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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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effect of tiquizium bromide in vitro and in vivo",{"VOID":1088},"10.1007\u002Fs002280050126",{"EN":1090},"Objective: We studied the bronchodilatory effect of tiquizium bromide [3-(di-2-thienylmethylene)-5-methyl-trans-quinolizidinium bromide; TQZ], an antimuscarinic agent, on airway smooth muscle in vitro, and also in patients with chronic obstructive pulmonary disease (COPD). Methods: In the first experiment, canine tracheal smooth muscle was used to measure the pA2 of TQZ in vitro. The selectivity of TQZ for muscarinic receptor subtypes was also examined with a radioligand binding assay. Results: The pA2 value of TQZ was 8.75. The pK\ni values of TQZ for M1, M2, and M3 were 8.70, 8.94, and 9.11, respectively. In an open pilot experiment, the effects of TQZ inhalation were studied in seven patients with COPD (seven men, mean age 68.5 years). TQZ significantly increased forced vital capacity (FVC) and forced expiratory volume in 1 s (FEV1) in a dose-dependent manner. The mean maximum increases in FVC and FEV1 caused by inhaled TQZ (2.0 mg) were 24% and 29%, respectively, and they were measured 1 h after the drug had been inhaled. The FVC and FEV1 were still significantly higher than the control values even 8 h after the drug had been inhaled. No adverse effects were observed after inhalation of TQZ. Conclusion: These data suggest that TQZ is an effective antimuscarinic agent, and that it causes significant bronchodilation in patients with COPD.","PUBLICATION","Auto Verify","http:\u002F\u002Flink.springer.com\u002F10.1007\u002Fs002280050126",[1095,1111,1124,1137,1150,1163],{"id":1096,"sortIndex":32,"researcher":28,"roles":1097,"affiliations":1099,"properties":1108,"displayName":1110,"givenName":28,"familyName":28},"fb4e33b7-0b84-4090-81b1-ea8d97d585e0",[1098],"AUTHOR",[1100],{"id":1101,"sortIndex":32,"affiliation":1102,"properties":28},"8f50fa80-b784-4143-ad01-5a89276eab73",{"id":1101,"createTime":28,"updateTime":28,"relativeEntities":1103,"slug":28,"properties":1104,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1107,"statistic":28},[],{"title":1105},{"VI":1106},"Second Department of Internal Medicine, Akita University School of Medicine, Japan",[],{"title":1109},{"VI":1110},"T. 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pharmacokinetics of pindolol were studied in six healthy individuals following a single 10 mg dose (SD) and multiple (5 mg tid over 6 days) doses (MD). The plasma elimination half-life was identical after SD (4.7±0,8 h) and MD (4.1±1.1 h). Steady state plasma concentrations were reached after 36 h and remained stable thereafter. The variation in steady state concentrations was small in each individual and also between individuals. The steady state concentration of pindolol can be predicted from the pharmacokinetic data obtained after a single dose. The results of the present study suggest that the disposition of pindolol is linear over the concentration range studied.",{"EN":1412},"Single and multiple dose pharmacokinetics of pindolol",{"VOID":1414},"Åblad, B., Borg, K.O., Johnsson, G., Regårdh, C.-G., Sölvell, L.: Combined pharmacokinetic and pharmacodynamic studies on alprenolol and 4-hydroxyalprenolol in man. Life Sci.14, 693–704 (1974)\nAellig, W.H.: β-Adrenoceptor blocking activity and duration of action of pindolol and propranolol in healthy volunteers. Brit. J. clin. Pharmacol.3, 251–257 (1976)\nBodem, G., Chidsey, C.A.: Pharmacokinetic studies of practolol, a beta adrenergic antagonist, in man. Clin. Pharmacol. Ther.14, 26–29 (1973)\nBranch, R.A., Shand, D.G.: Propranolol disposition in chronic liver disease: A physiological approach. Clin. Pharmacokin.1, 264–279 (1976)\nEvans, G.H., Shand, D.G.: Disposition of propranolol. V. Drug accumulation and steady state concentrations during chronic oral administration in man. Clin. Pharmacol. Ther.14, 487–493 (1973)\nGugler, R., Herold, W., Dengler, H.J.: Pharmacokinetics of pindolol in man. Europ. J. clin. Pharmacol.7, 17–24 (1974)\nGugler, R., Höbel, W., Bodem, G., Dengler, H.J.: The effect of pindolol on exercise-induced cardiac acceleration in relation to plasma levels in man. Clin. Pharmacol. Ther.17, 127–133 (1975)\nJohnsson, G., Regårdh, C.