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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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importance of systemic sclerosis (SSc) autoantibodies for diagnosis has become recognized by their incorporation into the 2013 ACR\u002FEULAR classification criteria. Clear prognostic and phenotypic associations with cutaneous subtype and internal organ involvement have been also described. However, little is known about the potential of autoantibodies to exert a direct pathogenic role in SSc. The aim of the study is to assess the pathogenic capacity of anti-DNA-topoisomerase I (anti-Topo-I) and anti-centromeric protein B (anti-Cenp-B) autoantibodies to induce pro-fibrotic markers in dermal fibroblasts. Dermal fibroblasts were isolated from unaffected and affected skin samples of (n = 10) limited cutaneous SSc (LcSSc) patients, from affected skin samples of diffuse cutaneous (DcSSc) patients (n = 10) and from healthy subjects (n = 20). Fibroblasts were stimulated with anti-Topo-I, anti-Cenp-B IgGs, and control IgGs in ratios 1:100 and 1:200 for 24 h. Cells were also incubated with 10% SSc anti-Topo-I+ and anti-Cenp-B+ whole serum and with 10% control serum for 24 h. Viability was assessed by MTT test, while apoptosis was assessed by flow cytometry. Activation of pro-fibrotic genes ACTA2, COL1A1, and TAGLN was evaluated by quantitative real-time PCR (qPCR), while the respective protein levels alpha-smooth-muscle actin (α-SMA), type-I-collagen (Col-I), and transgelin (SM22) were assessed by immunocytochemistry (ICC). MTT showed that anti-Cenp-B\u002Fanti-Topo-I IgGs and anti-Cenp-B+\u002Fanti-Topo-I+ sera reduced viability (in a dilution-dependent manner for IgGs) for all the fibroblast populations. Apoptosis is induced in unaffected LcSSc and control fibroblasts, while affected LcSSc\u002FDcSSc fibroblasts showed apoptosis resistance. Basal mRNA (ACTA2, COL1A1, and TAGLN) and protein (α-SMA, Col-1, and SM22) levels were higher in affected LcSSc\u002FDcSSc fibroblasts compared to LcSSc unaffected and to control ones. Stimulation with anti-Cenp-B\u002Fanti-Topo-I IgGs and with anti-Cenp-B+\u002Fanti-Topo-I+ sera showed a better induction in unaffected LcSSc and control fibroblasts. However, a statistically significant increase of all pro-fibrotic markers is reported also in affected LcSSc\u002FDcSSc fibroblasts upon stimulation with both IgGs and sera. This study suggests a pathogenic role of SSc-specific autoantibodies to directly induce pro-fibrotic activation in human dermal fibroblasts. Therefore, besides the diagnostic and prognostic use of those autoantibodies, these data might further justify the importance of immunosuppressive drugs in the early stages of the autoimmune disease, including SSc.",{"EN":940},"Antibodies against specific extractable nuclear antigens (ENAs) as diagnostic and prognostic tools and inducers of a profibrotic phenotype in cultured human skin fibroblasts: are they functional?",{"VOID":942},"Denton CP. Advances in pathogenesis and treatment of systemic sclerosis. Clin Med (Lond). 2016;16:55–60.\nRajkumar VS, Howell K, Csiszar K, Denton CP, Black CM, Abraham DJ. Shared expression of phenotypic markers in systemic sclerosis indicates a convergence of pericytes and fibroblasts to a myofibroblast lineage in fibrosis. Arthritis Res Ther. 2005;7:1113–23.\nLeRoy EC, Black C, Fleischmajer R, Jablonska S, Krieg T, Medsger TA Jr, et al. Scleroderma (systemic sclerosis): classification, subsets and pathogenesis. J Rheumatol. 1988;15:202–5.\nAllanore Y. Limited cutaneous systemic sclerosis: the unfairly neglected subset. J Scleroderma Relat Disord. 2016;1:241–6.\nPearson DR, Werth VP, Pappas-Taffer L. Systemic sclerosis: current concepts of skin and systemic manifestations. Clin Dermatol. 2018;36:459–74.\nStochmal, A., Czuwara, J., Trojanowska, M. et al. Clinic Rev Allerg Immunol. 2019; https:\u002F\u002Fdoi.org\u002F10.1007\u002Fs12016-018-8718-8.\nBanhuk FW, Pahim BC, Jorge AS, Menolli RA. Relationships among antibodies against extractable nuclear antigens, antinuclear antibodies, and autoimmune diseases in a Brazilian public hospital. Autoimmune Dis. 2018;2018:9856910.\nOkano Y. Antinuclear antibody in systemic sclerosis (scleroderma). Rheum Dis Clin N Am. 1996;22:709–35.\nTan EM. Antinuclear antibodies: diagnostic markers for autoimmune diseases and probes for cell biology. Adv Immunol. 1989;44:93–151.\nTartar DM, Chung L, Fiorentino DF. Clinical significance of autoantibodies in dermatomyositis and systemic sclerosis. Clin Dermatol. 2018;36:508–24.\nChoi MY, Fritzler MJ. Progress in understanding the diagnostic and pathogenic role of autoantibodies associated with systemic sclerosis. Curr Opin Rheumatol. 2016;28:586–94.\nLiaskos C, Marou E, Simopoulou T, Barmakoudi M, Efthymiou G, Scheper T, et al. Disease-related autoantibody profile in patients with systemic sclerosis. Autoimmunity. 2017;50:414–21.\nKuwana M. Circulating anti-nuclear antibodies in systemic sclerosis: utility in diagnosis and disease subsetting. J Nippon Med Sch. 2017;84:56–63.\nBoonstra M, Mertens BJA, Bakker JA, Ninaber MK, Ajmone Marsan N, van der Helm-van Mil AHM, et al. To what extent do autoantibodies help to identify high-risk patients in systemic sclerosis? Clin Exp Rheumatol. 2018;36 Suppl 113(4):109–17.\nVan den Hoogen F, Khanna D, Fransen J, Johnson SR, Baron M, Tyndall A, et al. 2013 classification criteria for systemic sclerosis: an American College of Rheumatology\u002FEuropean league against rheumatism collaborative initiative. Ann Rheum Dis. 2013;72:1747–55.\nVan den Hoogen F, Khanna D, Fransen J, Johnson SR, Baron M, Tyndall A, et al. 2013 classification criteria for systemic sclerosis: an American College of Rheumatology\u002FEuropean league against rheumatism collaborative initiative. Arthritis Rheum. 2013;65:2737–47.\nValentini G, Marcoccia A, Cuomo G, Vettori S, Iudici M, Bondanini F, et al. Early systemic sclerosis: analysis of the disease course in patients with marker autoantibody and\u002For capillaroscopic positivity. Arthritis Care Res. 2014;66:1520–7.\nSalazar GA, Assassi S, Wigley F, Hummers L, Varga J, Hinchcliff M, et al. Antinuclear antibody-negative systemic sclerosis. Semin Arthritis Rheum. 2015;44:680–6.\nChander R, Singh S, Kalantri SA, Charan S, Gupta A. Sero-negative systemic sclerosis: a rare presentation. J Clin Diagn Res. 2016;10:OD12–3.\nClements PJ, Lachenruch PA, Nq SC, Simmons M, Sterz M, Furst DE. Skin score. A semiquantitative measure of cutaneous involvement that improves prediction of prognosis in systemic sclerosis. Arthritis Rheum. 1990;33:1256–63.\nCheleschi S, Giordano N, Volpi N, Tenti S, Gallo I, Di Meglio M, et al. A complex relationship between Visfatin and Resistin and microRNA: an in vitro study on human chondrocyte cultures. Int J Mol Sci. 2018;19:3909.\nRamakers C, Ruijter JM, Deprez RH, Moorman AF. Assumption-free analysis of quantitative real-time polymerase chain reaction (PCR) data. Neurosci Lett. 2003;339:62–6.\nPfaffl MW. A new mathematical model for relative quantification in real RT-PCR. Nucleic Acid Res. 2001;29:e45.\nVandesompele J, de Preter K, Pattyn F, Poppe B, van Roy N, de Paepe A, et al. Accurate normalization of real-time quantitative RT-PCR data by geometric averaging of multiple internal control genes. Genome Biol. 2002;3:research0034.1.\nCorallo C, Franci B, Lucani B, Montella A, Chirico C, Gonnelli S, et al. From microvasculature to fibroblasts: contribution of anti-endothelial cell antibodies in systemic sclerosis. Int J Immunopathol Pharmacol. 2015;28:93–103.\nCorallo C, Santucci A, Bernardini G, Figura N, Leoncini R, Riolo G, et al. Proteomic investigation of dermal fibroblasts isolated from affected and unaffected skin samples from patients with limited cutaneous systemic sclerosis: 2 distinct entities? J Rheumatol. 2017;44:40–8.\nMehra S, Walker J, Patterson K, Fritzler MJ. Autoantibodies in systemic sclerosis. Autoimmun Rev. 2013;12:340–54.\nKranenburg P, van den Hombergh WM, Knaapen-Hans HK, van den Hoogen FH, Fransen J, Vonk MC. Survival and organ involvement in patients with limited cutaneous systemic sclerosis and anti-topoisomerase-I antibodies: determined by skin subtype or auto-antibody subtype? A long-term follow-up study. Rheumatology (Oxford). 2016;55:2001–8.\nSteen VD. Autoantibodies in systemic sclerosis. Semin Arthritis Rheum. 2005;35:35–42.\nCoghlan JG, Denton CP, Grunig E, Bonderman D, Distler O, Khanna D, et al. Evidence-based detection of pulmonary arterial hypertension in systemic sclerosis: the DETECT study. Ann Rheum Dis. 2014;73:1340–9.\nHesselstrand R, Scheja A, Shen GQ, Wiik A, Akesson A. The association of antinuclear antibodies with organ involvement and survival in systemic sclerosis. Rheumatology (Oxford). 2003;42:534–40.\nvan Caam A, Vonk M, van den Hoogen F, van Lent P, van der Kraan P. Unraveling SSc pathophysiology; the Myofibroblast. Front Immunol. 2018;9:2452.\nNunes JPL, Cunha AC, Meirinhos T, Nunes A, Araújo PM, Godinho AR, et al. Prevalence of auto-antibodies associated to pulmonary arterial hypertension in scleroderma - a review. Autoimmun Rev. 2018;17:1186–201.\nKim D, Peck A, Santer D, Patole P, Schwartz SM, Molitor JA, et al. Induction of interferon-alpha by scleroderma sera containing autoantibodies to topoisomerase I: association of higher interferon-alpha activity with lung fibrosis. Arthritis Rheum. 2008;58:2163–73.\nSchulz JN, Plomann M, Sengle G, Gullberg D, Krieg T, Eckes B. New developments on skin fibrosis - essential signals emanating from the extracellular matrix for the control of myofibroblasts. Matrix Biol. 2018;69:522–32.