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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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cells that accumulate with age have been shown to contribute to age-related diseases and organ dysfunction and have attracted attention as a target for anti-aging therapy. In particular, the use of senescent cell-depleting agents, or senolytics, has been shown to improve the aging phenotype in animal models. Since senescence has been implicated in the skin, particularly in fibroblasts, this study used aged human skin fibroblasts to investigate the effects of resibufogenin. A component of the traditional Chinese medicine toad venom, resibufogenin was investigated for senolytic and\u002For senomorphic activity. We found that the compound selectively caused senescent cell death without affecting proliferating cells, with a marked effect on the suppression of the senescence-associated secretory phenotype. We also found that resibufogenin causes senescent cell death by inducing a caspase-3-mediated apoptotic program. Administration of resibufogenin to aging mice resulted in an increase in dermal collagen density and subcutaneous fat, improving the phenotype of aging skin. In other words, resibufogenin ameliorates skin aging through selective induction of senescent cell apoptosis without affecting non-aged cells. This traditional compound may have potential therapeutic benefits in skin aging characterized by senescent cell accumulation.",{"EN":1004},"Identification of resibufogenin, a component of toad venom, as a novel senolytic compound in vitro and for potential skin rejuvenation in male mice",{"VOID":1006},"Al-Asmakh M, Bawadi H, Hamdan M, Gupta I, Kheraldine H, Jabeen A, Rizeq B, Al Moustafa AE (2021) Dasatinib and PD-L1 inhibitors provoke toxicity and inhibit angiogenesis in the embryo. Biomed Pharmacother 134:111134\nBaker DJ, Childs BG, Durik M, Wijers ME, Sieben CJ, Zhong J, Saltness RA, Jeganathan KB, Verzosa GC, Pezeshki A, Khazaie K, Miller JD, van Deursen JM (2016) Naturally occurring p16(Ink4a)-positive cells shorten healthy lifespan. Nature 530:184–189\nBeedholm R, Clark BFC, Rattan SIS (2004) Mild heat stress stimulates proteasome and its 11S activator in human fibroblasts undergoing aging in vitro. Cell Stress Chaperones 9:49–57\nBirch J, Gil J (2020) Senescence and the SASP: many therapeutic avenues. Genes Dev 34:1565–1576\nCalabrese EJ, Agathokleous E, Kapoor R, Kozumbo WJ, Rattan SIS (2019) Re-analysis of herbal extracts data reveals that inflammatory processes are mediated by hormetic mechanisms. Chem Biol Interact 314:108844\nChang J, Wang Y, Shao L et al (2016) Clearance of senescent cells by ABT263 rejuvenates aged hematopoietic stem cells in mice. Nat Med 22:78–83\nCoppé J-P, Desprez P-Y, Krtolica A, Campisi J (2010) The senescence-associated secretory phenotype: the dark side of tumor suppression. Annu Rev Pathol 5:99–118\nEzure T, Hosoi J, Amano S, Tsuchiya T (2009) Sagging of the cheek is related to skin elasticity, fat mass and mimetic muscle function. Skin Res Technol 15:299–305\nGao Y, Xu Z, Li X, Liu Z, Li W, Kang Y, Zhang X, Qi Y (2022) Resibufogenin, one of bufadienolides in toad venom, suppresses LPS-induced inflammation via inhibiting NF-κB and AP-1 pathways. Int Immunopharmacol 113:109312\nGuo Y, Liang F, Zhao F, Zhao J (2022) Retraction note: resibufogenin suppresses tumor growth and Warburg effect through regulating miR-143-3p\u002FHK2 axis in breast cancer. Mol Cell Biochem 477:2687\nHayflick L, Moorhead PS (1961) The serial cultivation of human diploid cell