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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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responses to ozone are reduced in immature rats",{"VOID":948},"Shore SA, Abraham JH, Schwartzman IN, Krishna Murthy GG, Laporte JD: Ventilatory responses to ozone are reduced in immature rats. J Appl Physiol. 2000, 88: 2023-2030.",{"VOID":950},"10.1186\u002Frr-2001-68585","PUBLICATION","https:\u002F\u002Frespiratory-research.biomedcentral.com\u002Farticles\u002F10.1186\u002Frr-2001-68585",[954],{"id":955,"sortIndex":32,"researcher":28,"roles":956,"affiliations":958,"properties":967,"displayName":969,"givenName":28,"familyName":28},"cd87c7c9-27f3-4956-a642-2b00cf6be3b7",[957],"AUTHOR",[959],{"id":960,"sortIndex":32,"affiliation":961,"properties":28},"1ccc44bd-1ce6-47f7-9e71-5f689c2f38a1",{"id":960,"createTime":28,"updateTime":28,"relativeEntities":962,"slug":28,"properties":963,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":966,"statistic":28},[],{"title":964},{"VI":965},"The Centers for Disease Control and Prevention, Georgia, USA",[],{"title":968},{"VI":969},"Jeff Fedan","ARTICLE",{"url":952,"publisher":972,"properties":1013},{"id":868,"createTime":869,"updateTime":870,"relativeEntities":973,"slug":872,"properties":974,"entityType":25,"verifyStatus":878,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":32,"subjectFields":977,"manageAffiliations":982,"indexDatabases":993,"url":930,"thumbnailPath":28,"statistic":1008,"gsStatistic":28,"type":55,"analyzePriority":28},[],{"issn":975,"title":976},{"VOID":875},{"EN":877},[978],{"id":881,"createTime":28,"updateTime":28,"relativeEntities":979,"label":980,"description":981,"parentId":28,"standard":28,"scholarHubFieldId":28},[],{"EN":884},{},[983,988],{"id":888,"createTime":28,"updateTime":28,"relativeEntities":984,"slug":28,"properties":985,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":987,"statistic":28},[],{"title":986},{"EN":892},[],{"id":895,"createTime":28,"updateTime":28,"relativeEntities":989,"slug":28,"properties":990,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":992,"statistic":28},[],{"title":991},{"EN":899},[],[994,1001],{"id":903,"indexDatabase":995,"url":909,"indexYears":910,"academicFieldIds":1000,"indexDatabaseRanking":913},{"id":786,"createTime":28,"updateTime":28,"relativeEntities":996,"label":997,"description":998,"key":792,"publicationTags":999,"standard":28},[],{"EN":789,"VI":789},{"EN":789,"VI":791},[794],[912],{"id":915,"indexDatabase":1002,"url":927,"indexYears":28,"academicFieldIds":1007,"indexDatabaseRanking":28},{"id":917,"createTime":28,"updateTime":28,"relativeEntities":1003,"label":1004,"description":1005,"key":924,"publicationTags":1006,"standard":28},[],{"EN":920,"VI":920},{"EN":922,"VI":923},[926,813],[929],{"impactFactor":32,"impactFactorByYear":1009,"i10Index":32,"i10IndexLast5Year":32,"totalPublication":40,"totalPublicationByYear":1010,"totalCitation":32,"totalCitationByYear":1011,"totalCitationPerPublication":32,"totalCitationPerPublicationByYear":1012,"hindexLast5Year":32,"hindex":32},{},{"2004":40},{},{},{"pages":1014,"volume":1016},{"VOID":1015},"1-1",{"VOID":1017},"2","2001-09-20",2001,[926,913],false,{"id":1023,"createTime":1024,"updateTime":1025,"relativeEntities":1026,"slug":1027,"properties":1028,"entityType":951,"verifyStatus":26,"verifyTime":1025,"verifyNote":1037,"languages":28,"translateLanguages":28,"viewCount":32,"primaryUrl":1038,"fullTextUrl":28,"authors":1039,"publicationType":970,"publisherRelationship":1096,"citationCount":28,"citationInfo":28,"publishDate":1143,"publishYear":1144,"citationAnalyzeStatus":878,"lastCitationAnalyze":28,"indexDatabases":1145,"openAccess":28,"references":28,"isForceReanalyzing":1021},"005541cc-44a2-4010-b1fa-ef7f46b73e21","2024-01-05T11:49:14.921+00:00","2025-02-21T15:03:16.875+00:00",[],"Protection-from-pulmonary-ischemia-reperfusion-injury-by-adenosine-A2A-receptor-activation",{"abstract":1029,"title":1031,"references":1033,"doi":1035},{"EN":1030},"Lung ischemia-reperfusion (IR) injury leads to significant morbidity and mortality which remains a major obstacle after lung transplantation. However, the role of various subset(s) of lung cell populations in the pathogenesis of lung IR injury and the mechanisms of cellular protection remain to be elucidated. In the present study, we investigated the effects of adenosine A2A receptor (A2AAR) activation on resident lung cells after IR injury using an isolated, buffer-perfused murine lung model. To assess the protective effects of A2AAR activation, three groups of C57BL\u002F6J mice were studied: a sham group (perfused for 2 hr with no ischemia), an IR group (1 hr ischemia + 1 hr reperfusion) and an IR+ATL313 group where ATL313, a specific A2AAR agonist, was included in the reperfusion buffer after ischemia. Lung injury parameters and pulmonary function studies were also performed after IR injury in A2AAR knockout mice, with or without ATL313 pretreatment. Lung function was assessed using a buffer-perfused isolated lung system. Lung injury was measured by assessing lung edema, vascular permeability, cytokine\u002Fchemokine activation and myeloperoxidase levels in the bronchoalveolar fluid. After IR, lungs from C57BL\u002F6J wild-type mice displayed significant dysfunction (increased airway resistance, pulmonary artery pressure and decreased pulmonary compliance) and significant injury (increased vascular permeability and edema). Lung injury and dysfunction after IR were significantly attenuated by ATL313 treatment. Significant induction of TNF-α, KC (CXCL1), MIP-2 (CXCL2) and RANTES (CCL5) occurred after IR which was also attenuated by ATL313 treatment. Lungs from A2AAR knockout mice also displayed significant dysfunction, injury and cytokine\u002Fchemokine production after IR, but ATL313 had no effect in these mice. Specific activation of A2AARs provides potent protection against lung IR injury via attenuation of inflammation. This protection occurs in the absence of circulating blood thereby indicating a protective role of A2AAR activation on resident lung cells such as alveolar macrophages. Specific A2AAR activation may be a promising therapeutic target for the prevention or treatment of pulmonary graft dysfunction in transplant patients.",{"EN":1032},"Protection from pulmonary ischemia-reperfusion injury by adenosine A2A receptor activation",{"VOID":1034},"Fiser SM, Tribble CG, Long SM, Kaza AK, Kern JA, Jones DR, Robbins MK, Kron IL: Ischemia-reperfusion injury after lung transplantation increases risk of late bronchiolitis obliterans syndrome. Ann Thorac Surg 2002, 73:1041–1047.\nde Perrot M, Liu M, Waddell TK, Keshavjee S: Ischemia-reperfusion-induced lung injury. Am J Respir Crit Care Med 2003, 167:490–511.\nBoehler A, Estenne M: Post-transplant bronchiolitis obliterans. Eur Respir J 2003, 22:1007–1018.\nZhao M, Fernandez LG, Doctor A, Sharma AK, Zarbock A, Tribble CG, Kron IL, Laubach VE: Alveolar macrophage activation is a key initiation signal for acute lung ischemia-reperfusion injury. Am J Physiol Lung Cell Mol Physiol 2006, 291:L1018–1026.\nSharma AK, Fernandez LG, Awad AS, Kron IL, Laubach VE: Proinflammatory response of alveolar epithelial cells is enhanced by alveolar macrophage-produced TNF-alpha during pulmonary ischemia-reperfusion injury. Am J Physiol Lung Cell Mol Physiol 2007, 293:L105–113.\nRoss SD, Tribble CG, Gaughen JR Jr, Shockey KS, Parrino PE, Kron IL: Reduced neutrophil infiltration protects against lung reperfusion injury after transplantation. Ann Thorac Surg 1999, 67:1428–1433.\nEppinger MJ, Deeb GM, Bolling SF, Ward PA: Mediators of ischemia-reperfusion injury of rat lung. Am J Pathol 1997, 150:1773–1784.\nEppinger MJ, Jones ML, Deeb GM, Bolling SF, Ward PA: Pattern of injury and the role of neutrophils in reperfusion injury of rat lung. J Surg Res 1995, 58:713–718.\nBando K, Paradis IL, Similo S, Konishi H, Komatsu K, Zullo TG, Yousem SA, Close JM, Zeevi A, Duquesnoy RJ, et al.: Obliterative bronchiolitis after lung and heart-lung transplantation. An analysis of risk factors and management. J Thorac Cardiovasc Surg 1995, 110:4–13.\nSnell GI, Esmore DS, Williams TJ: Cytolytic therapy for the bronchiolitis obliterans syndrome complicating lung transplantation. Chest 1996, 109:874–878.\nMal H, Dehoux M, Sleiman C, Boczkowski J, Leseche G, Pariente R, Fournier M: Early release of proinflammatory cytokines after lung transplantation. Chest 1998, 113:645–651.\nMaxey TS, Enelow RI, Gaston B, Kron IL, Laubach VE, Doctor A: Tumor necrosis factor-alpha from resident lung cells is a key initiating factor in pulmonary ischemia-reperfusion injury. J Thorac Cardiovasc Surg 2004, 127:541–547.\nNovick RJ, Gehman KE, Ali IS, Lee J: Lung preservation: the importance of endothelial and alveolar type II cell integrity. Ann Thorac Surg 1996, 62:302–314.\nCronstein BN, Daguma L, Nichols D, Hutchison AJ, Williams M: The adenosine\u002Fneutrophil paradox resolved: human neutrophils possess both A1 and A2 receptors that promote chemotaxis and inhibit O 2 generation, respectively. J Clin Invest 1990, 85:1150–1157.\nCronstein BN, Levin RI, Philips M, Hirschhorn R, Abramson SB, Weissmann G: Neutrophil adherence to endothelium is enhanced via adenosine A1 receptors and inhibited via adenosine A2 receptors. J Immunol 1992, 148:2201–2206.\nNolte D, Lorenzen A, Lehr HA, Zimmer FJ, Klotz KN, Messmer K: Reduction of postischemic leukocyte-endothelium interaction by adenosine via A2 receptor. Naunyn Schmiedebergs Arch Pharmacol 1992, 346:234–237.\nMullane K, Bullough D: Harnessing an endogenous cardioprotective mechanism: cellular sources and sites of action of adenosine. J Mol Cell Cardiol 1995, 27:1041–1054.\nMurphree LJ, Sullivan GW, Marshall MA, Linden J: Lipopolysaccharide rapidly modifies adenosine receptor transcripts in murine and human macrophages: role of NF-kappaB in A(2A) adenosine receptor induction. Biochem J 2005, 391:575–580.