\nOhyama K, Baba M, Tamai M, Aibara N, Ichinose K, Kishikawa N, et al. Proteomic profiling of antigens in circulating immune complexes associated with each of seven autoimmune diseases. Clin Biochem. 2015;48:181–5.\nRaschi E, Chighizola CB, Cesana L, Privitera D, Ingegnoli F, Mastaglio C, et al. Immune complexes containing scleroderma-specific autoantibodies induce a profibrotic and proinflammatory phenotype in skin fibroblasts. Arthritis Res Ther. 2018;20:187.\nHénault J, Robitaille G, Senécal JL, Raymond Y. DNA topoisomerase I binding to fibroblasts induces monocyte adhesion and activation in the presence of anti-topoisomerase I autoantibodies from systemic sclerosis patients. Arthritis Rheum. 2006;54:963–73.\nHénault J, Tremblay M, Clément I, Raymond Y, Senécal JL. Direct binding of anti-DNA topoisomerase I autoantibodies to the cell surface of fibroblasts in patients with systemic sclerosis. Arthritis Rheum. 2004;50:3265–74.\nGirstun A, Ishikawa T, Kowalska-Loth B, Czubaty A, Staron K. Subnuclear localization of human topoisomerase I. J Cell Biochem. 2017;118:407–19.\nOppenheim JJ, Dong HF, Plotz P, Caspi RR, Dykstra M, Pierce S, et al. Autoantigens act as tissue-specific chemoattractants. J Leukoc Biol. 2005;77:854–61.\nRobitaille G, Henault J, Christin MS, Senecal JL, Raymond Y. The nuclear autoantigen CENP-B displays cytokine-like activities toward vascular smooth muscle cells. Arthritis Rheum. 2007;56:3814–26.\nRobitaille G, Christin MS, Clement I, Senecal JL, Raymond Y. Nuclear autoantigen CENP-B transactivation of the epidermal growth factor receptor via chemokine receptor 3 in vascular smooth muscle cells. Arthritis Rheum. 2009;60:2805–16.\nHoward OZ. Autoantigen signalling through chemokine receptors. Curr Opin Rheumatol. 2006;18:642–6.\nIngegnoli F, Ughi N, Mihai C. Update on the epidemiology, risk factors, and disease outcomes of systemic sclerosis. Best Pract Res Clin Rheumatol. 2018;32:223–40.\nOrlandi M, Barsotti S, Lepri G, Codullo V, Di Battista M, Guiducci S, et al. One year in review 2018: systemic sclerosis. Clin Exp Rheumatol. 2018;36(Suppl 113):3–23.\nRudnicka L, Czuwara J, Barusińska A, Nowicka U, Makieła B, Jabłonska S. Implications for the use of topoisomerase I inhibitors in treatment of patients with systemic sclerosis. Ann N Y Acad Sci. 1996;803:318–20.\nGünther J, Rademacher J, van Laar JM, Siegert E, Riemekasten G. Functional autoantibodies in systemic sclerosis. Semin Immunopathol. 2015;37:529–42.\nMihai C, Tervaert JW. Anti-endothelial cell antibodies in systemic sclerosis. Ann Rheum Dis. 2010;69(2):319–24.\nVahidi Manesh P, Farazmand A, Gharibdoost F, Vanaki N, Mostafaei S, Kavosi H, et al. Downregulation of miR-542-3p contributes to apoptosis resistance in dermal fibroblasts from systemic sclerosis patients via Survivin overexpression. Iran J Allergy Asthma Immunol. 2019;18(2):173–81.\nLagares D, Santos A, Grasberger PE, Liu F, Probst CK, Rahimi RA, et al. Targeted apoptosis of myofibroblasts with the BH3 mimetic ABT-263 reverses established fibrosis. Sci Transl Med. 2017;9(420):eaal3765.",{"VOID":944},"10.1186\u002Fs13075-019-1931-x","PUBLICATION","Auto Verify","https:\u002F\u002Farthritis-research.biomedcentral.com\u002Farticles\u002F10.1186\u002Fs13075-019-1931-x",[949,965,980,995,1008,1021,1034,1047,1060],{"id":950,"sortIndex":32,"researcher":28,"roles":951,"affiliations":953,"properties":962,"displayName":964,"givenName":28,"familyName":28},"a24a6c68-fa07-4d81-a39b-2e0b8b8e72da",[952],"AUTHOR",[954],{"id":955,"sortIndex":32,"affiliation":956,"properties":28},"c3e21b73-96fc-4e04-a8a5-7ec9ececfed0",{"id":955,"createTime":28,"updateTime":28,"relativeEntities":957,"slug":28,"properties":958,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":961,"statistic":28},[],{"title":959},{"VI":960},"Scleroderma Unit, Department of Medicine, Surgery and Neurosciences, University of Siena, Siena, Italy",[],{"title":963},{"VI":964},"Claudio 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Tissue Analysis in Clinical Studies",{"VOID":1107},"Bresnihan B, Tak PP: Synovial tissue analysis in rheumatoid arthritis. Balliere's Clini Rheumatol. 1999, 13: 85-99.\nCunnane G, Grehan S, Geoghegan S, et al: Serum amyloid A in the assessment of early inflammatory arthritis. J Rheumatol . 1999,\nSteel DM, Whitehead AS: The major acute phase reactants: C-reactive protein, serum amyloid P component and serum amyloid A protein. Immunology Today. 1994, 15: 81-88. 10.1016\u002F0167-5699(94)90138-4.",{"VOID":1109},"10.1186\u002Far49","2025-01-08T20:52:45.247+00:00","https:\u002F\u002Farthritis-research.biomedcentral.com\u002Farticles\u002F10.1186\u002Far49",[1113],{"id":1114,"sortIndex":32,"researcher":28,"roles":1115,"affiliations":1116,"properties":1125,"displayName":1127,"givenName":28,"familyName":28},"417c707a-b44d-4c2a-9bd7-265fef799c31",[952],[1117],{"id":1118,"sortIndex":32,"affiliation":1119,"properties":28},"2b048f58-9931-4a1d-8f9d-518c24e328b5",{"id":1118,"createTime":28,"updateTime":28,"relativeEntities":1120,"slug":28,"properties":1121,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1124,"statistic":28},[],{"title":1122},{"VI":1123},"St Vincent's Hospital, Dublin, Ireland.",[],{"title":1126},{"VI":1127},"Barry Bresnihan",{"url":1111,"publisher":1129,"properties":1142},{"id":868,"createTime":869,"updateTime":870,"relativeEntities":1130,"slug":872,"properties":1131,"entityType":25,"verifyStatus":878,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":32,"subjectFields":1134,"manageAffiliations":1135,"indexDatabases":1136,"url":28,"thumbnailPath":28,"statistic":1137,"gsStatistic":28,"type":28,"analyzePriority":28},[],{"title":1132,"eissn":1133},{"EN":875},{"VOID":877},[],[],[],{"impactFactor":32,"impactFactorByYear":1138,"i10Index":889,"i10IndexLast5Year":600,"totalPublication":890,"totalPublicationByYear":1139,"totalCitation":899,"totalCitationByYear":1140,"totalCitationPerPublication":914,"totalCitationPerPublicationByYear":1141,"hindexLast5Year":434,"hindex":434},{"2012":884,"2013":588,"2015":106,"2016":120,"2017":173,"2018":885,"2019":886,"2020":172,"2021":887,"2022":888,"2023":173},{"1999":892,"2000":430,"2001":893,"2002":894,"2010":132,"2011":134,"2013":40,"2014":201,"2015":127,"2016":895,"2017":452,"2018":896,"2019":897,"2020":452,"2021":898,"2022":575,"2023":362,"2024":152},{"1999":40,"2000":901,"2001":902,"2002":903,"2010":904,"2011":905,"2014":129,"2015":906,"2016":907,"2017":908,"2018":909,"2019":910,"2020":911,"2021":912,"2022":913},{"1999":513,"2000":916,"2001":366,"2002":532,"2010":917,"2011":918,"2014":462,"2015":919,"2016":920,"2017":921,"2018":922,"2019":923,"2020":924,"2021":189,"2022":925},{"pages":1143,"volume":1145},{"VOID":1144},"1-24",{"VOID":1146},"1","1999-11-15",1999,[],{"id":1151,"createTime":1152,"updateTime":1153,"relativeEntities":1154,"slug":1155,"properties":1156,"entityType":945,"verifyStatus":26,"verifyTime":1153,"verifyNote":946,"languages":28,"translateLanguages":28,"viewCount":32,"primaryUrl":1163,"fullTextUrl":28,"authors":1164,"publicationType":1073,"publisherRelationship":1180,"citationCount":28,"citationInfo":28,"publishDate":1199,"publishYear":1200,"citationAnalyzeStatus":878,"lastCitationAnalyze":28,"indexDatabases":1201,"openAccess":28,"references":28,"isForceReanalyzing":1096},"00ce000d-eb40-4dac-9886-51ef2c7e9332","2024-01-15T20:18:28.952+00:00","2025-01-09T21:51:59.638+00:00",[],"Association-of-MHC-and-rheumatoid-arthritis-Why-is-rheumatoid-arthritis-associated-with-the-MHC-genetic-region-An-introduction",{"title":1157,"references":1159,"doi":1161},{"EN":1158},"Association of MHC and rheumatoid arthritis: Why is rheumatoid arthritis associated with the MHC genetic region? An introduction",{"VOID":1160},"Taneja V, David CS: Regulatory role of HLA class II molecules in animal models of RA: studies on transgenic\u002Fknockout mice. Arthritis Res. 2000, 2: 205-207. 10.1186\u002Far88.\nFugger L, Svejgaard A: HLA-DR4 and rheumatoid arthritis: studies in mice and men. Arthritis Res. 2000, 2: 208-211. 10.1186\u002Far89.\nWeyand CM, Goronzy JJ: HLA polymorphisms in phenotypic variants of rheumatoid arthritis. Arthritis Res. 2000, 2: 212-216. 10.1186\u002Far90.\nRoudier J: Association of RA with HLA-DR4: the role of repertoire selection. Arthritis Res. 2000, 2: 217-220. 10.1186\u002Far91.\nJirholt J, Cook A, Emahazion T: Genetic linkage analysis of collagen-induced arthritis in the mouse. Eur J Immunol . 1998, 28: 3321-3328. 10.1002\u002F(SICI)1521-4141(199810)28:10\u003C3321::AID-IMMU3321>3.0.CO;2-M.\nRosloniec EF, Brand DD, Whittington KB, Stuart JM, Ciubotaru M, Ward ES: Vaccination with a recombinant V alpha domain of a TCR prevents the development of collagen-induced arthritis. J Immunol. 1995, 155: 4504-4511.\nGoronzy JJ, Bartz Bazzanella P, Hu W, Jendro MC, Walser Kuntz DR, Weyand CM: Dominant clonotypes in the repertoire of peripheral CD4+ T cells in rheumatoid arthritis. J Clin Invest. 1994, 94: 2068-2076.\nKawahito Y, Cannon GW, Gulko PS: Localization of quantitative trait loci regulating adjuvant-induced arthritis in rats: evidence for genetic factors common to multiple autoimmune diseases. J Immunol. 1998, 161: 4411-4419.\nVingsbo C, Sahlstrand P, Brun JG, Jonsson R, Saxne T, Holmdahl R: Pristane-induced arthritis in rats: a new model for rheumatoid arthritis with a chronic disease course influenced by both major histocompatibility complex and non-major histocompatibility complex genes. Am J Pathol. 