-G., Sövell, L.: Combined pharmacokinetic and pharmacodynamic studies in man of the adrenergic β1-receptor antagonist metoprolol. Acta pharmacol. toxicol.36 Supp. V, 31–44 (1975)\nJohnsson, G., Regårdh, C.-G.: Clinical pharmacokinetics of β-adrenoceptor blocking drugs. Clin. Pharmacokin.1, 233–263 (1976)\nNies, A.S., Shand, D.G.: Clinical pharmacology of propranolol. Circulation52, 6–15 (1975)\nNies, A.S., Shand, D.G., Wilkinson, G.R.: Altered hepatic blood flow in drug disposition. Clin. Pharmacokin.1, 135–155 (1976)\nPacha, W.L.: A method for the fluorometric determination of 4(2-hydroxy-3-isopropylaminopropoxyl)indole, a β-blocking agent, in plasma and urine. Experientia25, 802–803 (1969)\nRawlins, M.D., Collste, P., Frisk-Holmberg, M., Lind, M., Östman, J., Sjöqvist, F.: Steady-state plasma concentrations of alprenolol in man. Europ. J. clin. Pharmacol.7, 353–356 (1974)\nShand, D.G., Rangno, R.E., Evans, G.H.: The disposition of propranolol. II. Hepatic elimination in the rat. Pharmacology8, 344–352 (1972)\nShand, D.G., Rangno, R.E.: The disposition of propranolol. I. Elimination during oral absorption in man. Pharmacology7, 159–168 (1972)\nShand, D.G.: Pharmacokinetic properties of the β-adrenergic receptor blocking drugs. Drugs7, 39–47 (1974)\nWagner, J.G., Northam, J.I., Alway, C.D., Carpenter, O.S.: Blood levels of drugs at equilibrium state after multiple dosing. Nature (Lond.)207, 1301–1302 (1965)",{"VOID":1416},"10.1007\u002FBF00606675","https:\u002F\u002Flink.springer.com\u002Farticle\u002F10.1007\u002FBF00606675",[1419,1434],{"id":1420,"sortIndex":32,"researcher":28,"roles":1421,"affiliations":1422,"properties":1431,"displayName":1433,"givenName":28,"familyName":28},"3ab99c0a-2d85-4983-80f4-9249ad618255",[1098],[1423],{"id":1424,"sortIndex":32,"affiliation":1425,"properties":28},"54d530e3-f7d4-4968-b150-5ccd133df425",{"id":1424,"createTime":28,"updateTime":28,"relativeEntities":1426,"slug":28,"properties":1427,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1430,"statistic":28},[],{"title":1428},{"VI":1429},"Department of Medicine, University of Bonn, Bonn, Germany",[],{"title":1432},{"VI":1433},"R. 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investigate the bioavailability of fluconazole (FLCZ) from fosfluconazole (phosphate pro-drug of FLCZ) and to compare the pharmacokinetics of fosfluconazole and FLCZ in Japanese and Caucasian subjects. In a randomised, double-blind, double-dummy, single-dose, two-period, crossover study, 12 Japanese and 12 Caucasian healthy subjects received a bolus intravenous injection of 1000 mg fosfluconazole or an intravenous infusion of 800 mg FLCZ in random order. Concentrations of fosfluconazole and FLCZ were determined in plasma and urine samples taken up to 144 h and 48 h post-dose, respectively. The bioavailability of FLCZ after administration of fosfluconazole was 95.2% (95% confidence interval: 89.0, 102.0) in Japanese subjects and 100.6% (94.0, 107.7) in Caucasian subjects. The ratio of bioavailabilities (Japanese\u002FCaucasian) was 94.7% (86.0, 104.3). There were no statistically significant differences in the pharmacokinetic parameters of fosfluconazole (except for AUCinf) and FLCZ between Japanese and Caucasian subjects. Although mean AUCinf of fosfluconazole was 25.6% (5.6, 49.2) greater in Japanese subjects, the lack of a statistically significant difference in weight-adjusted CL of fosfluconazole demonstrates that the difference in AUCinf was due to a difference in body weight. The adverse-event profile was similar in Japanese and Caucasian subjects after both fosfluconazole and FLCZ dosing, and both treatments were well tolerated in each group. The pharmacokinetics of fosfluconazole and FLCZ were similar in Japanese and Caucasian subjects. Fosfluconazole is almost completely converted to FLCZ and similar systemic exposure to FLCZ is achieved after single doses of fosfluconazole in both Japanese and Caucasian subjects.",{"EN":1516},"Comparison of the pharmacokinetics of fosfluconazole and fluconazole after single intravenous administration of fosfluconazole in healthy Japanese and Caucasian volunteers",{"VOID":1518},"Marriot MS, Richardson K (1987) The discovery and mode of action of fluconazole. 