\nCronstein BN: Adenosine, an endogenous anti-inflammatory agent. J Appl Physiol 1994, 76:5–13.\nDay YJ, Huang L, Ye H, Li L, Linden J, Okusa MD: Renal ischemia-reperfusion injury and adenosine 2A receptor-mediated tissue protection: the role of CD4+ T cells and IFN-gamma. J Immunol 2006, 176:3108–3114.\nDay YJ, Marshall MA, Huang L, McDuffie MJ, Okusa MD, Linden J: Protection from ischemic liver injury by activation of A2A adenosine receptors during reperfusion: inhibition of chemokine induction. Am J Physiol Gastrointest Liver Physiol 2004, 286:G285–293.\nOkusa MD, Linden J, Macdonald T, Huang L: Selective A2A adenosine receptor activation reduces ischemia-reperfusion injury in rat kidney. Am J Physiol 1999, 277:F404–412.\nPeart J, Flood A, Linden J, Matherne GP, Headrick JP: Adenosine-mediated cardioprotection in ischemic-reperfused mouse heart. J Cardiovasc Pharmacol 2002, 39:117–129.\nReece TB, Okonkwo DO, Ellman PI, Warren PS, Smith RL, Hawkins AS, Linden J, Kron IL, Tribble CG, Kern JA: The evolution of ischemic spinal cord injury in function, cytoarchitecture, and inflammation and the effects of adenosine A2A receptor activation. J Thorac Cardiovasc Surg 2004, 128:925–932.\nBullough DA, Magill MJ, Firestein GS, Mullane KM: Adenosine activates A2 receptors to inhibit neutrophil adhesion and injury to isolated cardiac myocytes. J Immunol 1995, 155:2579–2586.\nGazoni LM, Laubach VE, Mulloy DP, Bellizzi A, Unger EB, Linden J, Ellman PI, Lisle TC, Kron IL: Additive protection against lung ischemia-reperfusion injury by adenosine A2A receptor activation before procurement and during reperfusion. J Thorac Cardiovasc Surg 2008, 135:156–165.\nRoss SD, Tribble CG, Linden J, Gangemi JJ, Lanpher BC, Wang AY, Kron IL: Selective adenosine-A2A activation reduces lung reperfusion injury following transplantation. J Heart Lung Transplant 1999, 18:994–1002.\nSullivan GW, Linden J, Buster BL, Scheld WM: Neutrophil A2A adenosine receptor inhibits inflammation in a rat model of meningitis: synergy with the type IV phosphodiesterase inhibitor, rolipram. J Infect Dis 1999, 180:1550–1560.\nRieger JM, Brown ML, Sullivan GW, Linden J, Macdonald TL: Design, synthesis, and evaluation of novel A2A adenosine receptor agonists. J Med Chem 2001, 44:531–539.\nLinden J: Molecular approach to adenosine receptors: receptor-mediated mechanisms of tissue protection. Annu Rev Pharmacol Toxicol 2001, 41:775–787.\nLink AA, Kino T, Worth JA, McGuire JL, Crane ML, Chrousos GP, Wilder RL, Elenkov IJ: Ligand-activation of the adenosine A2a receptors inhibits IL-12 production by human monocytes. J Immunol 2000, 164:436–442.\nLappas CM, Rieger JM, Linden J: A2A adenosine receptor induction inhibits IFN-gamma production in murine CD4+ T cells. J Immunol 2005, 174:1073–1080.\nDuggan M, Kavanagh BP: Pulmonary atelectasis: a pathogenic perioperative entity. Anesthesiology 2005, 102:838–854.\nSaito S, Ogawa J, Minamiya Y: Pulmonary reexpansion causes xanthine oxidase-induced apoptosis in rat lung. Am J Physiol Lung Cell Mol Physiol 2005, 289:L400–406.\nCassada DC, Tribble CG, Long SM, Laubach VE, Kaza AK, Linden J, Nguyen BN, Rieger JM, Fiser SM, Kron IL, et al.: Adenosine A2A analogue ATL-146e reduces systemic tumor necrosing factor-alpha and spinal cord capillary platelet-endothelial cell adhesion molecule-1 expression after spinal cord ischemia. J Vasc Surg 2002, 35:994–998.\nReece TB, Laubach VE, Tribble CG, Maxey TS, Ellman PI, Warren PS, Schulman AM, Linden J, Kern JA, Kron IL: Adenosine A2A receptor agonist improves cardiac dysfunction from pulmonary ischemia-reperfusion injury. Ann Thorac Surg 2005, 79:1189–1195.\nRivo J, Zeira E, Galun E, Einav S, Linden J, Matot I: Attenuation of reperfusion lung injury and apoptosis by A2A adenosine receptor activation is associated with modulation of Bcl-2 and Bax expression and activation of extracellular signal-regulated kinases. Shock 2007, 27:266–273.\nSullivan GW: Adenosine A2A receptor agonists as anti-inflammatory agents. Curr Opin Investig Drugs 2003, 4:1313–1319.\nDay YJ, Li Y, Rieger JM, Ramos SI, Okusa MD, Linden J: A2A adenosine receptors on bone marrow-derived cells protect liver from ischemia-reperfusion injury. J Immunol 2005, 174:5040–5046.\nChunn JL, Young HW, Banerjee SK, Colasurdo GN, Blackburn MR: Adenosine-dependent airway inflammation and hyperresponsiveness in partially adenosine deaminase-deficient mice. J Immunol 2001, 167:4676–4685.\nMatherne GP, Linden J, Byford AM, Gauthier NS, Headrick JP: Transgenic A1 adenosine receptor overexpression increases myocardial resistance to ischemia. Proc Natl Acad Sci USA 1997, 94:6541–6546.\nLee HT, Xu H, Nasr SH, Schnermann J, Emala CW: A1 adenosine receptor knockout mice exhibit increased renal injury following ischemia and reperfusion. Am J Physiol Renal Physiol 2004, 286:F298–306.\nNeely CF, Keith IM: A1 adenosine receptor antagonists block ischemia-reperfusion injury of the lung. Am J Physiol 1995, 268:L1036–1046.\nYang D, Zhang Y, Nguyen HG, Koupenova M, Chauhan AK, Makitalo M, Jones MR, St Hilaire C, Seldin DC, Toselli P, et al.: The A2B adenosine receptor protects against inflammation and excessive vascular adhesion. J Clin Invest 2006, 116:1913–1923.\nRivo J, Zeira E, Galun E, Matot I: Activation of A3 adenosine receptor provides lung protection against ischemia-reperfusion injury associated with reduction in apoptosis. Am J Transplant 2004, 4:1941–1948.\nNakamura T, Abu-Dahab R, Menger MD, Schafer U, Vollmar B, Wada H, Lehr CM, Schafers HJ: Depletion of alveolar macrophages by clodronate-liposomes aggravates ischemia-reperfusion injury of the lung. J Heart Lung Transplant 2005, 24:38–45.\nNaidu BV, Krishnadasan B, Farivar AS, Woolley SM, Thomas R, Van Rooijen N, Verrier ED, Mulligan MS: Early activation of the alveolar macrophage is critical to the development of lung ischemia-reperfusion injury. J Thorac Cardiovasc Surg 2003, 126:200–207.\nDay YJ, Huang L, Ye H, Linden J, Okusa MD: Renal ischemia-reperfusion injury and adenosine 2A receptor-mediated tissue protection: role of macrophages. Am J Physiol Renal Physiol 2005, 288:F722–731.\nNaidu BV, Woolley SM, Farivar AS, Thomas R, Fraga CH, Goss CH, Mulligan MS: Early tumor necrosis factor-alpha release from the pulmonary macrophage in lung ischemia-reperfusion injury. J Thorac Cardiovasc Surg 2004, 127:1502–1508.\nKrishnadasan B, Naidu BV, Byrne K, Fraga C, Verrier ED, Mulligan MS: The role of proinflammatory cytokines in lung ischemia-reperfusion injury. 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disorders following ICU discharge",{"VOID":1156},"Chishti A, Batchelor AM, Bullock RE, Fulton B, Gascoigne AD, Baudouin SV: Sleep-related breathing disorders following discharge from intensive care. Intensive Care Med. 2000, 26: 426-433.",{"VOID":1158},"10.1186\u002Frr-2001-68588","https:\u002F\u002Frespiratory-research.biomedcentral.com\u002Farticles\u002F10.1186\u002Frr-2001-68588",[1161],{"id":1162,"sortIndex":32,"researcher":28,"roles":1163,"affiliations":1164,"properties":1173,"displayName":1175,"givenName":28,"familyName":28},"0ebf8fbc-daf4-4ac9-a45b-224b2aa9cd3f",[957],[1165],{"id":1166,"sortIndex":32,"affiliation":1167,"properties":28},"4537bf60-2c4f-419d-92ef-f0629da0c626",{"id":1166,"createTime":28,"updateTime":28,"relativeEntities":1168,"slug":28,"properties":1169,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1172,"statistic":28},[],{"title":1170},{"VI":1171},"St Georges' Hospital, England",[],{"title":1174},{"VI":1175},"Richard Venn",{"url":1159,"publisher":1177,"properties":1218},{"id":868,"createTime":869,"updateTime":870,"relativeEntities":1178,"slug":872,"properties":1179,"entityType":25,"verifyStatus":878,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":32,"subjectFields":1182,"manageAffiliations":1187,"indexDatabases":1198,"url":930,"thumbnailPath":28,"statistic":1213,"gsStatistic":28,"type":55,"analyzePriority":28},[],{"issn":1180,"title":1181},{"VOID":875},{"EN":877},[1183],{"id":881,"createTime":28,"updateTime":28,"relativeEntities":1184,"label":1185,"description":1186,"parentId":28,"standard":28,"scholarHubFieldId":28},[],{"EN":884},{},[1188,1193],{"id":888,"createTime":28,"updateTime":28,"relativeEntities":1189,"slug":28,"properties":1190,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1192,"statistic":28},[],{"title":1191},{"EN":892},[],{"id":895,"createTime":28,"updateTime":28,"relativeEntities":1194,"slug":28,"properties":1195,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1197,"statistic":28},[],{"title":1196},{"EN":899},[],[1199,1206],{"id":903,"indexDatabase":1200,"url":909,"indexYears":910,"academicFieldIds":1205,"indexDatabaseRanking":913},{"id":786,"createTime":28,"updateTime":28,"relativeEntities":1201,"label":1202,"description":1203,"key":792,"publicationTags":1204,"standard":28},[],{"EN":789,"VI":789},{"EN":789,"VI":791},[794],[912],{"id":915,"indexDatabase":1207,"url":927,"indexYears":28,"academicFieldIds":1212,"indexDatabaseRanking":28},{"id":917,"createTime":28,"updateTime":28,"relativeEntities":1208,"label":1209,"description":1210,"key":924,"publicationTags":1211,"standard":28},[],{"EN":920,"VI":920},{"EN":922,"VI":923},[926,813],[929],{"impactFactor":32,"impactFactorByYear":1214,"i10Index":32,"i10IndexLast5Year":32,"totalPublication":40,"totalPublicationByYear":1215,"totalCitation":32,"totalCitationByYear":1216,"totalCitationPerPublication":32,"totalCitationPerPublicationByYear":1217,"hindexLast5Year":32,"hindex":32},{},{"2004":40},{},{},{"pages":1219,"volume":1220},{"VOID":1015},{"VOID":1017},[926,913],{"id":1223,"createTime":1224,"updateTime":1225,"relativeEntities":1226,"slug":1227,"properties":1228,"entityType":951,"verifyStatus":26,"verifyTime":1225,"verifyNote":1037,"languages":28,"translateLanguages":28,"viewCount":32,"primaryUrl":1237,"fullTextUrl":28,"authors":1238,"publicationType":970,"publisherRelationship":1458,"citationCount":28,"citationInfo":28,"publishDate":1505,"publishYear":1506,"citationAnalyzeStatus":878,"lastCitationAnalyze":28,"indexDatabases":1507,"openAccess":28,"references":28,"isForceReanalyzing":1021},"0063be1c-cbac-4a8f-8803-0a9c822720b6","2024-01-11T07:31:17.955+00:00","2024-12-13T12:01:27.220+00:00",[],"Notch4-mediates-vascular-remodeling-via-ERK-JNK-P38-MAPK-signaling-pathways-in-hypoxic-pulmonary-hypertension",{"abstract":1229,"title":1231,"references":1233,"doi":1235},{"EN":1230},"Hypoxic