1996, 149: 1675-1683.",{"VOID":1162},"10.1186\u002Far87","https:\u002F\u002Farthritis-research.biomedcentral.com\u002Farticles\u002F10.1186\u002Far87",[1165],{"id":1166,"sortIndex":32,"researcher":28,"roles":1167,"affiliations":1168,"properties":1177,"displayName":1179,"givenName":28,"familyName":28},"76eef83b-81c4-4bea-a214-4b1e57780c6c",[952],[1169],{"id":1170,"sortIndex":32,"affiliation":1171,"properties":28},"4b8762b8-7335-49d7-963b-9a32b6a6becc",{"id":1170,"createTime":28,"updateTime":28,"relativeEntities":1172,"slug":28,"properties":1173,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1176,"statistic":28},[],{"title":1174},{"EN":1175},"Lund University, Lund, Sweden",[],{"title":1178},{"VI":1179},"Rikard Holmdahl",{"url":1163,"publisher":1181,"properties":1194},{"id":868,"createTime":869,"updateTime":870,"relativeEntities":1182,"slug":872,"properties":1183,"entityType":25,"verifyStatus":878,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":32,"subjectFields":1186,"manageAffiliations":1187,"indexDatabases":1188,"url":28,"thumbnailPath":28,"statistic":1189,"gsStatistic":28,"type":28,"analyzePriority":28},[],{"title":1184,"eissn":1185},{"EN":875},{"VOID":877},[],[],[],{"impactFactor":32,"impactFactorByYear":1190,"i10Index":889,"i10IndexLast5Year":600,"totalPublication":890,"totalPublicationByYear":1191,"totalCitation":899,"totalCitationByYear":1192,"totalCitationPerPublication":914,"totalCitationPerPublicationByYear":1193,"hindexLast5Year":434,"hindex":434},{"2012":884,"2013":588,"2015":106,"2016":120,"2017":173,"2018":885,"2019":886,"2020":172,"2021":887,"2022":888,"2023":173},{"1999":892,"2000":430,"2001":893,"2002":894,"2010":132,"2011":134,"2013":40,"2014":201,"2015":127,"2016":895,"2017":452,"2018":896,"2019":897,"2020":452,"2021":898,"2022":575,"2023":362,"2024":152},{"1999":40,"2000":901,"2001":902,"2002":903,"2010":904,"2011":905,"2014":129,"2015":906,"2016":907,"2017":908,"2018":909,"2019":910,"2020":911,"2021":912,"2022":913},{"1999":513,"2000":916,"2001":366,"2002":532,"2010":917,"2011":918,"2014":462,"2015":919,"2016":920,"2017":921,"2018":922,"2019":923,"2020":924,"2021":189,"2022":925},{"pages":1195,"volume":1197},{"VOID":1196},"1-2",{"VOID":1198},"2","2000-04-27",2000,[],{"id":1203,"createTime":1204,"updateTime":1205,"relativeEntities":1206,"slug":1207,"properties":1208,"entityType":945,"verifyStatus":26,"verifyTime":1217,"verifyNote":946,"languages":28,"translateLanguages":28,"viewCount":32,"primaryUrl":1218,"fullTextUrl":28,"authors":1219,"publicationType":1073,"publisherRelationship":1360,"citationCount":28,"citationInfo":28,"publishDate":1379,"publishYear":1380,"citationAnalyzeStatus":878,"lastCitationAnalyze":28,"indexDatabases":1381,"openAccess":28,"references":28,"isForceReanalyzing":1096},"00ef5ee3-8eda-4e23-9473-a9f9d7bffbf3","2024-02-20T15:14:01.758+00:00","2025-01-03T05:19:50.908+00:00",[],"Social-media-for-arthritis-related-comparative-effectiveness-and-safety-research-and-the-impact-of-direct-to-consumer-advertising",{"abstract":1209,"title":1211,"references":1213,"doi":1215},{"EN":1210},"Social media may complement traditional data sources to answer comparative effectiveness\u002Fsafety questions after medication licensure. The Treato platform was used to analyze all publicly available social media data including Facebook, blogs, and discussion boards for posts mentioning inflammatory arthritis (e.g. rheumatoid, psoriatic). Safety events were self-reported by patients and mapped to medical ontologies, resolving synonyms. Disease and symptom-related treatment indications were manually redacted. The units of analysis were unique terms in posts. Pre-specified conditions (e.g. herpes zoster (HZ)) were selected based upon safety signals from clinical trials and reported as pairwise odds ratios (ORs); drugs were compared with Fisher’s exact test. Empirically identified events were analyzed using disproportionality analysis and reported as relative reporting ratios (RRRs). The accuracy of a natural language processing (NLP) classifier to identify cases of shingles associated with arthritis medications was assessed. As of October 2015, there were 785,656 arthritis-related posts. Posts were predominantly US posts (75%) from patient authors (87%) under 40 years of age (61%). For HZ posts (n = 1815), ORs were significantly increased with tofacitinib versus other rheumatoid arthritis therapies. ORs for mentions of perforated bowel (n = 13) were higher with tocilizumab versus other therapies. RRRs associated with tofacitinib were highest in conditions related to baldness and hair regrowth, infections and cancer. The NLP classifier had a positive predictive value of 91% to identify HZ. There was a threefold increase in posts following television direct-to-consumer advertisement (p = 0.04); posts expressing medication safety concerns were significantly more frequent than favorable posts. Social media is a challenging yet promising data source that may complement traditional approaches for comparative effectiveness research for new medications.",{"EN":1212},"Social media for arthritis-related comparative effectiveness and safety research and the impact of direct-to-consumer advertising",{"VOID":1214},"Jain G, Sharma M. Social Media: A Review. In: Satapathy S, Mandal J, Udgata S, Bhateja V. (eds) Information Systems Design and Intelligent Applications. Advances in Intelligent Systems and Computing, vol 433. Springer: New Delhi; 2016. p. 387-95.\nLober WB, Flowers JL. Consumer empowerment in health care amid the internet and social media. Semin Oncol Nurs. 2011;27(3):169–82.\nMoorhead SA, Hazlett DE, Harrison L, Carroll JK, Hoving C. A new dimension of health care: systematic review of the uses, benefits, and limitations of social media for health communication. J Med Internet Res. 2013;15(4), e85.\nO'Neill RT, Szarfman A. Some FDA perspectives on data mining for pediatric safety assessment. Workshop on adverse drug events in pediatrics. Curr Ther Res Clin Exp. 2001;62:650–63.\nhttps:\u002F\u002Ftreato.com\u002F. Accessed 20 Feb 2017.\nhttp:\u002F\u002Fcorp.treato.com\u002Ftechnology. Accessed 20 Feb 2017.\nVan Holle L, Bauchau V. The upper bound to the relative reporting ratio–a measure of the impact of the violation of hidden assumptions underlying some disproportionality methods used in signal detection. Pharmacoepidemiol Drug Saf. 2014;23(8):787–94.\nEvans SJ, Waller PC, Davis S. Use of proportional reporting ratios (PRRs) for signal generation from spontaneous adverse drug reaction reports. Pharmacoepidemiol Drug Saf. 2001;10(6):483–6.\nThe Healthcare Hashtag Project. Symplur. N.p., n.d. Web. 26 May 2016.\nKim K, Kwon N. Profile of e-patients: analysis of their cancer information-seeking from a national survey. J Health Commun. 2010;15(7):712–33.\nRajagopalan MS, Khanna VK, Leiter Y, Stott M, Showalter TN, Dicker AP, et al. Patient-oriented cancer information on the internet: a comparison of Wikipedia and a professionally maintained database. J Oncol Pract. 2011;7(5):319–23.\nNordqvist C, Hanberger L, Timpka T, Nordfeldt S. Health professionals' attitudes towards using a Web 2.0 portal for child and adolescent diabetes care: qualitative study. J Med Internet Res. 2009;11(2):e12.\nGreene JA, Choudhry NK, Kilabuk E, Shrank WH. Online social networking by patients with diabetes: a qualitative evaluation of communication with Facebook. J Gen Intern Med. 2011;26(3):287–92.\nSanford A. “I can air my feelings instead of eating them”: blogging as social support for the morbidly obese. Communication Studies. 2010;61(5):567–84.\nSarker A, Ginn R, Nikfarjam A, O'Connor K, Smith K, Jayaraman S, et al. Utilizing social media data for pharmacovigilance: a review. J Biomed Inform. 2015;54:202–12.\nYang CC, Yang H, Jiang L. Postmarketing drug safety surveillance using publicly available health-consumer-contributed content in social media. TMIS. 2014;5(1):2.\nPierce CE, et al. Evaluation of Facebook and Twitter Monitoring to Detect Safety Signals for Medical Products: An Analysis of Recent FDA Safety Alerts. Drug Safety. 2017;1-15.\nBahk CY, Cumming M, Paushter L, Madoff LC, Thomson A, Brownstein JS. Publicly available online tool facilitates real-time monitoring of vaccine conversations and sentiments. Health Aff (Millwood). 2016;35(2):341–7.\nTopaz M, Lai K, Dhopeshwarkar N, Seger DL, Sa'adon R, Goss F, et al. Clinicians' reports in electronic health records versus patients' concerns in social media: a pilot study of adverse drug reactions of aspirin and atorvastatin. Drug Saf. 2016;39(3):241–50.\nLedford C, Anderson L. Online social networking in discussions of risk: applying the CAUSE model in a content analysis of Facebook. Health Risk Soc. 2013;15(3):251–64.\nHale TM, Pathipati AS, Zan S, Jethwani K. Representation of health conditions on Facebook: content analysis and evaluation of user engagement. J Med Internet Res. 2014;16(8), e182.\nGreene JA, Kesselheim AS. Pharmaceutical marketing and the new social media. N Engl J Med. 2010;363(22):2087–9.\nhttp:\u002F\u002Fpharmamkting.blogspot.com\u002F2016\u002F03\u002Fannual-spending-on-directto-consumer.html. Accessed 20 Feb 2017.\nhttps:\u002F\u002Fwww.emarketer.com\u002FReport\u002FUS-Healthcare-Pharma-Industry-2016-Digital-Ad-Spending-Forecast-Trends\u002F2001786. Accessed 20 Feb 2017.\nBravo CA, Hoffman-Goetz L. Social Media and Men’s Health A Content Analysis of Twitter Conversations During the 2013 Movember Campaigns in the United States, Canada, and the United Kingdom. Am J Mens Health. 2015;1557988315617826.\nTyrawski J, DeAndrea DC. Pharmaceutical companies and their drugs on social media: a content analysis of drug information on popular social media sites. J Med Internet Res. 2015;17(6), e130.