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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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We here report dizygotic twin sisters with OPLL of the cervical spine and propose a new pathogenesis of OPLL. This is the first report of dizygotic twins with OPLL. The twins suffered from schizophrenia, which might be related to the pathogenesis of OPLL. In addition, we investigated the occurrence of OPLL in 30 patients with schizophrenia who had been admitted to a mental hospital. OPLL of the cervical spine was found in six (20%) of them, with an incidence almost five times higher than the incidence of OPLL among the general population in Japan. Schizophrenia may have a increased susceptibility to OPLL.",{"EN":956},"Ossification of the posterior longitudinal ligament in dizygotic twins with schizophrenia: a case report",{"VOID":958},"Bakay L, Cares HL, Smith RJ. Ossification in the region of the posterior longitudinal ligament as a cause of cervical myelopathy. J Neurol Neurosurg Psychiatry. 1970;33:263–8.\nMinagi H, Gronner AT. Calcification of the posterior longitudinal ligament: a cause of cervical myelopathy. AJR Am J Roentgenol. 1969;105:365–9.\nNagashima C. Cervical myelopathy due to ossification of the posterior longitudinal ligament of the spine. J Neurosurg. 1972;37:653–60.\nOno K, Ota H, Tada K, Hamada H, Takaoka K. Ossified posterior longitudinal ligament: a clinicopathologic study. Spine. 1977;2:126–38.\nTsuyama N. Ossification of the posterior longitudinal ligament of the spine. Clin Orthop. 1984;184:71–84.\nKey GA. On paraplegia depending on the ligament of the spine. Guys Hosp Rep. 1838;3:17–34.\nTsukimoto H. A case report: autopsy of syndrome of compression of spinal cord owing to ossification within spinal canal of cervical spine. Atch Jpn Chir. 1960;29:1003–7.\nTerayama K. Genetic studies on ossification of the posterior longitudinal ligament of the spine. Spine. 1989;14:1184–91.\nMiura Y, Kawai K. Genetic studies of OPLL: analysis of twins. Seikeigeka. 1993;44:993–8. (in Japanese).\nMiyakawa T, Leiter LM, Gerber DJ, Gainetdinov RR, Sotnicova TD, et al. Conditional calcineurin knockout mice exhibit multiple abnormal behaviors related to schizophrenia. Proc Natl Acad Sci USA. 2003;100:8987–92.\nGerber DJ, Miyakawa T, Demars S, Gogos JA, Karayiorgou M, Tonegawa S. Evidence for association of schizophrenia with genetic variation in the 8p21.3 gene, PPP3CC, encoding the calcineurin gamma subunit. Proc Natl Acad Sci USA. 2003;100:8993–9.\nStern PH. The calcineurin-NFAT pathway and bone: intriguing new findings. Mol Interv. 2006;6:193–6.\nSun L, Blair HC, Peng Y, Zaidi N, Adebanio OA, Wu XB, et al. Calcineurin regulates bone formation by the osteoblast. Proc Natl Acad Sci USA. 2005;102:17130–5.\nMatsunaga S, Sakou T. OPLL: disease entity, incidence, literature search, and prognosis. In: Yonenobu K, Nakamura K, Toyama Y (eds). OPLL: ossification of the posterior longitudinal ligament. 2nd ed. Tokyo: Springer; 2006. pp 11–7.\nKitajima I, Une F, Kuriyama M, Nakashima H, Igata A. Mother and child cases of familial vitamin D resistant rickets: pathogenesis of ankylosing spinal hyperostosis. J Jpn Soc Intern Med. 1985;74:447–51.\nImamura K, Matsunaga S, Nagata M, Nakamura K, Yokouchi M, Yamamoto T, et al. Ossification of the posterior longitudinal ligament of the thoracic spine in association with polycystic ovary syndrome. Neurol India. 2006;54:448–50.",{"VOID":960},"10.1007\u002Fs10165-008-0036-1","PUBLICATION","Auto Verify","https:\u002F\u002Fdoi.org\u002F10.3109\u002Fs10165-008-0036-1",[965,981,994,1007,1020,1033,1046],{"id":966,"sortIndex":32,"researcher":28,"roles":967,"affiliations":969,"properties":978,"displayName":980,"givenName":28,"familyName":28},"518cf518-f266-482a-a8dc-0347e43af296",[968],"AUTHOR",[970],{"id":971,"sortIndex":32,"affiliation":972,"properties":28},"17a1e0a9-4479-42cd-83be-01e1e4770018",{"id":971,"createTime":28,"updateTime":28,"relativeEntities":973,"slug":28,"properties":974,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":977,"statistic":28},[],{"title":975},{"VI":976},"Department of Orthopaedic Surgery, Imakiire General Hospital, Kagoshima, Japan",[],{"title":979},{"VI":980},"Shunji 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activates D1-like and D2-like receptors (D1R and D2R). While D1R antagonists have ameliorated the severity of disease in some experimental autoimmune models of mice by promoting interferon (IFN)-γ and inhibiting interleukin (IL)-17 production by T cells, dopamine effects in the immune system are reportedly diverse. To investigate the impact of D1R blockade on an animal model of rheumatoid arthritis (RA), DBA\u002F1 mice with collagen-induced arthritis (CIA) were treated with a selective D1R antagonist, SCH23390, after the primary immunization. This treatment suppressed the severity of the CIA. Nevertheless, serum levels of antibodies to type II collagen were not affected by the treatment. Th1\u002FTh17 differentiation of splenic T cells in the treated animals was not biased. In vitro, when bone marrow-derived macrophages were stimulated in the presence of the D1R antagonist SCH23390, alteration of inflammatory cytokine expression was not observed, but their in vitro differentiation to osteoclasts was inhibited. Co-administration of a selective D1R agonist, A68930, abrogated the in vivo anti-arthritic effect and the in vitro suppression of osteoclastogenesis by the D1R antagonist. Our results argue that D1R blockade is potentially a new approach to the treatment of RA. Its effect could be partly attributable to the inhibition of osteoclastogenesis.",{"EN":1127},"Therapeutic effect of D1-like dopamine receptor antagonist on collagen-induced arthritis of mice",{"VOID":1129},"Missale C, Nash SR, Robinson SW, Jaber M, Caron MG. Dopamine receptors: from structure to function. Physiol Rev. 1998;78:188–225.\nSalah RS, Kuhn DM, Galloway MP. Dopamine autoreceptors modulate the phosphorylation of tyrosine hydroxylase in rat striatal slices. J Neurochem. 1989;52:1517–22.\nBasu S, Dasgupta PS. Dopamine, a neurotransmitter, influences the immune system. J Neuroimmunol. 2000;102:113–24.\nBeck GCh, Brinkkoetter P, Hanusch C, Schulte J, van Ackern K, van der Woude FJ, et al. Clinical review: immunomodulatory effects of dopamine in general inflammation. Crit Care. 2004;8:485–91.\nMeredith EJ, Chamba A, Holder MJ, Barnes NM, Gordon J. Close encounters of the monoamine kind: immune cells betray their nervous disposition. Immunology. 2005;115:289–95.\nMcKenna F, McLaughlin PJ, Lewis BJ, Sibbring GC, Cummerson JA, Bowen-Jones D, et al. Dopamine receptor expression on human T- and B-lymphocytes, monocytes, neutrophils, eosinophils and NK cells: a flowcytometric study. J Neuroimmunol. 2002;132:34–40.