strains. Exp Cell Res 25:585–621\nIchikawa M, Sowa Y, Iizumi Y, Aono Y, Sakai T (2015) Resibufogenin induces G1-Phase arrest through the proteasomal degradation of cyclin D1 in human malignant tumor cells. PLoS ONE 10:e0129851\nJanson DG, Saintigny G, van Adrichem A, Mahé C, El Ghalbzouri A (2012) Different gene expression patterns in human papillary and reticular fibroblasts. J Invest Dermatol 132:2565–2572\nJohmura Y, Yamanaka T, Omori S, Wang TW, Sugiura Y, Matsumoto M, Suzuki N, Kumamoto S, Yamaguchi K, Hatakeyama S, Takami T, Yamaguchi R, Shimizu E et al (2021) Senolysis by glutaminolysis inhibition ameliorates various age-associated disorders. Science 371:265–270\nKamiya Y, Odama M, Mizuguti A, Murakami S, Ito T (2021) Puerarin blocks the aging phenotype in human dermal fibroblasts. PLoS ONE 22:16:e0249367\nKim H, Jang J, Song MJ, Kim G, Park CH, Lee DH, Lee SH, Chung JH (2022) Attenuation of intrinsic ageing of the skin via elimination of senescent dermal fibroblasts with senolytic drugs. J Eur Acad Dermatol Venereol 36:1125–1135\nLi H, Liu L, Huang T, Jin M, Zheng Z, Zhang H, Ye M, Liu K (2021a) Establishment of a novel ferroptosis-related lncRNA pair prognostic model in colon adenocarcinoma. Aging 13:23072–23095\nLi FJ, Hu JH, Ren X, Zhou CM, Liu Q, Zhang YQ (2021b) Toad venom: a comprehensive review of chemical constituents, anticancer activities, and mechanisms. Arch Pharm 354:e2100060\nLiu L, Liu Y, Liu X, Zhang N, Mao G, Zeng Q, Yin M, Song D, Deng H (2018) Resibufogenin suppresses transforming growth factor-β-activated kinase 1-mediated nuclear factor-κB activity through protein kinase C-dependent inhibition of glycogen synthase kinase 3. Cancer Sci 109:3611–3622\nLu Z, Xu A, Yuan X, Chen K, Wang L, Guo T (2018) Anticancer effect of resibufogenin on gastric carcinoma cells through the phosphoinositide 3-kinase\u002Fprotein kinase B\u002Fglycogen synthase kinase 3β signaling pathway. Oncol Lett 16:3297–3302\nMamun AA, Sufian MA, Uddin MS, Sumsuzzman DM, Jeandet P, Islam MS, Zhang HJ, Kong AN, Sarwar MS (2022) Exploring the role of senescence inducers and senotherapeutics as targets for anticancer natural products. Eur J Pharmacol 928:174991\nNielsen ER, Eskildsen-Helmond Y, Rattan SIS (2006) MAP-kinases and heat shock-induced horme-sis in human fibroblasts during serial passaging in vitro. Ann NY Acad Sci U S A 1067:343–348\nPapanagnou ED, Gumeni S, Sklirou AD, Rafeletou A, Terpos E, Keklikoglou K, Kastritis E, Stamatelopoulos K, Sykiotis GP, Dimopoulos MA, Trougakos IP (2022) Autophagy activation can partially rescue proteasome dysfunction-mediated cardiac toxicity. Aging Cell 21:e13715\nRattan SIS (2005) Hormetic modulation of aging and longevity by mild heat stress. Dose-response 3:533–546\nRattan SIS, Clark BF (1994) Kinetin delays the onset of ageing characteristics in human fibroblasts. Biochem Biophys Res Commun 201:665–672\nRoos CM, Zhang B, Palmer AK, Ogrodnik MB, Pirtskhalava T, Thalji NM, Hagler M, Jurk D, Smith LA, Casaclang-Verzosa G, Zhu Y, Schafer MJ, Tchkonia T et al (2016) Chronic senolytic treatment alleviates established vasomotor dysfunction in aged or atherosclerotic mice. Aging Cell 15:973–977\nSaccon TD, Nagpal R, Yadav H, Cavalcante MB, Nunes ADC, Schneider A, Gesing A, Hughes B, Yousefzadeh M, Tchkonia T, Kirkland JL, Niedernhofer LJ, Robbins PD et al (2021) Senolytic Combination of Dasatinib and Quercetin alleviates intestinal senescence and inflammation and modulates the gut microbiome in aged mice. J Gerontol A Biol Sci Med Sci 76:1895–1905\nSharma AK, Roberts RL, Benson RD Jr, Pierce JL, Yu K, Hamrick