\nSzarfman A, Chen M, Blum MD. More on fluoroquinolone antibiotics and tendon rupture. N Engl J Med. 1995;332(3):193.\nSullivan HW, O'Donoghue AC, Amie C, Aikin KJ. Communicating benefit and risk information in direct-to-consumer print advertisements: a randomized study. Ther Innov Regul Sci. 2015;49(4):493–502.\nWest SL, Squiers LB, McCormack L, Southwell BG, Brouwer ES, Ashok M, et al. Communicating quantitative risks and benefits in promotional prescription drug labeling or print advertising. Pharmacoepidemiol Drug Saf. 2013;22(5):447–58.\nSullivan HW, Campbell M. Do prescription drug ads tell consumers enough about benefits and side effects? Results from the Health Information National Trends Survey, Fourth Administration. J Health Commun. 2015;20(12):1391–6.\nDuggan M. The Demographics of Social Media Users. Pew Research Center: Internet, Science & Tech. Pew Research Center, 19 Aug. 2015. Web. 20 Feb 2017.\nChou WY, Hunt YM, Beckjord EB, Moser RP, Hesse BW. Social media use in the United States: implications for health communication. J Med Internet Res. 2009;11(4), e48.\nMartinez O, Wu E, Shultz AZ, Capote J, Lopez Rios J, Sandfort T, et al. Still a hard-to-reach population? Using social media to recruit Latino gay couples for an HIV intervention adaptation study. J Med Internet Res. 2014;16(4), e113.\nKlint F. Twitter CEO Jack Dorsey Hints Its 140 Character Limit Could End. Wired. Conde Nast, 05 Jan. 2016. Web. 20 Feb 2017. http:\u002F\u002Fwww.wired.com\u002F2016\u002F01\u002Ftwitter-ceo-jack-dorsey-hints-its-140-character-limit-could-end\u002F. 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and Macrophages in Synovitis: Villains or Victims?",{"VOID":1392},"Hahn G, Stuhlmüller B, Hain N, Kalden JR, Pfizenmaier K, Burmester GR: Modulation of monocyte activation in patients with rheumatoid arthritis by leukapheresis therapy. J Clin Invest. 1993, 91: 862-870.\nBurmester GR, Stuhlmuller B, Keyszer G, Kinne RW: Mononuclear phagocytes and rheumatoid synovitis. Mastermind or workhorse in arthritis? . Arthritis Rheum. 1997, 40: 5-18.\nDörffel Y, Lätsch C, Stuhlmüller B, et al: Pre-activated peripheral blood monocytes in patients with essential hypertension. Hypertension. 1999\nStuhlmüller B, Ungethüm U, Scholze S, Backhaus M, Kinne RW, Burmester GR: Differential gene expression of activated and non-activated monocytes from patients with rheumatoid arthritis. . 1999\nSeki T, Selby J, Häupl T, Winchester R: Use of differential subtraction method to identify genes that characterize the phenotype of cultured rheumatoid arthritis synoviocytes. Arthritis Rheum. 1998, 41: 1356-1364. 10.1002\u002F1529-0131(199808)41:8\u003C1356::AID-ART4>3.0.CO;2-X.\nHäupl T, Ungethüm U, Bramlage C, et al: Bone morphogenetic proteins in synovial tissue from RA, OA and normal joints: implications for protective mechanisms. Arthritis Rheum. 1998, 41(suppl): S195-\nKeyszer G, Redlich A, Häupl T, et al: Differential expression of cathepsins B and L compared with matrix metalloproteinases and their respective inhibitors in rheumatoid arthritis and osteoarthritis: a parallel investigation by semiquantitative reverse transcriptase-polymerase chain reaction and immunohistochemistry. Arthritis Rheum. 1998, 41: 1378-1387. 10.1002\u002F1529-0131(199808)41:8\u003C1378::AID-ART6>3.0.CO;2-J.\nUngethüm U, Häupl T, Burmester G-R: Gene products identified by RDA subtraction in rheumatoid arthritis. J Autoimmunity. 1999, (suppl):",{"VOID":1394},"10.1186\u002Far29","https:\u002F\u002Farthritis-research.biomedcentral.com\u002Farticles\u002F10.1186\u002Far29",[1397,1412,1425],{"id":1398,"sortIndex":32,"researcher":28,"roles":1399,"affiliations":1400,"properties":1409,"displayName":1411,"givenName":28,"familyName":28},"60dbe76a-5f85-4795-b663-7f1bb6ca496c",[952],[1401],{"id":1402,"sortIndex":32,"affiliation":1403,"properties":28},"92900550-262f-42fb-8467-4bab8dfec020",{"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 Rheumatology, Humboldt University of Berlin, Germany",[],{"title":1410},{"VI":1411},"Gerd R Burmester",{"id":1413,"sortIndex":40,"researcher":28,"roles":1414,"affiliations":1415,"properties":1422,"displayName":1424,"givenName":28,"familyName":28},"07e24c4c-b6cd-40c4-ba06-6e3431a9daea",[952],[1416],{"id":1402,"sortIndex":32,"affiliation":1417,"properties":28},{"id":1402,"createTime":28,"updateTime":28,"relativeEntities":1418,"slug":28,"properties":1419,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1421,"statistic":28},[],{"title":1420},{"VI":1407},[],{"title":1423},{"VI":1424},"Thomas Häupl",{"id":1426,"sortIndex":123,"researcher":28,"roles":1427,"affiliations":1428,"properties":1435,"displayName":1437,"givenName":28,"familyName":28},"d75faff8-a54e-4a91-958a-7b3bc49f8bfd",[952],[1429],{"id":1402,"sortIndex":32,"affiliation":1430,"properties":28},{"id":1402,"createTime":28,"updateTime":28,"relativeEntities":1431,"slug":28,"properties":1432,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1434,"statistic":28},[],{"title":1433},{"VI":1407},[],{"title":1436},{"VI":1437},"Bruno Stuhlmüller",{"url":1395,"publisher":1439,"properties":1452},{"id":868,"createTime":869,"updateTime":870,"relativeEntities":1440,"slug":872,"properties":1441,"entityType":25,"verifyStatus":878,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":32,"subjectFields":1444,"manageAffiliations":1445,"indexDatabases":1446,"url":28,"thumbnailPath":28,"statistic":1447,"gsStatistic":28,"type":28,"analyzePriority":28},[],{"title":1442,"eissn":1443},{"EN":875},{"VOID":877},[],[],[],{"impactFactor":32,"impactFactorByYear":1448,"i10Index":889,"i10IndexLast5Year":600,"totalPublication":890,"totalPublicationByYear":1449,"totalCitation":899,"totalCitationByYear":1450,"totalCitationPerPublication":914,"totalCitationPerPublicationByYear":1451,"hindexLast5Year":434,"hindex":434},{"2012":884,"2013":588,"2015":106,"2016":120,"2017":173,"2018":885,"2019":886,"2020":172,"2021":887,"2022":888,"2023":173},{"1999":892,"2000":430,"2001":893,"2002":894,"2010":132,"2011":134,"2013":40,"2014":201,"2015":127,"2016":895,"2017":452,"2018":896,"2019":897,"2020":452,"2021":898,"2022":575,"2023":362,"2024":152},{"1999":40,"2000":901,"2001":902,"2002":903,"2010":904,"2011":905,"2014":129,"2015":906,"2016":907,"2017":908,"2018":909,"2019":910,"2020":911,"2021":912,"2022":913},{"1999":513,"2000":916,"2001":366,"2002":532,"2010":917,"2011":918,"2014":462,"2015":919,"2016":920,"2017":921,"2018":922,"2019":923,"2020":924,"2021":189,"2022":925},{"pages":1453,"volume":1454},{"VOID":1144},{"VOID":1146},[],{"id":1457,"createTime":1458,"updateTime":1459,"relativeEntities":1460,"slug":1461,"properties":1462,"entityType":945,"verifyStatus":26,"verifyTime":1459,"verifyNote":946,"languages":28,"translateLanguages":28,"viewCount":32,"primaryUrl":1471,"fullTextUrl":28,"authors":1472,"publicationType":1073,"publisherRelationship":1640,"citationCount":28,"citationInfo":28,"publishDate":1658,"publishYear":1659,"citationAnalyzeStatus":878,"lastCitationAnalyze":28,"indexDatabases":1660,"openAccess":28,"references":28,"isForceReanalyzing":1096},"0172f1c7-f1e7-40b4-8ef9-d6aeb0dc3925","2024-02-13T17:25:34.764+00:00","2024-12-25T01:10:15.898+00:00",[],"Serum-TNF%CE%B1-levels-at-24-h-after-certolizumab-pegol-predict-effectiveness-at-week-12-in-patients-with-rheumatoid-arthritis-from-TSUBAME-study",{"abstract":1463,"title":1465,"references":1467,"doi":1469},{"EN":1464},"To estimate the relationship between serum TNFα, IL-6, and serum CZP levels and the clinical response to CZP in RA patients in the TSUBAME study. One hundred patients with RA who received CZP were enrolled and multiple clinical parameters, serum TNFα, IL-6, and CZP levels, were assessed at 0, 24, and 48 h and 12 weeks after first administration of CZP. The CZP therapy significantly improved the DAS28(ESR) at 12 weeks. Serum TNFα and IL-6 levels significantly decreased from baseline at 24 h after the first administration of CZP. Serum TNFα levels at baseline were not related to clinical parameters at baseline and improvement in DAS28(ESR) at week 12 of the CZP therapy. However, serum levels of CZP at 24 h were strongly and negatively correlated with TNFα levels at 24 h, which were negatively correlated with improved rate in DAS28(ESR) at week 12. Only serum levels of TNFα, but not IL-6, at 24 h had a negative correlation with achievement of DAS28(ESR)\u003C2.6 at week 12 by the multivariate analysis (odds ratio 0.01, 95% confidence interval 0.04e−2–0.22, p \u003C 0.01). A receiver operating characteristic analysis was conducted to estimate the achievement of DAS28(ESR)\u003C2.6 at week 12 after the CZP therapy and cut-off value of 0.76 pg\u002Fml for serum levels of TNFα at 24 h was yielded (area under the curve=0.75). DAS28(ESR)\u003C2.6 was achieved at week 12 significantly more patients with lower serum TNF levels (≦0.76 pg\u002Fml) at 24 h than those with higher TNF levels. CZP was highly effective in RA patients who had low serum TNFα levels at 24 h after the initial administration of CZP. Therefore, we propose that serum TNFα levels at 24 h could serve as a biomarker predicting effectiveness to CZP at week 12 in patients with RA. Clinical trial registration number: \n                  UMIN ID:000022831\n                  \n                ",{"EN":1466},"Serum TNFα levels at 24 h after certolizumab pegol predict effectiveness at week 12 in patients with rheumatoid arthritis from TSUBAME study",{"VOID":1468},"Kvien TK. Epidemiology and burden of illness of rheumatoid arthritis. Pharmacoeconomics. 