\nTarazona R, González-García A, Zamzami N, Marchetti P, Frechin N, Gonzalo JA, et al. Chlorpromazine amplifies macrophage-dependent IL-10 production in vivo. J Immunol. 1995;154:861–70.\nBesser MJ, Ganor Y, Levite M. Dopamine by itself activates either D2, D3 or D1\u002FD5 dopaminergic receptors in normal human T-cells and triggers the selective secretion of either IL-10, TNF-α or both. J Neuroimmunol. 2005;169:161–71.\nCarapau D, Kruhofer M, Chatalbash A, Orengo JM, Mota MM, Rodriguez A. Transcriptome profile of dendritic cells during malaria: cAMP regulation of IL-6. Cell Microbiol. 2007;9:1738–52.\nPark YG, Kang SK, Noh SH, Park KK, Chang YC, Lee YC, et al. PGE2 induces IL-1β gene expression in mouse osteoblasts through a cAMP-PKA signaling pathway. Int Immunopharmacol. 2004;4:779–89.\nJaramillo M, Olivier M. Hydrogen peroxide induces murine macrophage chemokine gene transcription via extracellular signal-regulated kinase and cyclic adenosine 5-monophosphate (cAMP)-dependent pathways: involvement of NF-κB, activator protein 1, and cAMP response element binding protein. J Immunol. 2002;169:7026–38.\nNakano K, Higashi T, Hashimoto K, Takagi R, Tanaka Y, Matsushita S. Antagonizing dopamine D1-like receptor inhibits Th17 cell differentiation: preventive and therapeutic effects on experimental autoimmune encephalomyelitis. Biochem Biophys Res Commun. 2008;22:286–91.\nHashimoto K, Inoue T, Higashi T, Takei S, Awata T, Katayama S, et al. Dopamine D1-like receptor antagonist, SCH23390, exhibits a preventive effect on diabetes mellitus that occurs naturally in NOD mice. Biochem Biophys Res Commun. 2009;383:460–3.\nNakae S, Nambu A, Sudo K, Iwakura Y. Suppression of immune induction of collagen-induced arthritis IL-17-deficient mice. J Immunol. 2003;171:6173–7.\nSekine C, Sugihara T, Miyake S, Hirai H, Yoshida M, Miyasaka N, et al. Successful treatment of animal models of rheumatoid arthritis with small-molecule cyclin-dependent kinase inhibitors. J Immunol. 2008;180:1954–61.\nNakaya M, Tanaka M, Okabe Y, Hanayama R, Nagata S. Opposite effects of rho family GTPases on engulfment of apoptotic cells by macrophages. J Biol Chem. 2006;281:8836–42.\nKim Y, Sato K, Asagiri M, Morita I, Soma K, Takayanagi H. Contribution of nuclear factor of activated T cells c1 to the transcriptional control of immunoreceptor osteoclast-associated receptor but not triggering receptor expressed by myeloid cells-2 during osteoclastogenesis. J Biol Chem. 2005;280:32905–13.\nMurakami Y, Akahoshi T, Hayashi I, Endo H, Hashimoto A, Kono S, et al. Inhibition of monosodium urate monohydrate crystal-induced acute inflammation by retrovirally transfected prostaglandin D synthase. Arthritis Rheum. 2003;48:2931–41.\nMurakami Y, Kohsaka H, Kitasato H, Akahoshi T. Lipopolysaccharide-induced up-regulation of triggering receptor expressed on myeloid cells-1 expression on macrophages is regulated by endogenous prostaglandin E2. J Immunol. 2007;178:1144–50.\nOhata J, Miura T, Johnson TA, Hori S, Ziegler SF, Kohsaka H. Enhanced efficacy of regulatory T cell transfer against increasing resistance, by elevated Foxp3 expression induced in arthritic murine hosts. Arthritis Rheum. 2007;56:2947–56.\nBourne JA. SCH 23390: the first selective dopamine D1-like receptor antagonist. CNS Drug Rev. 2001;7:399–414.\nDeNinno MP, Schoenleber R, MacKenzie R, Britton DR, Asin KE, Briggs C, et al. A68930: a potent agonist selective for the dopamine D1 receptor. Eur J Pharmacol. 1991;25:209–19.\nTerato K, Hasty KA, Cremer MA, Stuart JM, Townes AS, Kang AH. Collagen-induced arthritis in mice. Localization of an arthritogenic determinant to fragment of the type II collagen molecule. J Exp Med. 1985;162:637–46.\nMukai E, Nagashima M, Hirano D, Yoshino S. Comparative study of symptoms and neuroendocrine–immune network mediator levels between rheumatoid arthritis patients and healthy subjects. Clin Exp Rheumatol. 2000;18:585–90.\nChan GL, Holden JE, Stoessl AJ, Doudet DJ, Wang Y, Dobko T, et al. Reproducibility of the distribution of carbon-11-SCH 23390, a dopamine D1 receptor tracer, in normal subjects. J Nucl Med. 1998;39:792–7.\nTanaka S, Matsunaga H, Kimura M, Tatsumi K, Hidaka Y, Takano T, et al. Autoantibodies against four kinds of neurotransmitter receptors in psychiatric disorders. J Neuroimmunol. 2003;141:155–64.",{"VOID":1131},"10.1007\u002Fs10165-010-0387-2","https:\u002F\u002Facademic.oup.com\u002Fmr\u002Farticle-abstract\u002F21\u002F3\u002F260\u002F6315588?redirectedFrom=fulltext",[1134,1167,1182,1195,1208,1221],{"id":1135,"sortIndex":32,"researcher":28,"roles":1136,"affiliations":1137,"properties":1164,"displayName":1166,"givenName":28,"familyName":28},"7dad5845-e88d-4c03-a7c1-acd3cfc9afd8",[968],[1138,1146,1155],{"id":1139,"sortIndex":32,"affiliation":1140,"properties":28},"3cbe6f33-0553-4dd4-b951-3b9406396b48",{"id":1139,"createTime":28,"updateTime":28,"relativeEntities":1141,"slug":28,"properties":1142,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1145,"statistic":28},[],{"title":1143},{"VI":1144},"Global Center of Excellence (GCOE) Program, Department of Medicine and Rheumatology, Graduate School of Medical and Dental Sciences, International Research Center for Molecular Science in Tooth and Bone Diseases, Tokyo Medical and Dental University, Tokyo, Japan",[],{"id":1147,"sortIndex":40,"affiliation":1148,"properties":1154},"998aadf5-b514-485f-b23c-b22a65017e4d",{"id":1147,"createTime":28,"updateTime":28,"relativeEntities":1149,"slug":28,"properties":1150,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1153,"statistic":28},[],{"title":1151},{"VI":1152},"Department of Biomolecular Science, Faculty of Science, Toho University, Funabashi, Japan",[],{},{"id":1156,"sortIndex":123,"affiliation":1157,"properties":1163},"5380619e-fa6e-4bcc-839c-2ff6673d4301",{"id":1156,"createTime":28,"updateTime":28,"relativeEntities":1158,"slug":28,"properties":1159,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1162,"statistic":28},[],{"title":1160},{"VI":1161},"Clinical Immunology, RIKEN Research Center of Allergy and Immunology, Yokohama, Japan",[],{},{"title":1165},{"VI":1166},"Hiroki Nakashioya",{"id":1168,"sortIndex":40,"researcher":28,"roles":1169,"affiliations":1170,"properties":1179,"displayName":1181,"givenName":28,"familyName":28},"a04c1649-a3d9-4229-a08c-ceb90bba3e5e",[968],[1171],{"id":1172,"sortIndex":32,"affiliation":1173,"properties":28},"f9e2e79b-e615-4582-b685-3a1763810132",{"id":1172,"createTime":28,"updateTime":28,"relativeEntities":1174,"slug":28,"properties":1175,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1178,"statistic":28},[],{"title":1176},{"VI":1177},"Department of Allergy and Immunology, Faculty of Medicine, Saitama Medical University, Iruma-gun, Japan",[],{"title":1180},{"VI":1181},"Kazuhisa