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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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Studies of renal function may be conducted using a wide range of approaches, such as biochemistry, immunology, genetics, mathematical modeling, molecular biology, as well as physiological and clinical methodologies.","PENDING",[886,892],{"id":887,"createTime":28,"updateTime":28,"relativeEntities":888,"label":889,"description":891,"parentId":28,"standard":28,"scholarHubFieldId":28},"317b242e-4e36-43ab-821e-f9755e22375e",[],{"EN":890},"Physiology",{},{"id":893,"createTime":28,"updateTime":28,"relativeEntities":894,"label":895,"description":897,"parentId":28,"standard":28,"scholarHubFieldId":28},"8e32f7cd-3445-43a4-981f-c8e55ee3064b",[],{"EN":896},"Urology",{},[899,906],{"id":900,"createTime":28,"updateTime":28,"relativeEntities":901,"slug":28,"properties":902,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":905,"statistic":28},"ee372727-4c87-4379-b8a3-771408d03bd0",[],{"title":903},{"EN":904},"AMER PHYSIOLOGICAL SOC",[],{"id":907,"createTime":28,"updateTime":28,"relativeEntities":908,"slug":28,"properties":909,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":912,"statistic":28},"b49c938d-bca1-4d52-9e02-c7bc2ebaea8a",[],{"title":910},{"EN":911},"American Physiological Society",[],[914,927],{"id":915,"indexDatabase":916,"url":921,"indexYears":922,"academicFieldIds":923,"indexDatabaseRanking":926},"8497d219-b3e4-4f80-92e0-f29cb2f6d875",{"id":775,"createTime":28,"updateTime":28,"relativeEntities":917,"label":918,"description":919,"key":781,"publicationTags":920,"standard":28},[],{"EN":778,"VI":778},{"EN":778,"VI":780},[783],"https:\u002F\u002Fwww.scopus.com\u002Fsourceid\u002F9500153964","1992-1996,2001,2009",[924,925],"f845e4fe-178d-4593-b013-715b3c1cc81c","45560ae3-6e73-4562-b98a-3bad7e554cef","SCOPUS__Q1",{"id":928,"indexDatabase":929,"url":940,"indexYears":28,"academicFieldIds":941,"indexDatabaseRanking":28},"942d2231-0ee0-4ec2-ab72-1481d3f23b83",{"id":930,"createTime":28,"updateTime":28,"relativeEntities":931,"label":932,"description":934,"key":937,"publicationTags":938,"standard":28},"a4921856-b128-4d9f-8f1f-e80813d3bbd4",[],{"EN":933,"VI":933},"ISI\u002FSCIE - Science Citation Index Expanded",{"EN":935,"VI":936},"SCIE database","Cơ sở dữ liệu SCIE","scie",[939,813],"SCIE","https:\u002F\u002Fmjl.clarivate.com\u002Fsearch-results?issn=1931-857X",[942,943],"08b1efac-a7b2-46c7-9e79-ef24d3d9025d","89bd3143-34da-4e0c-a662-528d683c514f","https:\u002F\u002Fjournals.physiology.org\u002Fjournal\u002Fajprenal",{"impactFactor":32,"impactFactorByYear":946,"i10Index":136,"i10IndexLast5Year":40,"totalPublication":140,"totalPublicationByYear":948,"totalCitation":949,"totalCitationByYear":950,"totalCitationPerPublication":960,"totalCitationPerPublicationByYear":961,"hindexLast5Year":122,"hindex":122},{"2013":947,"2014":49,"2017":357,"2018":51,"2020":205,"2021":47},4.5,{"1978":40,"1985":123,"1998":123,"2000":123,"2001":40,"2002":40,"2003":42,"2004":40,"2005":123,"2006":42,"2007":123,"2008":40,"2009":40,"2012":123,"2016":40,"2019":40},4533,{"1978":520,"1985":951,"1998":952,"2000":953,"2001":954,"2002":437,"2003":955,"2004":147,"2005":435,"2006":956,"2007":957,"2008":154,"2009":958,"2012":959,"2016":604,"2019":436},141,1417,711,69,757,139,191,127,131,174.35,{"1978":520,"1985":962,"1998":963,"2000":964,"2001":954,"2002":437,"2003":965,"2004":147,"2005":516,"2006":966,"2007":967,"2008":154,"2009":958,"2012":968,"2016":604,"2019":436},70.5,708.5,355.5,252.33,46.33,95.5,65.5,{"meta":970,"data":972},{"total":971},"190",[973,1787,2062,2400,3109,3550,4433,4636,5051,5699],{"id":974,"createTime":975,"updateTime":976,"relativeEntities":977,"slug":978,"properties":979,"entityType":996,"verifyStatus":26,"verifyTime":997,"verifyNote":998,"languages":999,"translateLanguages":1000,"viewCount":32,"primaryUrl":1001,"fullTextUrl":28,"authors":1002,"publicationType":1037,"publisherRelationship":1038,"citationCount":1093,"citationInfo":1094,"publishDate":1097,"publishYear":1095,"citationAnalyzeStatus":884,"lastCitationAnalyze":28,"indexDatabases":1098,"openAccess":28,"references":1099,"isForceReanalyzing":1786},"4132a1d1-9b18-4f14-bcec-f0069998766b","2024-09-19T00:52:52.624+00:00","2025-02-11T18:28:10.097+00:00",[],"Isozymes-of-the-Na-K-ATPase-heterogeneity-in-structure-diversity-in-function",{"mag":980,"keywords":982,"openalex":984,"abstract":986,"title":989,"pm":992,"doi":994},{"VOID":981},"2175631194",{"VI":983},"",{"VOID":985},"W2175631194",{"EN":987,"VI":988},"\u003Cjats:p>The Na-K-ATPase is characterized by a complex molecular heterogeneity that results from the expression and differential association of multiple isoforms of both its α- and β-subunits. At present, as many as four different α-polypeptides (α1, α2, α3, and α4) and three distinct β-isoforms (β1, β2, and β3) have been identified in mammalian cells. The stringent constraints on the structure of the Na pump isozymes during evolution and their tissue-specific and developmental pattern of expression suggests that the different Na-K-ATPases have evolved distinct properties to respond to cellular requirements. This review focuses on the functional properties, regulation, and possible physiological relevance of the Na pump isozymes. The coexistence of multiple α- and β-isoforms in most cells has hindered the understanding of the roles of the individual polypeptides. The use of heterologous expression systems has helped circumvent this problem. The kinetic characteristics of different Na-K-ATPase isozymes to the activating cations (Na\u003Cjats:sup>+\u003C\u002Fjats:sup>and K\u003Cjats:sup>+\u003C\u002Fjats:sup>), the substrate ATP, and the inhibitors Ca\u003Cjats:sup>2+\u003C\u002Fjats:sup>and ouabain demonstrate that each isoform has distinct properties. In addition, intracellular messengers differentially regulate the activity of the individual Na-K-ATPase isozymes. Thus the regulation of specific Na pump isozymes gives cells the ability to precisely coordinate Na-K-ATPase activity to their physiological requirements.