MW, McGee-Lawrence ME (2020) The Senolytic Drug Navitoclax (ABT-263) causes trabecular bone loss and impaired osteoprogenitor function in aged mice. Front Cell Dev Biol 8:354\nTakaya K, Ishii T, Asou T, Kishi K (2022) Glutaminase inhibitors rejuvenate human skin via clearance of senescent cells: a study using a mouse\u002Fhuman chimeric model. Aging 14:8914–8926\nTakaya K, Ishii T, Asou T, Kishi K (2023) Navitoclax (ABT-263) rejuvenates human skin by eliminating senescent dermal fibroblasts in a mouse\u002Fhuman chimeric model. Rejuvenation Res In Press 26:9–20\nTominaga K (2015) The emerging role of senescent cells in tissue homeostasis and pathophysiology. Pathobiol Aging Age Relat Dis 5:27743\nVelarde MC, Demaria M (2016) Targeting senescent cells: possible implications for delaying skin aging: a Mini-Review. Gerontology 62:513–518\nWang DL, Qi FH, Xu HL, Inagaki Y, Orihara Y, Sekimizu K, Kokudo N, Wang FS, Tang W (2010) Apoptosis-inducing activity of compounds screened and characterized from cinobufacini by bioassay-guided isolation. Mol Med Rep 3:717–722\nWang ZJ, Sun L, Heinbockel T (2014) Resibufogenin and cinobufagin activate central neurons through an ouabain-like action. PLoS ONE 9:e113272\nWei WL, An YL, Li ZW, Wang YY, Ji HJ, Hou JJ, Wu WY, Guo DA (2019) Simultaneous determination of resibufogenin and its eight metabolites in rat plasma by LC-MS\u002FMS for metabolic profiles and pharmacokinetic study. Phytomedicine 60:152971\nWesterheide SD, Bosman JD, Mbadugha BNA et al (2004) Celastrols as inducers of the heat shock response and cytoprotection. J Biol Chem 279:56053–56060\nXia W, Quan T, Hammerberg C, Voorhees JJ, Fisher GJ (2015) A mouse model of skin aging: fragmentation of dermal collagen fibrils and reduced fibroblast spreading due to expression of human matrix metalloproteinase-1. J Dermatol Sci 78:79–82\nXie JT, Wang H, Attele AS, Yuan CS (2000) Effects of resibufogenin from toad venom on isolated Purkinje fibers. Am J Chin Med 28:187–196\nXu M, Pirtskhalava T, Farr JN, Weigand BM, Palmer AK, Weivoda MM, Inman CL, Ogrodnik MB, Hachfeld CM, Fraser DG, Onken JL, Johnson KO, Verzosa GC et al (2018) Senolytics improve physical function and increase lifespan in old age. 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study investigates characteristics of aging in the central nervous system of the senescence accelerated prone mice (SAMP8). We examined 3 and 10-months old senescence-accelerated-prone mice (SAMP8) for functional and molecular changes in their brains, specifically in the hippocampus and somatosensory cortex. There was no statistically significant increase in the apoptosis indicators as revealed by Western Blotting for BAD and TUNEL experiments. However, the functional magnetic resonance imaging showed an increase in the area of BOLD images from the 3-month old to the 10-months old SAMP mice upon the application of tail stimulus. These results demonstrated a lack of neuronal deaths but an increase in the activated brain area with age.",{"EN":1135},"Changes of brain activity in the aged SAMP mouse",{"VOID":1137},"Adams I, Jones DG (1982) Synaptic remodeling and astrocytic hypertrophy in rat cerebral cortex from early to late adulthood. Neurobiol Aging 3:179–186\nBattaini F, Pascale A (2005) Protein kinase C signal transduction regulation in physiological and pathological aging. Ann N Y Acad Sci 1057:177–192\nBertoni-Freddari C, Fattoretti P, Meier-Ruge W, Ulrich J (1989) Computer-assisted morphometry of synaptic plasticity during aging and dementia. Pathol Res Pract 185:799–802\nBertoni-Freddari C, Fattoretti P, Casoli