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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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SCIE","scie",[934,813],"SCIE","https:\u002F\u002Fmjl.clarivate.com\u002Fsearch-results?issn=1476-9255",[937],"03744874-dcbd-436b-8d5c-f6fa955ce005",{"impactFactor":32,"impactFactorByYear":939,"i10Index":158,"i10IndexLast5Year":357,"totalPublication":943,"totalPublicationByYear":944,"totalCitation":945,"totalCitationByYear":946,"totalCitationPerPublication":952,"totalCitationPerPublicationByYear":953,"hindexLast5Year":133,"hindex":133},{"2012":582,"2013":840,"2014":696,"2015":696,"2016":287,"2017":940,"2018":941,"2019":222,"2020":231,"2021":942,"2022":232,"2023":696},1.13,0.8,1.77,492,{"2004":123,"2005":205,"2006":145,"2007":127,"2008":323,"2009":134,"2010":141,"2011":122,"2012":202,"2013":280,"2014":147,"2015":206,"2016":131,"2017":135,"2018":129,"2019":135,"2020":122,"2021":135,"2022":128,"2023":69,"2024":46},2451,{"2005":162,"2006":50,"2007":155,"2008":156,"2009":217,"2010":148,"2011":324,"2012":947,"2013":611,"2014":948,"2015":949,"2016":950,"2017":156,"2018":151,"2019":864,"2020":951,"2021":147,"2022":145},209,216,494,248,138,4.98,{"2005":954,"2006":955,"2007":956,"2008":957,"2009":958,"2010":173,"2011":959,"2012":960,"2013":961,"2014":962,"2015":963,"2016":964,"2017":965,"2018":966,"2019":967,"2020":48,"2021":175,"2022":368},5.8,5.89,5.24,5.14,11.59,4.65,6.53,1.51,6.97,9.15,9.92,3.43,3.42,10.38,{"meta":969,"data":971},{"total":970},"493",[972,1143,1267,1517,1738,1844,1977,2151,2299,2476],{"id":973,"createTime":974,"updateTime":975,"relativeEntities":976,"slug":977,"properties":978,"entityType":987,"verifyStatus":26,"verifyTime":975,"verifyNote":988,"languages":28,"translateLanguages":28,"viewCount":40,"primaryUrl":989,"fullTextUrl":28,"authors":990,"publicationType":1087,"publisherRelationship":1088,"citationCount":28,"citationInfo":28,"publishDate":1139,"publishYear":1140,"citationAnalyzeStatus":878,"lastCitationAnalyze":28,"indexDatabases":1141,"openAccess":28,"references":28,"isForceReanalyzing":1142},"0183e268-0158-4ea9-a195-debd5b5cbfb1","2024-01-13T15:34:09.949+00:00","2025-01-24T23:54:18.468+00:00",[],"The-role-of-the-purinergic-P2X7-receptor-in-inflammation",{"abstract":979,"title":981,"references":983,"doi":985},{"EN":980},"The inflammatory process, orchestrated against a variety of injurious stimuli, is composed of three inter-related phases; initiation, propagation and resolution. Understanding the interplay between these three phases and harnessing the beneficial properties of inflammation whilst preventing its damaging effects, will undoubtedly lead to the advent of much needed therapies, particularly in chronic disease states. The P2X7 receptor (P2X7R) is increasingly recognised as an important cell surface regulator of several key inflammatory molecules including IL-1β, IL-18, TNF-α and IL-6. Moreover, as P2X7R-dependent cytokine production is driven by activating the inflammasome, antagonists of this receptor are likely to have therapeutic potential as novel anti-inflammatory therapies. The function of the P2X7R in inflammation, immunity and its potential role in disease will be reviewed and discussed.",{"EN":982},"The role of the purinergic P2X7 receptor in inflammation",{"VOID":984},"Nathan C: Points of control in inflammation. 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inflammatory response to hepatic ischemia-reperfusion (I\u002FR) is associated with an increase in cytokine production. Studies have documented that sex hormones modulate both the innate and adaptive immune responses, and that females are more robust than males. The aim of this study was to determine whether a sex difference in cytokine response to hepatic I\u002FR exists under normal pathophysiologic condition without hormone intervention. Adult C57BL\u002F6 mice underwent 90 min of hepatic ischemia followed by various reperfusion periods (0, 1.5, 3, 6 hr). Plasma cytokine TNF-α, IL-6, MIP-2, and KC were measured. Liver injury was assessed by plasma alanine transaminase (ALT) levels and liver histopathology. A reperfusion time-dependent increase in hepatocellular injury was observed in both males and females, as indicated by increasing levels of plasma ALT and liver histopathology. The plasma cytokines were significantly increased in both female and male I\u002FR groups compared to their respective sham counterparts. However, there was a significant difference in cytokine kinetics between the female and male I\u002FR groups. Female mice initially had a higher level of IL-6, KC, and MIP-2 in response to I\u002FR, which began to decline after 3 hr of reperfusion and were significantly lower than the male I\u002FR counterparts by 6 hr of reperfusion. In contrast, the hepatocellular injury and TNF production were only moderately lower in female IR than male IR. The study underscores role of the gender in differential inflammatory cytokine expression in response to hepatic I\u002FR, which may reflect the host response outcome.",{"EN":1153},"Sex differences in inflammatory cytokine production in hepatic ischemia-reperfusion",{"VOID":1155},"Jaeschke H, Bautista AP, Spolarics A, Spiter JJ: Superoxide generation by Kupffer cells and priming of neutrophils during reperfusion after hepatic ischemia. Free Radic Res Commun. 1991, 15: 277-284.\nAngele MK, Chaudry IH: Surgical trauma and immunosuppression: pathophysiology and potential immunomodulatory approaches. Arch Surg. 2005, 390: 333-341. 10.1007\u002Fs00423-005-0557-4.\nSener G, Arbak S, Kurtaran P, Gedik N, Yegens BC: Estrogen protects the liver and intestines against sepsis-induced injury in rats. J Surg Res. 2005, 128: 70-78.\nZellweger R, Wichmann MW, Ayala A, Stein S, DeMaso CM, Chaudry IH: Females in proestrus state maintain splenic immune functions and tolerate sepsis better than males. Crit Care Med. 1997, 1: 106-110. 10.1097\u002F00003246-199701000-00021.\nWei M, Kuukasjarvi P, Kaukinen S, Laurikka J, Pehkonen E, Laine S, Moilanen E, Metsanoja R, Tarkka M: Anti-inflammatory effects of 17beta-estradiol pretreatment in men after coronary artery surgery. J Cardiothorac Vasc Anesth. 2001, 15: 455-459. 10.1053\u002Fjcan.2001.24981.\nSchröder J, Kahlke V, Staubach KH, Zabel P, Stüber F: Gender Differences in Human Sepsis. Arch Surg. 1998, 133: 1200-1205. 10.1001\u002Farchsurg.133.11.1200.\nShimizu I: Impact of oestrogens on the progression of liver disease. Liver Int. 2003, 23: 63-10.1034\u002Fj.1600-0676.2003.00811.x.\nPfeilschifter J, Koditz R, Pfohl M, Schatz H: Changes in proinflammatory cytokine activity after menopause. Endocr Rev. 2002, 23: 90-119. 