Nakano",{"id":1183,"sortIndex":123,"researcher":28,"roles":1184,"affiliations":1185,"properties":1192,"displayName":1194,"givenName":28,"familyName":28},"f241f851-b08a-42a6-9fe1-f92da37c9ee9",[968],[1186],{"id":1147,"sortIndex":32,"affiliation":1187,"properties":28},{"id":1147,"createTime":28,"updateTime":28,"relativeEntities":1188,"slug":28,"properties":1189,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1191,"statistic":28},[],{"title":1190},{"VI":1152},[],{"title":1193},{"VI":1194},"Naoko Watanabe",{"id":1196,"sortIndex":42,"researcher":28,"roles":1197,"affiliations":1198,"properties":1205,"displayName":1207,"givenName":28,"familyName":28},"31d42c4b-4012-4b38-b05e-896af2af303f",[968],[1199],{"id":1139,"sortIndex":32,"affiliation":1200,"properties":28},{"id":1139,"createTime":28,"updateTime":28,"relativeEntities":1201,"slug":28,"properties":1202,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1204,"statistic":28},[],{"title":1203},{"VI":1144},[],{"title":1206},{"VI":1207},"Nobuyuki Miyasaka",{"id":1209,"sortIndex":45,"researcher":28,"roles":1210,"affiliations":1211,"properties":1218,"displayName":1220,"givenName":28,"familyName":28},"e1f06f86-851c-499c-9501-3e1e335b7046",[968],[1212],{"id":1172,"sortIndex":32,"affiliation":1213,"properties":28},{"id":1172,"createTime":28,"updateTime":28,"relativeEntities":1214,"slug":28,"properties":1215,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1217,"statistic":28},[],{"title":1216},{"VI":1177},[],{"title":1219},{"VI":1220},"Sho Matsushita",{"id":1222,"sortIndex":46,"researcher":28,"roles":1223,"affiliations":1224,"properties":1238,"displayName":1240,"givenName":28,"familyName":28},"4784dc74-ad30-49f2-9333-de57b132f48a",[968],[1225,1231],{"id":1139,"sortIndex":32,"affiliation":1226,"properties":28},{"id":1139,"createTime":28,"updateTime":28,"relativeEntities":1227,"slug":28,"properties":1228,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1230,"statistic":28},[],{"title":1229},{"VI":1144},[],{"id":1156,"sortIndex":40,"affiliation":1232,"properties":1237},{"id":1156,"createTime":28,"updateTime":28,"relativeEntities":1233,"slug":28,"properties":1234,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1236,"statistic":28},[],{"title":1235},{"VI":1161},[],{},{"title":1239},{"VI":1240},"Hitoshi Kohsaka",{"url":1132,"publisher":1242,"properties":1287},{"id":868,"createTime":869,"updateTime":870,"relativeEntities":1243,"slug":872,"properties":1244,"entityType":25,"verifyStatus":878,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":32,"subjectFields":1247,"manageAffiliations":1256,"indexDatabases":1267,"url":28,"thumbnailPath":28,"statistic":1282,"gsStatistic":28,"type":28,"analyzePriority":28},[],{"issn":1245,"title":1246},{"VOID":875},{"EN":877},[1248,1252],{"id":881,"createTime":28,"updateTime":28,"relativeEntities":1249,"label":1250,"description":1251,"parentId":28,"standard":28,"scholarHubFieldId":28},[],{"EN":884},{},{"id":887,"createTime":28,"updateTime":28,"relativeEntities":1253,"label":1254,"description":1255,"parentId":28,"standard":28,"scholarHubFieldId":28},[],{"EN":890},{},[1257,1262],{"id":894,"createTime":28,"updateTime":28,"relativeEntities":1258,"slug":28,"properties":1259,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1261,"statistic":28},[],{"title":1260},{"EN":898},[],{"id":901,"createTime":28,"updateTime":28,"relativeEntities":1263,"slug":28,"properties":1264,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1266,"statistic":28},[],{"title":1265},{"EN":905},[],[1268,1275],{"id":909,"indexDatabase":1269,"url":921,"indexYears":28,"academicFieldIds":1274,"indexDatabaseRanking":28},{"id":911,"createTime":28,"updateTime":28,"relativeEntities":1270,"label":1271,"description":1272,"key":918,"publicationTags":1273,"standard":28},[],{"EN":914,"VI":914},{"EN":916,"VI":917},[920,813],[923],{"id":925,"indexDatabase":1276,"url":931,"indexYears":932,"academicFieldIds":1281,"indexDatabaseRanking":936},{"id":775,"createTime":28,"updateTime":28,"relativeEntities":1277,"label":1278,"description":1279,"key":781,"publicationTags":1280,"standard":28},[],{"EN":778,"VI":778},{"EN":778,"VI":780},[783],[934,935],{"impactFactor":32,"impactFactorByYear":1283,"i10Index":32,"i10IndexLast5Year":32,"totalPublication":47,"totalPublicationByYear":1284,"totalCitation":46,"totalCitationByYear":1285,"totalCitationPerPublication":284,"totalCitationPerPublicationByYear":1286,"hindexLast5Year":40,"hindex":40},{},{"2000":40,"2001":40,"2002":145},{"2000":40,"2002":45},{"2000":40,"2002":346},{"pages":1288,"volume":1290},{"VOID":1289},"260-266",{"VOID":1291},"21","2010-12-28",2010,[936,920],{"id":1296,"createTime":1297,"updateTime":1298,"relativeEntities":1299,"slug":1300,"properties":1301,"entityType":961,"verifyStatus":26,"verifyTime":1298,"verifyNote":962,"languages":28,"translateLanguages":28,"viewCount":32,"primaryUrl":1308,"fullTextUrl":28,"authors":1309,"publicationType":1061,"publisherRelationship":1325,"citationCount":28,"citationInfo":28,"publishDate":1376,"publishYear":1377,"citationAnalyzeStatus":878,"lastCitationAnalyze":28,"indexDatabases":1378,"openAccess":28,"references":28,"isForceReanalyzing":1116},"00ed3b4a-3cca-40bc-9e5a-e146ad3c64a2","2023-12-12T08:11:02.044+00:00","2025-01-19T15:37:47.024+00:00",[],"The-definition-and-clinical-features-of-the-mutilans-type-of-rheumatoid-arthritis",{"title":1302,"doi":1304,"abstract":1306},{"EN":1303},"The definition and clinical features of the mutilans type of rheumatoid arthritis",{"VOID":1305},"10.1007\u002Fs101650200023",{"EN":1307}," The mutilans type of rheumatoid arthritis (RA) is refractory to several treatments and involves many types of surgical application. It is difficult to prevent its progress, and it has a poor functional prognosis. However, the definition is not always distinct. In this report, I attempt to clarify the clinical features of the mutilans type of RA and establish an accurate definition of the disease. Previous definitions have been divided into three groups: (1) the mutilans group (Mu-G), which has more than three joints showing severe resorptive bone destruction and joint instability; (2) the suspected mutilans group (sMu-G) which has one to two joints with joint instability or showing no instability but with highly resorptive bone destruction; (3) the Larsen V group (LV-G), which has radiological findings indicating Larsen grade V disease. Patients suffering from rheumatoid arthritis for over 10 years and who do not fall into any of the above groups are referred to as the control group. Among 337 patients who suffered from RA for more than 10 years, 58 were classified as being in the mutilans group, 59 in the suspected Mu-G, 47 in the LV-G, and 173 in the control group. The mutilans group had distinctive features which were different from those of the other groups, which had a radiological finding