2004;22(2 Suppl 1):1–12. https:\u002F\u002Fdoi.org\u002F10.2165\u002F00019053-200422001-00002.\nLee DM, Weinblatt ME. Rheumatoid arthritis. Lancet. 2001;358(9285):903–11. https:\u002F\u002Fdoi.org\u002F10.1016\u002FS0140-6736(01)06075-5.\nSmolen JS, et al. Rheumatoid arthritis. Nat Rev Dis Primers. 2018;4:18001.\nMcInnes IB, Buckley CD, Isaacs JD. Cytokines in rheumatoid arthritis - shaping the immunological landscape. Nat Rev Rheumatol. 2016;12(1):63–8. https:\u002F\u002Fdoi.org\u002F10.1038\u002Fnrrheum.2015.171.\nMaini R, et al. Infliximab (chimeric anti-tumour necrosis factor alpha monoclonal antibody) versus placebo in rheumatoid arthritis patients receiving concomitant methotrexate: a randomised phase III trial. ATTRACT Study Group. Lancet. 1999;354(9194):1932–9.\nWeinblatt ME, Keystone EC, Furst DE, Moreland LW, Weisman MH, Birbara CA, et al. Adalimumab, a fully human anti-tumor necrosis factor alpha monoclonal antibody, for the treatment of rheumatoid arthritis in patients taking concomitant methotrexate: the ARMADA trial. Arthritis Rheum. 2003;48(1):35–45. https:\u002F\u002Fdoi.org\u002F10.1002\u002Fart.10697.\nNesbitt A, Fossati G, Bergin M, Stephens P, Stephens S, Foulkes R, et al. Mechanism of action of certolizumab pegol (CDP870): in vitro comparison with other anti-tumor necrosis factor alpha agents. Inflamm Bowel Dis. 2007;13(11):1323–32. https:\u002F\u002Fdoi.org\u002F10.1002\u002Fibd.20225.\nvan der Heide A, Jacobs JW, Bijlsma JW, Heurkens AH, van Booma-Frankfort C, van der Veen M, et al. The effectiveness of early treatment with \"second-line\" antirheumatic drugs. A randomized, controlled trial. Ann Intern Med. 1996;124(8):699–707. https:\u002F\u002Fdoi.org\u002F10.7326\u002F0003-4819-124-8-199604150-00001.\nTanaka Y, Yamanaka H, Ishiguro N, Miyasaka N, Kawana K, Hiramatsu K, et al. Adalimumab discontinuation in patients with early rheumatoid arthritis who were initially treated with methotrexate alone or in combination with adalimumab: 1 year outcomes of the HOPEFUL-2 study. RMD Open. 2016;2(1):e000189. https:\u002F\u002Fdoi.org\u002F10.1136\u002Frmdopen-2015-000189.\nTracey D, Klareskog L, Sasso EH, Salfeld JG, Tak PP. Tumor necrosis factor antagonist mechanisms of action: a comprehensive review. Pharmacol Ther. 2008;117(2):244–79. https:\u002F\u002Fdoi.org\u002F10.1016\u002Fj.pharmthera.2007.10.001.\nKeystone E, Heijde Dv, Mason D Jr, Landewé R, Vollenhoven RV, Combe B, et al. Certolizumab pegol plus methotrexate is significantly more effective than placebo plus methotrexate in active rheumatoid arthritis: findings of a fifty-two-week, phase III, multicenter, randomized, double-blind, placebo-controlled, parallel-group study. Arthritis Rheum. 2008;58(11):3319–29. https:\u002F\u002Fdoi.org\u002F10.1002\u002Fart.23964.\nYamamoto K, Takeuchi T, Yamanaka H, Ishiguro N, Tanaka Y, Eguchi K, et al. Efficacy and safety of certolizumab pegol plus methotrexate in Japanese rheumatoid arthritis patients with an inadequate response to methotrexate: the J-RAPID randomized, placebo-controlled trial. Mod Rheumatol. 2014;24(5):715–24. https:\u002F\u002Fdoi.org\u002F10.3109\u002F14397595.2013.864224.\nArnett FC, Edworthy SM, Bloch DA, McShane D, Fries JF, Cooper NS, et al. The American Rheumatism Association 1987 revised criteria for the classification of rheumatoid arthritis. Arthritis Rheum. 1988;31(3):315–24. https:\u002F\u002Fdoi.org\u002F10.1002\u002Fart.1780310302.\nAletaha D, et al. 2010 Rheumatoid arthritis classification criteria: an American College of Rheumatology\u002FEuropean League Against Rheumatism collaborative initiative. Arthritis Rheum. 2010;62(9):2569–81. https:\u002F\u002Fdoi.org\u002F10.1002\u002Fart.27584.\nPrevoo ML, van 't Hof M, Kuper HH, van Leeuwen M, van de Putte L, van Riel P. 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(1):44–8. https:\u002F\u002Fdoi.org\u002F10.1002\u002Fart.1780380107.\nKayakabe K, et al. Interleukin-1beta measurement in stimulated whole blood cultures is useful to predict response to anti-TNF therapies in rheumatoid arthritis. Rheumatology (Oxford). 2012;51(9):1639–43.\nChen DY, Chen YM, Chen HH, Hsieh CW, Lin CC, Lan JL. Increasing levels of circulating Th17 cells and interleukin-17 in rheumatoid arthritis patients with an inadequate response to anti-TNF-alpha therapy. Arthritis Res Ther. 2011;13(4):R126. https:\u002F\u002Fdoi.org\u002F10.1186\u002Far3431.\nAyubi E, Safiri S. Serum interleukin-6 and survivin levels predict clinical response to etanercept treatment in patients with established rheumatoid arthritis: methodological issues. Mod Rheumatol. 2018;28(2):380. https:\u002F\u002Fdoi.org\u002F10.1080\u002F14397595.2017.1387224.\nZhang B, Jiang W. IL-1beta, IL-17A, CRP and biologics history might serve as potential markers for clinical response to etanercept in rheumatoid arthritis patients. Inflammopharmacology. 2019;27(6):1123–30.\nTakeuchi T, Miyasaka N, Tatsuki Y, Yano T, Yoshinari T, Abe T, et al. Baseline tumour necrosis factor alpha levels predict the necessity for dose escalation of infliximab therapy in patients with rheumatoid arthritis. Ann Rheum Dis. 2011;70(7):1208–15. https:\u002F\u002Fdoi.org\u002F10.1136\u002Fard.2011.153023.\nAtsumi T, et al. Clinical benefit of 1-year certolizumab pegol (CZP) add-on therapy to methotrexate treatment in patients with early rheumatoid arthritis was observed following CZP discontinuation: 2-year results of the C-OPERA study, a phase III randomised trial. Ann Rheum Dis. 2017;76(8):1348–56.\nCarron P, Lambert B, van Praet L, de Vos F, Varkas G, Jans L, et al. Scintigraphic detection of TNF-driven inflammation by radiolabelled certolizumab pegol in patients with rheumatoid arthritis and spondyloarthritis. RMD Open. 2016;2(1):e000265. https:\u002F\u002Fdoi.org\u002F10.1136\u002Frmdopen-2016-000265.\nBerkhout LC, et al. The effect of certolizumab drug concentration and anti-drug antibodies on TNF neutralisation. Clin Exp Rheumatol. 2020;38(2):306–13.\nvan Schie KA, et al. Therapeutic TNF inhibitors can differentially stabilize trimeric TNF by inhibiting monomer exchange. Sci Rep. 2016;6:32747.\nPalframan R, Airey M, Moore A, Vugler A, Nesbitt A. Use of biofluorescence imaging to compare the distribution of certolizumab pegol, adalimumab, and infliximab in the inflamed paws of mice with collagen-induced arthritis. J Immunol Methods. 2009;348(1-2):36–41. https:\u002F\u002Fdoi.org\u002F10.1016\u002Fj.jim.2009.06.009.",{"VOID":1470},"10.1186\u002Fs13075-021-02547-2","https:\u002F\u002Farthritis-research.biomedcentral.com\u002Farticles\u002F10.1186\u002Fs13075-021-02547-2",[1473,1488,1501,1514,1527,1540,1553,1566,1579,1592,1605,1627],{"id":1474,"sortIndex":32,"researcher":28,"roles":1475,"affiliations":1476,"properties":1485,"displayName":1487,"givenName":28,"familyName":28},"8e025593-6518-471b-9989-89836a4a6ee3",[952],[1477],{"id":1478,"sortIndex":32,"affiliation":1479,"properties":28},"2e55dcdb-a993-48fd-afeb-4f465e98a203",{"id":1478,"createTime":28,"updateTime":28,"relativeEntities":1480,"slug":28,"properties":1481,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1484,"statistic":28},[],{"title":1482},{"VI":1483},"The First Department of Internal Medicine, School of Medicine, University of Occupational and 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lupus erythematosus (SLE) is the paradigm of a multisystem autoimmune disease in which genetic factors strongly influence susceptibility. Through genome scans and congenic dissection, numerous loci associated with lupus susceptibility have been defined and the complexity of the inheritance of this disease has been revealed. In this review, we provide a brief description of animal models of SLE, both spontaneous models and synthetic models, with an emphasis on the B6 congenic model derived from analyses of the NZM2410 strain. A hypothetical model of disease progression that organizes many of the identified SLE susceptibility loci in three distinct biological pathways that interact to mediate disease pathogenesis is also described. We finally discuss our recent fine mapping analysis, which revealed a cluster of loci that actually comprise the Sle1 locus.",{"EN":1671},"Susceptibility genes in the pathogenesis of murine lupus",{"VOID":1673},"Blatt NB, Glick GD: Anti-DNA autoantibodies and systemic lupus erythematosus. 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Arthritis Rheum. 1986, 29: 739-747.\nTakahashi K, Kozono Y, Waldschmidt TJ, Quigg RJ, Baron A, Holers VM: Mouse complement receptors type 1 (CR1;CD35) and type 2 (CR2;CD21): expression on normal B cell subpopulations and decreased levels during the development of autoimmunity in MRL\u002Flpr mice. J Immunol. 1997, 159: 1557-1569.\nBoackle SA, Holers VM, Chen X, Szakonyi G, Karp D, Wakeland EK, Morel L: Cr2, a candidate gene in the murine Sle1c lupus susceptibility locus, encodes a dysfunctional protein. Immunity. 2002, 15: 785-\nProdeus AP, Goerg S, Shen LM, Pozdnyakova OO, Chu L, Alicot EM, Goodnow CC, Carroll MC: A critical role for complement in maintenance of self-tolerance. Immunity. 1998, 9: 721-731.\nRozzo SJ, Allard JD, Choubey D, Vyse TJ, Izui S, Peltz G, Kotzin BL: Evidence for an interferon-inducible gene, Ifi202, in the susceptibility to systemic lupus. Immunity. 2001, 15: 435-443. 10.1016\u002FS1074-7613(01)00196-0.\nWakeland EK, Wandstrat AE, Liu K, Morel L: Genetic dissection of systemic lupus erythematosus. Curr Opin Immunol. 1999, 11: 701-707. 10.1016\u002FS0952-7915(99)00039-4.