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Multicentre European Study Group. Eur J Clin Microbiol Infect Dis 16:287–295\nBentley A, Butters M, Green SP, Learmonth WJ, Macrae JA, Morland MC, O’Connor G, Skuse J (2002) The discovery and process development of a commercial route to the water soluble prodrug, fosfluconazole. Org Process Res Dev 6:109–112\nSobue S, Sekiguchi K, Shimatani K, Tan K (2004) Pharmacokinetics and safety of fosfluconazole after single intravenous bolus injection in healthy male Japanese volunteers. J Clin Pharmacol 44:284–292\nShiba K, Saito A, Miyahara T (1990) Safety and pharmacokinetics of single oral and intravenous doses of fluconazole in healthy subjects. Clin Ther 12:206–215\nBrammer KW, Farrow PR, Faulkner JK (1990) Pharmacokinetics and tissue penetration of fluconazole in humans. Rev Infect Dis 12:S318–S326\nHumphrey MJ, Jevons S, Tarbit MH (1985) Pharmacokinetic evaluation of UK-49,858, a metabolically stable triazole antifungal drug, in animals and humans. 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studies in vitro or in rodent models have suggested a potential relationship between angiotensin-converting enzyme (ACE) inhibition and the insulin-like growth factor 1 (IGF-1) axis. However, this relationship has only rarely been investigated in humans. The aim of the present cross-sectional study was to assess the association of ACE inhibitors with free IGF-1 and IGFBP-3 in the blood of older hypertensive adults. Data are from the baseline evaluation of the ilSIRENTE study, which enrolled 364 subjects aged 80 or older. For the present study we selected a subpopulation of 264 hypertensive participants without congestive heart failure. Free IGF-1 and IGFBP-3 in the blood were measured by a radioimmunoassay method. Analyses of covariance were performed to evaluate the differences in free IGF-1 and IGFBP-3 levels according to the use of ACE inhibitors. The mean age of participants was 85.7 years (SD: 4.9), 170 (64%) were women and 123 (47%) were using an ACE inhibitor. Following adjustment for potential confounders, the concentration of free IGF-1 was slightly, but not significantly higher among ACE inhibitor users than among non-users (0.74 vs. 0.65 ng\u002FmL; p = 0.20). In contrast, ACE inhibitor users had a significantly higher IGFBP-3 serum levels than non-users (4821 vs. 4330 ng\u002FmL; p = 0.005). In addition, the concentration of IGFBP-3 was significantly higher among ACE inhibitors users than among non-users of antihypertensive drugs (p = 0.02) and users of other antihypertensive drugs (p = 0.01). Among hypertensive older adults, ACE inhibitors use is associated with higher IGFBP-3 levels.",{"EN":1798},"Use of ACE inhibitors is associated with elevated levels of IGFBP-3 among hypertensive older adults: results from the IlSIRENTE study",{"VOID":1800},"Kawachi S, Takeda N, Sasaki A, Kokubo Y, Takami K, Sarui H, Hayashi M, Yamakita N, Yasuda K (2005) Circulating insulin-like growth factor-1 and insulin-like growth factor binding protein-3 are associated with early carotid atherosclerosis. Arterioscler Thromb Vasc Biol 25:617–621\nNapoli R (2006) Growth hormone, vascular reactivity, and heart failure. Eur J Clin Pharmacol 62(Suppl 1):141–144\nJohnsen SP, Hundborg HH, Sorensen HT, Orskov H, Tjonneland A, Overvad K, Jorgensen JO (2005) Insulin-like growth factor (IGF) I, -II, and IGF binding protein-3 and risk of ischemic stroke. J Clin Endocrinol Metab 90:5937–5941\nBarbieri M, Bonafe M, Franceschi C, Paolisso G (2003) Insulin\u002FIGF-I-signaling pathway: an evolutionarily conserved mechanism of longevity from yeast to humans. Am J Physiol Endocrinol Metab 285:E1064–E1071\nMusaro A, McCullagh K, Paul A, Houghton L, Dobrowolny G, Molinaro M, Barton ER, Sweeney HL, Rosenthal N (2001) Localized Igf-1 transgene expression sustains hypertrophy and regeneration in senescent skeletal muscle. Nat Genet 27:195–200\nBarbieri M, Ferrucci L, Ragno E, Corsi A, Bandinelli S, Bonafe M, Olivieri F, Giovagnetti S, Franceschi C, Guralnik JM, Paolisso G (2003) Chronic inflammation and the effect of IGF-I on muscle strength and power in older persons. Am J Physiol Endocrinol Metab 284:E481–E487\nALLHAT Officers and Coordinators for