10.1210\u002Fer.23.1.90.\nRogers A, Eastell R: The effect of 17beta-estradiol on production of cytokines in cultures of peripheral blood. Bone. 2001, 29: 30-4. 10.1016\u002FS8756-3282(01)00468-9.\nYokoyama Y, Nimura Y, Nagion M, Bland KI, Chaudry IH: Current understanding of gender dimorphism in hepatic pathophysiology. J Surg Res. 2005, 1: 147-156.\nHarada H, Pavlick KP, Hines IN, Hoffman JM, Bharwani S, Gray L, Wolf RE, Grisham MB: Selected contribution: Effects of gender on reduced-size liver ischemia and reperfusion injury. J Appl Physiol. 2001, 91: 2816-2822.\nInaba K, Suzuki S, Ihara H, Sakaguchi T, Baba S, Urano T, Konno H, Nakamura S: Sexual dimorphism in endotoxin susceptibility after partial hepatectomy in rats. J Hepatol. 2005, 42: 719-27. 10.1016\u002Fj.jhep.2004.12.026.\nCrockett ET, Galligan JJ, Uhal BD, Roth JHR, Pandya K: Protection of Early Phase Hepatic Ischemia-Reperfusion Injury by cholinergic agonists. BMC Clin Pathol. 2006, 6: 1-13. 10.1186\u002F1472-6890-6-3.\nMosher B, Dean R, Harkema J, Remick D, Palma J, Crockett E: Inhibition of kupffer cells reduced CXC chemokine production and liver injury. J Surg Res. 2001, 99: 201-210. 10.1006\u002Fjsre.2001.6217.\nColleti LM, Kunkel SL, Walz A, Burdick MD, Kunkel RG, Wilke CA, Strieter RM: The role of cytokine networks in the local liver injury following hepatic ischemia\u002Freperfusion in the rat. Hepatology. 1996, 23: 506-513. 10.1002\u002Fhep.510230315.\nLentsch AB, Yoshidome H, Cheadle WG, Miller FN, Edwards MJ: Chemokine involvement in hepatic ischemia\u002Freperfusion injury in mice: Roles for macrophage inflammatory protein-2 and KC. Hepatology. 1998, 27: 563-568. 10.1002\u002Fhep.510270226.\nHarada H, Bharwani S, Pavlick KP, Korach KS, Grisham MB: Estrogen receptor-α, sexual dimorphism, and reduced-size liver ischemia and reperfusion injury in mice. Pediatr Res. 2004, 55: 450-456. 10.1203\u002F01.PDR.0000110524.88784.DD.\nFrancavilla A, Eagon PK, DiLeo A, Polimeno L, Panella C, Aquilino AM, Ingrosso M, Van Thiel DH, Starzl TE: Sex hormone-related functions in regenerating male rat liver. Gastroenterology. 1986, 91: 1263-70.\nKubala L, Ciz M, Vondracek J, Cizova H, Cerny J, Nemec P, Studenik P, Duskova M, Lojek A: Peri- and post-operative course of cytokines and the metabolic activity of neutrophils in human liver transplantation. Cytokine. 2001, 16: 97-101. 10.1006\u002Fcyto.2001.0952.\nScheingraber S, Dobbert D, Schmiedel P, Seliger E, Dralle H: Gender-specific differences in sex hormones and cytokines in patients undergoing major abdominal surgery. Surg Today. 2005, 35: 846-54. 10.1007\u002Fs00595-005-3044-1.\nSpeyer CL, Rancilio NJ, McClintock SD, Crawford JD, Gao H, Sarma JV, Ward PA: Regulatory effects of estrogen on acute lung inflammation in mice. Am J Physiol Cell Physiol. 2005, 288: 881-90. 10.1152\u002Fajpcell.00467.2004.\nColantoni A, Idilman R, De Maria N, La Paglia N, Belmonte J, Wezeman F, Emanuele N, Thiel V, DH Kovacs EJ, Emanuele MA: Hepatic apoptosis and proliferation in male and female rats fed alcohol: Role of cytokines. Alcohol Clin Exp Res. 2003, 27: 1184-1189. 10.1097\u002F01.ALC.0000075834.52279.F9.\nTeoh N, Field J, Farrell G: IL-6 is one likely mediator of the hepatoprotective and pro-proliferative effects of ischaemic preconditioning. J Hepatol. 2006, 45: 20-7. 10.1016\u002Fj.jhep.2006.01.039.\nJin X, Zimmers TA, Perez EA, Pierce RH, Zhang Z, Koniaris LG: Paradoxical effects of short- and long-term interleukin-6 exposure on liver injury and repair. Hepatology. 2006, 43: 474-84. 10.1002\u002Fhep.21087.\nWichmann MW, Zellweger R, DeMaso CM, Ayala A, Chaudry IH: Enhanced immune responses in females as opposed to decreased responses in males following hemorrhagic shock. Cytokine. 1996, 8: 853-863. 10.1006\u002Fcyto.1996.0114.\nZuckerman SH, Ahmari SE, Bryan-Poole N, Evans GF, Short L, Glasebrook AL: Estriol: a potent regulator of TNF and IL-6 expression in a murine model of endotoxemia. Inflammation. 1996, 20: 581-97. 10.1007\u002FBF01488797.\nStein B, Yang MX: Repression of the interleukin-6 promoto by estrogen receptor is mediated by NF-kB and C\u002FEBPB. J Mol Cell Biol. 1995, 15: 4971-4979.\nDinarello CA: The proinflammatory cytokines interleukin-1 and tumor necrosis factor and treatment of the septic shock syndrome. J Infect Dis. 1991, 163: 1177-1184.\nWoo CH, Eom YW, Yoo MH, You HJ, Han HJ, Song WK, Yoo YJ, Chun JS, Kim JH: Generates Reactive Oxygen Species via a Cytosolic Phospholipase A2-linked Cascade. J Biol Chem. 2000, 275: 32357-32363. 10.1074\u002Fjbc.M005638200.\nSquadrito F, Altavilla D, Squadrito G, Campo GM, Arlotta M, Arcoraci V, Minutoli L, Saitta A, Caputi AP: The involvement of of tumor necrosis factor-α in the 17 beta ostradiol in splanchnic ischemia-reperfusion injury. Br J Pharmacol. 1997, 121: 1782-1788. 10.1038\u002Fsj.bjp.0701288.\nDepshpande R, Khalili H, Pergolizzi RG, Michael SD, Change MY: Estradiol down-regulates LPS-induced cytokine production and NF-kB activation in murine macrophages. Am J Reprod Immunol. 1997, 38: 46-54.\nVegeto E, Belcredito S, Ghisletti S, Meda C, Etteri S, Maggi A: The endogenous estrogen status regulates microglia reactivity in animal models of neuroinflammation. Endocrinology. 2006, 147: 2263-72. 10.1210\u002Fen.2005-1330.\nKim HP, Lee JY, Jeong JK, Bae SW, Lee HK, Jo I: Nongenomic stimulation of nitric oxide release by estrogen is mediated by estrogen receptor α localized in caveolae. Biochem Biophys Res Commun. 1999, 263: 257-262. 10.1006\u002Fbbrc.1999.1348.\nArnal JF, Clamens S, Pechet C, Negre-Salvayre A, Allera C, Girolami JP, Salvayre R, Bayard F: Ethinylestradiol does not enhance the expression of nitric oxide synthase in bovine endothelial cells but increases the release of bioactive nitric oxide by inhibiting superoxide anion production. Proc Natl Acad Sci USA. 1996, 93: 4108-4113. 