\u003C\u002Fjats:p>","\u003Cjats:p>Na-K-ATPase được đặc trưng bởi sự không đồng nhất phân tử phức tạp, kết quả từ sự biểu hiện và sự kết hợp khác biệt của nhiều isoform cả của các tiểu đơn vị α và β. Hiện tại, đã có tới bốn polypeptide α khác nhau (α1, α2, α3 và α4) và ba isoform β khác biệt (β1, β2 và β3) được xác định trong tế bào có vú. Các ràng buộc nghiêm ngặt về cấu trúc của các isozym Na pump trong quá trình tiến hóa và mô hình biểu hiện đặc hiệu theo mô và phát triển cho thấy rằng các Na-K-ATPase khác nhau đã phát triển các đặc tính riêng biệt để phản ứng với nhu cầu của tế bào. Bài tổng quan này tập trung vào các đặc tính chức năng, sự điều chỉnh và khả năng liên quan sinh lý của các isozym Na pump. Sự tồn tại đồng thời của nhiều isoform α và β trong hầu hết các tế bào đã cản trở việc hiểu biết về vai trò của từng polypeptide. Việc sử dụng các hệ thống biểu hiện dị thể đã giúp khắc phục vấn đề này. Các đặc điểm động học của các isozym Na-K-ATPase khác nhau đối với các cation kích hoạt (Na\u003Cjats:sup>+\u003C\u002Fjats:sup> và K\u003Cjats:sup>+\u003C\u002Fjats:sup>), cơ chất ATP và các chất ức chế Ca\u003Cjats:sup>2+\u003C\u002Fjats:sup> và ouabain cho thấy mỗi isoform có các đặc tính riêng biệt. Ngoài ra, các tín hiệu tế bào nội bào điều chỉnh khác nhau hoạt động của các isozym Na-K-ATPase riêng lẻ. Do đó, việc điều chỉnh các isozym Na pump cụ thể cho phép tế bào phối hợp chính xác hoạt động Na-K-ATPase với các yêu cầu sinh lý của chúng.\u003C\u002Fjats:p>",{"EN":990,"VI":991},"Isozymes of the Na-K-ATPase: heterogeneity in structure, diversity in function","Các isozym của Na-K-ATPase: sự không đồng nhất trong cấu trúc, sự đa dạng trong chức năng",{"VOID":993},"9815123",{"VOID":995},"10.1152\u002Fajprenal.1998.275.5.f633","PUBLICATION","2024-09-19T00:52:52.623+00:00","Auto Verify",[31],[30],"https:\u002F\u002Fwww.physiology.org\u002Fdoi\u002F10.1152\u002Fajprenal.1998.275.5.F633",[1003,1022],{"id":1004,"sortIndex":32,"researcher":28,"roles":1005,"affiliations":1006,"properties":1015,"displayName":1019,"givenName":28,"familyName":28},"9046c9e5-5122-4617-9282-fdcf8fa179b3",[],[1007],{"id":1008,"sortIndex":32,"affiliation":1009,"properties":28},"b87538e5-5d70-4271-8366-3ca9b573dccc",{"id":1008,"createTime":28,"updateTime":28,"relativeEntities":1010,"slug":28,"properties":1011,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1014,"statistic":28},[],{"title":1012},{"VI":1013},"Department of Cell Biology and Physiology, Washington University School of Medicine, St. Louis, Missouri 63110",[],{"orcid":1016,"title":1018,"openalex":1020},{"VOID":1017},"https:\u002F\u002Forcid.org\u002F0000-0001-7721-9869",{"EN":1019},"Gustavo Blanco",{"VOID":1021},"A5037666188",{"id":1023,"sortIndex":40,"researcher":28,"roles":1024,"affiliations":1025,"properties":1032,"displayName":1034,"givenName":28,"familyName":28},"087aee04-168c-4ef6-bd80-db0aa50f35c0",[],[1026],{"id":1008,"sortIndex":32,"affiliation":1027,"properties":28},{"id":1008,"createTime":28,"updateTime":28,"relativeEntities":1028,"slug":28,"properties":1029,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1031,"statistic":28},[],{"title":1030},{"VI":1013},[],{"title":1033,"openalex":1035},{"EN":1034},"Robert W. 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C., 1992, J. Bioenerg. Biomembr., 24, 249, 10.1007\u002FBF00768846",{"doi":1691},"10.1007\u002FBF00768846",{"id":28,"text":1693,"url":28,"identifiers":1694},"10.1152\u002Fajpcell.1981.240.5.C207",{"doi":1693},{"id":28,"text":1696,"url":28,"identifiers":1697},"10.1016\u002F0014-5793(87)80677-4",{"doi":1696},{"id":28,"text":1699,"url":28,"identifiers":1700},"Sweadner K. J., 1979, J. Biol. Chem., 254, 6060, 10.1016\u002FS0021-9258(18)50519-6",{"doi":1701},"10.1016\u002FS0021-9258(18)50519-6",{"id":28,"text":1703,"url":28,"identifiers":1704},"Sweadner K. J., 1985, J. Biol. Chem., 260, 11508, 10.1016\u002FS0021-9258(17)39059-2",{"doi":1705},"10.1016\u002FS0021-9258(17)39059-2",{"id":28,"text":1707,"url":28,"identifiers":1708},"10.1016\u002F0304-4157(89)90019-1",{"doi":1707},{"id":28,"text":1710,"url":28,"identifiers":1711},"Sweadner K. J., 1991, Soc. Gen. Physiol. 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Physiol., 266, F240",{},{"id":28,"text":1740,"url":28,"identifiers":1741},"10.1016\u002F0006-291X(91)91513-C",{"doi":1740},{"id":28,"text":1743,"url":28,"identifiers":1744},"10.1093\u002Foxfordjournals.jbchem.a132654",{"doi":1743},{"id":28,"text":1746,"url":28,"identifiers":1747},"10.1016\u002FS0006-291X(88)80914-8",{"doi":1746},{"id":28,"text":1749,"url":28,"identifiers":1750},"10.1016\u002F0304-4157(93)90012-D",{"doi":1749},{"id":28,"text":1752,"url":28,"identifiers":1753},"10.1016\u002F0020-711X(80)90117-2",{"doi":1752},{"id":28,"text":1755,"url":28,"identifiers":1756},"10.1146\u002Fannurev.ph.50.030188.001451",{"doi":1755},{"id":28,"text":1758,"url":28,"identifiers":1759},"Yoon K. L., 1994, J. Biol. 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Chem., 268, 8019, 10.1016\u002FS0021-9258(18)53058-1",{"doi":1785},"10.1016\u002FS0021-9258(18)53058-1",false,{"id":1788,"createTime":1789,"updateTime":1790,"relativeEntities":1791,"slug":1792,"properties":1793,"entityType":996,"verifyStatus":26,"verifyTime":1789,"verifyNote":998,"languages":1809,"translateLanguages":1810,"viewCount":32,"primaryUrl":1811,"fullTextUrl":28,"authors":1812,"publicationType":1037,"publisherRelationship":1909,"citationCount":1963,"citationInfo":1964,"publishDate":1967,"publishYear":1965,"citationAnalyzeStatus":884,"lastCitationAnalyze":28,"indexDatabases":1968,"openAccess":28,"references":1969,"isForceReanalyzing":1786},"1357f6d7-69cb-411b-b830-522e1e20060b","2024-09-05T15:22:24.366+00:00","2025-02-11T18:29:07.071+00:00",[],"Glomerular-hemodynamics-in-severe-obesity",{"mag":1794,"keywords":1796,"openalex":1797,"abstract":1799,"title":1802,"pm":1805,"doi":1807},{"VOID":1795},"1826211555",{"VI":983},{"VOID":1798},"W1826211555",{"EN":1800,"VI":1801},"\u003Cjats:p>Differential solute clearances were used to characterize glomerular function in 12 nondiabetic subjects with severe obesity (body mass index >38). Nine healthy subjects served as the control group. In the obese group, glomerular filtration rate (GFR) and renal plasma flow (RPF) exceeded the control value by 51 and 31%, respectively. Consequently, filtration fraction increased. The augmented RPF suggested a state of renal vasodilatation involving, mainly or solely, the afferent arteriole. Albumin excretion rate and fractional albumin clearance increased by 89 and 78%, respectively. Oral glucose tolerance tests were suggestive of insulin resistance. Insulin resistance was positively correlated with GFR ( r = 0.88, P < 0.001) and RPF ( r = 0.72, P < 0.001). Mean arterial pressure was higher than in the control group. Fractional clearances of dextrans of broad size distribution tended to be lowered. The determinants of the GFR were estimated qualitatively by using a theoretical model of dextran transport through a heteroporous membrane. This analysis suggests that the high GFR in very obese subjects may be the result of an increase in transcapillary hydraulic pressure difference (ΔP). An abnormal transmission of increased arterial pressure to the glomerular capillaries through a dilated afferent arteriole could account for the augmentation in ΔP.