the ALLHAT Collaborative Research Group (2002) The Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial Major outcomes in high-risk hypertensive patients randomized to angiotensin-converting enzyme inhibitor or calcium channel blocker vs diuretic: The Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT). JAMA 288:2981–2997\nGarg R, Yusuf F (1995) Overview of randomized clinical trial of angiotensin converting enzyme on mortality and morbidity in patients with congestive heart failure. Collaborative group on ACE Inhibitor. JAMA 273:1450–1458\nOnder G, Penninx BW, Balkrishnan R, Fried LP, Chaves PH, Williamson J, Carter C, Di Bari M, Guralnik JM, Pahor M (2002) Relation between use of angiotensin-converting enzyme inhibitors and muscle strength and physical function in older women: an observational study. Lancet 359:926–930\nParmley WW (1998) Evolution of angiotensin-converting enzyme inhibition in hypertension, heart failure, and vascular protection. Am J Med 105:27S–31S\nDean RG, Bach LA, Burrell LM (2003) Upregulation of cardiac insulin-like growth factor-I receptor by ACE inhibition after myocardial infarction: potential role in remodeling. J Histochem Cytochem 51:831–839\nvan Eickels M, Vetter H, Grohe C (2000) Angiotensin-converting enzyme (ACE) inhibition attenuates insulin-like growth factor-I (IGF-I) induced cardiac fibroblast proliferation. Br J Pharmacol 131:1592–1596\nCorbalan R, Acevedo M, Godoy I, Jalil J, Campusano C, Klassen J (1998) Enalapril restores depressed circulating insulin-like growth factor 1 in patients with chronic heart failure. J Card Fail 4:115–119\nAnwar A, Gaspoz JM, Pampallona S, Zahid AA, Sigaud P, Pichard C, Brink M, Delafontaine P (2002) Effect of congestive heart failure on the insulin-like growth factor-1 system. Am J Cardiol 90:1402–1405\nLandi F, Russo A, Cesari M, Barillaro C, Onder G, Zamboni V, De Santis A, Pahor M, Ferrucci L, Bernabei R (2005) The ilSIRENTE study: a prospective cohort study on persons aged 80 years and older living in a mountain community of Central Italy. Aging Clin Exp Res 17:486–493\nMorris JN, Fries BE, Bernabei R, Ikegami N, Gilgen R, Steel K, Carpenter I (1996) RAI-Home Care assessment manual. InterRAI, Washington D.C.\nMorris JN, Fries BE, Steel K, Ikegami N, Bernabei R, Carpenter GI, Gilgen R, Hirdes JP, Topinkova E (1997) Comprehensive clinical assessment in community setting: applicability of the MDS-HC. J Am Geriatr Soc 45:1017–1024\nHawes C, Morris JN, Phillips CD, Mor V, Fries BE, Nonemaker S (1995) Reliability estimates for the Minimum Data Set for nursing home resident assessment and care screening (MDS). Gerontologist 35:172–178\nLandi F, Tua E, Onder G, Carrara B, Sgadari A, Rinaldi C, Gambassi G, Lattanzio F, Bernabei R (2000) Minimum data set for home care: a valid instrument to assess frail older people living in the community. Med Care 38:1184–1190\nOnder G, Liperoti R, Russo A, Soldato M, Capoluongo E, Volpato S, Cesari M, Ameglio F, Bernabei R, Landi F (2006) Body mass index, free Insulin Growth Factor 1 and physical function among older adults: results from the IlSIRENTE study. Am J Physiol Endocrinol Metab 291:E829–E834\nPsaty BM, Lee M, Savage PJ, Rutan GH, German PS, Lyles M (1992) Assessing the use of medications in the elderly: methods and initial experience in the Cardiovascular Health Study. The Cardiovascular Health Study Collaborative Research Group. J Clin Epidemiol 45:683–692\nPahor M, Chrischilles EA, Guralnik JM, Brown SL, Wallace RB, Carbonin PU (1994) Drug data coding and analysis in epidemiological studies. Eur J Epidemiol 10:405–411\nWorld Health Organisation Collaborating Centre for Drug Statistics Methodology Anatomical Therapeutical Chemical (ATC) (1994) classification index including defined daily doses (DDDs) for plain substances. Oslo: WHO (available on http:\u002F\u002Fwww.whocc.no\u002Fatcddd\u002F accessed on 01-15-2006)\nRechler MM (1997) Growth inhibition by insulin-like growth factor (IGF) binding protein-3-what’s IGF got to do with it? Endocrinology 138:2645–2647\nBrink M, Wellen J, Delafontaine P (1996) Angiotensin II causes weight loss and decreases circulating insulin-like growth factor I in rats through a pressor-independent mechanism. J Clin Invest 97:2509–2516\nDi Bari M, van de