTime":28,"updateTime":28,"relativeEntities":1934,"slug":28,"properties":1935,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1937,"statistic":28},[],{"title":1936},{"EN":908},[],[1939,1946],{"id":912,"indexDatabase":1940,"url":918,"indexYears":919,"academicFieldIds":1945,"indexDatabaseRanking":923},{"id":775,"createTime":28,"updateTime":28,"relativeEntities":1941,"label":1942,"description":1943,"key":781,"publicationTags":1944,"standard":28},[],{"EN":778,"VI":778},{"EN":778,"VI":780},[783],[921,922],{"id":925,"indexDatabase":1947,"url":937,"indexYears":28,"academicFieldIds":1952,"indexDatabaseRanking":28},{"id":927,"createTime":28,"updateTime":28,"relativeEntities":1948,"label":1949,"description":1950,"key":934,"publicationTags":1951,"standard":28},[],{"EN":930,"VI":930},{"EN":932,"VI":933},[936,813],[939,940,941],{"impactFactor":32,"impactFactorByYear":1954,"i10Index":32,"i10IndexLast5Year":32,"totalPublication":40,"totalPublicationByYear":1955,"totalCitation":32,"totalCitationByYear":1956,"totalCitationPerPublication":32,"totalCitationPerPublicationByYear":1957,"hindexLast5Year":32,"hindex":32},{},{"2017":40},{},{},{"pages":1959,"volume":1961},{"VOID":1960},"687-698",{"VOID":1962},"37","2014-07-17",2014,[923,936],{"id":1967,"createTime":1968,"updateTime":1969,"relativeEntities":1970,"slug":1971,"properties":1972,"entityType":961,"verifyStatus":26,"verifyTime":1969,"verifyNote":1112,"languages":28,"translateLanguages":28,"viewCount":32,"primaryUrl":1981,"fullTextUrl":28,"authors":1982,"publicationType":972,"publisherRelationship":2233,"citationCount":28,"citationInfo":28,"publishDate":2285,"publishYear":2286,"citationAnalyzeStatus":880,"lastCitationAnalyze":28,"indexDatabases":2287,"openAccess":28,"references":28,"isForceReanalyzing":1028},"0141a6d0-6a50-4aad-8767-10846a59d8e2","2024-02-11T19:21:32.537+00:00","2024-12-12T16:18:51.815+00:00",[],"Functional-and-electrophysiological-characterization-of-four-non-truncating-mutations-responsible-for-creatine-transporter-SLC6A8-deficiency-syndrome",{"abstract":1973,"title":1975,"references":1977,"doi":1979},{"EN":1974},"Intellectual disability coupled with epilepsy are clinical hallmarks of the creatine (Cr) transporter deficiency syndrome resulting from mutations in the SLC6A8 gene. So far characterization of pathogenic mutations of SLC6A8 has been limited to Cr uptake. The aim of our study was to characterize the electrogenic and pharmacological properties of non truncating SLC6A8 mutations identified in patients presenting variable clinical severity. Electrophysiological and pharmacological properties of four mutants (including two novel ones) were studied in X. laevis oocyte expression system. Creatine uptake was assessed with [14C]-Cr in X. laevis and patients’ fibroblasts. Subcellular localization was determined by immunofluorescence and western blot. All mutants were properly targeted to the plasma membrane in both systems. Mutations led to the complete loss of both electrogenic and transport activities in X. laevis and Cr uptake in patients’ fibroblasts. Among the Cr analogs tested, guanidinopropionate induced an electrogenic activity with the normal SLC6A8 transporter similar to creatine whereas a phosphocreatine derivative, PCr-Mg-CPLX, resulted in partial activity. SLC6A8 mutants displayed no electrogenic activity with all Cr analogs tested in X. laevis oocytes. Although the mutations altered various domains of SLC6A8 Cr uptake and electrogenic properties were completely inhibited and could not be dissociated. Besides the metabolic functions of Cr, the loss of SLC6A8 electrogenic activity, demonstrated here for the first time, may also play a role in the altered brain functions of the patients.",{"EN":1976},"Functional and electrophysiological characterization of four non-truncating mutations responsible for creatine transporter (SLC6A8) deficiency syndrome",{"VOID":1978},"Ardon O, di San A, Filippo C, Salomons GS et al (2010) Creatine transporter deficiency in two half-brothers. Am J Med Genet A 152A(8):1979–1983\nArias A, Corbella M, Fons C et al (2007) Creatine transporter deficiency: prevalence among patients with mental retardation and pitfalls in metabolite screening. Clin Biochem 40(16–17):1328–1331\nBen-Yona A, Bendahan A, Kanner BI (2011) A glutamine residue