\nTsao BP, Cantor RM, Kalunian C, Chen C-J, Badsha H, Singh R, Wallace DJ, Kitridou RC, Chen S, Shen N, Song YW, Isenberg DA, Yu C-L, Hahn BH, Rotter JI: Evidence for linkage of a candidate chromosome 1 region to human systemic lupus erythematosus. J ClinInvest. 1997, 99: 725-731.\nRahman ZS, Tin SK, Buenaventura PN, Ho CH, Yap EP, Yong RY, Koh DR: A novel susceptibility locus on chromosome 2 in the (New Zealand Black × New Zealand White)F1 hybrid mouse model of systemic lupus erythematosus. J Immunol. 2002, 168: 3042-3049.\nXie S, Chang S, Yang P, Jacob C, Kaliyaperumal A, Datta SK, Mohan C: Genetic contributions of nonautoimmune SWR mice toward lupus nephritis. J Immunol. 2001, 167: 7141-7149.",{"VOID":1675},"10.1186\u002Far583","2025-02-22T22:55:36.180+00:00","https:\u002F\u002Farthritis-research.biomedcentral.com\u002Farticles\u002F10.1186\u002Far583",[1679,1694,1707],{"id":1680,"sortIndex":32,"researcher":28,"roles":1681,"affiliations":1682,"properties":1691,"displayName":1693,"givenName":28,"familyName":28},"f4ed5db4-a580-4b43-b88a-8c88724bbc39",[952],[1683],{"id":1684,"sortIndex":32,"affiliation":1685,"properties":28},"97652d41-dfda-4370-9b1d-0d4628732263",{"id":1684,"createTime":28,"updateTime":28,"relativeEntities":1686,"slug":28,"properties":1687,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1690,"statistic":28},[],{"title":1688},{"VI":1689},"Center for Immunology, University of Texas Southwestern Medical Center, Dallas, USA",[],{"title":1692},{"VI":1693},"Charles Nguyen",{"id":1695,"sortIndex":40,"researcher":28,"roles":1696,"affiliations":1697,"properties":1704,"displayName":1706,"givenName":28,"familyName":28},"9020bf63-3caf-411c-9cc9-6cfc97326672",[952],[1698],{"id":1684,"sortIndex":32,"affiliation":1699,"properties":28},{"id":1684,"createTime":28,"updateTime":28,"relativeEntities":1700,"slug":28,"properties":1701,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1703,"statistic":28},[],{"title":1702},{"VI":1689},[],{"title":1705},{"VI":1706},"Nisha Limaye",{"id":1708,"sortIndex":123,"researcher":28,"roles":1709,"affiliations":1710,"properties":1717,"displayName":1719,"givenName":28,"familyName":28},"c3ee4f04-3442-4065-b8e9-c9e794460d79",[952],[1711],{"id":1684,"sortIndex":32,"affiliation":1712,"properties":28},{"id":1684,"createTime":28,"updateTime":28,"relativeEntities":1713,"slug":28,"properties":1714,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1716,"statistic":28},[],{"title":1715},{"VI":1689},[],{"title":1718},{"VI":1719},"Edward K Wakeland",{"url":1677,"publisher":1721,"properties":1734},{"id":868,"createTime":869,"updateTime":870,"relativeEntities":1722,"slug":872,"properties":1723,"entityType":25,"verifyStatus":878,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":32,"subjectFields":1726,"manageAffiliations":1727,"indexDatabases":1728,"url":28,"thumbnailPath":28,"statistic":1729,"gsStatistic":28,"type":28,"analyzePriority":28},[],{"title":1724,"eissn":1725},{"EN":875},{"VOID":877},[],[],[],{"impactFactor":32,"impactFactorByYear":1730,"i10Index":889,"i10IndexLast5Year":600,"totalPublication":890,"totalPublicationByYear":1731,"totalCitation":899,"totalCitationByYear":1732,"totalCitationPerPublication":914,"totalCitationPerPublicationByYear":1733,"hindexLast5Year":434,"hindex":434},{"2012":884,"2013":588,"2015":106,"2016":120,"2017":173,"2018":885,"2019":886,"2020":172,"2021":887,"2022":888,"2023":173},{"1999":892,"2000":430,"2001":893,"2002":894,"2010":132,"2011":134,"2013":40,"2014":201,"2015":127,"2016":895,"2017":452,"2018":896,"2019":897,"2020":452,"2021":898,"2022":575,"2023":362,"2024":152},{"1999":40,"2000":901,"2001":902,"2002":903,"2010":904,"2011":905,"2014":129,"2015":906,"2016":907,"2017":908,"2018":909,"2019":910,"2020":911,"2021":912,"2022":913},{"1999":513,"2000":916,"2001":366,"2002":532,"2010":917,"2011":918,"2014":462,"2015":919,"2016":920,"2017":921,"2018":922,"2019":923,"2020":924,"2021":189,"2022":925},{"pages":1735,"volume":1737},{"VOID":1736},"1-9",{"VOID":1738},"4","2002-05-09",2002,[],{"id":1743,"createTime":1744,"updateTime":1745,"relativeEntities":1746,"slug":1747,"properties":1748,"entityType":945,"verifyStatus":26,"verifyTime":1745,"verifyNote":946,"languages":28,"translateLanguages":28,"viewCount":32,"primaryUrl":1755,"fullTextUrl":28,"authors":1756,"publicationType":1073,"publisherRelationship":1772,"citationCount":28,"citationInfo":28,"publishDate":1791,"publishYear":1200,"citationAnalyzeStatus":878,"lastCitationAnalyze":28,"indexDatabases":1792,"openAccess":28,"references":28,"isForceReanalyzing":1096},"01b6990d-b384-4419-97b4-fd65a769825d","2024-01-27T16:34:22.795+00:00","2025-01-08T17:30:18.037+00:00",[],"Whole-genome-scan-of-a-murine-model-of-RA",{"title":1749,"references":1751,"doi":1753},{"EN":1750},"Whole genome scan of a murine model of RA",{"VOID":1752},"Otto JM, Cs-Szabo G, Gallagher J, Velins S, Mikecz K, Buzas EI, Enders JT, Li Y, Olsen BR, Glant TT: Identification of multiple loci linked to inflammation and autoantibody production by a genome scan of a murine model of rheumatoid arthritis. Arthritis Rheum. 2000, 42: 2524-2531.",{"VOID":1754},"10.1186\u002Far-2000-66780","https:\u002F\u002Farthritis-research.biomedcentral.com\u002Farticles\u002F10.1186\u002Far-2000-66780",[1757],{"id":1758,"sortIndex":32,"researcher":28,"roles":1759,"affiliations":1760,"properties":1769,"displayName":1771,"givenName":28,"familyName":28},"692f30da-9501-4c50-a4f8-f51566615ead",[952],[1761],{"id":1762,"sortIndex":32,"affiliation":1763,"properties":28},"0deca7ee-9e35-4def-841a-fb298b8dcf39",{"id":1762,"createTime":28,"updateTime":28,"relativeEntities":1764,"slug":28,"properties":1765,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1768,"statistic":28},[],{"title":1766},{"VI":1767},"Manchester University Medical School, MAnchester, UK",[],{"title":1770},{"VI":1771},"Ali Hajeer",{"url":1755,"publisher":1773,"properties":1786},{"id":868,"createTime":869,"updateTime":870,"relativeEntities":1774,"slug":872,"properties":1775,"entityType":25,"verifyStatus":878,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":32,"subjectFields":1778,"manageAffiliations":1779,"indexDatabases":1780,"url":28,"thumbnailPath":28,"statistic":1781,"gsStatistic":28,"type":28,"analyzePriority":28},[],{"title":1776,"eissn":1777},{"EN":875},{"VOID":877},[],[],[],{"impactFactor":32,"impactFactorByYear":1782,"i10Index":889,"i10IndexLast5Year":600,"totalPublication":890,"totalPublicationByYear":1783,"totalCitation":899,"totalCitationByYear":1784,"totalCitationPerPublication":914,"totalCitationPerPublicationByYear":1785,"hindexLast5Year":434,"hindex":434},{"2012":884,"2013":588,"2015":106,"2016":120,"2017":173,"2018":885,"2019":886,"2020":172,"2021":887,"2022":888,"2023":173},{"1999":892,"2000":430,"2001":893,"2002":894,"2010":132,"2011":134,"2013":40,"2014":201,"2015":127,"2016":895,"2017":452,"2018":896,"2019":897,"2020":452,"2021":898,"2022":575,"2023":362,"2024":152},{"1999":40,"2000":901,"2001":902,"2002":903,"2010":904,"2011":905,"2014":129,"2015":906,"2016":907,"2017":908,"2018":909,"2019":910,"2020":911,"2021":912,"2022":913},{"1999":513,"2000":916,"2001":366,"2002":532,"2010":917,"2011":918,"2014":462,"2015":919,"2016":920,"2017":921,"2018":922,"2019":923,"2020":924,"2021":189,"2022":925},{"pages":1787,"volume":1789},{"VOID":1788},"1-3",{"VOID":1790},"3","2000-02-04",[],{"id":1794,"createTime":1795,"updateTime":1796,"relativeEntities":1797,"slug":1798,"properties":1799,"entityType":945,"verifyStatus":26,"verifyTime":1796,"verifyNote":946,"languages":28,"translateLanguages":28,"viewCount":32,"primaryUrl":1808,"fullTextUrl":28,"authors":1809,"publicationType":1073,"publisherRelationship":1896,"citationCount":28,"citationInfo":28,"publishDate":1913,"publishYear":1380,"citationAnalyzeStatus":878,"lastCitationAnalyze":28,"indexDatabases":1914,"openAccess":28,"references":28,"isForceReanalyzing":1096},"01ddce71-39ed-454a-9712-e29a0b8d35a9","2024-02-13T05:10:03.082+00:00","2025-01-07T12:51:43.177+00:00",[],"Comparative-analyses-of-muscle-MRI-and-muscular-function-in-anti-synthetase-syndrome-patients-and-matched-controls-a-cross-sectional-study",{"abstract":1800,"title":1802,"references":1804,"doi":1806},{"EN":1801},"Magnetic resonance imaging (MRI) of thigh muscles is increasingly used to assess disease activity and damage extent in chronic myositis, but the validity of the findings is not clear. Here, the primary aim was to compare thigh MRI findings in patients having chronic myositis associated with anti-synthetase syndrome (ASS) and in matched healthy controls. Cross-sectional analyses of thigh muscle MRI, muscular function and creatinine kinase (CK) were performed in 68 ASS patients (median disease duration 71 months) and 67 controls matched for age and gender. MRI changes associated with disease activity (edema in muscles and fascia) and damage (fatty replacement and muscle volume reduction) were assessed semiquantitatively, giving a total MRI score of 0–78 (total edema 0–42 and total damage 0–36). ASS patients had higher total MRI score than the matched controls (14.1 versus 3.0; p \u003C 0.001) and less muscle strength (p \u003C 0.001). Muscle edema was more frequent in ASS patients than controls (38% versus 12%), as was fatty replacement (42% versus 4%). In ASS patients, we found that the total edema score correlated with CK, but 23% of the patients with normal CK had score > 18. Muscle compartment analyses in ASS patients showed that muscle edema was most pronounced anteriorly, while fatty replacement dominated posteriorly. This study showed, for the first time, the magnitude of difference in muscle MRI findings between chronic myositis cases and matched controls. In ASS patients, muscle MRI appeared to provide useful complementary information to muscle strength and CK levels in the assessment of myositis.",{"EN":1803},"Comparative analyses of muscle MRI and muscular function in anti-synthetase syndrome patients and matched controls: a cross-sectional study",{"VOID":1805},"Marguerie C, Bunn CC, Beynon HL, Bernstein RM, Hughes JM, So AK, et al. Polymyositis, pulmonary fibrosis and autoantibodies to aminoacyl-tRNA synthetase enzymes. Q J Med. 1990;77(282):1019–38.