Poll-Franse LV, Onder G, Kritchevsky SB, Newman A, Harris TB, Williamson JD, Marchionni N, Pahor M, Health, Aging and Body Composition Study (2004) Antihypertensive medications and differences in muscle mass in older persons: the Health, Aging and Body Composition Study. J Am Geriatr Soc 52:961–966\nBrink M, Price SR, Chrast J, Bailey JL, Anwar A, Mitch WE, Delafontaine P (2001) Angiotensin II induces skeletal muscle wasting through enhanced protein degradation and down-regulates autocrine insulin-like growth factor I. Endocrinology 142:1489–1496\nBrink M, Chrast J, Price SR, Mitch WE, Delafontaine P (1999) Angiotensin II stimulates gene expression of cardiac insulin-like growth factor I and its receptor through effects on blood pressure and food intake. Hypertension 34:1053–1059\nMaggio M, Ceda GP, Lauretani F, Pahor M, Bandinelli S, Najjar SS, Ling SM, Basarla S, Ruggiero C, Valenti G, Ferrucci L (2006) Relation of Angiotensin-Converting Enzyme inhibitor treatment to Insulin-Like Growth Factor-1 serum levels in subjects >65 years of age (the InChianti Study). Am J Cardiol 97:1525–1529\nChen JW, Hojlund K, Beck-Nielsen H, Sandahl Christiansen J, Orskov H, Frystyk J (2005) Free rather than total circulating insulin-like growth factor-I determines the feedback on growth hormone release in normal subjects. 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renal handling and effects of an intravenous bolus of frusemide with and without plasma volume expansion with dextran or albumin, and with large variations in plasma albumin concentration, have been studied in five patients with the nephrotic syndrome. Decreased renal sensitivity to frusemide was found in only one patient, who also had hypovolaemia and an activated renin-angiotensin-aldosterone system. Plasma volume expansion increased the diuresis but not the saluresis, and slightly increased renal sensitivity to frusemide. An increase in albuminuria after albumin infusion did not reduce the sensitivity to frusemide. A decrease in plasma albumin concentration from 33 g·l−1 after albumin infusion to 23 g·l−1 after infusion of dextran caused a substantial increase in the renal clearance (from 84 to 123 ml·min−1), non-renal clearance (from 72 to 138 ml·min−1), and apparent volume of distribution (from 13 to 23 l) of frusemide, probably as a consequence of an increase in the unbound fraction. The rate of urinary excretion of frusemide was highest after albumin infusion, despite the fact that its renal clearance was lowest then.",{"EN":2028},"Pharmacokinetics and effects of frusemide in patients with the nephrotic syndrome",{"VOID":2030},"Brater DC (1985) Resistance to loop diuretics. Why it happens and what to do about it. Drugs 30: 427–443\nOdlind B, Beermann B (1980) Renal tubular secretion and effects of furosemide. Clin Pharmacol Ther 27: 784–790\nKaojarern S, Day B, Brater DC (1982) The time course of delivery of furosemide into urine: An independent determinant of overall response. Kidney Int 22: 69–74\nRane A, Villeneuve JP, Stone WJ, Nies AS, Wilkinson GR, Branch RA (1978) Plasma binding and disposition of furosemide in the nephrotic syndrome and in uremia. Clin Pharmacol Ther 24: 199–207\nPrandota J (1983) Pharmacokinetics of furosemide urinary elimination by nephrotic children. Pediatr Res 17: 141–147\nKeller E, Hoppe-Seyler G, Schollmeyer P (1982) Disposition and diuretic effect of furosemide in the nephrotic syndrome. Clin Pharmacol Ther 32: 442–449\nSmith DE, Hyneck ML, Berardi RR, Port FK (1985) Urinary protein binding, kinetics, and dynamics of furosemide in nephrotic patients. J Pharm Sci 74: 603–607\nGreen TP, Mirkin BL (1980) Resistance of proteinuric rats to furosemide: urinary drug protein binding as a determinant of drug effect. Life Sci 26: 623–630\nEder HA, Lauson HD, Chinard FP, Greif RI, Cotzias GC, van Slyke DD (1954) A study of the mechanisms of edema formation in patients with the nephrotic syndrome. J Clin Invest 33: 636–656\nDorhout Mees EJ (1984) Edema formation in the nephrotic syndrome. Contrib Nephrol 43: 64–75\nBrown EA, Markandu ND, Sagnella GA, Jones BE, MacGregor GA (1985) Sodium retention in the nephrotic syndrome is due to an intrarenal defect: Evidence from steroid-induced remission. Nephron 39: 290–295\nKoomans HA, Boer