of Larsen grade V disease or severe resorptive bone destruction without instability. From these data, the definition of the mutilans type of RA should be specified as the Mu-G. Thus, the Mu-G shows a distinctive clinical picture which is unlike that in the other groups. It is important to define the mutilans type of RA clearly because it has a poor prognosis. Early identification will help in the establishment of a treatment plan.","https:\u002F\u002Fdoi.org\u002F10.3109\u002Fs101650200023",[1310],{"id":1311,"sortIndex":32,"researcher":28,"roles":1312,"affiliations":1313,"properties":1322,"displayName":1324,"givenName":28,"familyName":28},"63023b41-9768-49dd-935c-c48d5e745dce",[968],[1314],{"id":1315,"sortIndex":32,"affiliation":1316,"properties":28},"a7193b1d-061b-4f6a-907f-db433bdcefb0",{"id":1315,"createTime":28,"updateTime":28,"relativeEntities":1317,"slug":28,"properties":1318,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1321,"statistic":28},[],{"title":1319},{"VI":1320},"Department of Orthopaedic Surgery, Showa University School of Medicine, 1-5-8 Hatanodai, Shinagawa-ku, Tokyo 142-8666, Japan Tel. +81-3-3784-8543; Fax +81-3-3784-9005 e-mail: o-namiki@db3.so-net.ne.jp, , JP",[],{"title":1323},{"VI":1324},"O. Namiki",{"url":1308,"publisher":1326,"properties":1371},{"id":868,"createTime":869,"updateTime":870,"relativeEntities":1327,"slug":872,"properties":1328,"entityType":25,"verifyStatus":878,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":32,"subjectFields":1331,"manageAffiliations":1340,"indexDatabases":1351,"url":28,"thumbnailPath":28,"statistic":1366,"gsStatistic":28,"type":28,"analyzePriority":28},[],{"issn":1329,"title":1330},{"VOID":875},{"EN":877},[1332,1336],{"id":881,"createTime":28,"updateTime":28,"relativeEntities":1333,"label":1334,"description":1335,"parentId":28,"standard":28,"scholarHubFieldId":28},[],{"EN":884},{},{"id":887,"createTime":28,"updateTime":28,"relativeEntities":1337,"label":1338,"description":1339,"parentId":28,"standard":28,"scholarHubFieldId":28},[],{"EN":890},{},[1341,1346],{"id":894,"createTime":28,"updateTime":28,"relativeEntities":1342,"slug":28,"properties":1343,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1345,"statistic":28},[],{"title":1344},{"EN":898},[],{"id":901,"createTime":28,"updateTime":28,"relativeEntities":1347,"slug":28,"properties":1348,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1350,"statistic":28},[],{"title":1349},{"EN":905},[],[1352,1359],{"id":909,"indexDatabase":1353,"url":921,"indexYears":28,"academicFieldIds":1358,"indexDatabaseRanking":28},{"id":911,"createTime":28,"updateTime":28,"relativeEntities":1354,"label":1355,"description":1356,"key":918,"publicationTags":1357,"standard":28},[],{"EN":914,"VI":914},{"EN":916,"VI":917},[920,813],[923],{"id":925,"indexDatabase":1360,"url":931,"indexYears":932,"academicFieldIds":1365,"indexDatabaseRanking":936},{"id":775,"createTime":28,"updateTime":28,"relativeEntities":1361,"label":1362,"description":1363,"key":781,"publicationTags":1364,"standard":28},[],{"EN":778,"VI":778},{"EN":778,"VI":780},[783],[934,935],{"impactFactor":32,"impactFactorByYear":1367,"i10Index":32,"i10IndexLast5Year":32,"totalPublication":47,"totalPublicationByYear":1368,"totalCitation":46,"totalCitationByYear":1369,"totalCitationPerPublication":284,"totalCitationPerPublicationByYear":1370,"hindexLast5Year":40,"hindex":40},{},{"2000":40,"2001":40,"2002":145},{"2000":40,"2002":45},{"2000":40,"2002":346},{"pages":1372,"volume":1374},{"VOID":1373},"134-143",{"VOID":1375},"12","2002-06-01",2002,[936,920],{"id":1380,"createTime":1381,"updateTime":1381,"relativeEntities":1382,"slug":1383,"properties":1384,"entityType":961,"verifyStatus":878,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":32,"primaryUrl":1395,"fullTextUrl":28,"authors":1396,"publicationType":1061,"publisherRelationship":1509,"citationCount":28,"citationInfo":28,"publishDate":1555,"publishYear":1556,"citationAnalyzeStatus":878,"lastCitationAnalyze":28,"indexDatabases":1557,"openAccess":28,"references":28,"isForceReanalyzing":1116},"018f7fc5-5cf3-45cf-bb5a-6a8def129c49","2024-04-07T22:14:03.412+00:00",[],"Right-ventricular-endomyocardial-fibrosis-mimicking-Ebstein-anomaly-in-a-patient-with-Beh%C3%A7et-s-disease-case-report-and-review-of-the-literature",{"abstract":1385,"title":1387,"keywords":1389,"references":1391,"doi":1393},{"EN":1386},"Behçet’s disease is a multisystemic, chronic inflammatory disorder with diffuse clinical manifestations including the cardiovascular system. Endomyocardial fibrosis is a rarely seen complication of Behçet’s disease leading to progressive heart failure. We report a case of right ventricular endomyocardial fibrosis mimicking Ebstein anomaly in a 26-year-old male Turkish patient with Behçet’s disease, who had heart failure symptoms. In addition, the previously reported cases of endomyocardial fibrosis complicating Behçet’s disease are reviewed in this article.",{"EN":1388},"Right ventricular endomyocardial fibrosis mimicking Ebstein anomaly in a patient with Behçet’s disease: case report and review of the literature",{"EN":1390},"",{"VOID":1392},"Chae EJ, Do KH, Seo JB, Park SH, Kang JW, Jang YM, Lee JS, Song JW, Song KS, Lee JH, Kim AY, Lim TH. Radiologic and clinical findings of Behçet’s disease: comprehensive review of multisystemic involvement. Radiographics. 2008;28:e31.\nShimizu T, Ehrlich GE, Inaba G, Hayashi K. Behçet disease (Behçet syndrome). Semin Arthritis Rheum. 1979;8:223–60.\nHamza M. Les manifestations cardiovasculares de la maladie de Behçet (Abstract).1st Mediterranean Symposium on Behçet’s disease, Istanbul, June 4, 1988, p. 26.\nLakhanpal S, Tani K, Lie JT, Katoh K, Ishigatsubo Y, Ohokubo T. Pathologic features of Behçet’s syndrome: a review of Japanese registry data. Hum Pathol. 1985;16:790–5.\nHuong DL, Wechsler B, Papo T, de Zuttere D, Bletry O, Hernigou A, Delcourt A, Godeau P, Piette JC. Endomyocardial fibrosis in Behçet’s disease. Ann Rheum Dis. 1997;56:205–8.\nBuge A, Escourolle R, Chomette G, et al. Behçet’s disease with neurologic manifestations and endocardial fibrosis of the right heart. Anatomoclinical study of a case. Ann Med Interne. 1977;5:411–9.\nEl Ramahi KM, Fawzy ME, Sieck JO, Vanhaleweyk G. Cardiac and pulmonary involvement in Behçet’s disease. Scand J Rheumatol. 1991;20:373–6.\nPena JM, Garcia-Alegria J, Garcia-Fernandez F, Arnalich F, Barbado FJ, Vazquez JJ. Mitral and aortic regurgitation in Behçet’s disease. Ann Rheum Dis. 1985;44:637–79.\nBelmadani K, Dahreddine A, Benyass A, Hda A, Boukili MA, Ohayon V, Archane MI, Pavie A, Gandjbakhch I. Endomyocardial fibrosis in Behçet’s disease: a case report of a pseudo-tumoral form. Arch Mal Coeur Vaiss. 2001;4:282–6.