\nAndersson H, Sem M, Lund MB, Aalokken TM, Gunther A, Walle-Hansen R, et al. Long-term experience with rituximab in anti-synthetase syndrome-related interstitial lung disease. Rheumatology (Oxford). 2015;54(8):1420–8.\nConnors GR, Christopher-Stine L, Oddis CV, Danoff SK. Interstitial lung disease associated with the idiopathic inflammatory myopathies: what progress has been made in the past 35 years? Chest. 2010;138(6):1464–74.\nSolomon J, Swigris JJ, Brown KK. Myositis-related interstitial lung disease and antisynthetase syndrome. J Bras Pneumol. 2011;37(1):100–9.\nLega JC, Fabien N, Reynaud Q, Durieu I, Durupt S, Dutertre M, et al. The clinical phenotype associated with myositis-specific and associated autoantibodies: a meta-analysis revisiting the so-called antisynthetase syndrome. Autoimmun Rev. 2014;13(9):883–91.\nHervier B, Devilliers H, Stanciu R, Meyer A, Uzunhan Y, Masseau A, et al. Hierarchical cluster and survival analyses of antisynthetase syndrome: phenotype and outcome are correlated with anti-tRNA synthetase antibody specificity. Autoimmun Rev. 2012;12(2):210–7.\nHamaguchi Y, Fujimoto M, Matsushita T, Kaji K, Komura K, Hasegawa M, et al. Common and distinct clinical features in adult patients with anti-aminoacyl-tRNA synthetase antibodies: heterogeneity within the syndrome. PLoS One. 2013;8(4):e60442.\nCavagna L, Nuno L, Scire CA, Govoni M, Longo FJ, Franceschini F, et al. Clinical spectrum time course in anti Jo-1 positive antisynthetase syndrome: results from an international retrospective multicenter study. Medicine (Baltimore). 2015;94(32):e1144.\nDel Grande F, Carrino JA, Del Grande M, Mammen AL, Christopher SL. Magnetic resonance imaging of inflammatory myopathies. Top Magn Reson Imaging. 2011;22(2):39–43.\nMaurer B, Walker UA. Role of MRI in diagnosis and management of idiopathic inflammatory myopathies. Curr Rheumatol Rep. 2015;17(11):67.\nMorrow JM, Sinclair CD, Fischmann A, Machado PM, Reilly MM, Yousry TA, et al. MRI biomarker assessment of neuromuscular disease progression: a prospective observational cohort study. Lancet Neurol. 2016;15(1):65–77.\nWattjes MP, Kley RA, Fischer D. Neuromuscular imaging in inherited muscle diseases. Eur Radiol. 2010;20(10):2447–60.\nYoshida K, Kurosaka D, Joh K, Matsushima S, Takahashi E, Hirai K, et al. Fasciitis as a common lesion of dermatomyositis, demonstrated early after disease onset by en bloc biopsy combined with magnetic resonance imaging. Arthritis Rheum. 2010;62(12):3751–9.\nZheng Y, Liu L, Wang L, Xiao J, Wang Z, Lv H, et al. Magnetic resonance imaging changes of thigh muscles in myopathy with antibodies to signal recognition particle. Rheumatology (Oxford). 2015;54(6):1017–24.\nCox FM, Reijnierse M, van Rijswijk CS, Wintzen AR, Verschuuren JJ, Badrising UA. Magnetic resonance imaging of skeletal muscles in sporadic inclusion body myositis. Rheumatology (Oxford). 2011;50(6):1153–61.\nTomasova Studynkova J, Charvat F, Jarosova K, Vencovsky J. The role of MRI in the assessment of polymyositis and dermatomyositis. Rheumatology (Oxford). 2007;46(7):1174–9.\nVan De Vlekkert J, Maas M, Hoogendijk JE, De Visser M, Van Schaik IN. Combining MRI and muscle biopsy improves diagnostic accuracy in subacute-onset idiopathic inflammatory myopathy. Muscle Nerve. 2015;51(2):253–8.\nDastmalchi M, Grundtman C, Alexanderson H, Mavragani CP, Einarsdottir H, Helmers SB, et al. A high incidence of disease flares in an open pilot study of infliximab in patients with refractory inflammatory myopathies. Ann Rheum Dis. 2008;67(12):1670–7.\nCuriel RV, Jones R, Brindle K. Magnetic resonance imaging of the idiopathic inflammatory myopathies: structural and clinical aspects. Ann N Y Acad Sci. 2009;1154:101–14.\nAouizerate J, De Antonio M, Bassez G, Gherardi RK, Berenbaum F, Guillevin L, et al. Myofiber HLA-DR expression is a distinctive biomarker for antisynthetase-associated myopathy. Acta Neuropathol Commun. 2014;2:154.\nStenzel W, Preusse C, Allenbach Y, Pehl D, Junckerstorff R, Heppner FL, et al. Nuclear actin aggregation is a hallmark of anti-synthetase syndrome-induced dysimmune myopathy. Neurology. 2015;84(13):1346–54.\nFernandez C, Bardin N, De Paula AM, Salort-Campana E, Benyamine A, Franques J, et al. Correlation of clinicoserologic and pathologic classifications of inflammatory myopathies: study of 178 cases and guidelines for diagnosis. Medicine (Baltimore). 2013;92(1):15–24.\nAndersson H, Aalokken TM, Gunther A, Mynarek GK, Garen T, Lund MB, et al. Pulmonary involvement in the antisynthetase syndrome: a comparative cross-sectional study. J Rheumatol. 2016;43(6):1107–13.\nDobloug C, Garen T, Bitter H, Stjarne J, Stenseth G, Grovle L, et al. Prevalence and clinical characteristics of adult polymyositis and dermatomyositis; data from a large and unselected Norwegian cohort. Ann Rheum Dis. 2015;74(8):1551–6.\nAmerican Thoracic Society. Idiopathic pulmonary fibrosis: diagnosis and treatment. International consensus statement. American Thoracic Society (ATS), and the European Respiratory Society (ERS). Am J Respir Crit Care Med. 2000;161(2 Pt 1):646–64\nBohan A, Peter JB. Polymyositis and dermatomyositis (second of two parts). N Engl J Med. 1975;292(8):403–7.\nGoutallier D, Postel JM, Gleyze P, Leguilloux P, Van Driessche S. Influence of cuff muscle fatty degeneration on anatomic and functional outcomes after simple suture of full-thickness tears. J Shoulder Elbow Surg. 2003;12(6):550–4.\nKendall HO, Kendall FP, Wadsworth GE. Muscles: testing and function. 2nd ed. Baltimore: Williams and Wilkins; 1971.\nAlexanderson H, Broman L, Tollback A, Josefson A, Lundberg IE, Stenstrom CH. Functional index-2: validity and reliability of a disease-specific measure of impairment in patients with polymyositis and dermatomyositis. Arthritis Rheum. 2006;55(1):114–22.\nDion E, Cherin P, Payan C, Fournet JC, Papo T, Maisonobe T, et al. Magnetic resonance imaging criteria for distinguishing between inclusion body myositis and polymyositis. J Rheumatol. 2002;29(9):1897–906.\nMercuri E, Pichiecchio A, Allsop J, Messina S, Pane M, Muntoni F. Muscle MRI in inherited neuromuscular disorders: past, present, and future. J Magn Reson Imaging. 2007;25(2):433–40.\nYao L, Gai N. Fat-corrected T2 measurement as a marker of active muscle disease in inflammatory myopathy. AJR Am J Roentgenol. 2012;198(5):W475–81.\nBartlett ML, Ginn L, Beitz L, Villalba ML, Plotz P, Bacharach SL. Quantitative assessment of myositis in thigh muscles using magnetic resonance imaging. Magn Reson Imaging. 1999;17(2):183–91.\nYao L, Yip AL, Shrader JA, Mesdaghinia S, Volochayev R, Jansen AV, et al. Magnetic resonance measurement of muscle T2, fat-corrected T2 and fat fraction in the assessment of idiopathic inflammatory myopathies. Rheumatology (Oxford). 2015;55(3):441–9.\nKumar Y, Wadhwa V, Phillips L, Pezeshk P, Chhabra A. MR imaging of skeletal muscle signal alterations: systematic approach to evaluation. Eur J Radiol. 2016;85(5):922–35.\nGarcia J. MRI in inflammatory myopathies. Skeletal Radiol. 2000;29(8):425–38.\nBarsotti S, Zampa V, Talarico R, Minichilli F, Ortori S, Iacopetti V, et al. Thigh magnetic resonance imaging for the evaluation of disease activity in patients with idiopathic inflammatory myopathies followed in a single center. Muscle Nerve. 2016;54(4):666–72.\nRider LG, Koziol D, Giannini EH, Jain MS, Smith MR, Whitney-Mahoney K, et al. Validation of manual muscle testing and a subset of eight muscles for adult and juvenile idiopathic inflammatory myopathies. Arthritis Care Res (Hoboken). 2010;62(4):465–72.\nLa Corte R, Lo Mo Naco A, Locaputo A, Dolzani F, Trotta F. In patients with antisynthetase syndrome the occurrence of anti-Ro\u002FSSA antibodies causes a more severe interstitial lung disease. Autoimmunity. 2006;39(3):249–53.\nVancsa A, Csipo I, Nemeth J, Devenyi K, Gergely L, Danko K. Characteristics of interstitial lung disease in SS-A positive\u002FJo-1 positive inflammatory myopathy patients. Rheumatol Int. 2009;29(9):989–94.\nMarie I, Hatron PY, Dominique S, Cherin P, Mouthon L, Menard JF, et al. Short-term and long-term outcome of anti-Jo1-positive patients with anti-Ro52 antibody. Semin Arthritis Rheum. 