WH, Dorhout Mees EJ (1987) Renal function during recovery from minimal lesions nephrotic syndrome. Nephron 47: 173–178\nDorhout Mees EJ, Roos JC, Boer P, Yoe OH, Simatupang TA (1979) Observations on edema formation in nephrotic syndrome in adults with minimal lesions. Am J Med 67: 378–384\nGeers AB, Koomans HA, Roos JC, Boer P, Dorhout Mees EJ (1984) Functional relationships in the nephrotic syndrome. Kidney Int 26: 324–330\nKoomans HA, Geers AB, van der Meiracker AH, Roos JC, Boer P, Dorhout Mees EJ (1984) Effects of plasma volume expansion on renal salt handling in patients with the nephrotic syndrome. Am J Nephrol 4: 227–234\nBrown EA, Markandu ND, Sagnella GA, Squires M, Jones BE, MacGregor GA (1982) Evidence that some mechanism other than the renin system causes sodium retention in nephrotic syndrome. Lancet 2: 1237–1240\nBrown EA, Markandu ND, Sagnella GA, Jones BE, MacGregor GA (1984) Lack of effect of captopril on the sodium retention of the nephrotic syndrome. Nephron 37: 43–48\nChonko AM, Bay WH, Stein JH, Ferris TF (1977) The role of renin and aldosterone in the salt retention of edema. Am J Med 63: 881–889\nIchikawa HG, Rennke HG, Hoyer JR, Badr KF, Schor N, Troy JL, Lechene CP, Brenner BM (1983) Role for intrarenal mechanisms in the impaired salt excretion of experimental nephrotic syndrome. J Clin Invest 71: 91–103\nHammarlund MM, Paalzow LK, Odlind B (1984) Pharmacokinetics of furosemide in man after intravenous and oral administration. Application of moment analysis. Eur J Clin Pharmacol 26: 197–207\nMcKenzie JK, Clements JA (1974) Simplified radioimmunoassay for serum aldosterone utilizing increased antibody specificity. J Clin Endocrinol Metab 38: 622–627\nFühr J, Kaczmarczyk J, Krüttgen C-D (1955) Eine einfache colorimetrische Methode zur Inulinbestimmung für Nieren-Clearanceuntersuchungen bei Stoffwechselgesunden und Diabetikern. Klin Wochenschr 33: 729–730\nBrun C (1951) A rapid method for the determination of paraaminohippuric acid in kidney function test. J Lab Clin Med 37: 955–958\nAllgulander C, Beermann B, Sjögren A (1980) Frusemide pharmacokinetics in patients with liver disease. Clin Pharmacokinet 5: 570–575\nAndreasen F, Jakobsen P (1974) Determination of furosemide in blood plasma and its binding to proteins in normal plasma and in plasma from patients with acute renal failure. Acta Pharmacol Toxicol 35: 49–57\nSjöström P, Odlind B, Beermann B, Hammarlund-Udenaes M (1987) Changes in furosemide pharmacokinetics induced by dehydration. In: Andreucci VE, Dal Canton A (eds) Diuretics: Basic pharmacological, and clinical aspects. Martinus Nijhoff, Boston, USA, pp 107–109\nBowman RH (1975) Renal secretion [35S]furosemide and its depression by albumin binding. Am J Physiol 229: 93–98\nHall S, Rowland M (1985) Influence of fraction unbound upon the renal clearance of furosemide in the isolated perfused rat kidney. J Pharmacol Exp Ther 232: 263–268\nGreen TP, Mirkin BL (1981) Furosemide disposition in normal and proteinuric rats: urinary drug-protein binding as a determinant of drug excretion. J Pharmacol Exp Ther 218: 122–127\nAlván G, Beermann B, Hjelte L, Lind M, Lindholm A, Strandvik B (1988) Increased nonrenal clearance and increased diuretic efficiency of furosemide in cystic fibrosis. Clin Pharmacol Ther 44: 436–441\nRowland M, Tozer T (1980) Clinical pharmacokinetics concepts and applications. Lea and Febiger, Philadelphia\nInoue M, Okajima K, Itoh K, Ando Y, Watanabe N, Yasaka T, Nagase S, Morino Y (1987) Mechanism of furosemide resistance in analbuminemic rats and hypoalbuminemic patients. Kidney Int 32: 198–203\nDanielsen H, Pedersen EB, Madsen M, Jensen T (1985) Abnormal renal sodium excretion in the nephrotic syndrome after furosemide: relation to glomerular filtration rate. Acta Med Scand 217: 513–518\nAurell M (1969) Renal response in man to plasma volume expansion and angiotensin. Scand J Clin Lab Invest 24 [Suppl 112]: 13–31\nJames J, Gordillo G, Metcoff J (1954) Effects of infusion of hyperoncotic dextran in children with the nephrotic syndrome. J Clin Invest 33: 1346–1357\nOrloff J, Welt LG, Stowe L (1950) The effects of concentrated salt-poor albumin on the metabolism and excretion of water and electrolytes in nephrosis and toxemia of pregnancy. J Clin Invest 