pulmonary hypertension (HPH) is a chronic progressive advanced disorder pathologically characterized by pulmonary vascular remodeling. Notch4 as a cell surface receptor is critical for vascular development. However, little is known about the role and mechanism of Notch4 in the development of hypoxic vascular remodeling. Lung tissue samples were collected to detect the expression of Notch4 from patients with HPH and matched controls. Human pulmonary artery smooth muscle cells (HPASMCs) were cultured in hypoxic and normoxic conditions. Real-time quantitative PCR and western blotting were used to examine the mRNA and protein levels of Notch4. HPASMCs were transfected with small interference RNA (siRNA) against Notch4 or Notch4 overexpression plasmid, respectively. Cell viability, cell proliferation, apoptosis, and migration were assessed using Cell Counting Kit-8, Edu, Annexin-V\u002FPI, and Transwell assay. The interaction between Notch4 and ERK, JNK, P38 MAPK were analyzed by co-immunoprecipitation. Adeno-associated virus 1-mediated siRNA against Notch4 (AAV1-si-Notch4) was injected into the airways of hypoxic rats. Right ventricular systolic pressure (RVSP), right ventricular hypertrophy and pulmonary vascular remodeling were evaluated. In this study, we demonstrate that Notch4 is highly expressed in the media of pulmonary vascular and is upregulated in lung tissues from patients with HPH and HPH rats compared with control groups. In vitro, hypoxia induces the high expression of Delta-4 and Notch4 in HPASMCs. The increased expression of Notch4 promotes HPASMCs proliferation and migration and inhibits cells apoptosis via ERK, JNK, P38 signaling pathways. Furthermore, co-immunoprecipitation result elucidates the interaction between Notch4 and ERK\u002FJNK\u002FP38. In vivo, silencing Notch4 partly abolished the increase in RVSP and pulmonary vascular remodeling caused by hypoxia in HPH rats. These findings reveal an important role of the Notch4-ERK\u002FJNK\u002FP38 MAPK axis in hypoxic pulmonary remodeling and provide a potential therapeutic target for patients with HPH.",{"EN":1232},"Notch4 mediates vascular remodeling via ERK\u002FJNK\u002FP38 MAPK signaling pathways in hypoxic pulmonary hypertension",{"VOID":1234},"Hoeper MM, Ghofrani HA, Grünig E, Klose H, Olschewski H, Rosenkranz S. Pulmonary hypertension. Dtsch Arztebl Int. 2017;114:73–84.\nChen J, Sysol JR, Singla S, Zhao S, Yamamura A, Valdez-Jasso D, et al. Nicotinamide phosphoribosyltransferase promotes pulmonary vascular remodeling and is a therapeutic target in pulmonary arterial hypertension. Circulation. 2017;135:1532–46.\nSchermuly RT, Ghofrani HA, Wilkins MR, Grimminger F. Mechanisms of disease: pulmonary arterial hypertension. Nat Rev Cardiol. 2011;8:443–55.\nGaliè N, Humbert M, Vachiery JL, Gibbs S, Lang I, Torbicki A, et al. 2015 ESC\u002FERS Guidelines for the diagnosis and treatment of pulmonary hypertension: the Joint Task Force for the Diagnosis and Treatment of Pulmonary Hypertension of the European Society of Cardiology (ESC) and the European Respiratory Society (ERS): endorsed by: Association for European Paediatric and Congenital Cardiology (AEPC), International Society for Heart and Lung Transplantation (ISHLT). Eur Heart J. 2016;37:67–119.\nPagliaro L, Marchesini M, Roti G. Targeting oncogenic Notch signaling with SERCA inhibitors. J Hematol Oncol. 2021;14:8.\nArtavanis-Tsakonas S, Rand MD, Lake RJ. Notch signaling: cell fate control and signal integration in development. Science. 1999;284:770–6.\nBray SJ. Notch signalling in context. Nat Rev Mol Cell Biol. 2016;17:722–35.\nRamakrishnan G, Davaakhuu G, Chung WC, Zhu H, Rana A, Filipovic A, et al. AKT and 14-3-3 regulate Notch4 nuclear localization. Sci Rep. 2015;5:8782.\nMumm JS, Kopan R. Notch signaling: from the outside in. Dev Biol. 2000;228:151–65.\nBaron M. An overview of the Notch signalling pathway. Semin Cell Dev Biol. 2003;14:113–9.\nMeester JAN, Verstraeten A, Alaerts M, Schepers D, Van Laer L, Loeys BL. Overlapping but distinct roles for NOTCH receptors in human cardiovascular disease. Clin Genet. 2019;95:85–94.\nNoseda M, McLean G, Niessen K, Chang L, Pollet I, Montpetit R, et al. Notch activation results in phenotypic and functional changes consistent with endothelial-to-mesenchymal transformation. Circ Res. 2004;94:910–7.\nSasnauskienė A, Jonušienė V, Krikštaponienė A, Butkytė S, Dabkevičienė D, Kanopienė D, et al. NOTCH1, NOTCH3, NOTCH4, and JAG2 protein levels in human endometrial cancer. Medicina (Kaunas). 2014;50:14–8.\nNagamatsu I, Onishi H, Matsushita S, Kubo M, Kai M, Imaizumi A, et al. 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JNK regulates serotonin-mediated proliferation and migration of pulmonary artery smooth muscle cells. Am J Physiol Lung Cell Mol Physiol. 2010;298:L863-869.\nJin N, Hatton N, Swartz DR, Xia X, Harrington MA, Larsen SH, et al. Hypoxia activates jun-N-terminal kinase, extracellular signal-regulated protein kinase, and p38 kinase in pulmonary arteries. Am J Respir Cell Mol Biol. 2000;23:593–601.\nDas M, Bouchey DM, Moore MJ, Hopkins DC, Nemenoff RA, Stenmark KR. Hypoxia-induced proliferative response of vascular adventitial fibroblasts is dependent on g protein-mediated activation of mitogen-activated protein kinases. J Biol Chem. 2001;276:15631–40.\nYu X, Li T, Liu X, Yu H, Hao Z, Chen Y, et al. Modulation of pulmonary vascular remodeling in hypoxia: role of 15-LOX-2\u002F15-HETE-MAPKs pathway. Cell Physiol Biochem. 2015;35:2079–97.\nYan S, Wang Y, Liu P, Chen A, Chen M, Yao D, et al. Baicalin attenuates hypoxia-induced pulmonary arterial hypertension to improve hypoxic cor pulmonale by reducing the activity of the p38 MAPK signaling pathway and MMP-9. Evid Based Complement Alternat Med. 2016;2016:2546402.\nTian H, Liu L, Wu Y, Wang R, Jiang Y, Hu R, et al. Resistin-like molecule beta acts as a mitogenic factor in hypoxic pulmonary hypertension via the Ca(2+)-dependent PI3K\u002FAkt\u002FmTOR and PKC\u002FMAPK signaling pathways. Respir Res. 2021;22:8.\nMacKenzie F, Duriez P, Wong F, Noseda M, Karsan A. Notch4 inhibits endothelial apoptosis via RBP-Jkappa-dependent and -independent pathways. J Biol Chem. 2004;279:11657–63.\nKiec-Wilk B, Grzybowska-Galuszka J, Polus A, Pryjma J, Knapp A, Kristiansen K. The MAPK-dependent regulation of the Jagged\u002FNotch gene expression by VEGF, bFGF or PPAR gamma mediated angiogenesis in HUVEC. J Physiol Pharmacol. 2010;61:217–25.\nLai PY, Tsai CB, Tseng MJ. Active form Notch4 promotes the proliferation and differentiation of 3T3-L1 preadipocytes. Biochem Biophys Res Commun. 2013;430:1132–9.\nQian CJ, Chen YY, Zhang X, Liu FQ, Yue TT, Ye B, et al. Notch4 inhibition reduces migration and invasion and enhances sensitivity to docetaxel by inhibiting Akt\u002Ffascin in pancreatic cancer cells. Oncol Lett. 2016;12:3499–505.\nHadri L, Kratlian RG, Benard L, Maron BA, Dorfmüller P, Ladage D, et al. Therapeutic efficacy of AAV1.SERCA2a in monocrotaline-induced pulmonary arterial hypertension. Circulation. 2013;128:512–23.\nLi X, He Y, Xu Y, Huang X, Liu J, Xie M, et al. KLF5 mediates vascular remodeling via HIF-1alpha in hypoxic pulmonary hypertension. Am J Physiol Lung Cell Mol Physiol. 2016;310:L299-310.\nMorris HE, Neves KB, Montezano AC, MacLean MR, Touyz RM. Notch3 signalling and vascular remodelling in pulmonary arterial hypertension. Clin Sci (Lond). 2019;133:2481–98.\nAlexander MR, Owens GK. 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Unraveling the complex story of immune responses to AAV vectors trial after trial. Hum Gene Ther. 2017;28:1061–74.\nMingozzi F, High KA. Overcoming the host immune response to adeno-associated virus gene delivery vectors: the race between clearance, tolerance, neutralization, and escape. Annu Rev Virol. 2017;4:511–34.\nMair KM, Wright AF, Duggan N, Rowlands DJ, Hussey MJ, Roberts S, et al. Sex-dependent influence of endogenous estrogen in pulmonary hypertension. Am J Respir Crit Care Med. 2014;190:456–67.\nXu SL, Deng YS, Liu J, Xu SY, Zhao FY, Wei L, et al. Regulation of circular RNAs act as ceRNA in a hypoxic pulmonary hypertension rat model. Genomics. 