\u003C\u002Fjats:p>","\u003Cjats:p>Khả năng thanh thải các chất hòa tan được sử dụng để xác định chức năng cầu thận ở 12 đối tượng không tiểu đường có béo phì nghiêm trọng (chỉ số khối cơ thể >38). Chín đối tượng khỏe mạnh được chọn làm nhóm đối chứng. Trong nhóm béo phì, tỷ lệ lọc cầu thận (GFR) và lưu lượng máu thận (RPF) cao hơn giá trị đối chứng lần lượt là 51% và 31%. Do đó, tỷ lệ lọc tăng lên. Lưu lượng máu thận tăng cường gợi ý về một trạng thái giãn mạch thận liên quan, chủ yếu hoặc chỉ là, động mạch đi vào. Tỷ lệ bài xuất albumin và thanh thải albumin phân đoạn đều tăng lần lượt là 89% và 78%. Các bài kiểm tra dung nạp glucose đường miệng cho thấy dấu hiệu kháng insulin. Kháng insulin có mối tương quan dương với GFR (r = 0.88, P \u003C 0.001) và RPF (r = 0.72, P \u003C 0.001). Áp lực động mạch trung bình cao hơn so với nhóm đối chứng. Các thanh thải phân đoạn của dextran có phân bố kích thước rộng có xu hướng giảm. Các yếu tố quyết định của GFR được ước lượng một cách định tính bằng cách sử dụng một mô hình lý thuyết về sự vận chuyển dextran qua một màng cực phân. Phân tích này gợi ý rằng GFR cao ở các đối tượng béo phì rất có thể do sự gia tăng trong sự chênh lệch áp suất thủy tĩnh xuyên mạch (ΔP). Một sự truyền áp suất động mạch tăng lên không bình thường tới các mao mạch cầu thận thông qua động mạch đi vào giãn nở có thể là nguyên nhân cho sự tăng lên trong ΔP.\u003C\u002Fjats:p>",{"EN":1803,"VI":1804},"Glomerular hemodynamics in severe obesity","Hemodynamique cầu thận trong béo phì nghiêm 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574",{},{"id":2063,"createTime":2064,"updateTime":2065,"relativeEntities":2066,"slug":2067,"properties":2068,"entityType":996,"verifyStatus":26,"verifyTime":2085,"verifyNote":998,"languages":2086,"translateLanguages":2087,"viewCount":32,"primaryUrl":2088,"fullTextUrl":28,"authors":2089,"publicationType":1037,"publisherRelationship":2109,"citationCount":2164,"citationInfo":2165,"publishDate":2168,"publishYear":2166,"citationAnalyzeStatus":884,"lastCitationAnalyze":28,"indexDatabases":2169,"openAccess":28,"references":2170,"isForceReanalyzing":1786},"53ad729a-8066-42ed-beeb-1cd257162b20","2024-11-25T06:50:39.137+00:00","2025-02-11T18:30:05.029+00:00",[],"Renal-Na-sup-sup-glucose-cotransporters",{"mag":2069,"keywords":2071,"openalex":2073,"abstract":2075,"title":2078,"pm":2081,"doi":2083},{"VOID":2070},"2152211669",{"VI":2072},"Na\u003Csup>+\u003C\u002Fsup>-glucose, chất vận chuyển, thận, SGLT1, SGLT2, SGLT3",{"VOID":2074},"W2152211669",{"EN":2076,"VI":2077},"\u003Cjats:p>In humans, the kidneys filter ∼180 g of d-glucose from plasma each day, and this is normally reabsorbed in the proximal tubules. Although the mechanism of reabsorption is well understood, Na\u003Cjats:sup>+\u003C\u002Fjats:sup>-glucose cotransport across the brush-border membrane and facilitated diffusion across the basolateral membrane, questions remain about the identity of the genes responsible for cotransport across the brush border. Genetic studies suggest that two different genes regulate Na\u003Cjats:sup>+\u003C\u002Fjats:sup>-glucose cotransport, and there is evidence from animal studies to suggest that the major bulk of sugar is reabsorbed in the convoluted proximal tubule by a low-affinity, high-capacity transporter and that the remainder is absorbed in the straight proximal tubule by a high-affinity, low-capacity transporter. There are at least three different candidates for these human renal Na\u003Cjats:sup>+\u003C\u002Fjats:sup>-glucose cotransporters. This review will focus on the structure-function relationships of these three transporters, SGLT1, SGLT2, and SGLT3.\u003C\u002Fjats:p>","\u003Cjats:p>Ở người, thận lọc khoảng 180 g d-glucose từ huyết tương mỗi ngày, và đây thường được tái hấp thu ở ống lượn gần. Mặc dù cơ chế tái hấp thu đã được hiểu rõ, việc đồng vận chuyển Na\u003Cjats:sup>+\u003C\u002Fjats:sup>-glucose qua màng vi nhung mao và sự khuếch tán được hỗ trợ qua màng đáy bên vẫn còn những câu hỏi về danh tính của các gen chịu trách nhiệm cho đồng vận chuyển qua màng vi nhung mao. Các nghiên cứu di truyền cho thấy hai gen khác nhau điều hòa đồng vận chuyển Na\u003Cjats:sup>+\u003C\u002Fjats:sup>-glucose, và có bằng chứng từ các nghiên cứu trên động vật cho thấy rằng phần lớn đường được tái hấp thu ở ống lượn gần bởi một chất vận chuyển có độ ái lực thấp, dung tích cao, trong khi phần còn lại được hấp thu ở ống lượn gần thẳng bởi một chất vận chuyển có độ ái lực cao, dung tích thấp. Có ít nhất ba ứng viên khác nhau cho các chất vận chuyển Na\u003Cjats:sup>+\u003C\u002Fjats:sup>-glucose ở thận người này. Bài tổng quan này sẽ tập trung vào các mối quan hệ cấu trúc-chức năng của ba chất vận chuyển này, SGLT1, SGLT2, và SGLT3.\u003C\u002Fjats:p>",{"EN":2079,"VI":2080},"Renal Na\u003Csup>+\u003C\u002Fsup>-glucose cotransporters","Các chất vận chuyển Na\u003Csup>+\u003C\u002Fsup>-glucose ở thận",{"VOID":2082},"11133510",{"VOID":2084},"10.1152\u002Fajprenal.2001.280.1.f10","2024-11-25T06:50:39.136+00:00",[31],[30],"https:\u002F\u002Fwww.physiology.org\u002Fdoi\u002F10.1152\u002Fajprenal.2001.280.1.F10",[2090],{"id":2091,"sortIndex":32,"researcher":28,"roles":2092,"affiliations":2093,"properties":2102,"displayName":2106,"givenName":28,"familyName":28},"8c804f56-36f3-4a55-8ada-abb58965c3dc",[],[2094],{"id":2095,"sortIndex":32,"affiliation":2096,"properties":28},"949f5121-a157-4ced-b3dd-1bac70e3f346",{"id":2095,"createTime":28,"updateTime":28,"relativeEntities":2097,"slug":28,"properties":2098,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":2101,"statistic":28},[],{"title":2099},{"EN":2100},"Department of Physiology, University of California Los Angeles School of Medicine, Los Angeles, California 90095-1751",[],{"orcid":2103,"title":2105,"openalex":2107},{"VOID":2104},"https:\u002F\u002Forcid.org\u002F0000-0002-1023-4391",{"EN":2106},"Ernest M. 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E, 1994, J Biol Chem, 269, 15204, 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published epidemiological and outcome analysis studies have brought to our attention the important role played by acute kidney injury (AKI) in the progression of chronic kidney disease (CKD) to end-stage renal disease (ESRD). AKI accelerates progression in patients with CKD; conversely, CKD predisposes patients to AKI. This research gives credence to older, well-thought-out wisdom that recovery from AKI is often not complete and is marked by residual structural damage. It also mirrors older experimental observations showing that unilateral nephrectomy, a surrogate for loss of nephrons by disease, compromises structural recovery and worsens tubulointerstitial fibrosis after ischemic AKI. Moreover, review of a substantial body of work on the relationships among reduced renal mass, hypertension, and pathology associated with these conditions suggests that impaired myogenic autoregulation of blood flow in the setting of hypertension, the arteriolosclerosis that