10.1073\u002Fpnas.93.9.4108.",{"VOID":1157},"10.1186\u002F1476-9255-3-16","http:\u002F\u002Fjournal-inflammation.biomedcentral.com\u002Farticles\u002F10.1186\u002F1476-9255-3-16",[1160,1175,1188,1201],{"id":1161,"sortIndex":32,"researcher":28,"roles":1162,"affiliations":1163,"properties":1172,"displayName":1174,"givenName":28,"familyName":28},"fd3e9d3f-e07e-4941-8c47-60c9a4b07278",[994],[1164],{"id":1165,"sortIndex":32,"affiliation":1166,"properties":28},"dadd0dd3-0078-434f-a94e-f439a0f2b184",{"id":1165,"createTime":28,"updateTime":28,"relativeEntities":1167,"slug":28,"properties":1168,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1171,"statistic":28},[],{"title":1169},{"VI":1170},"Departments of Physiology & Division of Human Pathology-College of Human Medicine, Michigan State University, East Lansing, USA",[],{"title":1173},{"VI":1174},"Elahé T 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pulmonary fibrosis (IPF) is an orphan disease characterized by progressive loss of lung function resulting in shortness of breath and often death within 3–4 years of diagnosis. Repetitive lung injury in susceptible individuals is believed to promote chronic oxidative stress, inflammation, and uncontrolled collagen deposition. Several preclinical and retrospective clinical studies in IPF have reported beneficial outcomes associated with the use of proton pump inhibitors (PPIs) such as esomeprazole. Accordingly, we sought to investigate molecular mechanism(s) by which PPIs favorably regulate the disease process. We stimulated oxidative stress, pro-inflammatory and profibrotic phenotypes in primary human lung epithelial cells and fibroblasts upon treatment with bleomycin or transforming growth factor β (TGFβ) and assessed the effect of a prototype PPI, esomeprazole, in regulating these processes. Our study shows that esomeprazole controls pro-inflammatory and profibrotic molecules through nuclear translocation of the transcription factor nuclear factor-like 2 (Nrf2) and induction of the cytoprotective molecule heme oxygenase 1 (HO1). Genetic deletion of Nrf2 or pharmacological inhibition of HO1 impaired esomeprazole-mediated regulation of proinflammatory and profibrotic molecules. Additional studies indicate that activation of Mitogen Activated Protein Kinase (MAPK) pathway is involved in the process. Our experimental data was corroborated by bioinformatics studies of an NIH chemical library which hosts gene expression profiles of IPF lung fibroblasts treated with over 20,000 compounds including esomeprazole. Intriguingly, we found 45 genes that are upregulated in IPF but downregulated by esomeprazole. Pathway analysis showed that these genes are enriched for profibrotic processes. Unbiased high throughput RNA-seq study supported antifibrotic effect of esomeprazole and revealed several novel targets. Taken together, PPIs may play antifibrotic role in IPF through direct regulation of the MAPK\u002FNrf2\u002FHO1 pathway to favorably influence the disease process in IPF.",{"EN":1277},"Esomeprazole attenuates inflammatory and fibrotic response in lung cells through the MAPK\u002FNrf2\u002FHO1 pathway",{"VOID":1279},"Raghu G, Chen SY, Yeh WS, Maroni B, Li Q, Lee YC, et al. Idiopathic pulmonary fibrosis in US Medicare beneficiaries aged 65 years and older: incidence, prevalence, and survival, 2001-11. Lancet Respir Med. 2014;2(7):566–72. https:\u002F\u002Fdoi.org\u002F10.1016\u002FS2213-2600(14)70101-8.\nHodgson U, Laitinen T, Tukiainen P. Nationwide prevalence of sporadic and familial idiopathic pulmonary fibrosis: evidence of founder effect among multiplex families in Finland. Thorax. 2002;57(4):338–42. https:\u002F\u002Fdoi.org\u002F10.1136\u002Fthorax.57.4.338.\nKing TE Jr, Bradford WZ, Castro-Bernardini S, Fagan EA, Glaspole I, Glassberg MK, et al. 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Investig New Drugs. 2014;32(6):1269–77. https:\u002F\u002Fdoi.org\u002F10.1007\u002Fs10637-014-0159-5.",{"VOID":1281},"10.1186\u002Fs12950-021-00284-6","2024-12-12T01:27:55.447+00:00","https:\u002F\u002Fjournal-inflammation.biomedcentral.com\u002Farticles\u002F10.1186\u002Fs12950-021-00284-6",[1285,1302,1315,1330,1345,1360,1375,1390,1405,1418,1431,1444],{"id":1286,"sortIndex":32,"researcher":28,"roles":1287,"affiliations":1288,"properties":1299,"displayName":1301,"givenName":28,"familyName":28},"c42154df-416f-49d8-88f6-6e248da7826b",[994],[1289],{"id":1290,"sortIndex":32,"affiliation":1291,"properties":1297},"6606367d-9026-42cf-aff1-5aafdd3ee439",{"id":1290,"createTime":28,"updateTime":28,"relativeEntities":1292,"slug":28,"properties":1293,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1296,"statistic":28},[],{"title":1294},{"VI":1295},"Department of Radiation Oncology, Baylor College of Medicine, Houston, USA",[],{"title":1298},{"VI":1295},{"title":1300},{"VI":1301},"Afshin Ebrahimpour",{"id":1303,"sortIndex":40,"researcher":28,"roles":1304,"affiliations":1305,"properties":1312,"displayName":1314,"givenName":28,"familyName":28},"545b45d3-38d0-4562-94a4-651f2bc8ebd8",[994],[1306],{"id":1290,"sortIndex":32,"affiliation":1307,"properties":28},{"id":1290,"createTime":28,"updateTime":28,"relativeEntities":1308,"slug":28,"properties":1309,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1311,"statistic":28},[],{"title":1310},{"VI":1295},[],{"title":1313},{"VI":1314},"Min Wang",{"id":1316,"sortIndex":123,"researcher":28,"roles":1317,"affiliations":1318,"properties":1327,"displayName":1329,"givenName":28,"familyName":28},"2ad794e2-c535-4435-bf9f-0f643c21c500",[994],[1319],{"id":1290,"sortIndex":32,"affiliation":1320,"properties":1325},{"id":1290,"createTime":28,"updateTime":28,"relativeEntities":1321,"slug":28,"properties":1322,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1324,"statistic":28},[],{"title":1323},{"VI":1295},[],{"title":1326},{"VI":1295},{"title":1328},{"VI":1329},"Li Li",{"id":1331,"sortIndex":42,"researcher":28,"roles":1332,"affiliations":1333,"properties":1342,"displayName":1344,"givenName":28,"familyName":28},"bdbca541-e407-429c-aa3e-942513ed0481",[994],[1334],{"id":1335,"sortIndex":32,"affiliation":1336,"properties":28},"6b866ca5-cf06-494f-a0bb-49d8199be32b",{"id":1335,"createTime":28,"updateTime":28,"relativeEntities":1337,"slug":28,"properties":1338,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1341,"statistic":28},[],{"title":1339},{"VI":1340},"Division of Biomedical Informatics, Cincinnati Children’s Hospital Medical Center, Department of Pediatrics, University of Cincinnati College of Medicine, Cincinnati, USA",[],{"title":1343},{"VI":1344},"Anil G. Jegga",{"id":1346,"sortIndex":45,"researcher":28,"roles":1347,"affiliations":1348,"properties":1357,"displayName":1359,"givenName":28,"familyName":28},"00cf601a-5b41-4de3-af7b-2c580703afc5",[994],[1349],{"id":1290,"sortIndex":32,"affiliation":1350,"properties":1355},{"id":1290,"createTime":28,"updateTime":28,"relativeEntities":1351,"slug":28,"properties":1352,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1354,"statistic":28},[],{"title":1353},{"VI":1295},[],{"title":1356},{"VI":1295},{"title":1358},{"VI":1359},"Mark D. 