2021;113:11–9.",{"VOID":1236},"10.1186\u002Fs12931-022-01927-9","https:\u002F\u002Frespiratory-research.biomedcentral.com\u002Farticles\u002F10.1186\u002Fs12931-022-01927-9",[1239,1263,1283,1298,1318,1338,1358,1378,1398,1418,1438],{"id":1240,"sortIndex":32,"researcher":28,"roles":1241,"affiliations":1242,"properties":1260,"displayName":1262,"givenName":28,"familyName":28},"8ca19a76-31e8-44f7-83dc-072a8660aada",[957],[1243,1251],{"id":1244,"sortIndex":32,"affiliation":1245,"properties":28},"f76106d1-344a-4c11-82c4-a20163e02c80",{"id":1244,"createTime":28,"updateTime":28,"relativeEntities":1246,"slug":28,"properties":1247,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1250,"statistic":28},[],{"title":1248},{"VI":1249},"Department of Pulmonary and Critical Care Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 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allergic asthma is a complex area with many interacting factors involved, the ‘hygiene hypothesis’ proposes that a lack of exposure to infection during childhood may polarise the immune system towards allergen-reactive Th2-type responses in genetically susceptible individuals. Toll-like receptors (TLRs) play a key role within the innate immune system and TLR7 agonists have previously been shown to up-regulate Th1 responses and down-regulate Th2 responses to allergens in murine models of allergic or chronic asthma. This study aimed to examine the efficacy and safety of the novel TRL7 agonist AZD8848, which has been developed as an antedrug. In this double-blind, randomised, parallel-group study, AZD8848 60 μg or placebo was administered intranasally once-weekly for 8 weeks in patients with mild-to-moderate allergic asthma (NCT00999466). Efficacy assessments were performed at 1 and 4 weeks after the last dose. The primary outcome was the late asthmatic response (LAR) fall in forced expiratory volume in 1 s (FEV1) after allergen challenge at 1-week post-treatment. AZD8848 significantly reduced average LAR fall in FEV1 by 27% vs. placebo at 1 week after treatment (p = 0.035). This effect was sustained at 4 weeks post-treatment; however, it did not reach clinical significance. AZD8848 reduced post-allergen challenge methacholine-induced airway hyper-responsiveness (AHR) vs. placebo at 1 week post-dosing (treatment ratio: 2.20, p = 0.024), with no effect at 4 weeks. There was no significant difference between the two groups in plasma cytokine, sputum Th2 cytokine or eosinophil responses post-allergen challenge at 1 week after treatment. The incidence of adverse events was similar in the two groups. AZD8848 was generally well tolerated. In patients with allergic asthma, TLR7 agonists could potentially reduce allergen responsiveness by stimulating Type 1 interferon responses to down-regulate the dominant Th2 responses. clinicaltrials.gov identifier NCT00999466.",{"EN":1674},"Effects of the Toll-like receptor 7 (TLR7) agonist, AZD8848, on allergen-induced responses in patients with mild asthma: a double-blind, randomised, parallel-group study",{"EN":1676},"",{"VOID":1678},"10.1186\u002Fs12931-019-1252-2",[31],"https:\u002F\u002Frespiratory-research.biomedcentral.com\u002Farticles\u002F10.1186\u002Fs12931-019-1252-2",[1682,1699,1714,1729,1742,1757,1772],{"id":1683,"sortIndex":32,"researcher":28,"roles":1684,"affiliations":1685,"properties":1694,"displayName":1698,"givenName":28,"familyName":28},"07b420c9-0307-41f4-ab9d-7440dee70380",[],[1686],{"id":1687,"sortIndex":32,"affiliation":1688,"properties":28},"5098a836-5e67-404e-b31f-88602f360988",{"id":1687,"createTime":28,"updateTime":28,"relativeEntities":1689,"slug":28,"properties":1690,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1693,"statistic":28},[],{"title":1691},{"EN":1692},"Respiratory Clinical Trials Ltd, Queen Anne Street Medical Centre, London, UK",[],{"email":1695,"title":1697},{"VOID":1696},"brian.leaker@qasmc.com",{"EN":1698},"Brian R. 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Br J Pharmacol. 2012;166:573–86.",{"id":28,"text":1862,"url":28,"identifiers":28},"Moisan J, Camateros P, Thuraisingam T, Marion D, Koohsari H, Martin P, Boghdady ML, Ding A, Gaestel M, Guiot MC, et al. TLR7 ligand prevents allergen-induced airway hyperresponsiveness and eosinophilia in allergic asthma by a MYD88-dependent and MK2-independent pathway. Am J Physiol Lung Cell Mol Physiol. 2006;290:L987–95.",{"id":28,"text":1864,"url":28,"identifiers":28},"Sel S, Wegmann M, Bauer S, Garn H, Alber G, Renz H. Immunomodulatory effects of viral TLR ligands on experimental asthma depend on the additive effects of IL-12 and IL-10. J Immunol. 2007;178:7805–13.",{"id":28,"text":1866,"url":28,"identifiers":28},"Huang T-J, MacAry PA, Eynott P, Moussavi A, Daniel KC, Askenase PW, Kemeny DM, Chung KF. Allergen-specific Th1 cells counteract efferent Th2 cell-dependent bronchial hyperresponsiveness and eosinophilic inflammation partly via IFN-γ. 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J Immunol. 2009;182:880–89.",{"id":28,"text":1896,"url":28,"identifiers":28},"Dudek AZ, Yunis C, Harrison LI, Kumar S, Hawkinson R, Cooley S, Vasilakos JP, Gorski KS, Miller JS. First in human phase I trial of 852A, a novel systemic toll-like receptor 7 agonist, to activate innate immune responses in patients with advanced cancer. Clin Cancer Res. 2007;13:7119–25.",{"id":28,"text":1898,"url":28,"identifiers":28},"Pockros PJ, Guyader D, Patton H, Tong MJ, Wright T, McHutchison JG, Meng TC. Oral resiquimod in chronic HCV infection: safety and efficacy in 2 placebo-controlled, double-blind phase IIa studies. J Hepatol. 2007;47:174–82.",{"id":28,"text":1900,"url":28,"identifiers":28},"Bell J, Britt J, Biffen M, Ferguson D, Aoki M, Eiho K, Bahl AK, Takaku H, Murray C. AZD8848\u002FDSP-3025 is a novel potent TLR7 agonist ante-drug that demonstrates negligible systemic activity and a prolonged period of control after cessation of weekly dosing in a Brown Norway rat ovalbumin challenge model. Am J Respir Crit Care Med. 2010;181:A5688.",{"id":28,"text":1902,"url":28,"identifiers":28},"Aoki M, Bell JP, Ikeda K, Onishi M, Eiho K, Tomizawa H, Takaku H, Kitaura M. Weekly dosing of AZD8848\u002FDSP-3025, a novel TLR7 agonist ante-drug, demonstrates a prolonged period of control against markers of pulmonary inflammation in an allergen challenge model in the mouse. Am J Respir Crit Care Med. 2010;181:A5689.",{"id":28,"text":1904,"url":28,"identifiers":28},"O'Byrne PM, Gauvreau GM, Brannan JD. Provoked models of asthma: what have we learnt? Clin Exp Allergy. 2009;39:181–92.",{"id":28,"text":1906,"url":28,"identifiers":28},"Weersink EJM, Postma DS, Aalbers R, de Monchy JGR. Early and late asthmatic reaction after allergen challenge. Respir Med. 1994;88:103–14.",{"id":28,"text":1908,"url":28,"identifiers":28},"Gauvreau GM, Hessel EM, Boulet LP, Coffman RL, O'Byrne PM. Immunostimulatory sequences regulate interferon-inducible genes but not allergic airway responses. Am J Respir Crit Care Med. 2006;174:15–20.",{"id":28,"text":1910,"url":28,"identifiers":28},"Bao M, Liu YJ. Regulation of TLR7\u002F9 signaling in plasmacytoid dendritic cells. Protein Cell. 2013;4:40–52.",{"id":28,"text":1912,"url":28,"identifiers":28},"Gordon S, Martinez FO. Alternative activation of macrophages: mechanism and functions. Immun. 2010;32:593–604.",{"id":28,"text":1914,"url":28,"identifiers":28},"Mosser DM, Edwards JP. Exploring the full spectrum of macrophage activation. Nat Rev Immunol. 2008;8:958–69.",{"id":28,"text":1916,"url":28,"identifiers":28},"Lv J, Yu Q, Lv J, Di C, Lin X, Su W, Wu M, Xia Z. Airway epithelial TSLP production of TLR2 drives type 2 immunity in allergic airway inflammation. Eur J Immunol. 2018. Epub ahead of print.",{"id":28,"text":1918,"url":28,"identifiers":28},"Gauvreau GM, O'Byrne PM, Boulet LP, Wang Y, Cockcroft D, Bigler J, M. F J, Boedigheimer M, Davis BE, Dias C, et al. Effects of an anti-TSLP antibody on allergen-induced asthmatic responses. N Engl J Med. 2014;370:2102–10.",{"id":28,"text":1920,"url":28,"identifiers":28},"Barnig C, Cernadas M, Dutile S, Liu X, Perrella MA, Kazani S, Wechsler ME, Israel E, Levy BD. Lipoxin A4 regulates Natural Killer cell and Type 2 innate lymphoid cell activation in asthma. Sci Translat Med. 2013;5:174ra126.",{"id":28,"text":1922,"url":28,"identifiers":28},"Kawai T, Akira S. The roles of TLRs, RLRs and NLRs in pathogen recognition. Int Immunol. 2009;21:317–37.",{"id":28,"text":1924,"url":28,"identifiers":28},"Fili L, Ferri S, Guarna F, Sampognaro S, Manuelli C, Liotta F, Cosmi L, Matucci A, Vultaggio A, Annunziato F, et al. Redirection of allergen-specific TH2 responses by a modified adenine through toll-like receptor 7 interaction and IL-12\u002FIFN release. J Allergy Clin Immunol. 2006;118:511–17.",{"id":28,"text":1926,"url":28,"identifiers":28},"Empey D, Laitinen L, Jacobs L, Gold W, Nadel J. Mechanisms of bronchial hyperreactivity in normal subjects after upper respiratory tract infection. Am Rev Respir Dis. 1976;113:131–39.",{"id":1928,"createTime":1929,"updateTime":1930,"relativeEntities":1931,"slug":1932,"properties":1933,"entityType":951,"verifyStatus":26,"verifyTime":1930,"verifyNote":1037,"languages":28,"translateLanguages":28,"viewCount":32,"primaryUrl":1942,"fullTextUrl":28,"authors":1943,"publicationType":970,"publisherRelationship":2087,"citationCount":28,"citationInfo":28,"publishDate":2134,"publishYear":2135,"citationAnalyzeStatus":878,"lastCitationAnalyze":28,"indexDatabases":2136,"openAccess":28,"references":28,"isForceReanalyzing":1021},"008e43bf-a8d9-4a68-9378-ada6a8ad7801","2024-01-27T02:26:46.720+00:00","2025-01-01T12:09:30.615+00:00",[],"Hypoxia-inducible-factor-1-%CE%B1-platelet-derived-growth-factor-axis-in-HIV-associated-pulmonary-vascular-remodeling",{"abstract":1934,"title":1936,"references":1938,"doi":1940},{"EN":1935},"Human immunodeficiency virus (HIV) infected patients are at increased risk for the development of pulmonary arterial hypertension (PAH). Recent reports have demonstrated that HIV associated viral proteins induce reactive oxygen species (ROS) with resultant endothelial cell dysfunction and related vascular injury. In this study, we explored the impact of HIV protein induced oxidative stress on production of hypoxia inducible factor (HIF)-1α and platelet-derived growth factor (PDGF), critical mediators implicated in the pathogenesis of HIV-PAH. The lungs from 4-5 months old HIV-1 transgenic (Tg) rats were assessed for the presence of pulmonary vascular remodeling and HIF-1α\u002FPDGF-BB expression in comparison with wild type controls. Human primary pulmonary arterial endothelial cells (HPAEC) were treated with HIV-associated proteins in the presence or absence of pretreatment with antioxidants, for 24 hrs followed by estimation of ROS levels and western blot analysis of HIF-1α or PDGF-BB. HIV-Tg rats, a model with marked viral protein induced vascular oxidative stress in the absence of active HIV-1 replication demonstrated significant medial thickening of pulmonary vessels and increased right ventricular mass compared to wild-type controls, with increased expression of HIF-1α and PDGF-BB in HIV-Tg rats. The up-regulation of both HIF-1α and PDGF-B chain mRNA in each HIV-Tg rat was directly correlated with an increase in right ventricular\u002Fleft ventricular+septum ratio. Supporting our in-vivo findings, HPAECs treated with HIV-proteins: Tat and gp120, demonstrated increased ROS and parallel increase of PDGF-BB expression with the maximum induction observed on treatment with R5 type gp-120CM. Pre-treatment of endothelial cells with antioxidants or transfection of cells with HIF-1α small interfering RNA resulted in abrogation of gp-120CM mediated induction of PDGF-BB, therefore, confirming that ROS generation and activation of HIF-1α plays critical role in gp120 mediated up-regulation of PDGF-BB. In summary, these findings indicate that viral protein induced oxidative stress results in HIF-1α dependent up-regulation of PDGF-BB and suggests the possible involvement of this pathway in the development of HIV-PAH.",{"EN":1937},"Hypoxia-inducible factor-1 α\u002Fplatelet derived growth factor axis in HIV-associated pulmonary vascular remodeling",{"VOID":1939},"Humbert M, Montani D, Perros F, Dorfmuller P, Adnot S, Eddahibi S: Endothelial cell dysfunction and cross talk between endothelium and smooth muscle cells in pulmonary arterial hypertension. 