T, Pieroni M, Meier-Ruge W, Ulrich J (1991) Neurobiology of the aging brain: morphological alterations at synaptic regions. Arch Gerontol Geriatr 12:253–259\nDluzniewska J, Beresewicz M, Wojewodzka U, Gajkowska B, Zablocka B (2005) Transient cerebral ischemia induces delayed proapoptotic BAD translocation to mitochondria in CA1 sector of hippocampus. Brain Res Mol Brain Res 133:274–280\nDriscoll I, Sutherland RJ (2005) The aging hippocampus: navigating between rat and human experiments. Rev Neurosci 16:87–121\nFang M, Li J, Lu G, Gong X, Yew DT (2005) A fMRI study of age-related differential cortical patterns during cued motor movement. Brain Topogr 17:127–137\nFlood JF, Morley JE (1992) Early onset of age-related impairment of aversive and appetitive learning in the SAM-P\u002F8 mouse. J Gerontol 47:B52–B59\nFlood JF, Morley JE (1993) Age-related changes in footshock avoidance acquisition and retention in senescence accelerated mouse (SAM). Neurobiol Aging 14:153–157\nGrigoriou V, Shapiro IM, Cavalcanti-Adam EA, Composto RJ, Ducheyne P, Adams CS (2005) Apoptosis and survival of osteoblast-like cells are regulated by surface attachment. J Biol Chem 280:1733–1739\nGroh C, Ahrens D, Rosseler W (2006) Environment and age-dependent plasticity of synaptic complexes in the mushroom bodies of honeybee queens. Brain Behav Evol 68:1–14\nHalpain S, Spencer K, Graber S (2005) Dynamics and pathology of dendritic spines. Prog Brain Res 147:29–37\nHof PR, Morrison JH (2004) The aging brain: morphomolecular senescence of cortical circuits. Trends Neurosci 27:607–613\nKarasawa N, Nagatsu I, Sakai K, Nagatsu T, Watanabe K, Onozuka M (1997) Immunocytochemical study of catecholaminergic neurons in the senescence-accelerated mouse (SAM-P8) brain. J Neural Transm 104:1267–1275\nLarner SF, McKinsey DM, Hayes RL, Wang KKW (2005) Caspase 7: increased expression and activation after traumatic brain injury in rats. J Neurochem 94:97–108\nLi WP, Chan WY, Lai HW, Yew DT (1997) Terminal dUTP nick end labeling (TUNEL) positive cells in the different regions of the brain in normal aging and Alzheimer patients. J Mol Neurosci 8:75–82\nLores-Arnaiz S, Bustamante J, Arismendi M, Vilas S, Paglia N, Basso N, Capani F, Coirini H, Costa JJ, Arnaiz MR (2006) Extensive enriched environments protect old rats from the aging dependent impairment of spatial cognition, synaptic plasticity and nitric oxide production. Behav Brain Res 169:294–302\nMarcilhac A (2004) Intracellular signaling pathways, apoptosis and neurodegenerative diseases. Psychol Neuropsychiatr Vieil 2:203–214\nMiyamoto M (1997) Characteristics of age related behavioral changes in senescence accelerated mouse SAMP8 and SAMP10. Exp Gerontol 32:139–148\nMiyamoto M, Kiyota Y, Yamazaki N, Nagaoka A, Matsuo T, Nagawa Y, Takeda T (1986) Age-related changes in learning and memory in the senescence-accelerated mouse (SAM). Physiol Behav 38:399–406\nMiyamoto M, Kiyota Y, Nishiyama M, Nagaoka A (1992) Senescence-accelerated mouse (SAM): age related reduced anxiety-like behavior in the SAM-P\u002F8 strain. Physiol Behav 51:979–985\nMoolman DL, Vitolo OV, Vonsattel JP, Shelanski ML (2004) Dendrite and dendritic spine alterations in Alzheimer models. J Neurocytol 33:377–387\nMorley JE, Kumar VB, Bernardo AE, Farr SA, Uezu K, Tumosa N, Flood JF (2000) Beta-amyloid precursor polypeptide in SAMP8 mice affects learning and memory. Peptides 21:1761–1767\nMorley JE, Farr SA, Kumar VB, Banks WA (2002) Alzheimer’s disease through the eye of a mouse: acceptance lecture for the 2001 Gayle A. Olson and Richard D. Olson Prize Peptides 23:589–599\nOhta