2012;41(6):890–9.",{"VOID":1807},"10.1186\u002Fs13075-017-1219-y","https:\u002F\u002Farthritis-research.biomedcentral.com\u002Farticles\u002F10.1186\u002Fs13075-017-1219-y",[1810,1825,1840,1855,1870,1883],{"id":1811,"sortIndex":32,"researcher":28,"roles":1812,"affiliations":1813,"properties":1822,"displayName":1824,"givenName":28,"familyName":28},"15cab182-443d-45b2-a1b5-eb9836a8a55f",[952],[1814],{"id":1815,"sortIndex":32,"affiliation":1816,"properties":28},"ac616fbc-6c66-463d-81db-75a65fab4b6c",{"id":1815,"createTime":28,"updateTime":28,"relativeEntities":1817,"slug":28,"properties":1818,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1821,"statistic":28},[],{"title":1819},{"VI":1820},"Institute of Clinical Medicine, Department of Rheumatology, Oslo University Hospital, Oslo, Norway",[],{"title":1823},{"VI":1824},"Helena 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Kirkhus",{"id":1841,"sortIndex":123,"researcher":28,"roles":1842,"affiliations":1843,"properties":1852,"displayName":1854,"givenName":28,"familyName":28},"42ed9b0a-6bb1-4c48-83d8-01eee190edd1",[952],[1844],{"id":1845,"sortIndex":32,"affiliation":1846,"properties":28},"0f3ba479-4dd2-4d9b-979c-013e78743842",{"id":1845,"createTime":28,"updateTime":28,"relativeEntities":1847,"slug":28,"properties":1848,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1851,"statistic":28},[],{"title":1849},{"EN":1850},"Department of Rheumatology, Oslo University Hospital, Oslo, Norway",[],{"title":1853},{"VI":1854},"Torhild 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cứu hoạt động của con đường mục tiêu của rapamycin ở động vật có vú (mTOR) và các điều chỉnh viên của nó, yếu tố tăng trưởng chuyển hóa (TGF)-β1 và phosphatase và homolog tensin (PTEN), trong các mẫu sinh thiết tuyến nước bọt nhỏ của bệnh nhân hội chứng Sjogren (SS) và xơ cứng hệ thống (SSc). Chúng tôi đã đánh giá hồi cứu các bệnh nhân SS, SSc và chồng chéo SS-SSc được nhập viện tại phòng khám rheumatology ngoại trú của chúng tôi từ tháng 1 năm 2007 đến tháng 12 năm 2015, những người đã thực hiện sinh thiết tuyến nước bọt nhỏ. Thông tin nhân khẩu học của bệnh nhân và một số đặc điểm lâm sàng đã được thu thập từ hồ sơ bệnh viện. Phương pháp nhuộm miễn dịch hóa học được sử dụng để phân tích sự biểu hiện của mTOR tổng thể, PTEN tổng thể và TGF-β1 trong các mô được sinh thiết. Các mẫu sinh thiết cũng được kiểm tra sự hiện diện và mức độ xơ hóa. Tổng cộng 58 bệnh nhân SS, 14 bệnh nhân SSc và 23 bệnh nhân chồng chéo SS-SSc đã được đưa vào nghiên cứu. Không có sự khác biệt đáng kể trong sự biểu hiện của mTOR giữa các nhóm này (P = 0.622). Protein PTEN được biểu hiện ở 87,2% bệnh nhân SS, 57,9% bệnh nhân mắc hội chứng chồng chéo và 100% bệnh nhân SSc, và sự khác biệt này là có ý nghĩa thống kê (P = 0.023). Mặc dù biểu hiện TGF-β1 của tế bào biểu mô ống đã tương tự giữa các nhóm (P = 0.345), nhưng sự biểu hiện của tế bào acinar lại thường gặp hơn ở bệnh nhân SSc (72,7%) và bệnh nhân chồng chéo (85,7%) so với các trường hợp SS (58,2%; P = 0.004). mTOR có thể là một trong những con đường chung trong bệnh lý của cả SS và SSc. Do đó, có thể có vai trò của các chất ức chế mTOR trong điều trị cả hai bệnh. Ngoài ra, sự biểu hiện của PTEN và TGF-β1 có thể là một đặc điểm phân biệt của SSc.","To examine the activity of the mammalian target of rapamycin (mTOR) pathway and its regulators, transforming growth factor (TGF)-β1 and phosphatase and tensin homolog (PTEN), in minor salivary gland biopsies of Sjogren’s syndrome (SS) and systemic sclerosis (SSc) patients. We retrospectively evaluated SS, SSc, and SS-SSc overlap patients admitted to our outpatient rheumatology clinic between January 2007 and December 2015 who underwent a minor salivary gland biopsy. Patient demographics and some clinical features were obtained from hospital records. Immunohistochemistry was used to analyze total mTOR, total PTEN, and TGF-β1 expression in the biopsied tissues. The biopsy specimens were also examined for the presence and degree of fibrosis. Minor salivary gland biopsies of 58 SS, 14 SSc, and 23 SS-SSc overlap patients were included in the study. There was no significant difference in mTOR expression between these groups (P = 0.622). PTEN protein was expressed in 87.2% of patients with SS, 57.9% with overlap syndrome, and 100% of the SSC patients, and these differences were statistically different (P = 0.023). Although ductal epithelial TGF-β1 expression was similar between the groups (P = 0.345), acinar cell expression was found to be more frequent in the SSc (72.7%) and overlap patients (85.7%) in comparison with the SS cases (58.2%; P = 0.004). mTOR may be one of the common pathways in the pathology of both SS and SSc. Hence, there may be a role for mTOR inhibitors in the treatment of both diseases. Additionally, PTEN and TGF-β1 expression may be a distinctive feature of SSc.",{"EN":1926,"VI":1927},"Role of the mTOR pathway in minor salivary gland changes in Sjogren’s syndrome and systemic sclerosis","Vai trò của con đường mTOR trong những thay đổi ở tuyến nước bọt nhỏ trong hội chứng Sjogren và xơ cứng hệ thống",{"VI":1929},"mTOR, PTEN, TGF-β1, hội chứng Sjogren, xơ cứng hệ thống, sinh thiết tuyến nước bọt nhỏ",{"VOID":1931},"Kassan SS, Moutsopoulos HM. Clinical manifestations and early diagnosis of Sjögren syndrome. Arch Intern Med. 2004;164(12):1275–84. https:\u002F\u002Fdoi.org\u002F10.1001\u002Farchinte.164.12.1275.\nMoriyama M, Tanaka A, Maehara T, Furukawa S, Nakashima H, Nakamura S. T helper subsets in Sjögren’s syndrome and IgG4-related dacryoadenitis and sialoadenitis: a critical review. J Autoimmun. 2014; https:\u002F\u002Fdoi.org\u002F10.1016\u002Fj.jaut.2013.07.007.\nManno R, Boin F. Immunotherapy of systemic sclerosis. Immunotherapy. 2010;2(6):863–78. https:\u002F\u002Fdoi.org\u002F10.2217\u002Fimt.10.69.\nGilbane AJ, Denton CP, Holmes AM. Scleroderma pathogenesis: a pivotal role for fibroblasts as effector cells. Arthritis Res Ther. 2013;15(3):215. https:\u002F\u002Fdoi.org\u002F10.1186\u002Far4230.\nLiang M, Lv J, Chu H, Wang J, Chen X, Zhu X, et al. Vertical inhibition of PI3K\u002FAkt\u002FmTOR signaling demonstrates in vitro and in vivo anti-fibrotic activity. J Dermatol Sci. 2014;76(2):104–11. https:\u002F\u002Fdoi.org\u002F10.1016\u002Fj.jdermsci.2014.08.002.\nPopulo H, Lopes JM, Soares P. The mTOR signalling pathway in human cancer. Int J Mol Sci. 2012;13(2):1886–918. https:\u002F\u002Fdoi.org\u002F10.3390\u002Fijms13021886.\nAssinder SJ, Dong Q, Kovacevic Z, Richardson DR. The TGF-beta, PI3K\u002FAkt and PTEN pathways: established and proposed biochemical integration in prostate cancer. Biochem J. 2009;417(2):411–21. https:\u002F\u002Fdoi.org\u002F10.1042\u002FBJ20081610.\nXu J, Lamouille S, Derynck R. TGF-beta-induced epithelial to mesenchymal transition. Cell Res. 2009;19(2):156–72. https:\u002F\u002Fdoi.org\u002F10.1038\u002Fcr.2009.\nLamouille S, Connolly E, Smyth JW, Akhurst RJ, Derynck R. TGF-β-induced activation of mTOR complex 2 drives epithelial-mesenchymal transition and cell invasion. J Cell Sci. 2012; https:\u002F\u002Fdoi.org\u002F10.1242\u002Fjcs.095299.\nWu T, Mohan C. The AKT axis as a therapeutic target in autoimmune diseases. Endocrine, Metab immune Disord -drug Targets. 2009;9(2):145–50.\nShah M, Edman MC, Janga SR, Shi P, Dhandhukia J, Liu S, et al. A rapamycin-binding protein polymer nanoparticle shows potent therapeutic activity in suppressing autoimmune dacryoadenitis in a mouse model of Sjogren’s syndrome. J Control Release. 2013;171(3):269–79. https:\u002F\u002Fdoi.org\u002F10.1016\u002Fj.jconrel.2013.07.016.\nVitali C, Bombardieri S, Jonsson R, Moutsopoulos HM, Alexander EL, Carsons SE, et al. Classification criteria for Sjögren's syndrome: a revised version of the European criteria proposed by the American-European consensus group. Ann Rheum Dis. 2002;61(6):554–8.\nvan den Hoogen F, Khanna D, Fransen J, Johnson SR, Baron M, Tyndall A, et al. 2013 classification criteria for systemic sclerosis: an American College of Rheumatology\u002FEuropean league against rheumatism collaborative initiative. Ann Rheum Dis. 2013;72(11):1747–55. https:\u002F\u002Fdoi.org\u002F10.1136\u002Fannrheumdis-2013-204424.\nChisholm DM, Mason DK. Labial salivary gland biopsy in Sjögren’s disease. J Clin Pathol. 1968;21(5):656–60.\nMutee AF, Kaur G, Kumar G, Muhammad TST, Khalid IA, Tan ML. Immunohistochemical evaluation of mTOR and Beclin-1 protein expression in human breast cancer and adjacent normal tissues, a study in Malaysian patients. Open Pathol J. 2009;3:111–7. https:\u002F\u002Fdoi.org\u002F10.2174\u002F1874375700903010111.\nSakr RA, Barbashina V, Morrogh M, Chandarlapaty S, Andrade VP, Arroyo CD, et al. Protocol for PTEN expression by immunohistochemistry in formalin-fixed paraffin-embedded human breast carcinoma. Appl Immunohistochem Mol Morphol. 2010;18(4):371–4. https:\u002F\u002Fdoi.org\u002F10.1097\u002FPAI.0b013e3181d50bd5.\nXie S, Macedo P, Hew M, Nassenstein C, Lee KY, Chung KF. Expression of transforming growth factor-β in idiopathic cough. Respir Res 2009; doi: https:\u002F\u002Fdoi.org\u002F10.1186\u002F1465-9921-10-40.\nHunzelmann N, Genth E, Krieg T, Lehmacher W, Malchers I, Meurer M, et al. The registry of the German network for systemic scleroderma: frequency of disease subsets and patterns of organ involvement. Rheumatology (Oxford). 2008;47(8):1185–92. https:\u002F\u002Fdoi.org\u002F10.1093\u002Frheumatology\u002Fken179.\nForestier A, Guerrier T, Jouvray M, Giovannelli J, Lefèvre G, Sobanski V, et al. Altered B lymphocyte homeostasis and functions in systemic sclerosis. Autoimmun Rev. 2018;17(3):244–55. https:\u002F\u002Fdoi.org\u002F10.1016\u002Fj.autrev.2017.10.015.",{"VOID":1933},"10.1186\u002Fs13075-018-1662-4","2025-01-10T04:27:23.419+00:00",[30],"https:\u002F\u002Farthritis-research.biomedcentral.com\u002Farticles\u002F10.1186\u002Fs13075-018-1662-4",[1938,1953,1968,1983,1998,2011,2024,2037],{"id":1939,"sortIndex":32,"researcher":28,"roles":1940,"affiliations":1941,"properties":1950,"displayName":1952,"givenName":28,"familyName":28},"5add9687-6e4e-465b-a71d-4ef6813f65a2",[952],[1942],{"id":1943,"sortIndex":32,"affiliation":1944,"properties":28},"b87cf758-81a0-4922-ae07-fee66192634d",{"id":1943,"createTime":28,"updateTime":28,"relativeEntities":1945,"slug":28,"properties":1946,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1949,"statistic":28},[],{"title":1947},{"VI":1948},"Department of Internal Medicine, Division of Nephrology, Izmir Katip Celebi 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