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Proc Natl Acad Sci USA. 2006, 103 (10): 3746-3751. 10.1073\u002Fpnas.0511237103.",{"VOID":1941},"10.1186\u002F1465-9921-12-103","https:\u002F\u002Frespiratory-research.biomedcentral.com\u002Farticles\u002F10.1186\u002F1465-9921-12-103",[1944,1959,1974,1987,2009,2024,2039,2054,2067],{"id":1945,"sortIndex":32,"researcher":28,"roles":1946,"affiliations":1947,"properties":1956,"displayName":1958,"givenName":28,"familyName":28},"9db966c1-5c95-49cb-8d0c-1bd0c38bc949",[957],[1948],{"id":1949,"sortIndex":32,"affiliation":1950,"properties":28},"8ed4af6e-730d-4e78-861f-cbac1a34572d",{"id":1949,"createTime":28,"updateTime":28,"relativeEntities":1951,"slug":28,"properties":1952,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1955,"statistic":28},[],{"title":1953},{"VI":1954},"Division of Pulmonary and Critical Care Medicine, Department of Medicine, University of Kansas Medical Center, Kansas City, USA",[],{"title":1957},{"VI":1958},"Joel Mermis",{"id":1960,"sortIndex":40,"researcher":28,"roles":1961,"affiliations":1962,"properties":1971,"displayName":1973,"givenName":28,"familyName":28},"93f382f4-3e5b-4442-8e7f-240b418a6525",[957],[1963],{"id":1964,"sortIndex":32,"affiliation":1965,"properties":28},"96831d76-b15a-4761-b485-528e31ef05d5",{"id":1964,"createTime":28,"updateTime":28,"relativeEntities":1966,"slug":28,"properties":1967,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1970,"statistic":28},[],{"title":1968},{"VI":1969},"Department of Molecular & Integrative Physiology, University of Kansas Medical Center, Kansas City, USA",[],{"title":1972},{"VI":1973},"Haihua Gu",{"id":1975,"sortIndex":123,"researcher":28,"roles":1976,"affiliations":1977,"properties":1984,"displayName":1986,"givenName":28,"familyName":28},"63fa19dc-a878-47f0-a736-c648fc7beb46",[957],[1978],{"id":1964,"sortIndex":32,"affiliation":1979,"properties":28},{"id":1964,"createTime":28,"updateTime":28,"relativeEntities":1980,"slug":28,"properties":1981,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1983,"statistic":28},[],{"title":1982},{"VI":1969},[],{"title":1985},{"VI":1986},"Bing Xue",{"id":1988,"sortIndex":42,"researcher":28,"roles":1989,"affiliations":1990,"properties":2006,"displayName":2008,"givenName":28,"familyName":28},"85e6ee51-9607-4be2-9a63-931e7dadc0f7",[957],[1991,1997],{"id":1964,"sortIndex":32,"affiliation":1992,"properties":28},{"id":1964,"createTime":28,"updateTime":28,"relativeEntities":1993,"slug":28,"properties":1994,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1996,"statistic":28},[],{"title":1995},{"VI":1969},[],{"id":1998,"sortIndex":40,"affiliation":1999,"properties":2005},"7614fad6-b2fd-42d1-8904-d86fee3b6e45",{"id":1998,"createTime":28,"updateTime":28,"relativeEntities":2000,"slug":28,"properties":2001,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":2004,"statistic":28},[],{"title":2002},{"VI":2003},"The Affiliated Hospital of Ningxia Medical College, Yinchuan, People's Republic of China",[],{},{"title":2007},{"VI":2008},"Fang Li",{"id":2010,"sortIndex":45,"researcher":28,"roles":2011,"affiliations":2012,"properties":2021,"displayName":2023,"givenName":28,"familyName":28},"10e18c65-93dd-4938-b8d2-83d704649818",[957],[2013],{"id":2014,"sortIndex":32,"affiliation":2015,"properties":28},"0a0cf97e-a9d5-4557-add8-6349b7122854",{"id":2014,"createTime":28,"updateTime":28,"relativeEntities":2016,"slug":28,"properties":2017,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":2020,"statistic":28},[],{"title":2018},{"VI":2019},"Pathology & Laboratory Medicine, University of Kansas Medical Center, Kansas City, USA",[],{"title":2022},{"VI":2023},"Ossama 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with fibrotic interstitial lung disease (ILD) are frequently physically inactive and many ILD subtypes are characterized by risk factors for myopathy; however, the importance of body composition, muscle strength, and physical performance in this population is largely unknown. Patients were prospectively recruited from a specialized ILD clinic, baseline characteristics were collected from the clinical record, pulmonary function tests were performed per established protocols, and dyspnea was measured using the University of California San Diego Shortness of Breath Questionnaire. Dual-energy X-ray absorptiometry (DXA) was used to assess body composition; handgrip strength to determine muscle strength, and 4-m gait speed to measure physical performance. One hundred and fifteen patients with fibrotic ILD including 40 patients with idiopathic pulmonary fibrosis were recruited. The mean age was 69+\u002F− 10 years in men (62% of the cohort), and 66+\u002F− 9 years in women, with mild and moderate reduction in FVC and DLCO, respectively, for both sexes. ILD severity (measured by FVC %-predicted, DLCO %-predicted, or the Composite Physiologic Index in separate models) significantly predicted muscle mass and percent body fat including with adjustment for age, sex, and weight. ILD severity was associated with grip strength and gait speed independent from body composition. ILD severity has an important impact on body composition, particularly in men. Future studies are needed to confirm and further explore the possibility of additional pathways through which ILD directly impacts limb muscle function and physical performance.",{"EN":2147},"Body composition, muscle function, and physical performance in fibrotic interstitial lung disease: a prospective cohort study",{"VOID":2149},"Marshall DC, Salciccioli JD, Shea BS, Akuthota P. Trends in mortality from idiopathic pulmonary fibrosis in the European Union: an observational study of the WHO mortality database from 2001-2013. Eur Respir J. 2018;51(1).\nNavaratnam V, Fogarty AW, Glendening R, McKeever T, Hubbard RB. The increasing secondary care burden of idiopathic pulmonary fibrosis: hospital admission trends in England from 1998 to 2010. Chest. 143(4):1078–84.\nGlaspole IN, Watson AL, Allan H, Chapman S, Cooper WA, Corte TJ, Ellis S, Grainge C, Goh N, Hopkins P, Keir G, Macansh S, Mahar A, Moodley Y, Reynolds PN, Ryerson CJ, Walters EH, Zappala CJ, Holland AE. Determinants and outcomes of prolonged anxiety and depression in idiopathic pulmonary fibrosis. Eur Respir J. 2017;50(2).\nRoot ED, Graney B, Baird S, Churney T, Fier K, Korn M, McCormic M, Sprunger D, Vierzba T, Wamboldt FS, Swigris JJ. Physical activity and activity space in patients with pulmonary fibrosis not prescribed supplemental oxygen. BMC Pulm Med. 2017;17(1):154.\nNishiyama O, Yamazaki R, Sano H, Iwanaga T, Higashimoto Y, Kume H, Tohda Y. Physical activity in daily life in patients with idiopathic pulmonary fibrosis. Respir Investig. 2018;56(1):57–63.\nJones SE, Maddocks M, Kon SS, Canavan JL, Nolan CM, Clark AL, Polkey MI, Man WD. Sarcopenia in COPD: prevalence, clinical correlates and response to pulmonary rehabilitation. Thorax. 2015;70(3):213–8.\nMorino A, Takahashi H, Chiba H, Ishiai S. Daily physical activity affects exercise capacity in patients with idiopathic pulmonary fibrosis. J Phys Ther Sci. 2017;29(8):1323–8.\nLeong DP, Teo KK, Rangarajan S, Lopez-Jaramillo P, Avezum A Jr, Orlandini A, Seron P, Ahmed SH, Rosengren A, Kelishadi R, Rahman O, Swaminathan S, Iqbal R, Gupta R, Lear SA, Oguz A, Yusoff K, Zatonska K, Chifamba J, Igumbor E, Mohan V, Anjana RM, Gu H, Li W, Yusuf S. Prognostic value of grip strength: findings from the prospective urban rural epidemiology (PURE) study. Lancet. 2015;386(9990):266–73.\nBurtin C, Ter Riet G, Puhan MA, Waschki B, Garcia-Aymerich J, Pinto-Plata V, Celli B, Watz H, Spruit MA. Handgrip weakness and mortality risk in COPD: a multicentre analysis. Thorax. 2016;71(1):86–7.\nAlakhras M, Decker PA, Nadrous HF, Collazo-Clavell M, Ryu JH. Body mass index and mortality in patients with idiopathic pulmonary fibrosis. Chest. 2007;131(5):1448–53.\nRahman I, Skwarska E, Henry M, Davis M, O’Connor CM, FitzGerald MX, Greening A, MacNee W. Systemic and pulmonary oxidative stress in idiopathic pulmonary fibrosis. Free Radic Biol Med. 1999;27(1–2):60–8.\nSnetselaar R, van Moorsel CH, Kazemier KM, van der Vis JJ, Zanen P, van Oosterhout MF, Grutters JC. Telomere length in interstitial lung diseases. Chest. 2015;148(4):1011–8.\nSchaap LA, Pluijm SM, Deeg DJ, Visser M. Inflammatory markers and loss of muscle mass (sarcopenia) and strength. Am J Med. 2006;119(6):526.e529–17.\nHoppeler H, Kleinert E, Schlegel C, Claassen H, Howald H, Kayar SR, Cerretelli P. Morphological adaptations of human skeletal muscle to chronic hypoxia. Int J Sports Med. 1990;11(Suppl 1):S3–9.