\nAouba A, Nebie L, Fabiani JL, Bruneval P, Patri B, Bandt MD. Tricuspid aseptic endocarditis revealing right endomyocardial fibrosis during an unrecognized Behçet’s disease: a case report. Presse Med. 2004;33:1367–9.\nDarie C, Knezinsky M, Demolombe-Rague S, Pinède L, Périnetti M, Ninet JF, Ninet J. Cardiac pseudotumor revealing Behçet’s disease. Rev Med Interne. 2005;5:420–4.\nEl Houari T, Oukerraj L, Ghzaiel L, Fellat I, Azeroual M, Serraj K, Mezalek ZT, Cherti M, Zarzur J, Arharbi M. Management of Behçet’s disease with multiple complications. Hellenic J Cardiol. 2009;5:420–2.\nSacre K, Ducrocq G, Hernigou A, Laissy JP, Papo T. Unusual cardiovascular events in Behçet’s disease. Clin Exp Rheumatol. 2010;28:582–5.\nHouman M, Ksontini I, Ben Ghorbel I, Lamloum M, Braham A, Mnif E, Miled M. Association of right heart thrombosis, endomyocardial fibrosis, and pulmonary artery aneurysm in Behçet’s disease. Eur J Int Med. 2002;13:455–7.\nBenveniste MFK, Truong MT, Almeida DR, Szarf G. Endomyocardial fibrosis mimicking right ventricular mass. Eur J Radiol Extra 2010;73(1):e9–11.\nGeri G, Weschler B, Huong DL, Isnard R, Piette JC, Amoura Z, Rigon MR, Cacoub P, Saadoun D. Spectrum of cardiac lesions in Behçet’s disease: a series of 52 patients and review. Medicine. 2012;91(1):25–34.",{"VOID":1394},"10.1007\u002Fs10165-012-0801-z","https:\u002F\u002Flink.springer.com\u002Farticle\u002F10.1007\u002Fs10165-012-0801-z",[1397,1412,1427,1440,1455,1470,1483,1496],{"id":1398,"sortIndex":32,"researcher":28,"roles":1399,"affiliations":1400,"properties":1409,"displayName":1411,"givenName":28,"familyName":28},"830f258d-5021-4eaf-a8e6-4af032b273cc",[968],[1401],{"id":1402,"sortIndex":32,"affiliation":1403,"properties":28},"402bfe96-a5dc-4d64-863a-b7a495c74809",{"id":1402,"createTime":28,"updateTime":28,"relativeEntities":1404,"slug":28,"properties":1405,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1408,"statistic":28},[],{"title":1406},{"VI":1407},"Department of Cardiology, Acıbadem University School of Medicine, Istanbul, Turkey",[],{"title":1410},{"VI":1411},"Ali 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investigate the point prevalence of major depressive disorder (MDD) as diagnosed by the Mini-International Neuropsychiatric Interview (M.I.N.I) in patients with rheumatoid arthritis (RA) and to determine whether MDD is related to features of RA disease, such as disease activity or physical dysfunction. Of the patients with RA who participated in the IORRA survey conducted in October 2005, 162 were evaluated using the M.I.N.I., the Center for Epidemiologic Studies-Depression (CES-D) scale, and the two-question depression screen for MDD. RA clinical features were obtained from the concomitant IORRA cohort database. Relationships between MDD and RA disease features were analyzed by the Wilcoxon rank sum test and Pearson’s chi-square test. The point prevalence of MDD as diagnosed by the M.I.N.I. was 6.8 % in our Japanese patients with RA. The percentage of depressive patients was determined to be 23.5, 17.3, or 7.4 % according to the CES-D scale with cut-off points of 16, 19, or 27, respectively, and 14.2 % according to the two-question depression screen. The best cut-off point for CES-D for risk of MDD diagnosed by M.I.N.I. in this study was determined to be 23, with 11.7 % depressive patients having the highest sum of sensitivity and specificity. No relationship between MDD and RA disease activity was detected. By using the well-established structural interview instrument M.I.N.I., we determined the point prevalence of MDD in the RA patients enrolled in this study to be 6.8 %, leading to the conclusion that concomitant MDD does not seem to influence disease activity in RA patients.",{"EN":1568},"Major depressive disorder in patients with rheumatoid arthritis",{"VOID":1570},"Pincus T, Griffith J, Pearce S, Isenberg D. Prevalence of self-reported depression in patients with rheumatoid arthritis. Br J Rheumatol. 1996;35:879–83.\nDickens C, Jackson J, Tomenson B, Hay E, Creed F. Association of depression and rheumatoid arthritis. Psychosomatics. 2003;44:209–15.\nFrank RG, Beck NC, Parker JC, Kashani JH, Elliott TR, Haut AE, et al. Depression in rheumatoid arthritis. J Rheumatol. 1988;15:920–5.\nMartens MP, Parker JC, Smarr KL, Hewett JE, Slaughter JR, Walker SE. Assessment of depression in rheumatoid arthritis: a modified version of the center for epidemiologic studies depression scale. Arthritis Rheum. 2003;49:549–55.\nMurphy S, Creed F, Jayson MI. Psychiatric disorder and illness behaviour in rheumatoid arthritis. Br J Rheumatol. 1988;27:357–63.\nOhtsuki T, Inagaki M, Oikawa Y, Saitoh A, Kurosawa M, Muramatsu K, et al. Multiple barriers against successful care provision for depressed patients in general internal medicine in a Japanese rural hospital: a cross-sectional study. BMC Psychiatry. 2010;10:30.\nOhayon MM, Schatzberg AF. Chronic pain and major depressive disorder in the general population. J Psychiatr Res. 2010;44:454–61.\nWilliams JW Jr, Mulrow CD, Kroenke K, Dhanda R, Badgett RG, Omori D, et al. Case-finding for depression in primary care: a randomized trial. Am J Med. 1999;106:36–43.\nPeck JR, Smith TW, Ward JR, Milano R. Disability and depression in rheumatoid arthritis. A multi-trait, multi-method investigation. Arthritis Rheum. 1989;32:1100–6.\nKojima M, Kojima T, Suzuki S, Oguchi T, Oba M, Tsuchiya H, et al. Depression, inflammation, and pain in patients with rheumatoid arthritis. Arthritis Rheum. 2009;61:1018–24.\nDowlati Y, Herrmann N, Swardfager W, Liu H, Sham L, Reim EK, et al. A meta-analysis of cytokines in major depression. Biol Psychiatry. 2010;67:446–57.\nSchiepers OJ, Wichers MC, Maes M. Cytokines and major depression. Prog Neuropsychopharmacol Biol Psychiatry. 2005;29:201–17.\nSheehan DV, Lecrubier Y, Sheehan KH, Amorim P, Janavs J, Weiller E, et al. The Mini-International Neuropsychiatric Interview (M.I.N.I.): the development and validation of a structured diagnostic psychiatric interview for DSM-IV and ICD-10. J Clin Psychiatry. 1998;59 Suppl 20:22–33 (quiz 4–57).\nRadloff L. The CES-D Scale: a self-report depression scale for research in the general population. Appl Psychol Meas. 1977;1:385–401.\nWhooley MA, Avins AL, Miranda J, Browner WS. Case-finding instruments for depression. Two questions are as good as many. J Gen Intern Med. 1997;12:439–45.\nYamanaka H, Inoue E, Singh G, Tanaka E, Nakajima A, Taniguchi A, et al. Improvement of disease activity of rheumatoid arthritis patients from 2000 to 2006 in a large observational cohort study IORRA in Japan. Mod Rheumatol. 2007;17:283–9.\nYamada T, Nakajima A, Inoue E, Tanaka E, Hara M, Tomatsu T, et al. Increased risk of tuberculosis in patients with rheumatoid arthritis in Japan. Ann Rheum Dis. 2006;65:1661–3.\nNakajima A, Inoue E, Tanaka E, Singh G, Sato E, Hoshi D, et al. Mortality and cause of death in Japanese patients with rheumatoid arthritis based on a large observational cohort. Scand J Rheumatol. 