conserved in the neurotransmitter:sodium:symporters is essential for the interaction of chloride with the GABA transporter GAT-1. J Biol Chem 286(4):2826–2833\nBetsalel OT, van de Kamp JM, Martinez-Munoz C et al (2008) Detection of low-level somatic and germline mosaicism by denaturing high-performance liquid chromatography in a EURO-MRX family with SLC6A8 deficiency. Neurogenetics 9(3):183–190\nBetsalel OT, Rosenberg EH, Almeida LS et al (2011) Characterization of novel SLC6A8 variants with the use of splice-site analysis tools and implementation of a newly developed LOVD database. Eur J Hum Genet 19(1):56–63\nBizzi A, Bugiani M, Salomons GS et al (2002) X-linked creatine deficiency syndrome: a novel mutation in creatine transporter gene SLC6A8. Ann Neurol 52(2):227–231\nBrosnan ME, Edison EE, da Silva R et al (2007) New insights into creatine function and synthesis. Adv Enzyme Regul 47:252–260\nCecil KM, Salomons GS, Ball WS Jr et al (2001) Irreversible brain creatine deficiency with elevated serum and urine creatine: a creatine transporter defect? Ann Neurol 49(3):401–404\nChen NH, Reith ME, Quick MW (2004) Synaptic uptake and beyond: the sodium- and chloride-dependent neurotransmitter transporter family SLC6. Pflugers Arch 447(5):519–531\nClark AJ, Rosenberg EH, Almeida LS et al (2006) X-linked creatine transporter (SLC6A8) mutations in about 1% of males with mental retardation of unknown etiology. Hum Genet 119(6):604–610\nCougnon M, Benammou S, Brouillard F et al (2002) Effect of reactive oxygen species on NH4+ permeation in Xenopus laevis oocytes. Am J Physiol Cell Physiol 282(6):C1445–C1453\nDai W, Vinnakota S, Qian X et al (1999) Molecular characterization of the human CRT-1 creatine transporter expressed in Xenopus oocytes. Arch Biochem Biophys 361(1):75–84\nDinour D, Chang MH, Satoh J et al (2004) A novel missense mutation in the sodium bicarbonate cotransporter (NBCe1\u002FSLC4A4) causes proximal tubular acidosis and glaucoma through ion transport defects. J Biol Chem 279(50):52238–52246\nDodd JR, Christie DL (2007) Selective amino acid substitutions convert the creatine transporter to a gamma-aminobutyric acid transporter. J Biol Chem 282(21):15528–15533\nGether U, Andersen PH, Larsson OM et al (2006) Neurotransmitter transporters: molecular function of important drug targets. Trends Pharmacol Sci 27(7):375–383\nGuimbal C, Kilimann MW (1993) A Na(+)-dependent creatine transporter in rabbit brain, muscle, heart, and kidney. cDNA cloning and functional expression. J Biol Chem 268(12):8418–8421\nHahn KA, Salomons GS, Tackels-Horne D et al (2002) X-linked mental retardation with seizures and carrier manifestations is caused by a mutation in the creatine-transporter gene (SLC6A8) located in Xq28. Am J Hum Genet 70(5):1349–1356\nKathofer S, Zhang W, Karle C et al (2000) Functional coupling of human beta 3-adrenoreceptors to the KvLQT1\u002FMinK potassium channel. J Biol Chem 275(35):26743–26747\nLion-Francois L, Cheillan D, Pitelet G et al (2006) High frequency of creatine deficiency syndromes in patients with unexplained mental retardation. Neurology 67(9):1713–1714\nLunardi G, Parodi A, Perasso L et al (2006) The creatine transporter mediates the uptake of creatine by brain tissue, but not the uptake of two creatine-derived compounds. Neuroscience 142(4):991–997\nNessler S, Friedrich O, Bakouh N et al (2004) Evidence for activation of endogenous transporters in Xenopus laevis oocytes expressing the Plasmodium falciparum chloroquine resistance transporter, PfCRT. J Biol Chem 279(38):39438–39446\nNewmeyer A, Cecil KM, Schapiro M et al (2005) Incidence of brain creatine transporter deficiency in males with developmental delay referred for brain magnetic resonance imaging. J Dev Behav Pediatr 26(4):276–282\nOhana E, Shcheynikov N, Yang D et al (2011) Determinants of coupled transport and uncoupled current by the electrogenic SLC26 transporters. J Gen Physiol 137(2):239–251\nPuusepp H, Kall K, Salomons GS et al (2009) The screening of SLC6A8 deficiency among Estonian families with X-linked mental retardation. J Inherit Metab Dis\nReith ME, Zhen J, Chen N (2006) The importance of company: Na+ and Cl- influence substrate interaction with SLC6 transporters and other proteins. 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