\nMeyer A, Salewsky B, Spira D, Steinhagen-Thiessen E, Norman K, Demuth I. Leukocyte telomere length is related to appendicular lean mass: cross-sectional data from the Berlin aging study II (BASE-II). Am J Clin Nutr. 2016;103(1):178–83.\nRaghu G, Collard HR, Egan JJ, Martinez FJ, Behr J, Brown KK, Colby TV, Cordier JF, Flaherty KR, Lasky JA, Lynch DA, Ryu JH, Swigris JJ, Wells AU, Ancochea J, Bouros D, Carvalho C, Costabel U, Ebina M, Hansell DM, Johkoh T, Kim DS, King TE, Jr., Kondoh Y, Myers J, Muller NL, Nicholson AG, Richeldi L, Selman M, Dudden RF, Griss BS, Protzko SL, Schunemann HJ: An official ATS\u002FERS\u002FJRS\u002FALAT statement: idiopathic pulmonary fibrosis: evidence-based guidelines for diagnosis and management. Am J Respir Crit Care Med 2011, 183(6):788–824.\nTravis WD, Costabel U, Hansell DM, King TE, Jr., Lynch DA, Nicholson AG, Ryerson CJ, Ryu JH, Selman M, Wells AU, Behr J, Bouros D, Brown KK, Colby TV, Collard HR, Cordeiro CR, Cottin V, Crestani B, Drent M, Dudden RF, Egan J, Flaherty K, Hogaboam C, Inoue Y, Johkoh T, Kim DS, Kitaichi M, Loyd J, Martinez FJ, Myers J, Protzko S, Raghu G, Richeldi L, Sverzellati N, Swigris J, Valeyre D, Pneumonias AECoII: An official American Thoracic Society\u002FEuropean Respiratory Society statement: update of the international multidisciplinary classification of the idiopathic interstitial pneumonias. Am J Respir Crit Care Med, 188(6):733–748.\nLukaski HC, Marchello MJ, Hall CB, Schafer DM, Siders WA. Soft tissue composition of pigs measured with dual x-ray absorptiometry: comparison with chemical analyses and effects of carcass thicknesses. Nutrition. 1999;15(9):697–703.\nCruz-Jentoft AJ, Baeyens JP, Bauer JM, Boirie Y, Cederholm T, Landi F, Martin FC, Michel JP, Rolland Y, Schneider SM, Topinkova E, Vandewoude M, Zamboni M. European working group on sarcopenia in older P: sarcopenia: European consensus on definition and diagnosis: report of the European working group on sarcopenia in older people. Age Ageing. 2010;39(4):412–23.\nWong SL. Grip strength reference values for Canadians aged 6 to 79: Canadian health measures survey, 2007 to 2013. Health Reports. 2016;27(10):3–10.\nNolan CM, Maddocks M, Maher TM, Canavan JL, Jones SE, Barker RE, Patel S, Jacob J, Cullinan P, Man WD. Phenotypic characteristics associated with slow gait speed in idiopathic pulmonary fibrosis. Respirology. 2017.\nMacintyre N, Crapo RO, Viegi G, Johnson DC, van der Grinten CP, Brusasco V, Burgos F, Casaburi R, Coates A, Enright P, Gustafsson P, Hankinson J, Jensen R, McKay R, Miller MR, Navajas D, Pedersen OF, Pellegrino R, Wanger J. Standardisation of the single-breath determination of carbon monoxide uptake in the lung. Eur Respir J. 2005;26(4):720–35.\nMiller MR, Hankinson J, Brusasco V, Burgos F, Casaburi R, Coates A, Crapo R, Enright P, van der Grinten CP, Gustafsson P, Jensen R, Johnson DC, MacIntyre N, McKay R, Navajas D, Pedersen OF, Pellegrino R, Viegi G, Wanger J. Standardisation of spirometry. Eur Respir J. 2005;26(2):319–38.\nWells AU, Desai SR, Rubens MB, Goh NS, Cramer D, Nicholson AG, Colby TV, du Bois RM, Hansell DM. Idiopathic pulmonary fibrosis: a composite physiologic index derived from disease extent observed by computed tomography. Am J Respir Crit Care Med. 2003;167(7):962–9.\nEakin EG, Resnikoff PM, Prewitt LM, Ries AL, Kaplan RM. Validation of a new dyspnea measure: the UCSD shortness of breath questionnaire. University of California, San Diego. Chest. 1998;113(3):619–24.\nTeam RC. R: a language and environment for statistical computing. Vienna: R Foundation for Statistical Computing; 2016.\nKelly TL, Wilson KE, Heymsfield SB. Dual energy X-ray absorptiometry body composition reference values from NHANES. PLoS One. 2009;4(9):e7038.\nNewman AB, Kupelian V, Visser M, Simonsick E, Goodpaster B, Nevitt M, Kritchevsky SB, Tylavsky FA, Rubin SM, Harris TB. Sarcopenia: alternative definitions and associations with lower extremity function. J Am Geriatr Soc. 2003;51(11):1602–9.\nKon SS, Canavan JL, Nolan CM, Clark AL, Jones SE, Cullinan P, Polkey MI, Man WD. The 4-metre gait speed in COPD: responsiveness and minimal clinically important difference. Eur Respir J. 2014;43(5):1298–305.\nGuadalupe-Grau A, Carnicero JA, Losa-Reyna J, Tresguerres J, Gomez-Cabrera MD, Castillo C, Alfaro-Acha A, Rosado-Artalejo C, Rodriguez-Manas L, Garcia-Garcia FJ. Endocrinology of aging from a muscle function point of view: results from the Toledo study for healthy aging. J Am Med Dir Assoc. 2016.\nValenti G, Denti L, Maggio M, Ceda G, Volpato S, Bandinelli S, Ceresini G, Cappola A, Guralnik JM, Ferrucci L. Effect of DHEAS on skeletal muscle over the life span: the InCHIANTI study. J Gerontol A Biol Sci Med Sci. 2004;59(5):466–72.\nJu CR, Chen RC. Serum myostatin levels and skeletal muscle wasting in chronic obstructive pulmonary disease. Respir Med. 2012;106(1):102–8.\nCreutzberg EC, Wouters EF, Mostert R, Pluymers RJ, Schols AM. A role for anabolic steroids in the rehabilitation of patients with COPD? A double-blind, placebo-controlled, randomized trial. Chest. 2003;124(5):1733–42.\nCasaburi R, Bhasin S, Cosentino L, Porszasz J, Somfay A, Lewis MI, Fournier M, Storer TW. Effects of testosterone and resistance training in men with chronic obstructive pulmonary disease. Am J Respir Crit Care Med. 2004;170(8):870–8.\nMendoza-Milla C, Valero Jimenez A, Rangel C, Lozano A, Morales V, Becerril C, Chavira R, Ruiz V, Barrera L, Montano M, Pardo A, Selman M. Dehydroepiandrosterone has strong antifibrotic effects and is decreased in idiopathic pulmonary fibrosis. Eur Respir J. 2013;42(5):1309–21.\nLandbo C, Prescott E, Lange P, Vestbo J, Almdal TP. Prognostic value of nutritional status in chronic obstructive pulmonary disease. Am J Respir Crit Care Med. 1999;160(6):1856–61.\nCelli BR, Cote CG, Marin JM, Casanova C, Montes de Oca M, Mendez RA, Pinto Plata V, Cabral HJ. The body-mass index, airflow obstruction, dyspnea, and exercise capacity index in chronic obstructive pulmonary disease. N Engl J Med. 2004;350(10):1005–12.\nLey B, Ryerson CJ, Vittinghoff E, Ryu JH, Tomassetti S, Lee JS, Poletti V, Buccioli M, Elicker BM, Jones KD, King TE Jr, Collard HR. A multidimensional index and staging system for idiopathic pulmonary fibrosis. Ann Intern Med. 2012;156(10):684–91.\nNishiyama O, Yamazaki R, Sano H, Iwanaga T, Higashimoto Y, Kume H, Tohda Y. Fat-free mass index predicts survival in patients with idiopathic pulmonary fibrosis. Respirology. 2016.\nSuzuki Y, Yoshimura K, Enomoto Y, Yasui H, Hozumi H, Karayama M, Furuhashi K, Enomoto N, Fujisawa T, Nakamura Y, Inui N, Suda T. Distinct profile and prognostic impact of body composition changes in idiopathic pulmonary fibrosis and idiopathic pleuroparenchymal fibroelastosis. Sci Rep. 2018;8(1):14074.\nBuckinx F, Reginster JY, Dardenne N, Croisiser JL, Kaux JF, Beaudart C, Slomian J, Bruyere O. Concordance between muscle mass assessed by bioelectrical impedance analysis and by dual energy X-ray absorptiometry: a cross-sectional study. BMC Musculoskelet Disord. 2015;16:60.\nSchols AM, Broekhuizen R, Weling-Scheepers CA, Wouters EF. Body composition and mortality in chronic obstructive pulmonary disease. Am J Clin Nutr. 2005;82(1):53–9.\nPuhan MA, Siebeling L, Zoller M, Muggensturm P, ter Riet G. Simple functional performance tests and mortality in COPD. Eur Respir J. 2013;42(4):956–63.\nMartinez CH, Diaz AA, Meldrum CA, McDonald MN, Murray S, Kinney GL, Hokanson JE, Curtis JL, Bowler RP, Han MK, Washko GR, Regan EA. Handgrip strength in chronic obstructive pulmonary disease. Associations with acute exacerbations and body composition. Ann Am Thorac Soc. 2017;14(11):1638–45.\nTonelli R, Cocconcelli E, Lanini B, Romagnoli I, Florini F, Castaniere I, Andrisani D, Cerri S, Luppi F, Fantini R, Marchioni A, Beghe B, Gigliotti F, Clini EM. Effectiveness of pulmonary rehabilitation in patients with interstitial lung disease of different etiology: a multicenter prospective study. BMC Pulm Med. 2017;17(1):130.\nDolmage TE, Goldstein RS. Effects of one-legged exercise training of patients with COPD. Chest. 2008;133(2):370–6.\nMaddocks M, Nolan CM, Man WD, Polkey MI, Hart N, Gao W, Rafferty GF, Moxham J, Higginson IJ. Neuromuscular electrical stimulation to improve exercise capacity in patients with severe COPD: a randomised double-blind, placebo-controlled trial. Lancet Respir Med. 2016;4(1):27–36.\nMaltais F, Decramer M, Casaburi R, Barreiro E, Burelle Y, Debigare R, Dekhuijzen PN, Franssen F, Gayan-Ramirez G, Gea J, Gosker HR, Gosselink R, Hayot M, Hussain SN, Janssens W, Polkey MI, Roca J, Saey D, Schols AM, Spruit MA, Steiner M, Taivassalo T, Troosters T, Vogiatzis I, Wagner PD. An official American Thoracic Society\u002FEuropean Respiratory Society statement: update on limb muscle dysfunction in chronic obstructive pulmonary disease. Am J Respir Crit Care Med. 2014;189(9):e15–62.",{"VOID":2151},"10.1186\u002Fs12931-019-1019-9","https:\u002F\u002Frespiratory-research.biomedcentral.com\u002Farticles\u002F10.1186\u002Fs12931-019-1019-9",[2154,2187,2200,2222,2244],{"id":2155,"sortIndex":32,"researcher":28,"roles":2156,"affiliations":2157,"properties":2184,"displayName":2186,"givenName":28,"familyName":28},"9fccec45-5d33-4679-bd4a-6ead417fd93b",[957],[2158,2166,2175],{"id":2159,"sortIndex":32,"affiliation":2160,"properties":28},"38499dc8-b319-41b8-813b-d198ab4388b8",{"id":2159,"createTime":28,"updateTime":28,"relativeEntities":2161,"slug":28,"properties":2162,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":2165,"statistic":28},[],{"title":2163},{"VI":2164},"Department of Medicine, University of British Columbia, Vancouver, Canada",[],{"id":2167,"sortIndex":40,"affiliation":2168,"properties":2174},"7ee7fb52-e557-4b7e-8b45-28daf751f3fb",{"id":2167,"createTime":28,"updateTime":28,"relativeEntities":2169,"slug":28,"properties":2170,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":2173,"statistic":28},[],{"title":2171},{"VI":2172},"Centre for Heart Lung Innovation, University of British Columbia, Vancouver, Canada",[],{},{"id":2176,"sortIndex":123,"affiliation":2177,"properties":2183},"18b02587-8aab-4967-8511-93ab9dbcd3be",{"id":2176,"createTime":28,"updateTime":28,"relativeEntities":2178,"slug":28,"properties":2179,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":2182,"statistic":28},[],{"title":2180},{"VI":2181},"Department of Pulmonary Medicine, University Hospital and University of Bern, Bern, Switzerland",[],{},{"title":2185},{"VI":2186},"Sabina A. 