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Tony Eissa",{"id":1376,"sortIndex":48,"researcher":28,"roles":1377,"affiliations":1378,"properties":1387,"displayName":1389,"givenName":28,"familyName":28},"9927d22e-a500-4ea6-b75d-592b9f12aca6",[994],[1379],{"id":1380,"sortIndex":32,"affiliation":1381,"properties":28},"a15fff52-4b35-46fe-b749-97729de46fdd",{"id":1380,"createTime":28,"updateTime":28,"relativeEntities":1382,"slug":28,"properties":1383,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1386,"statistic":28},[],{"title":1384},{"VI":1385},"Division of Pulmonary and Critical Care Medicine, Center for Interstitial Lung Disease, University of Washington, Seattle, USA",[],{"title":1388},{"VI":1389},"Ganesh Raghu",{"id":1391,"sortIndex":49,"researcher":28,"roles":1392,"affiliations":1393,"properties":1402,"displayName":1404,"givenName":28,"familyName":28},"901b0b7a-8ab7-4505-9aad-251d4188ea6e",[994],[1394],{"id":1395,"sortIndex":32,"affiliation":1396,"properties":28},"cfdf4f21-e967-432f-b504-d3e547a77ebc",{"id":1395,"createTime":28,"updateTime":28,"relativeEntities":1397,"slug":28,"properties":1398,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1401,"statistic":28},[],{"title":1399},{"EN":1400},"Department of Internal Medicine, The University of Texas Health Science Center at Houston, Houston, USA",[],{"title":1403},{"VI":1404},"Soma Jyothula",{"id":1406,"sortIndex":357,"researcher":28,"roles":1407,"affiliations":1408,"properties":1415,"displayName":1417,"givenName":28,"familyName":28},"269bb865-3ca7-4779-b021-be964899de10",[994],[1409],{"id":1365,"sortIndex":32,"affiliation":1410,"properties":28},{"id":1365,"createTime":28,"updateTime":28,"relativeEntities":1411,"slug":28,"properties":1412,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1414,"statistic":28},[],{"title":1413},{"VI":1370},[],{"title":1416},{"VI":1417},"Farrah Kheradmand",{"id":1419,"sortIndex":145,"researcher":28,"roles":1420,"affiliations":1421,"properties":1428,"displayName":1430,"givenName":28,"familyName":28},"85048969-86fa-401e-99e4-d1fe3c26837f",[994],[1422],{"id":1365,"sortIndex":32,"affiliation":1423,"properties":28},{"id":1365,"createTime":28,"updateTime":28,"relativeEntities":1424,"slug":28,"properties":1425,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1427,"statistic":28},[],{"title":1426},{"VI":1370},[],{"title":1429},{"VI":1430},"Nicola A. 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We tested the ability of this novel synthetic steroid with improved pharmacological properties to limit non-productive lung inflammation in rodents and attempted to gauge its immunological impact. In mice, oral treatment with HE3286 (40 mg\u002Fkg) significantly (p \u003C 0.05) decreased neutrophil counts and exudate volumes (~50%) in carrageenan-induced pleurisy, and myeloperoxidase in lipopolysaccharide-induced lung injury. HE3286 (40 mg\u002Fkg) was not found to be profoundly immune suppressive in any of the classical animal models of immune function, including those used to evaluate antigen specific immune responses in vivo (ovalbumin immunization). When mice treated for two weeks with HE3286 were challenged with K. pneumoniae, nearly identical survival kinetics were observed in vehicle-treated, HE3286-treated and untreated groups. HE3286 represents a novel, first-in-class anti-inflammatory agent that may translate certain benefits of β-AET observed in rodents into treatments for chronic inflammatory pulmonary disease.",{"EN":1527},"HE3286, an oral synthetic steroid, treats lung inflammation in mice without immune suppression",{"EN":1529},"",{"VOID":1531},"Barnes PJ: Mediators of chronic obstructive pulmonary disease. Pharmacol Rev. 2004, 56: 515-48. 10.1124\u002Fpr.56.4.2.\nBrusselle GG, Bracke KR, Maes T, D'Hulst AI, Moerloose KB, Joos GF: Murine models of COPD. Pulm Pharmacol Ther. 2006, 19: 155-65. 10.1016\u002Fj.pupt.2005.06.001.\nFujita M, Nakanishi Y: The pathogenesis of COPD: lessons learned from in vivo animal models. Med Sci Monit. 2007, 13: RA19-24.\nKoehler DR, Downey GP, Sweezey NB, Tanswell AK, Hu J: Lung inflammation as a therapeutic target in cystic fibrosis. 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Am J Respir Crit Care Med. 2000, 161: 271-9.\nSAS Institute Inc: SAS\u002FSTAT user's guide, SAS OnlineDoc 9.1. 2004, SAS Institute, Inc\nOffner H, Firestein GS, Boyle DL, Pieters R, Frincke JM, Garsd A: An orally bioavailable synthetic analog of an active dehydroepiandrosterone metabolite reduces established disease in rodent models of rheumatoid arthritis. J Pharmacol Exp Ther. 2009, 329: 1100-9. 10.1124\u002Fjpet.108.145086.\nShang XZ, Ma KY, Radewonuk J, Li J, Song XY, Griswold DE: IgE isotype switch and IgE production are enhanced in IL-21-deficient but not IFN-gamma-deficient mice in a Th2-biased response. Cell Immunol. 2006, 241: 66-74. 10.1016\u002Fj.cellimm.2006.07.011.\nWang E, Ouellet N, Simard M, Fillion I, Bergeron Y, Beauchamp D: Pulmonary and systemic host response to Streptococcus pneumoniae and Klebsiella pneumoniae bacteremia in normal and immunosuppressed mice. 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Am J Physiol Endocrinol Metab. 2010, 298: E1036-48. 10.1152\u002Fajpendo.00668.2009.\nWebb SJ, Geoghegan TE, Prough RA, Michael Miller KK: The biological actions of dehydroepiandrosterone involves multiple receptors. Drug Metab Rev. 2006, 38: 89-116. 10.1080\u002F03602530600569877.\nEbeling P, Koivisto VA: Physiological importance of dehydroepiandrosterone. Lancet. 1994, 343: 1479-81. 10.1016\u002FS0140-6736(94)92587-9.\nWang T, Villegas S, Huang Y, White SK, Ahlem C, Lu M: Amelioration of glucose intolerance by the synthetic androstene HE3286: link to inflammatory pathways. J Pharmacol Exp Ther. 2010, 333: 70-80. 10.1124\u002Fjpet.109.161182.\nAhlem C, Auci D, Mangano K, Reading C, Frincke J, Stickney D: HE3286: a novel synthetic steroid as an oral treatment for autoimmune disease. Ann N Y Acad Sci. 2009, 1173: 781-90. 10.1111\u002Fj.1749-6632.2009.04798.x.\nCosta M, Potvin S, Berthiaume Y, Gauthier L, Jeanneret A, Lavoie A: Diabetes: a major co-morbidity of cystic fibrosis. Diabetes Metab. 2005, 31: 221-32. 10.1016\u002FS1262-3636(07)70189-1.\nMilla CE, Billings J, Moran A: Diabetes is associated with dramatically decreased survival in female but not male subjects with cystic fibrosis. Diabetes Care. 2005, 28: 2141-4. 10.2337\u002Fdiacare.28.9.2141.\nSjoholm A, Nystrom T: Inflammation and the etiology of type 2 diabetes. 