A, Hirano T, Yagi H, Tanaka S, Hosokawa M, Takeda T (1989) Behavioral characteristics of the SAM-P\u002F8 strain in Sidman active avoidance task. Brain Res 498:195–198\nOkuma Y, Nomura Y (1998) Senescence-accelerated mouse (SAM) as an animal model of senile dementia: pharmacological, neurochemical and molecular biological approach. Jpn J Pharmacol 78:399–404\nPetrella JR, Townsend BA, Jha AP, Ziajko LA, Slavin MJ, Lustig C, Hart SJ, Doraiswamy PM (2005) Increasing memory load modulates regional brain activity in older adults as measured by fMRI. J Neuropsychiatry Clin Neurosci 17:75–83\nRombouts SA, Barkhof F, Goekoop R, Stam CJ, Scheltens P (2005) Altered resting state networks in mild cognitive impairment and mild Alzheimer’s disease: an fMRI study. Hum Brain Mapp 26:231–239\nSheng W, Wang G, Wang Y, Liang J, Wen J, Zheng PS, Wu Y, Lee V, Slingerland J, Dumont D, Yang BB (2005) The roles of versican V1 and V2 isoforms in cell proliferation and apoptosis. Mol Biol Cell 16:1330–1340\nSprott RL, Austad SN, Schneider EL, Rowe JW (1995) Handbook of the biology of aging. Academic, San Diego\nStrong R, Reddy V, Morley JE (2003) Cholinergic deficits in the septal-hippocampal pathway of the SAM-P\u002F8 senescence accelerated mouse. Brain Res 966:150–156\nSun X, Zhang X, Chen X, Zhang P, Bao M, Zhang D, Chen J, He S, Hu X (2005) Age-dependent brain activation during forward and backward digit recall revealed by fMRI. Neuroimage 26:36–47\nSureda FX, Gutierrez-Cuesta J, Romeu M, Mulero M, Canudas AM, Camins A, Mallol J, Pallas M (2006) Changes in oxidative stress parameters and neurodegeneration markers in the brain of the senescence-accelerated mice SAMP-8. Exp Gerontol 41:360–367\nTakeda T, Hosokawa M, Takeshita S, Irino M, Higuchi K, Matsushita T, Tomita Y, Yasuhira K, Hamamoto H, Shimizu K, Ishii M, Yamamuro T (1981) A new murine model of accelerated senescence. Mech Ageing Dev 17(2):183–194\nTakeda T, Hosokawa M, Higuchi K (1991) Senescence-accelerated mice (SAM): a novel murine model of accelerated senescence. J Am Geriatr Soc 39:911–919\nTessitore A, Hariri AR, Fera F, Smith WG, Das S, Weinberger DR, Mattay VS (2005) Functional changes in the activity of brain regions underlying emotion processing in the elderly. Psychiatry Res 139:9–18\nTonkikh A, Janus C, El-Beheiry H, Pennefather PS, Samoilova M, McDonald P, Ouanounou A, Carlen PL (2006) Calcium chelation improves spatial learning and synaptic plasticity in aged rats. Exp Neurol 197:291–300\nVantler M, Caglayan E, Zimmermann WH, Baumer AT, Rosenkranz S (2005) Systematic evaluation of anti-apoptotic growth factor signaling in vascular smooth muscle cells. Only phosphatidylinositol 3′-kinase is important. J Biol Chem 280:14168–14176\nvon Gunten A, Kovari E, Rivara CB, Bouras C, Hof PR, Giannakopoulos P (2005) Stereologic analysis of hippocampal Alzheimer’s disease pathology in the oldest-old: evidence for sparing of the entorhinal cortex and CA1 field. Exp Neurol 193:198–206\nWang J, Eslinger PJ, Smith MB, Yang QX (2005) Functional magnetic resonance imaging study of human olfaction and normal aging. J Gerontol A Biol Sci Med Sci 60:510–514\nWu Y, Zhang AQ, Wai MS, Lai HW, Wu SX, Yew DT (2006) Changes of apoptosis-related proteins in hippocampus of SAM mouse in development and aging. Neurobiol Aging 27:782.e1–782.e10\nYagi H, Katoh S, Akiguchi I, Takeda T (1988) Age-related deterioration of ability of acquisition in memory and learning in senescence accelerated mouse: SAM-P8 as an animal model of disturbances in recent memory. Brain Res 474:86–93\nZhang A, Lorke DE, Lai HW, Chu X, Wu Y, Yew DT (2004) Age-related alterations in cytochrome c-mediated caspase activation in rhesus macaque monkey (Macaca mulatta) brains. Brain Res Mol Brain Res 123:112–120\nZuo Y, Lin A, Chang P, Gan WB (2005) Development of long-term dendritic spine stability in diverse regions of cerebral cortex. 