2010;39:360–7.\nNakajima A, Kamitsuji S, Saito A, Tanaka E, Nishimura K, Horikawa N, et al. Disability and patient’s appraisal of general health contribute to depressed mood in rheumatoid arthritis in a large clinical study in Japan. Mod Rheumatol. 2006;16:151–7.\nPrevoo ML, van’t Hof MA, Kuper HH, van Leeuwen MA, van de Putte LB, van Riel PL. Modified disease activity scores that include twenty-eight-joint counts. Development and validation in a prospective longitudinal study of patients with rheumatoid arthritis. Arthritis Rheum. 1995;38:44–8.\nMatsuda Y, Singh G, Yamanaka H, Tanaka E, Urano W, Taniguchi A, et al. Validation of a Japanese version of the Stanford Health Assessment Questionnaire in 3,763 patients with rheumatoid arthritis. Arthritis Rheum. 2003;49:784–8.\nTurk DC, Okifuji A. Detecting depression in chronic pain patients: adequacy of self-reports. Behav Res Ther. 1994;32:9–16.\nGeisser ME, Roth RS, Robinson ME. Assessing depression among persons with chronic pain using the Center for Epidemiological Studies-Depression Scale and the Beck Depression Inventory: a comparative analysis. Clin J Pain. 1997;13:163–70.\nAyuso-Mateos JL, Vazquez-Barquero JL, Dowrick C, Lehtinen V, Dalgard OS, Casey P, et al. Depressive disorders in Europe: prevalence figures from the ODIN study. Br J Psychiatry. 2001;179:308–16.\nKawakami N, Takeshima T, Ono Y, Uda H, Hata Y, Nakane Y, et al. Twelve-month prevalence, severity, and treatment of common mental disorders in communities in Japan: preliminary finding from the World Mental Health Japan Survey 2002–2003. Psychiatry Clin Neurosci. 2005;59:441–52.\nLok EY, Mok CC, Cheng CW, Cheung EF. Prevalence and determinants of psychiatric disorders in patients with rheumatoid arthritis. Psychosomatics. 2010;51:338-e8.\nZautra AJ, Yocum DC, Villanueva I, Smith B, Davis MC, Attrep J, et al. Immune activation and depression in women with rheumatoid arthritis. J Rheumatol. 2004;31:457–63.\nEl-Tantawy AM, El-Sayed AE, Kora BA, Amin RT. Psychiatric morbidity associated with some cytokines (IL-1beta, IL-12, IL-18 and TNF-alpha) among rheumatoid arthritis patients. Egypt J Immunol. 2008;15:1–11.",{"VOID":1572},"10.1007\u002Fs10165-012-0643-8","https:\u002F\u002Fdoi.org\u002F10.3109\u002Fs10165-012-0643-8",[1575,1590,1605,1618,1631,1644,1657,1670,1683],{"id":1576,"sortIndex":32,"researcher":28,"roles":1577,"affiliations":1578,"properties":1587,"displayName":1589,"givenName":28,"familyName":28},"c9904209-da11-46c7-a64e-3d13085c58ec",[968],[1579],{"id":1580,"sortIndex":32,"affiliation":1581,"properties":28},"41ff4ea7-9bf2-4bad-a793-275a843e6d94",{"id":1580,"createTime":28,"updateTime":28,"relativeEntities":1582,"slug":28,"properties":1583,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1586,"statistic":28},[],{"title":1584},{"VI":1585},"Institute of Rheumatology, Tokyo Women’s Medical University, Shinjuku-ku, Tokyo, Japan",[],{"title":1588},{"VI":1589},"Eri 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54-year-old woman presented with painless subcutaneous masses on her right hand and spontaneous loss of extension of her ring finger. Surgical exploration of the wrist showed hypertrophic white-colored crystal deposits that both surrounded and invaded into the extensor tendons (intratendinous invasion). Histopathologic examination of the specimen demonstrated findings consistent with gouty tophi. We conclude that tophaceous gout needs to be included in the differential diagnosis of chronic extensor tenosynovitis of the hand.",{"EN":1759},"Multiple extensor tendon ruptures caused by tophaceous gout",{"VOID":1761},"Mannerfelt L, Oetker R, Ostlund B, Elbert B. Rupture of the extensor pollicis longus tendon after Colles fracture and by rheumatoid arthritis. J Hand Surg [Br]. 1990;15(1):49–50.\nCarr AJ, Burge PD. Rupture of extensor tendons due to osteoarthritis of the distal radio-ulnar joint. J Hand Surg [Br]. 1992;17(6):694–6.\nWeniger FG, Davison SP, Risin M, Salyapongse AN, Manders EK. Gouty flexor tenosynovitis of the digits: report of three cases. J Hand Surg [Am]. 2003;28(4):669–72.\nWurapa RK, Zelouf DS. Flexor tendon rupture caused by gout: a case report. J Hand Surg [Am]. 2002;27(4):591–3.\nMoore JR, Weiland AJ. Gouty tenosynovitis in the hand. J Hand Surg [Am]. 1985;10(2):291–5.\nHung JY, Wang SJ, Wu SS. Spontaneous rupture of extensor pollicis longus tendon with tophaceous gout infiltration. Arch Orthop Trauma Surg. 2005;125(4):281–4.\nStraub LR, Smith JW, Carpenter GK Jr, Dietz GH. The surgery of gout in the upper extremity. 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41-year-old woman presented with continuous fever, and her laboratory data suggested the recrudescence of systemic lupus erythematosus. She was treated with 60 mg\u002Fday prednisolone. With a dose reduction of prednisolone, high fever and pancytopenia were observed again. A bone marrow biopsy revealed hemophagocytosis. The effects of steroid pulse therapy, high-dose intravenous immunoglobulin, cyclosporine A, and methotrexate were insufficient. However, after four injections of etanercept (25 mg, twice a week) subcutaneously, her symptoms had completely resolved. In such cases, therapy with etanercept may be effective.",{"EN":1893},"Etanercept for the treatment of intractable hemophagocytic syndrome with systemic lupus erythematosus",{"VOID":1895},"Larroche C, Mouthon L. Pathogenesis of hemophagocytic syndrome (HPS). Autoimmune Rev. 2004;3:69–75.\nWong KF, Hui PK, Chan JKC, Chan YW, Ha SY. The acute lupus hemophagocytic syndrome. Ann Intern Med. 1991;114:387–90.\nKumakura S, Ishikura H, Kondo M, Murakawa Y, Masuda J, Kobayashi S. Autoimmune-associated hemophagocytic syndrome. Mod Rheumatol. 2004;14:205–15.\nQian J, Yang CD. Hemophagocytic syndrome as one of main manifestations in untreated systemic lupus erythematosus: two case reports and literature review. Clin Rheumatol. 2007;26:807–10.\nLambotte O, Khellaf M, Harmouche H, Bader-Meunier B, Manceron V, Goujard C, et al. Characteristics and long-term outcome of 15 episodes of systemic lupus erythematosus-associated hemophagocytic syndrome. Medicine. 2006;85:169–82.\nFautrel B. Adult-onset Still disease. Best Pract Res Clin Rheumatol. 2008;22:773–92.\nIdeguchi H, Ohno S, Takase K, Hattori H, Kirino Y, Takeno M, et al. Successful treatment of refractory lupus-associated haemophagocytic lymphohistiocytosis with infliximab. Rheumatology. 2007;46:1621–2.\nHenzan T, Nagafuji K, Tsukamoto H, Miyamoto T, Gondo H, Imashuku S, Harada M. Success with infliximab in treating refractory hemophagocytic lymphohistiocytosis. Am J Hematol. 2006;81:59–61.\nTakahashi N, Naniwa T, Banno S. Successful use of etanercept in the treatment of acute lupus hemophagocytic syndrome. Mod Rheumatol. 