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nephropathy is characterized by an inflammatory state in the kidney, that is promoted by cytokines and growth factors produced by damaged tubular cells, infiltrated macrophages and accumulated myofibroblasts. This inflammatory state contributes to tubular atrophy and interstitial fibrosis characteristic of obstructive nephropathy. Accumulation of leukocytes, especially macrophages and T lymphocytes, in the renal interstitium is strongly associated to the progression of renal injury. Proinflammatory cytokines, NF-κB activation, adhesion molecules, chemokines, growth factors, NO and oxidative stress contribute in different ways to progressive renal damage induced by obstructive nephropathy, as they induce leukocytes recruitment, tubular cell apoptosis and interstitial fibrosis. Increased angiotensin II production, increased oxidative stress and high levels of proinflammatory cytokines contribute to NF-κB activation which in turn induce the expression of adhesion molecules and chemokines responsible for leukocyte recruitment and iNOS and cytokines overexpression, which aggravates the inflammatory response in the damaged kidney. 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Mediators Inflamm. 2006, 2006: Article ID 12919, 9 pages.\nLenda DM, Kikawada E, Stanley ER, Kelley VR: Reduced macrophage recruitment, proliferation, and activation in colony-stimulating factor-1-deficient mice results in decreased tubular apoptosis during renal inflammation. J Immunol. 2003, 170: 3254-3262.\nLange-Sperandio B, Forbes MS, Thornhill B, Okusa MD, Linden J, Chevalier RL: A2A adenosine receptor agonist and PDE4 inhibition delays inflammation but fails to reduce injury in experimental obstructive nephropathy. Nephron Exp Nephrol. 2005, 100: e113-e123. 10.1159\u002F000085057.\nXaus J, Valledor AF, Cardo M, Marquès L, Beleta J, Palacios JM, Celada A: Adenosine inhibits macrophage colony-stimulating factor-dependent proliferation of macrophages through the induction of p27kip-1 expression. 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Kidney Int. 2004, 66: 1709-1710. 10.1111\u002Fj.1523-1755.2004.00984.x.\nWu JT, Kral JG: The NF-kappaB\u002FIkappaB signaling system: a molecular target in breast cancer therapy. J Surg Res. 2005, 123: 158-169. 10.1016\u002Fj.jss.2004.06.006.\nTamada S, Asai T, Kuwabara N, Iwai T, Uchida J, Teramoto K, Kaneda N, Yukimura T, Komiya T, Nakatani T, Miura K: Molecular mechanisms and therapeutic strategies of chronic renal injury: the role of nuclear factor kappaB activation in the development of renal fibrosis. J Pharmacol Sci. 2006, 100: 17-21. 10.1254\u002Fjphs.FMJ05003X4.\nGoncalves RG, Biato MA, Colosimo RD, Martinusso CA, Pecly ID, Farias EK, Cardoso LR, Takiya CM, Ornellas JF, Leite M: Effects of mycophenolate mofetil and lisinopril on collagen deposition in unilateral ureteral obstruction in rats. Am J Nephrol. 2004, 24: 527-536. 10.1159\u002F000081706.\nWu MJ, Wen MC, Chiu YT, Chiou YY, Shu KH, Tang MJ: Rapamycin attenuates unilateral ureteral obstruction-induced renal fibrosis. Kidney Int. 2006, 69: 2029-2036. 10.1038\u002Fsj.ki.5000161.",{"VOID":1858},"10.1186\u002F1476-9255-7-19","https:\u002F\u002Fjournal-inflammation.biomedcentral.com\u002Farticles\u002F10.1186\u002F1476-9255-7-19",[1861,1885,1905],{"id":1862,"sortIndex":32,"researcher":28,"roles":1863,"affiliations":1864,"properties":1882,"displayName":1884,"givenName":28,"familyName":28},"8d87acc2-6fc4-412a-92a3-2c0f1feccb4b",[994],[1865,1873],{"id":1866,"sortIndex":32,"affiliation":1867,"properties":28},"9fb91d63-6d00-442e-b1b9-fc77c92ee271",{"id":1866,"createTime":28,"updateTime":28,"relativeEntities":1868,"slug":28,"properties":1869,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1872,"statistic":28},[],{"title":1870},{"VI":1871},"Instituto \"Reina Sofía\" de Investigación Nefrológica, Departamento de Fisiología y Farmacología, Universidad de Salamanca, Salamanca, 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Pérez-Barriocanal",{"id":1906,"sortIndex":123,"researcher":28,"roles":1907,"affiliations":1908,"properties":1922,"displayName":1924,"givenName":28,"familyName":28},"cbfe2bad-977a-4cdb-ae72-b62e417a859e",[994],[1909,1915],{"id":1866,"sortIndex":32,"affiliation":1910,"properties":28},{"id":1866,"createTime":28,"updateTime":28,"relativeEntities":1911,"slug":28,"properties":1912,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1914,"statistic":28},[],{"title":1913},{"VI":1871},[],{"id":1874,"sortIndex":40,"affiliation":1916,"properties":1921},{"id":1874,"createTime":28,"updateTime":28,"relativeEntities":1917,"slug":28,"properties":1918,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1920,"statistic":28},[],{"title":1919},{"VI":1879},[],{},{"title":1923},{"VI":1924},"José M 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disease (BD) is a multisystem autoinflammatory disease characterised by mucosal ulceration, ocular, neural, joint and skin inflammation. The cause of BD is not known but there is a strong genetic association with HLA-B*51, IL10 and IL23R. Neutrophils are a first line of defence against invading pathogens and have been described as activated in patients with BD. Neutrophils can now be separated into different subsets, such as low density (LDN) and normal density (NDN) that have diverse functional roles. We wished to address neutrophil heterogeneity in patients with BD. Peripheral blood neutrophils were obtained from 32 BD patients and 37 healthy aged-matched controls. Percoll isolation was used to isolate all neutrophils, while Ficol-Hypaque was used to obtain LDN and NDN. Phagocytic capacity and production of reactive oxygen species (ROS), and neutrophil extracellular traps (NET) stimulated with phorbol 12-myristate 13-acetate (PMA) and Escherichia coli (E.coli) were assessed in both groups. We have demonstrated reduced phagocytic capacity and ROS production but greater NET production by total neutrophils stimulated with PMA or E.coli from BD patients in comparison with healthy controls. Patients with BD had elevated numbers of LDN and lower number of NDN compared with healthy controls. However, both neutrophil subsets showed the same reduced ROS production and phagocytic function as total neutrophils in both groups. Our novel findings indicate that the neutrophil population in BD is heterogeneous and the increased number of LDN in combination with greater NET production may contribute to the inflammatory response and pathogenesis.",{"EN":1987},"Low density neutrophils are increased in patients with Behçet’s disease but do not explain differences in neutrophil function",{"VOID":1989},"Tong B, Liu X, Xiao J, Su G. Immunopathogenesis of Behcet’s disease. 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J Am Acad Dermatol. 1995;32:968–76. https:\u002F\u002Fdoi.org\u002F10.1016\u002F0190-9622(95)91333-5.\nErgun T, Gürbüz O, Dogusoy G, et al. Histopathologic features of the spontaneous pustular lesions of Behçet’s syndrome. Int J Dermatol. 1998;37:194–6. https:\u002F\u002Fdoi.org\u002F10.1046\u002Fj.1365-4362.1998.00276.x.