results, and associated recurrent ischemic AKI in microscopic foci play important roles in the development of progressively increasing tubulointerstitial fibrosis. How nutrition, an additional factor that profoundly affects renal disease progression, influences these events needs reevaluation in light of information on the effects of calories vs. protein and animal vs. vegetable protein on injury and progression. Considerations based on published and emerging data suggest that a pathology that develops in regenerating tubules after AKI characterized by failure of differentiation and persistently high signaling activity is the proximate cause that drives downstream events in the interstitium: inflammation, capillary rarefaction, and fibroblast proliferation. In light of this information, we advance a comprehensive hypothesis regarding the pathophysiology of AKI as it relates to the progression of kidney disease. We discuss the implications of this pathophysiology for developing efficient therapeutic strategies to delay progression and avert ESRD.\u003C\u002Fjats:p>","\u003Cjats:p>Các nghiên cứu gần đây về dịch tễ học và phân tích kết quả đã làm nổi bật vai trò quan trọng của chấn thương thận cấp (AKI) trong sự tiến triển của bệnh thận mãn tính (CKD) đến bệnh thận giai đoạn cuối (ESRD). AKI làm tăng tốc độ tiến triển ở bệnh nhân bị CKD; ngược lại, CKD làm cho bệnh nhân dễ mắc AKI hơn. Nghiên cứu này xác nhận một triết lý cũ, từng được suy xét kỹ càng rằng sự phục hồi sau AKI thường không hoàn toàn và có dấu hiệu của tổn thương cấu trúc còn sót lại. Nó cũng phản ánh những quan sát thí nghiệm trước đây cho thấy rằng phẫu thuật cắt thận một bên, một sự thay thế cho tổn thất nephrons do bệnh lý, làm suy giảm khả năng phục hồi cấu trúc và làm trầm trọng thêm xơ hóa ống kẽ sau AKI thiếu máu cục bộ. Hơn nữa, việc xem xét một số lượng lớn công trình nghiên cứu về mối quan hệ giữa khối lượng thận giảm, tăng huyết áp và bệnh lý liên quan đến các tình trạng này cho thấy rằng việc điều hòa tự động huyết động học của máu bị suy giảm trong bối cảnh tăng huyết áp, chứng xơ động mạch nhỏ xảy ra và AKI thiếu máu cục bộ tái phát trong các ổ vi thể đóng vai trò quan trọng trong sự phát triển của xơ hóa ống kẽ gia tăng dần dần. Cách mà dinh dưỡng, một yếu tố bổ sung sâu sắc ảnh hưởng đến sự tiến triển của bệnh thận, tác động đến những sự kiện này cần được xem xét lại dựa trên thông tin về ảnh hưởng của calo so với protein và protein động vật so với protein thực vật đối với tổn thương và sự phát triển. Các xem xét dựa trên dữ liệu đã công bố và dữ liệu mới nổi gợi ý rằng một bệnh lý phát triển trong các ống tái sinh sau AKI, được đặc trưng bởi sự thất bại trong phân hóa và hoạt động tín hiệu cao liên tục, là nguyên nhân gần gũi thúc đẩy các sự kiện tiếp theo trong khoang kẽ: viêm, thưa mạch và sự phát triển của nguyên bào sợi. Dựa trên thông tin này, chúng tôi đưa ra một giả thuyết toàn diện về sinh lý bệnh của AKI liên quan đến sự tiến triển của bệnh thận. Chúng tôi thảo luận về các tác động của sinh lý bệnh này đối với việc phát triển các chiến lược điều trị hiệu quả nhằm làm chậm sự tiến triển và ngăn ngừa bệnh thận giai đoạn cuối.\u003C\u002Fjats:p>",{"EN":2418,"VI":2419},"Acute kidney injury: a springboard for progression in chronic kidney disease","Chấn thương thận cấp: một bàn đạp cho sự tiến triển trong bệnh thận mãn tính",{"VOID":2421},"20200097",{"VOID":2423},"10.1152\u002Fajprenal.00017.2010",[31],[30],"https:\u002F\u002Fwww.physiology.org\u002Fdoi\u002F10.1152\u002Fajprenal.00017.2010",[2428,2453,2472,2487,2504,2519],{"id":2429,"sortIndex":32,"researcher":28,"roles":2430,"affiliations":2431,"properties":2448,"displayName":2450,"givenName":28,"familyName":28},"8a108d50-7177-43ba-81dc-6eb4d006d45b",[],[2432,2440],{"id":2433,"sortIndex":32,"affiliation":2434,"properties":28},"55a06451-6b9b-493e-b5eb-6da2104101c9",{"id":2433,"createTime":28,"updateTime":28,"relativeEntities":2435,"slug":28,"properties":2436,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":2439,"statistic":28},[],{"title":2437},{"VI":2438},"Department of Pathology and",[],{"id":2441,"sortIndex":40,"affiliation":2442,"properties":28},"f48c6872-23e7-4f99-aad1-1a2d8d248941",{"id":2441,"createTime":28,"updateTime":28,"relativeEntities":2443,"slug":28,"properties":2444,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":2447,"statistic":28},[],{"title":2445},{"EN":2446},"Departments of Biochemistry and Medicine, University of Texas Health Science Center, San Antonio, Texas; and",[],{"title":2449,"openalex":2451},{"EN":2450},"Manjeri A. 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10.1016\u002FS0021-9258(19)50234-4",{"doi":3105},"10.1016\u002FS0021-9258(19)50234-4",{"id":28,"text":3107,"url":28,"identifiers":3108},"10.1152\u002Fajprenal.00324.2004",{"doi":3107},{"id":3110,"createTime":3111,"updateTime":3112,"relativeEntities":3113,"slug":3114,"properties":3115,"entityType":996,"verifyStatus":26,"verifyTime":3111,"verifyNote":998,"languages":3131,"translateLanguages":3132,"viewCount":32,"primaryUrl":3133,"fullTextUrl":28,"authors":3134,"publicationType":1037,"publisherRelationship":3194,"citationCount":3249,"citationInfo":3250,"publishDate":3252,"publishYear":2166,"citationAnalyzeStatus":884,"lastCitationAnalyze":28,"indexDatabases":3253,"openAccess":28,"references":3254,"isForceReanalyzing":1786},"4e036345-1ff4-4204-b810-f6aa0e41d83e","2024-10-11T06:43:21.175+00:00","2025-02-11T18:32:04.757+00:00",[],"Structural-determinants-of-glomerular-permeability",{"mag":3116,"keywords":3118,"openalex":3119,"abstract":3121,"title":3124,"pm":3127,"doi":3129},{"VOID":3117},"2126394082",{"VI":983},{"VOID":3120},"W2126394082",{"EN":3122,"VI":3123},"\u003Cjats:p>Recent progress in relating the functional properties of the glomerular capillary wall to its unique structure is reviewed. The fenestrated endothelium, glomerular basement membrane (GBM), and epithelial filtration slits form a series arrangement in which the flow diverges as it enters the GBM from the fenestrae and converges again at the filtration slits. A hydrodynamic model that combines morphometric findings with water flow data in isolated GBM has predicted overall hydraulic permeabilities that are consistent with measurements in vivo. The resistance of the GBM to water flow, which accounts for roughly half that of the capillary wall, is strongly dependent on the extent to which the GBM surfaces are blocked by cells. The spatial frequency of filtration slits is predicted to be a very important determinant of the overall hydraulic permeability, in keeping with observations in several glomerular diseases in humans. Whereas the hydraulic resistances of the cell layers and GBM are additive, the overall sieving coefficient for a macromolecule (its concentration in Bowman's space divided