2008;18:72–5.\nAouba A, De Bandt M, Aslangul E, Atkhen N, Patri B. Haemophagocytic syndrome in a rheumatoid arthritis patient treated with infliximab. Rheumatology. 2003;42:800–2.\nRamanan AV, Schneider R. Macrophage activation syndrome following initiation of etanercept in a child with systemic onset juvenile rheumatoid arthritis. J Rheumatol. 2003;30:401–3.\nMatsui T, Ohsumi K, Ozawa N, Shimada K, Sumitomo S, Shimane K, et al. CD64 on neutrophils is a sensitive and specific marker for detection of infection in patients with rheumatoid arthritis. J Rheumatol. 2006;33:2416–24.\nAikawa N, Fujishima S, Endo S, Sekine I, Kogawa K, Yamamoto Y, et al. Multicenter prospective study of procalcitonin as an indicator of sepsis. J Infect Chemother. 2005;11:152–9.\nOsugi Y, Hara J, Tagawa S, Takai K, Hosoi G, Matsuda Y, et al. Cytokine production regulating Th1 and Th2 cytokines in hemophagocytic lymphohistiocytosis. Blood. 1997;89:4100–3.\nBilliau AD, Roskams T, Damme-Lombaerts RV, Matthys P, Wouters C. Macrophage activation syndrome: characteristic findings on liver biopsy illustrating the key role of activated, IFN-γ-producing lymphocytes and IL-6- and TNF-α-producing macrophages. 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analyze the relationship between the progression of disability and disease activity in patients with rheumatoid arthritis (RA) in daily practice. Patients from an observational cohort, IORRA, who completed surveys during 2009–2011 were eligible. Linear regression of disease activity score 28 (DAS28), Japanese version of Health Assessment Questionnaire (J-HAQ), and EQ-5D from baseline were calculated, and the angles of the regression lines were designated DAS28 slope, J-HAQ slope, and EQ-5D slope, respectively, in each patient; averages were compared between treatment groups. A total of 5,038 patients [84.0 % female, mean age 59.4 (SD 13.1) years, disease duration 13.2 (9.6) years, DAS28 3.29 (1.14), and J-HAQ 0.715 (0.760)] were analyzed. The average DAS28 slope indicated improvement in all groups, whereas J-HAQ slopes were negative in patients on methotrexate (MTX), biologics, combination biologics\u002Fdisease-modifying antirheumatic drugs (DMARDs), and combination biologics\u002FMTX at baseline, but positive in patients on prednisolone >5 mg\u002Fday [0.010 (0.153)] and not on MTX at baseline [0.007 (0.122)], representing a worsening of disability. There is some disparity between improvement of disease activity and progression of disability, suggesting that quality of remission must be considered.",{"EN":2060},"Functional disability can deteriorate despite suppression of disease activity in patients with rheumatoid arthritis: a large observational cohort study",{"VOID":2062},"Smolen JS, Aletaha D. Monitoring rheumatoid arthritis. Curr Opin Rheumatol. 2011;23:252–8.\nYamanaka H, Inoue E, Singh G, et al. Improvement of disease activity of rheumatoid arthritis patients from 2000 to 2006 in a large observational cohort study IORRA in Japan. Mod Rheumatol. 2007;17:283–9.\nJayakumar K, Norton S, Dixey J, et al. Sustained clinical remission in rheumatoid arthritis: prevalence and prognostic factors in an inception cohort of patients treated with conventional DMARDS. Rheumatology (Oxford). 2012;51:169–75.\nTanaka Y. Intensive treatment and treatment holiday of TNF-inhibitors in rheumatoid arthritis. Curr Opin Rheumatol. 2012;24:319–26.\nAletaha D, Ward MM, Machold KP, et al. Remission and active disease in rheumatoid arthritis: defining criteria for disease activity states. Arthritis Rheum. 2005;52:2625–36.\nTanaka E, Mannalithara A, Inoue E, et al. Efficient management of rheumatoid arthritis significantly reduces long-term functional disability. Ann Rheum Dis. 2008;67:1153–8.\nSmolen JS, Aletaha D, Bijlsma JW, et al. Treating rheumatoid arthritis to target: recommendations of an international task force. Ann Rheum Dis. 2010;69:631–7.\nVermeer M, Kuper HH, Hoekstra M, et al. Implementation of a treat-to-target strategy in very early rheumatoid arthritis: results of the Dutch Rheumatoid Arthritis Monitoring remission induction cohort study. Arthritis Rheum. 2011;63:2865–72.\nYamanaka H, Seto Y, Tanaka E, et al. Management of rheumatoid arthritis: the 2012 perspective. Mod Rheumatol. 2012. doi:10.1007\u002Fs10165-012-0702-1.\nIikuni N, Inoue E, Tanaka E, et al. Low disease activity state with corticosteroid may not represent ‘true’ low disease activity state in patients with rheumatoid arthritis. Rheumatology (Oxford). 2008;47:519–21.\nTanaka E, Mannalithara A, Inoue E, et al. Effects of long-term corticosteroid usage on functional disability in patients with early rheumatoid arthritis, regardless of controlled disease activity. Rheumatol Int. 2010;32:749–57.\nMatsuda Y, Singh G, Yamanaka H, et al. Validation of a Japanese version of the Stanford Health Assessment Questionnaire in 3,763 patients with rheumatoid arthritis. Arthritis Rheum. 2003;49:784–8.\nYamanaka H, Inoue E, Tanaka E, et al. Influence of methotrexate dose on its efficacy and safety in rheumatoid arthritis patients: evidence based on the variety of prescribing approaches among practicing Japanese rheumatologists in a single institute-based large observational cohort (IORRA). Mod Rheumatol. 2007;17:98–105.\nPrevoo ML, van’t Hof MA, Kuper HH, et al. Modified disease activity scores that include twenty-eight-joint counts: development and validation in a prospective longitudinal study of patients with rheumatoid arthritis. Arthritis Rheum. 1995;38:44–8.\nHurst NP, Kind P, Ruta D, et al. Measuring health-related quality of life in rheumatoid arthritis: validity, responsiveness and reliability of EuroQol (EQ-5D). Br J Rheumatol. 1997;36:551–9.\nEmery P, Genovese MC, van Vollenhoven R, et al. Less radiographic progression with adalimumab plus methotrexate versus methotrexate monotherapy across the spectrum of clinical response in early rheumatoid arthritis. J Rheumatol. 2009;36:1429–41.\nTakeuchi T, Tanaka Y, Kaneko Y, et al. Effectiveness and safety of adalimumab in Japanese patients with rheumatoid arthritis: retrospective analyses of data collected during the first year of adalimumab treatment in routine clinical practice (HARMONY study). Mod Rheumatol. 2011;22:327–38.\nKameda H, Kanbe K, Sato E, et al. Continuation of methotrexate resulted in better clinical and radiographic outcomes than discontinuation upon starting etanercept in patients with rheumatoid arthritis: 52-week results from the JESMR study. J Rheumatol. 2011;38:1585–92.\nFurst DE. Observational cohort studies and well controlled clinical trials—we need them both! J Rheumatol. 2004;31:1476–7.\nOzminkowski RJ, Burton WN, Goetzel RZ, et al. The impact of rheumatoid arthritis on medical expenditures, absenteeism, and short-term disability benefits. J Occup Environ Med. 2006;48:135–48.