\nSensi A, Gavioli R, Spisani S, et al. HLA B51 antigen associated with neutrophil hyper-reactivity. Dis Markers. 1991;9:327–31.\nNeves FS, Carrasco S, Goldenstein-Schainberg C, et al. Neutrophil hyperchemotaxis in Behçet's disease: a possible role for monocytes orchestrating bacterial-induced innate immune responses. Clin Rheumatol. 2009;28:1403–10. https:\u002F\u002Fdoi.org\u002F10.1007\u002Fs10067-009-1261-1265.\nYamashita N, Kaneoka H, Kaneko S, et al. Role of gammadelta T lymphocytes in the development of Behçet’s disease. Clin Exp Immunol. 1997;107:241–7. https:\u002F\u002Fdoi.org\u002F10.1111\u002Fj.1365-2249.1997.274-ce1159.x.\nGogus F, Fresko I, Elbir Y, Eksioglu-Demiralp E, Direskeneli H. Oxidative burst response to monosodium urate crystals in patients with Behçet’s syndrome. Clin Exp Rheumatol. 2005;23:S81–5.\nEksioglu-Demiralp E, Direskeneli H, Kibaroglu A, et al. Neutrophil activation in Behçet's disease. Clin Exp Rheumatol. 2001;19:S19–24.\nSafi R, Kallas R, Bardawil T, et al. Neutrophils contribute to vasculitis by increased release of neutrophil extracellular traps in Behçet’s disease. J Dermatol Sci. 2018;92:143–50. https:\u002F\u002Fdoi.org\u002F10.1016\u002Fj.jdermsci.2018.08.010.\nLe Joncour A, Martos R, Loyau S, et al. Critical role of neutrophil extracellular traps (NETs) in patients with Behcet’s disease. Ann Rheum Dis. 2019;78:1274–82. https:\u002F\u002Fdoi.org\u002F10.1136\u002Fannrheumdis-2018-214335.\nMacey M, Hagi-Pavli E, Stewart J, et al. Age, gender and disease-related platelet and neutrophil activation ex vivo in whole blood samples from patients with Behçet’s disease. Rheumatology (Oxford). 2011;50:1849–59. https:\u002F\u002Fdoi.org\u002F10.1093\u002Frheumatology\u002Fker17.\nAvci A, Avci D, Erden F, et al. Can we use the neutrophil-to-lymphocyte ratio, platelet-to-lymphocyte ratio, and mean platelet volume values for the diagnosis of anterior uveitis in patients with Behcet’s disease? Ther Clin Risk Manag. 2017;13:881–6. https:\u002F\u002Fdoi.org\u002F10.2147\u002FTCRM.S135260.\nSaleh Z, Arayssi T. Update on the therapy of Behçet disease. Ther Adv Chronic Dis. 2014;5:112–34. https:\u002F\u002Fdoi.org\u002F10.1177\u002F2040622314523062.\nPark UC, Kim TW, Yu HG. Immunopathogenesis of ocular Behçet's disease. J Immunol Res. 2014;2014:653539. https:\u002F\u002Fdoi.org\u002F10.1155\u002F2014\u002F653539 Epub 2014 Jul 2.\nWright HL, Makki FA, Moots RJ, Edwards SW. 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Clin Exp Rheumatol. 2015;33:S85–95.\nEmmi G, Becatti M, Bettiol A, et al. Behçet’s syndrome as a model of thrombo-inflammation: the role of neutrophils. Front Immunol. 2019;10:1085. https:\u002F\u002Fdoi.org\u002F10.3389\u002Ffimmu.2019.01085.\nBecatti M, Emmi G, Bettiol A, et al. Behçet’s syndrome as a tool to dissect the mechanisms of thrombo-inflammation: clinical and pathogenetic aspects. Clin Exp Immunol. 2019;195:322–33. https:\u002F\u002Fdoi.org\u002F10.1111\u002Fcei.13243 Epub 2018 Dec 18.\nJohansson Å, Ohlsson S, Pettersson Å, et al. Impaired phagocytosis and reactive oxygen species production in phagocytes is associated with systemic vasculitis. Arthritis Res Ther. 2016;18:18–92.\nElloumi N, Ben Mansour R, Marzouk S, et al. Differential reactive oxygen species production of neutrophils and their oxidative damage in patients with active and inactive systemic lupus erythematosus. Immunol Lett. 2017;184:1–6. https:\u002F\u002Fdoi.org\u002F10.1016\u002Fj.imlet.2017.01.018.\nCarmona-Rivera C, Kaplan M. Low-density granulocytes: a distinct class of neutrophils in systemic autoimmunity. Semin Immunopathol. 2013;35:455–63. https:\u002F\u002Fdoi.org\u002F10.1007\u002Fs00281-013-0375-7.\nDenny M, Yalavarthi S, Zhao W, et al. A distinct subset of proinflammatory neutrophils isolated from patients with systemic lupus erythematosus induces vascular damage and synthesizes type I IFNs. J Immunol. 2010;184:3284–97.\nSagiv YJ, Michaeli J, Assi S, et al. Phenotypic diversity and plasticity in circulating neutrophil subpopulations in cancer. Cell Rep. 2015;10:562–73. https:\u002F\u002Fdoi.org\u002F10.1016\u002Fj.celrep.2014.12.039.\nFresneda Alarcon M, McLaren Z, Wright HL. Neutrophils in the pathogenesis of rheumatoid arthritis and systemic lupus erythematosus: same foe different M.O. 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Pondering neutrophil extracellular traps with healthy skepticism. Cell Microbiol. 2016;18:1349–57. https:\u002F\u002Fdoi.org\u002F10.1111\u002Fcmi.12652.\nHemmers S, Teijaro JR, Arandjelovic S, Mowen KA. PAD4-mediated neutrophil extracellular trap formation is not required for immunity against influenza infection. PLoS One. 2011;6:e22043. https:\u002F\u002Fdoi.org\u002F10.1371\u002Fjournal.pone.0022043.\nPieterse E, Rother N, Yanginlar C, et al. Neutrophils discriminate between lipopolysaccharides of different bacterial sources and selectively release neutrophil extracellular trap. Arterioscler Thromb Vasc Biol. 2017;37(7):1371–9. https:\u002F\u002Fdoi.org\u002F10.1161\u002FATVBAHA.117.309002.\nGrieshaber-Bouyer R, Nigrovic PA. Neutrophil heterogeneity as therapeutic opportunity in immune-mediated disease. Front Immunol. 2019;10:346. https:\u002F\u002Fdoi.org\u002F10.3389\u002Ffimmu.2019.00346.\nWright HL, Lyon M, Chapman EA. 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is a complex disease involving different cell types, including macrophages that play a major role in the inflammatory events occurring in atherogenesis. C-Reactive Protein (CRP) is a sensitive systemic marker of inflammation and was identified as a biomarker of cardiovascular diseases. Histological studies demonstrate CRP presence in human atherosclerotic lesions, and we have previously shown that macrophages express CRP mRNA. CRP could be locally secreted in the atherosclerotic lesion by arterial macrophages and local regulation of CRP could affect its pro-atherogenic effects. Moreover, human blood derived macrophages (HMDM) expression of CRP could reflect atherosclerotic lesion secretion of CRP. Ten type 2 diabetic patients and ten non-diabetic patients scheduled to undergo carotid endarterectomy were enrolled in this study, and their blood samples were used for serum CRP, lipid determination, and for preparation of HMDM further analyzed for their CRP mRNA expression and CRP content. Carotid lesions obtained from the patients were analyzed for their CRP and interleukin 6 (IL-6) content by immunohistochemistry. Lesions from diabetic patients showed substantially higher CRP levels by 62% (p = 0.05) than lesions from non diabetic patients, and CRP staining that co-localized with arterial macrophages. CRP carotid lesion levels positively correlated with CRP mRNA expression (r2 = 0.661) and with CRP content (r2 = 0.611) in the patient’s HMDM. Diabetes up-regulated carotid plaques CRP levels and CRP measurements in HMDM could reflect atherosclerotic lesion macrophages secretion of CRP. Understanding the regulation of locally produced macrophage CRP in the arterial wall during atherogenesis could be of major importance in identifying the underlying mechanisms of inflammatory response pathways during atherogenesis.",{"EN":2309},"A significant correlation between C - reactive protein levels in blood monocytes derived macrophages versus content in carotid atherosclerotic lesions",{"VOID":2311},"Libby P: Inflammation in atherosclerosis. Arterioscler Thromb Vasc Biol. 2012, 32: 2045-2051. 