by that in plasma) is the product of the sieving coefficients for the individual layers. Models for macromolecule filtration reveal that the individual sieving coefficients are influenced by one another and by the filtrate velocity, requiring great care in extrapolating in vitro observations to the living animal. The size selectivity of the glomerular capillary has been shown to be determined largely by the cellular layers, rather than the GBM. Controversial findings concerning glomerular charge selectivity are reviewed, and it is concluded that there is good evidence for a role of charge in restricting the transmural movement of albumin. Also discussed is an effect of albumin that has received little attention, namely, its tendency to increase the sieving coefficients of test macromolecules via steric interactions. Among the unresolved issues are the specific contributions of the endothelial glycocalyx and epithelial slit diaphragm to the overall hydraulic resistance and macromolecule selectivity and the nanostructural basis for the observed permeability properties of the GBM.\u003C\u002Fjats:p>","\u003Cjats:p>Tiến bộ gần đây trong việc liên kết các thuộc tính chức năng của thành mạch cầu thận với cấu trúc đặc trưng của nó đã được xem xét. Nội mô có lỗ, màng đáy cầu thận (GBM), và các khe lọc biểu mô tạo thành một chuỗi sắp xếp mà trong đó dòng chảy phân kỳ khi đi vào GBM từ các lỗ và hội tụ lại ở các khe lọc. Một mô hình thủy động lực học kết hợp các phát hiện hình học với dữ liệu dòng nước trong GBM cô lập đã dự đoán các độ thấm thủy lực tổng thể phù hợp với các đo đạc in vivo. Sự kháng cự của GBM đối với dòng nước, chiếm khoảng một nửa so với thành mạch, phụ thuộc mạnh vào mức độ mà bề mặt của GBM bị chặn bởi các tế bào. Tần số không gian của khe lọc được dự đoán là một yếu tố rất quan trọng xác định độ thấm thủy lực tổng thể, phù hợp với các quan sát ở một số bệnh cầu thận ở người. Trong khi các trở kháng thủy lực của các lớp tế bào và GBM là cộng dồn, hệ số lọc tổng thể cho một đại phân tử (nồng độ của nó trong không gian Bowman chia cho nồng độ trong huyết tương) là tích của các hệ số lọc cho các lớp riêng lẻ. Các mô hình cho lọc đại phân tử cho thấy rằng các hệ số lọc riêng lẻ bị ảnh hưởng lẫn nhau và bởi tốc độ dòng lọc, đòi hỏi sự cẩn trọng lớn trong việc suy diễn các quan sát in vitro sang động vật sống. Tính chọn lọc về kích thước của cầu thận đã được chứng minh chủ yếu được xác định bởi các lớp tế bào, chứ không phải bởi GBM. Các phát hiện gây tranh cãi liên quan đến tính chọn lọc về điện tích cầu thận đã được xem xét, và kết luận rằng có bằng chứng tốt về vai trò của điện tích trong việc hạn chế sự di chuyển xuyên mạch của albumin. Cũng được thảo luận là hiệu ứng của albumin nhận được ít sự chú ý, đó là có xu hướng tăng các hệ số lọc của các đại phân tử thử nghiệm thông qua các tương tác hình học. Giữa những vấn đề còn chưa được giải quyết là các đóng góp cụ thể của glycocalyx nội mô và diaphagm khe biểu mô đối với tổng thể kháng thủy lực và tính chọn lọc đại phân tử, cũng như cơ sở nano cấu trúc cho các thuộc tính thấm quan sát được của GBM.\u003C\u002Fjats:p>",{"EN":3125,"VI":3126},"Structural determinants of glomerular permeability","Các yếu tố cấu trúc xác định độ thấm của cầu thận",{"VOID":3128},"11553505",{"VOID":3130},"10.1152\u002Fajprenal.2001.281.4.f579",[31],[30],"https:\u002F\u002Fwww.physiology.org\u002Fdoi\u002F10.1152\u002Fajprenal.2001.281.4.F579",[3135,3160,3177],{"id":3136,"sortIndex":32,"researcher":28,"roles":3137,"affiliations":3138,"properties":3155,"displayName":3157,"givenName":28,"familyName":28},"46c19f68-ba48-468f-9cdb-11ff23ce842c",[],[3139,3147],{"id":3140,"sortIndex":32,"affiliation":3141,"properties":28},"79f2ad54-e4f5-490b-ae85-bef7d9af7686",{"id":3140,"createTime":28,"updateTime":28,"relativeEntities":3142,"slug":28,"properties":3143,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":3146,"statistic":28},[],{"title":3144},{"EN":3145},"‡Department of Chemical Engineering, and",[],{"id":3148,"sortIndex":40,"affiliation":3149,"properties":28},"d85d0aa9-067d-4fe7-b1d2-4d8ed47a5421",{"id":3148,"createTime":28,"updateTime":28,"relativeEntities":3150,"slug":28,"properties":3151,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":3154,"statistic":28},[],{"title":3152},{"EN":3153},"Division of Bioengineering and Environmental Health, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139; and",[],{"title":3156,"openalex":3158},{"EN":3157},"William M. 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humans and experimental models of renal ischemia, tubular cells in various nephron segments undergo necrotic and\u002For apoptotic cell death. Various factors, including nucleotide depletion, electrolyte imbalance, reactive oxygen species, endonucleases, disruption of mitochondrial integrity, and activation of various components of the apoptotic machinery, have been implicated in renal cell vulnerability. Several approaches to limit the injury and augment the regeneration process, including nucleotide repletion, administration of growth factors, reactive oxygen species scavengers, and inhibition of inducers and executioners of cell death, proved to be effective in animal models. Nevertheless, an effective approach to limit or prevent ischemic renal injury in humans remains elusive, primarily because of an incomplete understanding of the mechanisms of cellular injury. Elucidation of cell death pathways in animal models in the setting of renal injury and extrapolation of the findings to humans will aid in the design of potential therapeutic strategies. This review evaluates our understanding of the molecular signaling events in apoptotic and necrotic cell death and the contribution of various molecular components of these pathways to renal injury.\u003C\u002Fjats:p>","\u003Cjats:p>Ở người và các mô hình thí nghiệm của thiếu máu thận, các tế bào ống trong nhiều đoạn nephron trải qua cái chết tế bào do hoại tử và\u002Fhoặc apoptosis. Nhiều yếu tố, bao gồm sự thiếu hụt nucleotide, mất cân bằng điện giải, các tác nhân oxy phản ứng, endonucleases, sự phá vỡ tính toàn vẹn của ti thể, và việc kích hoạt các thành phần khác nhau của cơ chế apoptotic, đã được đề cập đến trong khả năng tổn thương tế bào thận. Nhiều phương pháp nhằm hạn chế tổn thương và gia tăng quá trình tái sinh, bao gồm việc bổ sung nucleotide, cung cấp các yếu tố tăng trưởng, các chất dọn dẹp oxy phản ứng, và ức chế các tác nhân gây ra và thực hiện cái chết tế bào, đã chứng tỏ hiệu quả trong các mô hình động vật. Tuy nhiên, một phương pháp hiệu quả để giới hạn hoặc ngăn ngừa tổn thương thận do thiếu máu ở người vẫn còn khó khăn, chủ yếu vì sự thiếu hiểu biết về các cơ chế gây tổn thương tế bào. Việc làm sáng tỏ các con đường chết tế bào trong các mô hình động vật trong bối cảnh tổn thương thận và suy diễn các phát hiện đó cho người sẽ giúp thiết kế các chiến lược điều trị tiềm năng. Bài đánh giá này xem xét sự hiểu biết của chúng tôi về các sự kiện tín hiệu phân tử trong cái chết tế bào do apoptosis và hoại tử cũng như sự đóng góp của các thành phần phân tử khác nhau của những con đường này đối với tổn thương thận.