29: 770–780\nSjöström P, Beermann B, Odlind B (1988) Delayed tolerance to furosemide diuresis. Influence of ACE inhibition by lisinopril. Scand J Urol Nephrol 22: 317–325",{"VOID":2032},"10.1007\u002FBF00558227","https:\u002F\u002Flink.springer.com\u002Farticle\u002F10.1007\u002FBF00558227",[2035,2050,2065,2080],{"id":2036,"sortIndex":32,"researcher":28,"roles":2037,"affiliations":2038,"properties":2047,"displayName":2049,"givenName":28,"familyName":28},"8efdf5f1-0616-44f8-9a1a-568f0293186f",[1098],[2039],{"id":2040,"sortIndex":32,"affiliation":2041,"properties":28},"64f5fb30-df83-49a2-b556-b0b4e50adad1",{"id":2040,"createTime":28,"updateTime":28,"relativeEntities":2042,"slug":28,"properties":2043,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":2046,"statistic":28},[],{"title":2044},{"VI":2045},"Department of Internal Medicine, Örebro Medical Center Hospital, Örebro, Sweden",[],{"title":2048},{"VI":2049},"P. A. 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study of the factors affecting the metabolic clearance of quinine in malaria",{"VOID":2164},"10.1007\u002Fs002280050323",{"EN":2166},"\n\n                        Objective: To assess the factors that contribute to impaired quinine clearance in acute falciparum malaria. \n\n                        Patients: Sixteen adult Thai patients with severe or moderately severe falciparum malaria were studied, and 12 were re-studied during convalescence. \n\n                        Methods: The clearance of quinine, dihydroquinine (an impurity comprising up to 10% of commercial quinine formulations), antipyrine (a measure of hepatic mixed-function oxidase activity), indocyanine green (ICG) (a measure of liver blood flow), and iothalamate (a measure of glomerular filtration rate) were measured simultaneously, and the relationship of these values to the␣biotransformation of quinine to the active metabolite 3-hydroxyquinine was assessed. \n\n                        Results: During acute malaria infection, the systemic clearance of quinine, antipyrine and ICG and the biotransformation of quinine to 3-hydroxyquinine were all reduced significantly when compared with values during convalescence. Iothalamate clearance was not affected significantly and did not correlate with the clearance of any of the other compounds. The clearance of total and free quinine correlated significantly with antipyrine clearance (r\n\n                        s = 0.70, P = 0.005 and r\n\n                        s = 0.67, P = 0.013, respectively), but not with ICG clearance (r\n\n                        s = 0.39 and 0.43 respectively, P > 0.15). In a multiple regression model, antipyrine clearance and plasma protein binding accounted for 71% of the variance in total quinine clearance in acute malaria. The pharmacokinetic properties of dihydroquinine were generally similar to those of quinine, although dihydroquinine clearance was less affected by acute malaria. The mean ratio of quinine to 3-hydroxyquinine area under the plasma concentration-time curve (AUC) values in acute malaria was 12.03 compared with 6.92 during convalescence P=0.01. The mean plasma protein binding of 3-hydroxyquinine was 46%, which was significantly lower than that of quinine (90.5%) or dihydroquinine (90.5%). \n\n                        Conclusion: The reduction in quinine clearance in acute malaria results predominantly from a disease-induced dysfunction in hepatic mixed-function oxidase activity (principally CYP 3A) which impairs the conversion of quinine to its major metabolite, 3-hydroxyquinine. The metabolite contributes approximately 5% of the antimalarial activity of the parent compound in malaria, but up to 10% during convalescence.","http:\u002F\u002Flink.springer.com\u002F10.1007\u002Fs002280050323",[2169,2184,2197,2212,2225,2238,2253,2268,2281,2294],{"id":2170,"sortIndex":32,"researcher":28,"roles":2171,"affiliations":2172,"properties":2181,"displayName":2183,"givenName":28,"familyName":28},"7c793f0f-c442-40a6-85bf-d1f9fa41b61b",[1098],[2173],{"id":2174,"sortIndex":32,"affiliation":2175,"properties":28},"d2520512-232e-4851-8c1c-0315d5747920",{"id":2174,"createTime":28,"updateTime":28,"relativeEntities":2176,"slug":28,"properties":2177,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":2180,"statistic":28},[],{"title":2178},{"VI":2179},"Faculty of Tropical Medicine, Mahidol University,  420\u002F6 Rajvithi Road, Bangkok 10400, Thailand Fax +66-2-246-7795, , TH",[],{"title":2182},{"VI":2183},"S. 