10.1161\u002FATVBAHA.108.179705.\nBarton M, Minotti R, Haas E: Inflammation and atherosclerosis. Circ Res. 2007, 101: 750-751. 10.1161\u002FCIRCRESAHA.107.162487.\nLusis AJ: Atherosclerosis. Nature. 2000, 407: 233-241. 10.1038\u002F35025203.\nKaplan M, Aviram M, Hayek T: Oxidative stress and macrophage foam cell formation during diabetes mellitus-induced atherogenesis: Role of insulin therapy. Pharmacol Ther. 2012, 136: 175-185. 10.1016\u002Fj.pharmthera.2012.08.002.\nPepys MB, Hirschfield GM: C-reactive protein: a critical update. J Clin Invest. 2003, 111: 1805-1812. 10.1172\u002FJCI200318921.\nPaul A, Yeh ET, Chan L: A proatherogenic role for C-reactive protein in vivo. Curr Opin Lipidol. 2005, 16: 512-517. 10.1097\u002F01.mol.0000180164.70077.a7.\nAbd TT, Eapen DJ, Bajpai A, Goyal A, Dollar A, Sperling L: The role of C-reactive protein as a risk predictor of coronary atherosclerosis: implications from the JUPITER trial. Curr Atheroscler Rep. 2011, 13: 154-161. 10.1007\u002Fs11883-011-0164-5.\nRidker PM: High-sensitivity C-reactive protein, inflammation, and cardiovascular risk: from concept to clinical practice to clinical benefit. Am Heart J. 2004, 148: S19-S26. 10.1016\u002Fj.ahj.2004.04.028.\nWensley F, Gao P, Burgess S, Kaptoge S, Di Angelantonio E, Shah T, Engert JC, Clarke R, Davey-Smith G, Nordestgaard BG, Saleheen D, Samani NJ, Sandhu M, Anand S, Pepys MB, Smeeth L, Whittaker J, Casas JP, Thompson SG, Hingorani AD, Danesh J, C Reactive Protein Coronary Heart Disease Genetics Collaboration (CCGC): Association between C reactive protein and coronary heart disease: mendelian randomisation analysis based on individual participant data. BMJ. 2011, 342: d548-\nVerma S, Devaraj S, Jialal I: Is C-reactive protein an innocent bystander or proatherogenic culprit? C-reactive protein promotes atherothrombosis. Circulation. 2006, 113: 2135-2150.\nDanesh J, Pepys MB: C-reactive protein and coronary disease: is there a causal link?. Circulation. 2009, 120: 2036-2039. 10.1161\u002FCIRCULATIONAHA.109.907212.\nEklund CM: Proinflammatory cytokines in CRP baseline regulation. Adv Clin Chem. 2009, 48: 111-136.\nAbeywardena MY, Leifert WR, Warnes KE, Varghese JN, Head RJ: Cardiovascular biology of interleukin-6. Curr Pharm Des. 2009, 15: 1809-1821. 10.2174\u002F138161209788186290.\nZhang YX, Cliff WJ, Schoefl GI, Higgins G: Coronary C-reactive protein distribution: its relation to development of atherosclerosis. Atherosclerosis. 1999, 145: 375-379. 10.1016\u002FS0021-9150(99)00105-7.\nYasojima K, Schwab C, McGeer EG, McGeer PL: Generation of C-reactive protein and complement components in atherosclerotic plaques. Am J Pathol. 2001, 158: 1039-1051. 10.1016\u002FS0002-9440(10)64051-5.\nKaplan M, Tendler Y, Mahamid R, Shiner M, Aviram M, Hayek T: High glucose regulates C-reactive protein production in macrophages. Clin Chem. 2010, 56: 1036-1038. 10.1373\u002Fclinchem.2009.136838.\nCiubotaru I, Potempa LA, Wander RC: Production of modified CRP in U937-derived macrophages. Exp Biol Med. 2005, 230: 762-770.\nJabs WJ, Theissing E, Nitschke M, Bechtel JF, Duchrow M, Mohamed S, Jahrbeck B, Sievers HH, Steinhoff J, Bartels C: Local Generation of C-Reactive Protein in Diseased Coronary Artery Venous Bypass Grafts and Normal Vascular Tissue. Circulation. 2003, 108: 1428-1431. 10.1161\u002F01.CIR.0000092184.43176.91.\nTorzewski J, Torzewski M, Bowyer DE, Fröhlich M, Koenig W, Waltenberger J, Fitzsimmons C, Hombach V: C-reactive protein frequently colocalizes with the terminal complement complex in the intima of early atherosclerotic lesions of human coronary Arteries. Arterioscler Thromb Vasc Biol. 1998, 18: 1386-1392. 10.1161\u002F01.ATV.18.9.1386.\nKeidar S, Gamliel-Lazarovich A, Kaplan M, Pavlotzky E, Hamoud S, Hayek T, Karry R, Abassi Z: Mineralocorticoid receptor blocker increases Angiotensin-converting enzyme 2 activity in congestive heart failure patients. Circ Res. 2005, 97: 946-953. 10.1161\u002F01.RES.0000187500.24964.7A.\nGiorno R: A comparison of two immunoperoxidase staining methods based on the avidin –biotin interaction. Diagn Immunol. 1984, 2: 161-166.\nGreen FJ: The Sigma-Aldrich Handbook of Stains, Dyes & Indicators. Edited by: Green FJ. 1990, Milwaukee, WI: Published by Aldrich Chemical Co, 565-567.\nBasta G, Schmidt AM, De Caterina R: Advanced end products and vascular inflammation: Implications for accelerated atherosclerosis in diabetes. Cardiovasc Res. 2004, 63: 582-592. 10.1016\u002Fj.cardiores.2004.05.001.\nKaraduman M, Oktenli C, Musabak U, Sengul A, Yesilova Z, Cingoz F, Olgun A, Sanisoglu SY, Baysan O, Yildiz O, Taslipinar A, Tatar H, Kutlu M, Ozata M: Leptin, soluble interleukin-6 receptor, C-reactive protein and soluble vascular cell adhesion molecule-1 levels in human coronary atherosclerotic plaque. Clin Exp Immunol. 2006, 143: 452-457. 10.1111\u002Fj.1365-2249.2006.03025.x.\nTurk JR, Carroll JA, Laughlin MH, Thomas TR, Casati J, Bowles DK, Sturek M: C-reactive protein correlates with macrophage accumulation in coronary arteries of hypercholesterolemic pigs. J Appl Physiol. 2003, 95: 1301-1304.\nVenugopal SK, Devaraj S, Jialal I: Effect of C-reactive protein on vascular cells: evidence for a proinflammatory, proatherogenic role. Curr Opin Nephrol Hypert. 2005, 14: 33-37. 10.1097\u002F00041552-200501000-00006.\nJialal I, Devaraj S, Singh U: Sources of CRP in atherosclerotic lesions. Am J Pathol. 2006, 168: 1054-1055. 10.2353\u002Fajpath.2006.051175.\nYeh ET: CRP as mediator of disease. Circulation. 2004, 109 (II): 11-14.\nWaldo SW, Li Y, Buono C, Zhao B, Billings EM, Chang J, Kruth HS: Heterogeneity of human macrophages in culture and in atherosclerotic plaques. Am J Pathol. 2008, 172: 1112-1126. 10.2353\u002Fajpath.2008.070513.\nLey K, Miller YI, Hedrick CC: Monocyte and macrophage dynamics during atherogenesis. Arterioscler Thromb Vasc Biol. 2011, 31: 1506-1516. 