\u003C\u002Fjats:p>",{"EN":3566,"VI":3567},"Cell death induced by acute renal injury: a perspective on the contributions of apoptosis and necrosis","Sự chết tế bào gây ra bởi tổn thương thận cấp tính: một cái nhìn về những đóng góp của quá trình apoptosis và hoại tử",{"VOID":3569},"12620919",{"VOID":3571},"10.1152\u002Fajprenal.00284.2002",[31],[30],"https:\u002F\u002Fwww.physiology.org\u002Fdoi\u002F10.1152\u002Fajprenal.00284.2002",[3576],{"id":3577,"sortIndex":32,"researcher":28,"roles":3578,"affiliations":3579,"properties":3588,"displayName":3592,"givenName":28,"familyName":28},"b4fa3cc6-d09e-4e68-bcab-22d2220afc93",[],[3580],{"id":3581,"sortIndex":32,"affiliation":3582,"properties":28},"d7d0e9d7-8eb4-46af-a213-22c497506512",{"id":3581,"createTime":28,"updateTime":28,"relativeEntities":3583,"slug":28,"properties":3584,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":3587,"statistic":28},[],{"title":3585},{"VI":3586},"Department of Physiology and Biophysics, University of Nebraska Medical Center, Omaha, Nebraska 68198-4575",[],{"orcid":3589,"title":3591,"openalex":3593},{"VOID":3590},"https:\u002F\u002Forcid.org\u002F0000-0003-0985-3213",{"EN":3592},"Babu J. 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junctions (TJ) regulate paracellular ionic charge selectivity and conductance across epithelial tissues and cell lines. These properties vary among epithelia, and recent evidence implicates the claudins, a family of TJ transmembrane proteins, as important determinants of both characteristics. To test the hypothesis that each claudin contributes a characteristic charge discrimination to the TJ, we expressed claudins-2, -4, -11, and -15 in both cation-selective Madin-Darby canine kidney (MDCK) II cells and in anion-selective LLC-PK\u003Cjats:sub>1\u003C\u002Fjats:sub>cells and examined changes in transepithelial electrical resistance (TER) and paracellular charge selectivity. Regulated expression and localization were verified by immunoblot analysis and immunofluorescence microscopy, respectively. Expression of claudin-4 increased TER in both cell lines, whereas effects of the others on TER were variable. Claudin-4 and -11 decreased paracellular permeability for Na\u003Cjats:sup>+\u003C\u002Fjats:sup>in MDCK II cells, whereas neither claudin-2 nor -15 had an effect. Conversely, in LLC-PK\u003Cjats:sub>1\u003C\u002Fjats:sub>cells, claudin-2 and -15 increased the permeability for Na\u003Cjats:sup>+\u003C\u002Fjats:sup>, whereas claudin-4 and -11 were without effect. We conclude that the contribution of each claudin is most easily detectable when it reverses the direction of monolayer charge selectivity. These results are consistent with a model in which exogenous claudins add new charge-selective pores, leading to a physiological phenotype that combines endogenous and exogenous contributions. Additionally, it is possible to rationalize the direction of charge selectivity conferred by the individual claudins on the basis of electrostatic effects of the charged amino acids in their first extracellular loops.\u003C\u002Fjats:p>","\u003Cjats:p> Các khớp chặt (TJ) điều chỉnh tính chọn lọc điện tích ion qua trung gian tế bào và độ dẫn điện trong các mô biểu mô và dòng tế bào. Các thuộc tính này khác nhau giữa các loại mô biểu mô, và bằng chứng gần đây cho thấy các claudin, một họ protein xuyên màng của TJ, là những yếu tố quan trọng quyết định cả hai đặc tính này. Để kiểm tra giả thuyết rằng mỗi claudin sẽ góp phần vào sự phân biệt điện tích của TJ, chúng tôi đã biểu hiện claudins-2, -4, -11 và -15 trong cả hai dòng tế bào Madin-Darby thận chó (MDCK) II chọn lọc cation và tế bào LLC-PK\u003Cjats:sub>1\u003C\u002Fjats:sub> chọn lọc anion, và xem xét sự thay đổi trong điện trở xuyên biểu mô (TER) và tính chọn lọc điện tích qua trung gian tế bào. Việc điều chỉnh biểu hiện và định vị đã được xác minh bằng phân tích immunoblot và kính hiển vi huỳnh quang, tương ứng. Biểu hiện của claudin-4 đã làm tăng TER ở cả hai dòng tế bào, trong khi ảnh hưởng của các claudin khác đến TER có sự biến thiên. Claudin-4 và -11 đã làm giảm tính thấm qua trung gian tế bào đối với Na\u003Cjats:sup>+\u003C\u002Fjats:sup> trong các tế bào MDCK II, trong khi claudin-2 và -15 không có tác động. Ngược lại, trong các tế bào LLC-PK\u003Cjats:sub>1\u003C\u002Fjats:sub>, claudin-2 và -15 đã làm tăng tính thấm đối với Na\u003Cjats:sup>+\u003C\u002Fjats:sup>, trong khi claudin-4 và -11 không có tác động. Chúng tôi kết luận rằng sự đóng góp của mỗi claudin được phát hiện một cách dễ dàng nhất khi nó đảo ngược hướng chọn lọc điện tích của lớp đơn. Các kết quả này phù hợp với mô hình mà trong đó các claudin ngoại lai tạo thêm các lỗ chân lông chọn lọc điện tích mới, dẫn đến hình thái sinh lý kết hợp các đóng góp nội tại và ngoại lai. Hơn nữa, có khả năng giải thích hướng chọn lọc điện tích mà từng claudin áp đặt dựa trên các hiệu ứng tĩnh điện của các axit amin mang điện trong các vòng ngoại bào đầu tiên của chúng.\u003C\u002Fjats:p>",{"EN":4449,"VI":4450},"Reversal of charge selectivity in cation or anion-selective epithelial lines by expression of different claudins","Sự đảo ngược tính chọn lọc điện tích trong các dòng biểu mô chọn lọc cation hoặc anion thông qua việc biểu hiện các claudin khác nhau",{"VOID":4452},"13129853",{"VOID":4454},"10.1152\u002Fajprenal.00116.2003","Author affiliation is blank",[31],[30],"https:\u002F\u002Fwww.physiology.org\u002Fdoi\u002F10.1152\u002Fajprenal.00116.2003",[4460,4477,4486],{"id":4461,"sortIndex":32,"researcher":28,"roles":4462,"affiliations":4463,"properties":4472,"displayName":4474,"givenName":28,"familyName":28},"3ff1d563-187f-494e-885e-93427e605b83",[],[4464],{"id":4465,"sortIndex":32,"affiliation":4466,"properties":28},"2215a18d-7af6-4c3f-8963-07b3fa8fdc3d",{"id":4465,"createTime":28,"updateTime":28,"relativeEntities":4467,"slug":28,"properties":4468,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":4471,"statistic":28},[],{"title":4469},{"EN":4470},"Department of Medicine, 6312 MBRB, CB#7545, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599-7545, USA. vitallie@med.unc.edu",[],{"title":4473,"openalex":4475},{"EN":4474},"Christina M. 