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The purpose of this study is to determine whether there is an association between anxiety and functional measures, quality of life and dyspnea. Data from 1828 patients with moderate to severe emphysema enrolled in the National Emphysema Treatment Trial (NETT), collected prior to rehabilitation and randomization, were used in linear regression models to test the association between anxiety symptoms, measured by the Spielberger State Trait Anxiety Inventory (STAI) and: (a) six-minute walk distance test (6 MWD), (b) cycle ergometry peak workload, (c) St. Georges Respiratory Questionnaire (SRGQ), and (d) UCSD Shortness of Breath Questionnaire (SOBQ), after controlling for potential confounders including age, gender, FEV1 (% predicted), DLCO (% predicted), and the Beck Depression Inventory (BDI). Anxiety was significantly associated with worse functional capacity [6 MWD (B = -0.944, p \u003C .001), ergometry peak workload (B = -.087, p = .04)], quality of life (B = .172, p \u003C .001) and shortness of breath (B = .180, p \u003C .001). Regression coefficients show that a 10 point increase in anxiety score is associated with a mean decrease in 6 MWD of 9 meters, a 1 Watt decrease in peak exercise workload, and an increase of almost 2 points on both the SGRQ and SOBQ. In clinically stable patients with moderate to severe emphysema, anxiety is associated with worse exercise performance, quality of life and shortness of breath, after accounting for the influence of demographic and physiologic factors known to affect these outcomes. ClinicalTrials.gov NCT00000606",{"EN":2329},"Anxiety is associated with diminished exercise performance and quality of life in severe emphysema: a cross-sectional study",{"VOID":2331},"Prigatano GP, Wright EC, Levin D: Quality of life and its predictors in patients with mild hypoxemia and chronic obstructive pulmonary disease. Arch Intern Med 1984, 144:1613–1619.\nMonso E, Fiz JM, Izquierdo J, Alonso J, Coll R, Rosell A, Morera J: Quality of life in severe chronic obstructive pulmonary disease: correlation with lung and muscle function. Respir Med 1998, 92:221–227.\nMcSweeny AJ, Grant I, Heaton RK, Adams KM, Timms RM: Life quality of patients with chronic obstructive pulmonary disease. Arch Intern Med 1982, 142:473–478.\nFelker B, Katon W, Hedrick SC, Rasmussen J, McKnight K, McDonnell MB, Fihn SD: The association between depressive symptoms and health status in patients with chronic pulmonary disease. 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Am Rev Respir Dis 1981, 123:659–664.\nSciurba F, Criner GJ, Lee SM, Mohsenifar Z, Shade D, Slivka W, Wise RA: Six-minute walk distance in chronic obstructive pulmonary disease: reproducibility and effect of walking course layout and length. Am J Respir Crit Care Med 2003, 167:1522–1527.\nHimmelfarb S, Murrell SA: The prevalence and correlates of anxiety symptoms in older adults. J Psychol 1984, 116:159–167.\nMurrell SA, Himmelfarb S, Wright K: Prevalence of depression and its correlates in older adults. Am J Epidemiol 1983, 117:173–185.\nCohen-Cole SA, Stoudemire A: Major depression and physical illness. Special considerations in diagnosis and biologic treatment. Psychiatr Clin North Am 1987, 10:1–17.\nCavanaugh S, Clark DC, Gibbons RD: Diagnosing depression in the hospitalized medically ill. Psychosomatics 1983, 24:809–815.\nFerrer M, Villasante C, Alonso J, Sobradillo V, Gabriel R, Vilagut G, Masa JF, Viejo JL, Jimenez-Ruiz CA, Miravitlles M: Interpretation of quality of life scores from the St George's Respiratory Questionnaire. Eur Respir J 2002, 19:405–413.\nSteffen TM, Hacker TA, Mollinger L: Age- and gender-related test performance in community-dwelling elderly people: Six-Minute Walk Test, Berg Balance Scale, Timed Up & Go Test, and gait speeds. Phys Ther 2002, 82:128–137.\nvon Leupoldt A, Ambruzsova R, Nordmeyer S, Jeske N, Dahme B: Sensory and affective aspects of dyspnea contribute differentially to the Borg scale's measurement of dyspnea. Respiration 2006, 73:762–768.\nCarrieri-Kohlman V, Gormley JM, Douglas MK, Paul SM, Stulbarg MS: Differentiation between dyspnea and its affective components. 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Psychosomatics 1992, 33:190–201.\nArgyropoulou P, Patakas D, Koukou A, Vasiliadis P, Georgopoulos D: Buspirone effect on breathlessness and exercise performance in patients with chronic obstructive pulmonary disease. Respiration 1993, 60:216–220.\nPapp LA, Weiss JR, Greenberg HE, Rifkin A, Scharf SM, Gorman JM, Klein DF: Sertraline for chronic obstructive pulmonary disease and comorbid anxiety and mood disorders. Am J Psychiatry 1995, 152:1531.\nSmoller JW, Pollack MH, Systrom D, Kradin RL: Sertraline effects on dyspnea in patients with obstructive airways disease. Psychosomatics 1998, 39:24–29.\nKunik ME, Braun U, Stanley MA, Wristers K, Molinari V, Stoebner D, Orengo CA: One session cognitive behavioural therapy for elderly patients with chronic obstructive pulmonary disease. Psychol Med 2001, 31:717–723.\nde Godoy DV, de Godoy RF: A randomized controlled trial of the effect of psychotherapy on anxiety and depression in chronic obstructive pulmonary disease. Arch Phys Med Rehabil 2003, 84:1154–1157.\nEmery CF: Effects of age on physiological and psychological functioning among COPD patients in an exercise program. J Aging Health 1994, 6:3–16.\nEmery CF, Schein RL, Hauck ER, MacIntyre NR: Psychological and cognitive outcomes of a randomized trial of exercise among patients with chronic obstructive pulmonary disease. Health Psychol 1998, 17:232–240.\nEmery CF, Shermer RL, Hauck ER, Hsiao ET, MacIntyre NR: Cognitive and psychological outcomes of exercise in a 1-year follow-up study of patients with chronic obstructive pulmonary disease. Health Psychol 2003, 22:598–604.\nGuell R, Resqueti V, Sangenis M, Morante F, Martorell B, Casan P, Guyatt GH: Impact of pulmonary rehabilitation on psychosocial morbidity in patients with severe COPD. Chest 2006, 129:899–904.\nKayahan B, Karapolat H, Atyntoprak E, Atasever A, Ozturk O: Psychological outcomes of an outpatient pulmonary rehabilitation program in patients with chronic obstructive pulmonary disease. Respir Med 2006, 100:1050–1057.\nATS statement: guidelines for the six-minute walk testAm J Respir Crit Care Med 2002, 166:111–117.",{"VOID":2333},"10.1186\u002F1465-9921-11-29","http:\u002F\u002Frespiratory-research.biomedcentral.com\u002Farticles\u002F10.1186\u002F1465-9921-11-29",[2336,2362,2386,2399,2414,2427,2448,2463,2478,2493,2508,2521,2536,2551,2572],{"id":2337,"sortIndex":32,"researcher":28,"roles":2338,"affiliations":2339,"properties":2359,"displayName":2361,"givenName":28,"familyName":28},"06896f6a-dd5f-40ca-8cd8-26ce9b2af7ca",[957],[2340,2348],{"id":2341,"sortIndex":32,"affiliation":2342,"properties":28},"c95ad8ad-d831-414e-a1ca-29c91e431adf",{"id":2341,"createTime":28,"updateTime":28,"relativeEntities":2343,"slug":28,"properties":2344,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":2347,"statistic":28},[],{"title":2345},{"VI":2346},"Mental Health Service, VA Ann Arbor Healthcare 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could prevent Pseudomonas aeruginosa colonization in lower respiratory tract (LRT) and reduced P. aeruginosa ventilator-associated pneumonia (VAP) rate. Recent studies also suggested that probiotics could improve lung inflammation in mice infected with P. aeruginosa. It seems that microbiota regulation may be a potential therapy for P. aeruginosa VAP patients. However, we know less about the LRT microbial composition and its correlation with prognosis in P. aeruginosa VAP patients. This study aimed to characterize LRT microbiota in P. aeruginosa VAP patients and explore the relationship between microbiota and patient prognosis. Deep endotracheal secretions were sampled from subjects via intubation. Communities were identified by 16S ribosomal RNA gene sequencing. The relationship between microbiota and the prognosis of P. aeruginosa VAP patients were evaluated. Clinical pulmonary infection score and the survival of intensive care unit were both the indicators of patient prognosis. In this study, the LRT microbial composition of P. aeruginosa VAP patients was significantly different from non-infected intubation patients, and showed significant individual differences, forming two clusters. According to the predominant phylum of each cluster, these two clusters were named Pro cluster and Fir-Bac cluster respectively. Patients from Pro cluster were dominated by Proteobacteria (adj.P \u003C 0.001), while those from Fir-Bac cluster were dominated by Firmicutes, and Bacteroidetes (both adj.P \u003C 0.001). These two varied clusters (Pro and Fir-Bac cluster) were associated with the patients’ primary disease (χ2-test, P \u003C 0.0001). The primary disease of the Pro cluster mainly included gastrointestinal disease (63%), and the Fir-Bac cluster was predominantly respiratory disease (89%). During the two-week dynamic observation period, despite the use of antibiotics, the dominant genera and Shannon diversity of the LRT microbiota did not change significantly in patients with P. aeruginosa VAP. In prognostic analysis, we found a significant negative correlation between Lactobacillus and clinical pulmonary infection score on the day of diagnosis (P = 0.014); but we found no significant difference of microbial composition between survivors and non-survivors. LRT microbial composition was diversified among P. aeruginosa VAP patients, forming two clusters which were associated with the primary diseases of the patients.",{"EN":2643},"Lower respiratory tract microbial composition was diversified in Pseudomonas aeruginosa ventilator-associated pneumonia patients",{"VOID":2645},"American Thoracic S. Infectious diseases Society of a: guidelines for the management of adults with hospital-acquired, ventilator-associated, and healthcare-associated pneumonia. Am J Respir Crit Care Med. 2005;171:388–416.