\nSmolen JS, Aletaha D, Grisar JC, et al. Estimation of a numerical value for joint damage-related physical disability in rheumatoid arthritis clinical trials. Ann Rheum Dis. 2010;69:1058–64.\nAletaha D, Smolen JS. Joint damage in rheumatoid arthritis progresses in remission according to the Disease Activity Score in 28 joints and is driven by residual swollen joints. Arthritis Rheum. 2011;63:3702–11.\nAletaha D, Alasti F, Smolen JS. Rheumatoid arthritis near remission: clinical rather than laboratory inflammation is associated with radiographic progression. 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Chest X-ray films showed diffuse mottled infiltrates and bronchial wall thickness in both lungs. Computed tomography revealed opacities along the thickening of the bronchovascular bundles. The pathologic findings were indistinguishable from those of diffuse panbronchiolitis. After discontinuation of gold compounds and initiation of steroid administration, her subjective symptoms immediately subsided. We conclude that our patient, who had suffered from chronic sinusitis and had a predisposition to bronchiolar disease, had bronchiolar disease induced by gold compounds.","https:\u002F\u002Facademic.oup.com\u002Fmr\u002Farticle-abstract\u002F15\u002F2\u002F148\u002F6296344?redirectedFrom=fulltext",[2274,2289,2302],{"id":2275,"sortIndex":32,"researcher":28,"roles":2276,"affiliations":2277,"properties":2286,"displayName":2288,"givenName":28,"familyName":28},"cb255a92-ccaa-4ff6-980a-06a19fb39ead",[968],[2278],{"id":2279,"sortIndex":32,"affiliation":2280,"properties":28},"434df1d4-00ba-43f3-8c1d-8c5d6cc32903",{"id":2279,"createTime":28,"updateTime":28,"relativeEntities":2281,"slug":28,"properties":2282,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":2285,"statistic":28},[],{"title":2283},{"VI":2284},"Department of Internal Medicine, Kawasaki Kyodo Hospital, Kawasaki, 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She was clinically diagnosed with Wegener’s granulomatosis, although vasculitis was not diagnosed due to the lack of typical histological findings. We discuss the differential diagnosis in this patient, and the association of MPO-ANCA with periaortitis or epidural spinal tumor.",{"EN":2379},"Epidural spinal tumor and periaortitis as rare complications of Wegener’s granulomatosis",{"VOID":2381},"Schilder AM. Wegener’s granulomatosis vasculitis and granuloma. Autoimmun Rev. 2010;9(7):483–7.\nSeo P, Stone JH. The antineutrophil cytoplasmic antibody-associated vasculitides. Am J Med. 2004;117(1):39–50.\nLeavitt RY, Fauci AS, Bloch DA, Michel BA, Hunder GG, Arend WP, et al. The American College of Rheumatology 1990 criteria for the classification of Wegener’s granulomatosis. Arthritis Rheum. 1990;33(8):1101–7.\nWatts R, Lane S, Hanslik T, Hauser T, Hellmich B, Koldingsnes W, et al. Development and validation of a consensus methodology for the classification of the ANCA-associated vasculitides and polyarteritis nodosa for epidemiological studies. Ann Rheum Dis. 2007;66(2):222–7.\nRao JK, Allen NB, Feussner JR, Weinberger M. A prospective study of antineutrophil cytoplasmic antibody (c-ANCA) and clinical criteria in diagnosing Wegener’s granulomatosis. Lancet. 1995;346(8980):926–31.\nBaranger TA, Audrain MA, Testa A, Besnier D, Guillevin L, Esnault VL. Anti-neutrophil cytoplasm antibodies in patients with ACR criteria for polyarteritis nodosa: help for systemic vasculitis classification? Autoimmunity. 1995;20(1):33–7.\nShaheen H, Abubakar S, Malik I, Altafullah I, Alam F, Khan A. Epidural spinal cord compression from metastatic cancer: clinical features and management. J Pak Med Assoc. 1991;41(3):60–2.\nMurphy JM, Gomez-Anson B, Gillard JH, Antoun NM, Cross J, Elliott JD, et al. Wegener granulomatosis: MR imaging findings in brain and meninges. Radiology. 1999;213(3):794–9.\nArroyo IL, Barron KS, Brewer EJ Jr. Spinal cord compression by epidural lipomatosis in juvenile rheumatoid arthritis. Arthritis Rheum. 1988;31(3):447–51.\nWeissman MN, Lange R, Kelley C, Belgea K, Abel L. Intraspinal epidural sarcoidosis: case report. Neurosurgery. 1996;39(1):179–81.\nHausler M, Schaade L, Ramaekers VT, Doenges M, Heimann G, Sellhaus B. Inflammatory pseudotumors of the central nervous system: report of 3 cases and a literature review. Hum Pathol. 2003;34(3):253–62.\nPradilla G, Ardila GP, Hsu W, Rigamonti D. Epidural abscesses of the CNS. Lancet Neurol. 2009;8(3):292–300.\nMuraszko KM, Oldfield EH. Vascular malformations of the spinal cord and dura. Neurosurg Clin North Am. 1990;1(3):631–52.\nPalmisano A, Vaglio A. Chronic periaortitis: a fibro-inflammatory disorder. Best Pract Res Clin Rheumatol. 2009;23(3):339–53.\nCarels T, Verbeken E, Blockmans D. p-ANCA-associated periaortitis with histological proof of Wegener’s granulomatosis: case report. Clin Rheumatol. 2005;24(1):83–6.\nVaglio A, Corradi D, Manenti L, Ferretti S, Garini G, Buzio C. Evidence of autoimmunity in chronic periaortitis: a prospective study. Am J Med. 2003;114(6):454–62.\nDehner LP, Coffin CM. Idiopathic fibrosclerotic disorders and other inflammatory pseudotumors. Semin Diagn Pathol. 1998;15(2):161–73.\nLui PC, Fan YS, Wong SS, Chan AN, Wong G, Chau TK, et al. Inflammatory pseudotumors of the central nervous system. Hum Pathol. 2009;40(11):1611–7.\nYamamoto H, Yamaguchi H, Aishima S, Oda Y, Kohashi K, Oshiro Y, et al. Inflammatory myofibroblastic tumor versus IgG4-related sclerosing disease and inflammatory pseudotumor: a comparative clinicopathologic study. Am J Surg Pathol. 2009;33(9):1330–40.\nMasaki Y, Dong L, Kurose N, Kitagawa K, Morikawa Y, Yamamoto M, et al. Proposal for a new clinical entity, IgG4-positive multiorgan lymphoproliferative syndrome: analysis of 64 cases of IgG4-related disorders. Ann Rheum Dis. 2009;68(8):1310–5.\nLevin A, Kasem S, Mader R, Naparstek Y, Friedman G, Ben-Yehuda A. Wegener granulomatosis with back pain, periaortitis, and dural inflammation developing while receiving monthly cyclophosphamide. J Clin Rheumatol. 2006;12(6):294–7.\nNagashima T, Maguchi S, Terayama Y, Horimoto M, Nemoto M, Nunomura M, et al. P-ANCA-positive Wegener’s granulomatosis presenting with hypertrophic pachymeningitis and multiple cranial neuropathies: case report and review of literature. Neuropathology. 2000;20(1):23–30.\nWang DC, Wei JW, Liu JH, Hu YG. The upper thoracic spinal cord compression as the initial manifestation of Wegener’s granulomatosis: a case report. Eur Spine J. 2007;16(Suppl 3):296–300.\nKerkeni S, Bardin T, Richette P. Back pain in a patient with Wegener’s granulomatosis. J Rheumatol. 2008;35(11):2292–4.\nMentzel HJ, Neumann T, Fitzek C, Sauner D, Reichenbach JR, Kaiser WA. MR imaging in Wegener granulomatosis of the spinal cord. 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