10.1161\u002FATVBAHA.110.221127.\nPepys MB: CRP or not CRP? That is the question. Arterioscler Thromb Vasc Biol. 2005, 25: 1091-1094. 10.1161\u002F01.ATV.0000169644.88847.28.\nKaptoge S, Di Angelantonio E, Pennells L, Wood AM, White IR, Gao P, Walker M, Thompson A, Sarwar N, Caslake M, Butterworth AS, Amouyel P, Assmann G, Bakker SJ, Barr EL, Barrett-Connor E, Benjamin EJ, Björkelund C, Brenner H, Brunner E, Clarke R, Cooper JA, Cremer P, Cushman M, Dagenais GR, D’Agostino RB, Dankner R, Davey-Smith G, Deeg D, Emerging Risk Factors Collaboration: C-reactive protein, fibrinogen, and cardiovascular disease prediction. N Engl J Med. 2012, 367: 1310-1320.\nHammond DJ, Singh SK, Thompson JA, Beeler BW, Rusiñol AE, Pangburn MK, Potempa LA, Agrawal A: Identification of acidic pH-dependent ligands of pentameric C-reactive protein. J Biol Chem. 2010, 285: 36235-36244. 10.1074\u002Fjbc.M110.142026.\nSingh SK, Thirumalai A, Hammond DJ, Pangburn MK, Mishra VK, Johnson DA, Rusiñol AE, Agrawal A: Exposing a hidden functional site of C-reactive protein by site-directed mutagenesis. J Biol Chem. 2012, 287: 3550-3558. 10.1074\u002Fjbc.M111.310011.\nAhrens I, Domeij H, Eisenhardt SU, Topcic D, Albrecht M, Leitner E, Viitaniemi K, Jowett JB, Lappas M, Bode C, Haviv I, Peter K: Opposing effects of monomeric and pentameric C-reactive protein on endothelial progenitor cells. Basic Res Cardiol. 2011, 106: 879-895. 10.1007\u002Fs00395-011-0191-y.",{"VOID":2313},"10.1186\u002F1476-9255-11-7","https:\u002F\u002Fjournal-inflammation.biomedcentral.com\u002Farticles\u002F10.1186\u002F1476-9255-11-7",[2316,2331,2346,2359,2374,2387,2402],{"id":2317,"sortIndex":32,"researcher":28,"roles":2318,"affiliations":2319,"properties":2328,"displayName":2330,"givenName":28,"familyName":28},"4e134f73-d6c9-4854-a12c-7958e8b6e91e",[994],[2320],{"id":2321,"sortIndex":32,"affiliation":2322,"properties":28},"5c32afa5-3fcd-482c-89ee-16bdc031fcca",{"id":2321,"createTime":28,"updateTime":28,"relativeEntities":2323,"slug":28,"properties":2324,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":2327,"statistic":28},[],{"title":2325},{"VI":2326},"Laboratory of Clinical Biochemistry, Rambam Health Care Campus, Haifa, Israel",[],{"title":2329},{"VI":2330},"Marielle 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disease (BD) is a systemic inflammatory disease with manifestations including recurrent oral and genital ulcerations, and vasculitis involving the skin, mucosa, joints, eyes, veins, arteries, nervous and gastrointestinal systems. BD is seen as a disease at the crossroad between autoimmune and autoinflammatory syndromes, possibly triggered by an aberrant response to infectious stimuli. The relevance of Gram negative bacteria-mediated oral inflammation with the increased expression of NACHT, LRR, and PYD domains-containing protein 3 (NLRP3), leading to systemic inflammation, prompted us to investigate the expression of NLRP3 inflammasome components and its link with IL-1β hypersecretion. When peripheral blood mononuclear cells (PBMCs) from 15 active, 15 stable BD patients and 15 healthy volunteers were stimulated, the basal and LPS-induced expressions of NLRP3 inflammasome components were significantly increased at both mRNA and protein levels in BD patients compared to healthy controls. Also, increased expression of NLRP3 and ASC was observed in 25 BD skin lesions compared to 25 erythema nodosum patients. Compatible with this, secretion of IL-1β by PBMCs stimulated with LPS alone or LPS plus ATP was increased in BD compared to healthy controls, which was suppressed by caspase-1 inhibitor. Our findings suggest the possible link between increased IL-1β secretion and increased expression of NLRP3 inflammasome components in BD patients with skin manifestations.",{"EN":2486},"Increased expression of the NLRP3 inflammasome components in patients with Behçet’s disease",{"VOID":2488},"Direskeneli H. Autoimmunity vs autoinflammation in Behcet’s disease: do we oversimplify a complex disorder? Rheumatology (Oxford). 2006;45:1461–5.\nPineton de Chambrun M, Wechsler B, Geri G, Cacoub P, Saadoun D. New insights into the pathogenesis of Behcet’s disease. Autoimmun Rev. 2012;11:687–98.\nYamaguchi Y, Kurita-Ochiai T, Kobayashi R, Suzuki T, Ando T. Activation of the NLRP3 inflammasome in Porphyromonas gingivalis-accelerated atherosclerosis. Pathog Dis. 2015;73:epub. doi:10.1093\u002Ffemspd\u002Fftv011.\nLiang L, Tan X, Zhou Q, Zhu Y, Tian Y, Yu H, et al. IL-1beta triggered by peptidoglycan and lipopolysaccharide through TLR2\u002F4 and ROS-NLRP3 inflammasome-dependent pathways is involved in ocular Behcet’s disease. Invest Ophthalmol Vis Sci. 2013;54:402–14.\nMitroulis I, Skendros P, Ritis K. Targeting IL-1beta in disease; the expanding role of NLRP3 inflammasome. Eur J Intern Med. 2010;21:157–63.\nQiao Y, Wang P, Qi J, Zhang L, Gao C. TLR-induced NF-kappaB activation regulates NLRP3 expression in murine macrophages. FEBS Lett. 2012;586:1022–6.\nNetea MG, Simon A, van de Veerdonk F, Kullberg BJ, Van der Meer JW, Joosten LA. IL-1beta processing in host defense: beyond the inflammasomes. PLoS Pathog. 2010;6, e1000661.\nBauernfeind F, Hornung V. Of inflammasomes and pathogens–sensing of microbes by the inflammasome. EMBO Mol Med. 2013;5:814–26.\nGogus F, Fresko I, Elbir Y, Eksioglu-Demiralp E, Direskeneli H. Oxidative burst response to monosodium urate crystals in patients with Behcet’s syndrome. Clin Exp Rheumatol. 2005;23 Suppl 38:S81–5.\nKaneko F, Oyama N, Nishibu A. Streptococcal infection in the pathogenesis of Behcet’s disease and clinical effects of minocycline on the disease symptoms. Yonsei Med J. 1997;38:444–54.\nCalguneri M, Kiraz S, Ertenli I, Benekli M, Karaarslan Y, Celik I. The effect of prophylactic penicillin treatment on the course of arthritis episodes in patients with Behcet’s disease. A randomized clinical trial. Arthritis Rheum. 1996;39:2062–5.\nDo JE, Kwon SY, Park S, Lee ES. Effects of vitamin D on expression of toll-like receptors of monocytes from patients with Behcet’s disease. Rheumatology (Oxford). 2008;47:840–8.\nDinarello CA. Immunological and inflammatory functions of the interleukin-1 family. Annu Rev Immunol. 2009;27:519–50.\nGul A, Tugal-Tutkun I, Dinarello CA, Reznikov L, Esen BA, Mirza A, et al. Interleukin-1beta-regulating antibody XOMA 052 (gevokizumab) in the treatment of acute exacerbations of resistant uveitis of Behcet’s disease: an open-label pilot study. Ann Rheum Dis. 2012;71:563–6.\nKeller M, Sollberger G, Beer HD. Thalidomide inhibits activation of caspase-1. 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