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Y, Gotoh S, Furuse M, Takasuga A, Tano Y, and Tsukita S.Differential expression patterns of claudins, tight junction membrane proteins, in mouse nephron segments.J Am Soc Nephrol13: 875–886, 2002.",{"doi":4594},"10.1681\u002FASN.V134875",{"id":28,"text":4596,"url":28,"identifiers":4597},"10.1007\u002Fs00418-001-0359-x",{"doi":4596},{"id":28,"text":4599,"url":28,"identifiers":4600},"Kottra Gand Fromter E.Functional properties of the paracellular pathway in some leaky epithelia.J Exp Biol106: 217–229, 1983.",{"doi":4601},"10.1242\u002Fjeb.106.1.217",{"id":28,"text":4603,"url":28,"identifiers":4604},"MacInnes D.The Principles of Electrochemistry. 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Recent experimental evidence suggests that at least five of the seven members of this family, FXYD1 (phospholemman), FXYD2 (γ-subunit of Na-K-ATPase), FXYD3 (Mat-8), FXYD4 (CHIF), and FXYD7, are auxiliary subunits of Na-K-ATPase and regulate Na-K-ATPase activity in a tissue- and isoform-specific way. These results highlight the complexity of the regulation of Na\u003Cjats:sup>+\u003C\u002Fjats:sup>and K\u003Cjats:sup>+\u003C\u002Fjats:sup>handling by Na-K-ATPase, which is necessary to ensure appropriate tissue functions such as renal Na\u003Cjats:sup>+\u003C\u002Fjats:sup>reabsorption, muscle contractility, and neuronal excitability. Moreover, a mutation in FXYD2 has been linked to cases of human hypomagnesemia, indicating that perturbations in the regulation of Na-K-ATPase by FXYD proteins may be critically involved in pathophysiological states. A better understanding of this novel regulatory mechanism of Na-K-ATPase should help in learning more about its role in pathophysiological states. This review summarizes the present knowledge of the role of FXYD proteins in the modulation of Na-K-ATPase as well as of other proteins, their regulation, and their structure-function relationship.\u003C\u002Fjats:p>","\u003Cjats:p>Các protein FXYD thuộc về một gia đình protein màng nhỏ. Bằng chứng thực nghiệm gần đây cho thấy ít nhất năm trong số bảy thành viên của gia đình này, FXYD1 (phospholemman), FXYD2 (chuỗi γ của Na-K-ATPase), FXYD3 (Mat-8), FXYD4 (CHIF) và FXYD7, là các tiểu đơn vị bổ trợ của Na-K-ATPase và điều chỉnh hoạt động của Na-K-ATPase theo từng mô và isoform cụ thể. Những kết quả này làm nổi bật sự phức tạp trong việc điều chỉnh việc xử lý Na\u003Cjats:sup>+\u003C\u002Fjats:sup> và K\u003Cjats:sup>+\u003C\u002Fjats:sup> bởi Na-K-ATPase, điều này cần thiết để đảm bảo các chức năng mô phù hợp như tái hấp thu Na\u003Cjats:sup>+\u003C\u002Fjats:sup> của thận, tính co bóp của cơ và sự hưng phấn của nơron. Hơn nữa, một đột biến trong FXYD2 đã được liên kết với các trường hợp giảm magiê ở người, cho thấy rằng những rối loạn trong việc điều chỉnh Na-K-ATPase bởi các protein FXYD có thể liên quan đến các trạng thái bệnh lý. Một sự hiểu biết tốt hơn về cơ chế điều chỉnh mới này của Na-K-ATPase nên giúp tìm hiểu thêm về vai trò của nó trong các trạng thái bệnh lý. Tổng quan này tóm tắt các kiến thức hiện tại về vai trò của các protein FXYD trong việc điều chỉnh Na-K-ATPase cũng như các protein khác, sự điều chỉnh của chúng và mối quan hệ cấu trúc-chức năng của chúng.\u003C\u002Fjats:p>",{"EN":4652,"VI":4653},"FXYD proteins: new regulators of Na-K-ATPase","Protein FXYD: Những người điều chỉnh mới của Na-K-ATPase",{"VOID":4655},"16403837",{"VOID":4657},"10.1152\u002Fajprenal.00126.2005",[31],[30],"https:\u002F\u002Fwww.physiology.org\u002Fdoi\u002F10.1152\u002Fajprenal.00126.2005",[4662],{"id":4663,"sortIndex":32,"researcher":28,"roles":4664,"affiliations":4665,"properties":4674,"displayName":4676,"givenName":28,"familyName":28},"9dc42a0c-154c-48b0-9f2c-438ec55a70e4",[],[4666],{"id":4667,"sortIndex":32,"affiliation":4668,"properties":28},"27cb363c-ecbb-401d-b185-a80af81f6bb7",{"id":4667,"createTime":28,"updateTime":28,"relativeEntities":4669,"slug":28,"properties":4670,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":4673,"statistic":28},[],{"title":4671},{"EN":4672},"Dept. of Pharmacology and Toxicology, Univ. of Lausanne, Rue du Bugnon 27, 1005 Lausanne, Switzerland. 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membrane substrate for cAMP-dependent protein kinase and protein kinase C in myocardium.J Biol Chem266: 11126–11130, 1991.",{"doi":1590},{"id":28,"text":4954,"url":28,"identifiers":4955},"Pihakaski-Maunsbach K, Tokonabe S, Vorum H, Rivard CJ, Capasso JM, Berl T, and Maunsbach AB.The γ-subunit of Na-K-ATPase is incorporated into plasma membranes of mouse IMCD3 cells in response to hypertonicity.Am J Physiol Renal Physiol288: F650–F657, 2005.",{"doi":4956},"10.1152\u002Fajprenal.00162.2004",{"id":28,"text":4958,"url":28,"identifiers":4959},"10.1074\u002Fjbc.M010836200",{"doi":4958},{"id":28,"text":4961,"url":28,"identifiers":4962},"10.1074\u002Fjbc.M201009200",{"doi":4961},{"id":28,"text":4964,"url":28,"identifiers":4965},"10.1016\u002FS0272-6386(00)70257-5",{"doi":4964},{"id":28,"text":4967,"url":28,"identifiers":4968},"Rose AMand Valdes R.Understanding the sodium pump and its relevance to disease.Clin Chem40: 1674–1685, 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extracellular calcium-sensing receptor (CaSR) plays a major role in the maintenance of a physiological serum ionized calcium (Ca\u003Cjats:sup>2+\u003C\u002Fjats:sup>) concentration by regulating the circulating levels of parathyroid hormone. It was molecularly identified in 1993 by Brown et al. in the laboratory of Dr. Steven Hebert with an expression cloning strategy. Subsequent studies have demonstrated that the CaSR is highly expressed in the kidney, where it is capable of integrating signals deriving from the tubular fluid and\u002For the interstitial plasma. Additional studies elucidating inherited and acquired mutations in the CaSR gene, the existence of activating and inactivating autoantibodies, and genetic polymorphisms of the CaSR have greatly enhanced our understanding of the role of the CaSR in mineral ion metabolism. Allosteric modulators of the CaSR are the first drugs in their class to become available for clinical use and have been shown to treat successfully hyperparathyroidism secondary to advanced renal failure. In addition, preclinical and clinical studies suggest the possibility of using such compounds in various forms of hypercalcemic hyperparathyroidism, such as primary and lithium-induced hyperparathyroidism and that occurring after renal transplantation. This review addresses the role of the CaSR in kidney physiology and pathophysiology as well as current and in-the-pipeline treatments utilizing CaSR-based therapeutics.