\nKalil AC, Metersky ML, Klompas M, Muscedere J, Sweeney DA, Palmer LB, Napolitano LM, O'Grady NP, Bartlett JG, Carratala J, et al. Management of Adults With Hospital-acquired and Ventilator-associated Pneumonia: 2016 Clinical practice guidelines by the Infectious Diseases Society of America and the American Thoracic Society. Clin Infect Dis. 2016;63:e61–e111.\nVincent JL, Sakr Y, Sprung CL, Ranieri VM, Reinhart K, Gerlach H, Moreno R, Carlet J, Le Gall JR, Payen D. Sepsis occurrence in acutely ill patients I: Sepsis in European intensive care units: results of the SOAP study. Crit Care Med. 2006;34:344–53.\nKlompas M, Kleinman K, Murphy MV. Descriptive epidemiology and attributable morbidity of ventilator-associated events. Infect Control Hosp Epidemiol. 2014;35:502–10.\nBorgatta B, Gattarello S, Mazo CA, Imbiscuso AT, Larrosa MN, Lujan M, Rello J. The clinical significance of pneumonia in patients with respiratory specimens harbouring multidrug-resistant Pseudomonas aeruginosa: a 5-year retrospective study following 5667 patients in four general ICUs. Eur J Clin Microbiol Infect Dis. 2017;36(11):2155–63.\nTao L, Hu B, Rosenthal VD, Gao X, He L. Device-associated infection rates in 398 intensive care units in shanghai, China: international nosocomial infection control consortium (INICC) findings. Int J Infect Dis. 2011;15:e774–80.\nDing C, Yang Z, Wang J, Liu X, Cao Y, Pan Y, Han L, Zhan S. Prevalence of Pseudomonas aeruginosa and antimicrobial-resistant Pseudomonas aeruginosa in patients with pneumonia in mainland China: a systematic review and meta-analysis. Int J Infect Dis. 2016;49:119–28.\nRosenthal VD, Bijie H, Maki DG, Mehta Y, Apisarnthanarak A, Medeiros EA, Leblebicioglu H, Fisher D, Alvarez-Moreno C, Khader IA, et al. International nosocomial infection control consortium (INICC) report, data summary of 36 countries, for 2004-2009. Am J Infect Control. 2012;40:396–407.\nGupta R, Malik A, Rizvi M, Ahmed M, Singh A. Epidemiology of multidrug-resistant gram-negative pathogens isolated from ventilator-associated pneumonia in ICU patients. J Glob Antimicrob Resist. 2017;9:47–50.\nKelly BJ, Imai I, Bittinger K, Laughlin A, Fuchs BD, Bushman FD, Collman RG. Composition and dynamics of the respiratory tract microbiome in intubated patients. Microbiome. 2016;4:7.\nZakharkina T, Martin-Loeches I, Matamoros S, Povoa P, Torres A, Kastelijn JB, Hofstra JJ, de Wever B, de Jong M, Schultz MJ, et al. The dynamics of the pulmonary microbiome during mechanical ventilation in the intensive care unit and the association with occurrence of pneumonia. Thorax. 2017;72:803–10.\nMan WH, de Steenhuijsen Piters WA, Bogaert D. The microbiota of the respiratory tract: gatekeeper to respiratory health. Nat Rev Microbiol. 2017;15:259–70.\nForestier C, Guelon D, Cluytens V, Gillart T, Sirot J, De Champs C. Oral probiotic and prevention of Pseudomonas aeruginosa infections: a randomized, double-blind, placebo-controlled pilot study in intensive care unit patients. Crit Care. 2008;12:R69.\nMorrow LE, Kollef MH, Casale TB. Probiotic prophylaxis of ventilator-associated pneumonia: a blinded, randomized, controlled trial. Am J Respir Crit Care Med. 2010;182:1058–64.\nSiempos II, Ntaidou TK, Falagas ME. Impact of the administration of probiotics on the incidence of ventilator-associated pneumonia: a meta-analysis of randomized controlled trials. Crit Care Med. 2010;38:954–62.\nKhailova L, Baird CH, Rush AA, McNamee EN, Wischmeyer PE. Lactobacillus rhamnosus GG improves outcome in experimental pseudomonas aeruginosa pneumonia: potential role of regulatory T cells. Shock. 2013;40:496–503.\nKollef MH, Ricard JD, Roux D, Francois B, Ischaki E, Rozgonyi Z, Boulain T, Ivanyi Z, Janos G, Garot D, et al. A randomized trial of the amikacin Fosfomycin inhalation system for the adjunctive therapy of gram-negative ventilator-associated pneumonia: IASIS trial. Chest. 2017;151:1239–46.\nLuna CM, Blanzaco D, Niederman MS, Matarucco W, Baredes NC, Desmery P, Palizas F, Menga G, Rios F, Apezteguia C. Resolution of ventilator-associated pneumonia: prospective evaluation of the clinical pulmonary infection score as an early clinical predictor of outcome. Crit Care Med. 2003;31:676–82.\nGodon JJ, Zumstein E, Dabert P, Habouzit F, Moletta R. Molecular microbial diversity of an anaerobic digestor as determined by small-subunit rDNA sequence analysis. Appl Environ Microbiol. 1997;63:2802–13.\nSalter SJ, Cox MJ, Turek EM, Calus ST, Cookson WO, Moffatt MF, Turner P, Parkhill J, Loman NJ, Walker AW. Reagent and laboratory contamination can critically impact sequence-based microbiome analyses. BMC Biol. 2014;12:87.\nZhang X, Zhao Y, Xu J, Xue Z, Zhang M, Pang X, Zhang X, Zhao L. Modulation of gut microbiota by berberine and metformin during the treatment of high-fat diet-induced obesity in rats. Sci Rep. 2015;5:14405.\nFujimura KE, Sitarik AR, Havstad S, Lin DL, Levan S, Fadrosh D, Panzer AR, LaMere B, Rackaityte E, Lukacs NW, et al. Neonatal gut microbiota associates with childhood multisensitized atopy and T cell differentiation. Nat Med. 2016;22:1187–91.\nDogra S, Sakwinska O, Soh SE, Ngom-Bru C, Bruck WM, Berger B, Brussow H, Lee YS, Yap F, Chong YS, et al. Dynamics of infant gut microbiota are influenced by delivery mode and gestational duration and are associated with subsequent adiposity. MBio. 2015;6\nde Steenhuijsen Piters WA, Heinonen S, Hasrat R, Bunsow E, Smith B, Suarez-Arrabal MC, Chaussabel D, Cohen DM, Sanders EA, Ramilo O, et al. Nasopharyngeal microbiota, host transcriptome, and disease severity in children with respiratory syncytial virus infection. Am J Respir Crit Care Med. 2016;194:1104–15.\nLiu R, Hong J, Xu X, Feng Q, Zhang D, Gu Y, Shi J, Zhao S, Liu W, Wang X, et al. Gut microbiome and serum metabolome alterations in obesity and after weight-loss intervention. Nat Med. 2017;23:859–68.\nFalony G, Joossens M, Vieira-Silva S, Wang J, Darzi Y, Faust K, Kurilshikov A, Bonder MJ, Valles-Colomer M, Vandeputte D, et al. Population-level analysis of gut microbiome variation. Science. 2016;352:560–4.\nBurke DG, Fouhy F, Harrison MJ, Rea MC, Cotter PD, O'Sullivan O, Stanton C, Hill C, Shanahan F, Plant BJ, Ross RP. The altered gut microbiota in adults with cystic fibrosis. BMC Microbiol. 2017;17:58.\nTan C, Ling Z, Huang Y, Cao Y, Liu Q, Cai T, Yuan H, Liu C, Li Y, Xu K. Dysbiosis of intestinal microbiota associated with inflammation involved in the progression of acute pancreatitis. Pancreas. 2015;44:868–75.\nLankelma JM, van Vught LA, Belzer C, Schultz MJ, van der Poll T, de Vos WM, Wiersinga WJ. Critically ill patients demonstrate large interpersonal variation in intestinal microbiota dysregulation: a pilot study. Intensive Care Med. 2017;43:59–68.\nTang R, Wei Y, Li Y, Chen W, Chen H, Wang Q, Yang F, Miao Q, Xiao X, Zhang H, et al. Gut microbial profile is altered in primary biliary cholangitis and partially restored after UDCA therapy. Gut. 2018;67:534–41.\nKlingensmith NJ, Coopersmith CM. The gut as the Motor of Multiple Organ Dysfunction in critical illness. Crit Care Clin. 2016;32:203–12.\nCharlson ES, Bittinger K, Haas AR, Fitzgerald AS, Frank I, Yadav A, Bushman FD, Collman RG. Topographical continuity of bacterial populations in the healthy human respiratory tract. Am J Respir Crit Care Med. 2011;184:957–63.\nBron PA, van Baarlen P, Kleerebezem M. Emerging molecular insights into the interaction between probiotics and the host intestinal mucosa. Nat Rev Microbiol. 2011;10:66–78.\nMatsumoto T, Ishikawa H, Tateda K, Yaeshima T, Ishibashi N, Yamaguchi K. Oral administration of Bifidobacterium longum prevents gut-derived Pseudomonas aeruginosa sepsis in mice. J Appl Microbiol. 2008;104:672–80.\nRao KP, Chennappa G, Suraj U, Nagaraja H, Raj AP, Sreenivasa MY. Probiotic potential of lactobacillus strains isolated from sorghum-based traditional fermented food. Probiotics Antimicrob Proteins. 2015;7:146–56.\nShokri D, Khorasgani MR, Mohkam M, Fatemi SM, Ghasemi Y, Taheri-Kafrani A. The inhibition effect of lactobacilli against growth and biofilm formation of Pseudomonas aeruginosa. Probiotics Antimicrob Proteins. 2017;10(1):34–42.\nCotar AI, Saviuc C, Nita RA, Bezirtzoglou E, Lazar V, Chifiriuc MC. Anti-pathogenic strategies for fighting Pseudomonas aeruginosa infections- probiotic soluble compounds as inhibitors of quorum sensing genes expression. Curr Org Chem. 2013;17:155–61.\nWang Z, Bafadhel M, Haldar K, Spivak A, Mayhew D, Miller BE, Tal-Singer R, Johnston SL, Ramsheh MY, Barer MR, et al. Lung microbiome dynamics in COPD exacerbations. Eur Respir J. 2016;47:1082–92.\nHeirali AA, Workentine ML, Acosta N, Poonja A, Storey DG, Somayaji R, Rabin HR, Whelan FJ, Surette MG, Parkins MD. The effects of inhaled aztreonam on the cystic fibrosis lung microbiome. Microbiome. 2017;5:51.\nRogers GB, Bruce KD, Martin ML, Burr LD, Serisier DJ. The effect of long-term macrolide treatment on respiratory microbiota composition in non-cystic fibrosis bronchiectasis: an analysis from the randomised, double-blind, placebo-controlled BLESS trial. 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