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between a bid and a tid regimen: improved compliance with no improved antihypertensive effect",{"VOID":2376},"10.1007\u002Fs002280050070",{"EN":2378},"\nObjectives: To compare compliance with an antihypertensive treatment administered either twice daily or three times daily. The two formulations of the antihypertensive treatment used (nicardipine) “regular tablets” (t.d.) and “slow release tablets” (b.d.) are bioequivalent at the daily dosage used in the study.  Study design: Open, controlled, parallel designed study with centralised, randomised allocation to the treatment groups: TID group: A nicardipine 20 mg tablet, three times daily for 3 months. BID group: A capsule of slow release (SR) nicardipine, 50 mg twice daily for 3 months.  Patients: 7274 hypertensive patients were investigated by 2.651 general practitioners. Compliance with the nicardipine was assessed by means of standardised interviews with the patients and by a questionnaire for the investigators.  Results: Compliance was slightly higher in the BID than in the TID group; 71.2% and 24.5% of patients in the first group declared their compliance was 100% and 80% compared to 82.3% and 15% in the second group. A statistically significant relationship was shown between compliance with nicardipine and the decrease in blood pressure after three months of therapy. However, no significant difference was noticed between the two groups of patients in the absolute decrease in blood pressure after the treatment period: 25.7\u002F14.7 mm Hg in the TID group compared with 25.9\u002F15.0 mm Hg in the BID group.  Conclusions: A difference in compliance between the bioequivalent BID and TID formulations of the same active agent was shown in hypertensive patients. However, the difference was not large enough to lead to a difference either in the number of controlled patients or in the decrease in blood pressure. Reducing the number of daily doses does not automatically lead to greater efficacy of treatment. 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J Pharm Sci 74: 1037–1040\nde Vries JX, Harenberg J, Zimmermann R, Simon M (1984) Phenprocoumon metabolic studies in patients. J Exp Clin Haematol 49: 138\nHaddock RE, Trager WF, Pohl LR (1975) Biotransformation of phenprocoumon in the rat. J Med Chem 18: 519–523\nPorter WR, Wheeler C, Trager WF (1981) Changes in the metabolic profiles of R- and S-Warfarin and R- and S-Phenprocoumon as a probe to categorize the effect of inducing agents on microsomal hydroxylases. Biochem Pharmacol 30: 3099–3104\nWheeler C, Trager WF, Porter WR (1981) Stereochemical aspects of the metabolism of phenprocoumon in rat liver microsomes. Biochem Pharmacol 30: 1785–1790\nHeimark LD, Trager WF (1985) A stable isotope assay for phenprocoumon and its metabolites. Biomed Mass Spectrom 12: 67–71\nHewick DS, Shepherd AMM (1976) The plasma elimination of enantiomers of phenprocoumon in man. J Pharm Pharmacol 28: 257–258\nKaiser R (1968) Chromatographie in der Gasphase. Bibliographisches Institut Mannheim, vol 4, part 2, pp 211, 216\nRowland M, Tozer TN (1980) Clinical pharmacokinetics: Concepts and applications. Lea and Febiger, Philadelphia, pp 130, 133\nTrager WF, Lewis RJ, Garland WA (1970) Mass spectral analysis in the identification of human metabolites of warfarin. J Med Chem 13: 1196–1204\nChan KK, Lewis RJ, Trager WF (1972) Absolute configuration of the four warfarin alcohols. J Med Chem 15: 1265–1270\nLewis RJ, Trager WF (1970) The metabolic fate of warfarin: Studies on the metabolites in plasma. Ann NY Acad Sci 179: 205–212\nLewis RJ, Trager WF, Chan KK, Breckenridge A, Orme M, Rowland M, Schary W (1974) Warfarin. Stereochemical aspects of its metabolism and the interaction with phenylbutazone. J Clin Invest 53: 1607–1617\nLee SJ, Field LR, Howald WN, Trager WF (1981) High performance liquid chromatographic separation and fluorescence detection of warfarin and its metabolites by post column acid\u002Fbase manipulation. 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