\u003C\u002Fjats:p>","Thụ thể cảm nhận canxi ngoại bào (CaSR) đóng vai trò chủ chốt trong việc duy trì nồng độ canxi ion hóa trong huyết thanh (Ca\u003Csup>2+\u003C\u002Fsup>) ở mức sinh lý bằng cách điều chỉnh các mức hormone cận giáp trong tuần hoàn. Nó được xác định một cách phân tử vào năm 1993 bởi Brown và cộng sự trong phòng thí nghiệm của Tiến sĩ Steven Hebert thông qua chiến lược nhân bản biểu hiện. Các nghiên cứu sau đó đã chứng minh rằng CaSR được biểu hiện cao ở thận, nơi nó có khả năng tích hợp các tín hiệu từ dịch ống và\u002Fhoặc huyết tương kẽ. Các nghiên cứu bổ sung làm sáng tỏ các đột biến di truyền và thu nhận trong gen CaSR, sự tồn tại của các kháng thể tự động hoạt hóa và không hoạt hóa, cũng như các đa hình gen của CaSR đã nâng cao đáng kể hiểu biết của chúng ta về vai trò của CaSR trong chuyển hóa ion khoáng. Các chất điều chỉnh allosteric của CaSR là những loại thuốc đầu tiên trong lớp của chúng được đưa vào sử dụng lâm sàng và đã chứng minh hiệu quả trong việc điều trị chứng cường cận giáp thứ phát do suy thận tiến triển. Ngoài ra, các nghiên cứu tiền lâm sàng và lâm sàng gợi ý khả năng sử dụng các hợp chất này trong các dạng chứng cường cận giáp tăng canxi trong máu, như cường cận giáp nguyên phát và cường cận giáp do lithium cũng như tình trạng xảy ra sau ghép thận. Bài tổng quan này đề cập đến vai trò của CaSR trong sinh lý và bệnh lý thận cũng như các phương pháp điều trị hiện tại và đang trong quá trình nghiên cứu sử dụng các liệu pháp dựa trên CaSR.",{"EN":5069,"VI":5070},"Physiology and pathophysiology of the calcium-sensing receptor in the kidney","Sinh lý và bệnh sinh của thụ thể cảm nhận canxi trong thận",{"VOID":5072},"19923405",{"VOID":5074},"10.1152\u002Fajprenal.00608.2009","2024-10-13T18:08:35.551+00:00",[31],[30],"https:\u002F\u002Fwww.physiology.org\u002Fdoi\u002F10.1152\u002Fajprenal.00608.2009",[5080,5099],{"id":5081,"sortIndex":32,"researcher":28,"roles":5082,"affiliations":5083,"properties":5092,"displayName":5096,"givenName":28,"familyName":28},"f56d84e1-0ea9-470f-8929-a7204b6a1bfd",[],[5084],{"id":5085,"sortIndex":32,"affiliation":5086,"properties":28},"82fd79ed-7100-44d6-bb8a-3e2c5ef3a754",{"id":5085,"createTime":28,"updateTime":28,"relativeEntities":5087,"slug":28,"properties":5088,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":5091,"statistic":28},[],{"title":5089},{"EN":5090},"School of Biosciences, Cardiff University, Cardiff, United Kingdom; and",[],{"orcid":5093,"title":5095,"openalex":5097},{"VOID":5094},"https:\u002F\u002Forcid.org\u002F0000-0002-7322-3163",{"EN":5096},"Daniela Riccardi",{"VOID":5098},"A5062022173",{"id":5100,"sortIndex":40,"researcher":28,"roles":5101,"affiliations":5102,"properties":5111,"displayName":5115,"givenName":28,"familyName":28},"80d979e3-45d1-48e8-81ba-74e03648c172",[],[5103],{"id":5104,"sortIndex":32,"affiliation":5105,"properties":28},"245f63d7-42bb-4f3b-a51f-e9260d713119",{"id":5104,"createTime":28,"updateTime":28,"relativeEntities":5106,"slug":28,"properties":5107,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":5110,"statistic":28},[],{"title":5108},{"VI":5109},"Division of Endocrinology, Diabetes, and Hypertension, Brigham and Women's Hospital, Boston, Massachusetts",[],{"orcid":5112,"title":5114,"openalex":5116},{"VOID":5113},"https:\u002F\u002Forcid.org\u002F0000-0002-5012-7988",{"EN":5115},"Edward M. 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bệnh cầu thận, nước tiểu, tế bào biểu mô tạng cầu thận, apoptosis, chức năng thận",{"VOID":5711},"3368602",{"VOID":5713},"W2159099277",{"EN":5715,"VI":5716},"\u003Cjats:p>The loss of glomerular visceral epithelial cells (podocytes) has been associated with the development of glomerular sclerosis and loss of renal function. Viability of podocytes recovered from urine of subjects with glomerular disease and of healthy controls was investigated by propidium iodide exclusion and TUNEL staining. Podocyte loss was quantified by cytospin. The growth behavior in culture of urinary cells and their expression of specific markers were examined. The majority of urinary podocytes are viable, although apoptosis occurs in about one-half of the cells. Patients with active glomerular disease excreted up to 388 podocytes\u002Fmg creatinine, whereas healthy controls and patients with quiescent disease generally excreted <0.5 podocytes\u002Fmg creatinine. The identity of cultured cells was confirmed by their morphology, growth behavior, and expression of podocyte-specific markers. The difference in growth behavior between healthy controls and subjects with active glomerular disease suggests that in active disease viable podocytes detach from the glomerular tuft due to local environmental factors rather than defects in the podocytes per se, whereas in healthy individuals mostly senescent podocytes are shed.\u003C\u002Fjats:p>","\u003Cjats:p>Sự mất mát tế bào biểu mô tạng cầu thận (podocytes) đã được liên kết với sự phát triển của xơ hóa cầu thận và mất chức năng thận. Tính khả thi của podocytes thu được từ nước tiểu của các đối tượng mắc bệnh cầu thận và các đối tượng lành mạnh đã được điều tra thông qua việc loại trừ iod propidium và nhuộm TUNEL. Mất mát podocytes được định lượng bằng kỹ thuật cytospin. Hành vi phát triển trong môi trường nuôi cấy của các tế bào trong nước tiểu và sự biểu hiện của các dấu hiệu đặc hiệu đã được xét nghiệm. Phần lớn podocytes trong nước tiểu vẫn còn khả thi, mặc dù sự apoptosis xảy ra trong khoảng một nửa số tế bào. Bệnh nhân mắc bệnh cầu thận cấp tính tiết ra tới 388 podocytes\u002Fmg creatinine, trong khi đó các đối tượng lành mạnh và bệnh nhân có bệnh ở thể ngủ thường tiết ra \u003C0.5 podocytes\u002Fmg creatinine. Danh tính của các tế bào nuôi cấy đã được xác nhận thông qua hình thái, hành vi phát triển và biểu hiện các dấu hiệu đặc hiệu của podocyte. Sự khác biệt trong hành vi phát triển giữa các đối tượng lành mạnh và những người mắc bệnh cầu thận cấp tính gợi ý rằng trong bệnh cấp tính, các podocytes sống sẽ tách rời khỏi cụm cầu thận do các yếu tố môi trường tại chỗ, thay vì do các khiếm khuyết ở chính các podocytes, trong khi đó ở những cá thể khỏe mạnh, chủ yếu là các podocytes lão hóa được thải ra.",{"EN":5718,"VI":5719},"Urinary excretion of viable podocytes in health and renal disease","Sự bài tiết podocytes sống trong nước tiểu ở tình trạng sức khỏe và bệnh thận",{"VOID":5721},"12631553",{"VOID":5723},"10.1152\u002Fajprenal.00404.2002",[31],[30],"https:\u002F\u002Fwww.physiology.org\u002Fdoi\u002F10.1152\u002Fajprenal.00404.2002",[5728,5745,5754,5761],{"id":5729,"sortIndex":32,"researcher":28,"roles":5730,"affiliations":5731,"properties":5740,"displayName":5742,"givenName":28,"familyName":28},"0f79f024-a464-43ca-bad9-5470ef09efb3",[],[5732],{"id":5733,"sortIndex":32,"affiliation":5734,"properties":28},"34f24702-4d62-4496-a5c1-a2298bd07ff8",{"id":5733,"createTime":28,"updateTime":28,"relativeEntities":5735,"slug":28,"properties":5736,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":5739,"statistic":28},[],{"title":5737},{"EN":5738},"Division of Nephrology, Department of Medicine, Stanford University School of Medicine, CA 94305, USA.",[],{"title":5741,"openalex":5743},{"EN":5742},"Stefanie U. 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