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A common G\u002FC polymorphism has been identified at position −174 of the IL6 gene promoter (IL6−174G>C), but its associations with sIL6 and mortality are still unclear. Data from a population-based elderly cohort (n = 824) were used to study the associations of baseline sIL6 with the IL6−174 C-allele (C+) carrier status and all-cause mortality at 4 years, in the presence and absence of preexisting major diseases (PMD). Analyses were adjusted for socio-demographic factors and body-mass-index. Three-hundred-eighty-eight participants (47.1%) had PMD. Compared to the bottom sIL6 quartile, mortality increased both in presence [Hazard Ratio (HR) = 3.04; 95% confidence interval (CI): 1.48–6.25] and absence of PMD [HR = 3.91; 95%CI: 1.42–10.72] for the third higher sIL6 quartile, but only in presence of PMD for the top sIL6 quartile [HR = 2.30; 95%CI: 1.09–4.83]. In absence of PMD, C+ carrier status did not affect both sIL6 and mortality. In presence of PMD, C+ carrier status was associated with increased baseline sIL6 [odds ratio 2.01; 95%CI: 1.25–3.22, for all sIL6 quartiles above the bottom] but not with increased mortality risk. A survival advantage was even found for C+ carriers with PMD and sIL6 in the top quartile [HR = 0.31, 95%CI: 0.13–0.76]. In conclusion, although associated with increased sIL6 levels in presence of major diseases, the IL6−174 C-allele does not seem to have direct detrimental effects on survival in older age.",{"EN":1332},"Associations of the −174 G\u002FC Interleukin-6 Gene Promoter Polymorphism with Serum Interleukin 6 and Mortality in the Elderly",{"VOID":1334},"M Bennermo C Held F Green LE Strandberg CG Ericsson LO Hansson H Watkins A Hamsten P Tornvall (2004) ArticleTitlePrognostic value of plasma interleukin-6 concentrations and the −174 G > C and −572 G > C promoter polymorphisms of the interleukin-6 gene in patients with acute myocardial infarction treated with thrombolysis Atherosclerosis 174 157–163 Occurrence Handle10.1016\u002Fj.atherosclerosis.2004.01.019 Occurrence Handle1:CAS:528:DC%2BD2cXjvVGqtLw%3D Occurrence Handle15135265\nM Bonafè F Olivieri L Cavallone S Giovagnetti F Marchegiani M Cardelli C Pieri M Marra R Antonicelli R Lisa MR Rizzo G Paolisso D Monti C Franceschi (2001) ArticleTitleA gender-dependent genetic predisposition to produce high levels of IL-6 is detrimental for longevity Eur J Immunol 31 2357–2361 Occurrence Handle10.1002\u002F1521-4141(200108)31:8\u003C2357::AID-IMMU2357>3.0.CO;2-X Occurrence Handle11500818\nDJ Brull HE Montgomery J Sanders S Dhamrait L Luong A Rumley GD Lowe SE Humphries (2001) ArticleTitleInterleukin-6 gene −174 g>c and −572 g>c promoter polymorphisms are strong predictors of plasma interleukin-6 levels after coronary artery bypass surgery Arterioscler Thromb Vasc Biol 21 1458–1463 Occurrence Handle1:CAS:528:DC%2BD3MXntVGku7o%3D Occurrence Handle11557672\nH Bruunsgaard S Ladelund AN Pedersen M Schroll T Jorgensen (2003) ArticleTitlePredicting death from tumor necrosis factor-alpha and interleukin-6 in 80-year-old people Clin Exp Immunol 132 24–31 Occurrence Handle10.1046\u002Fj.1365-2249.2003.02137.x Occurrence Handle1:CAS:528:DC%2BD3sXjtlKrs70%3D Occurrence Handle12653832\nH Bruunsgaard L Christiansen AN Pedersen M Schroll T Jorgensen BK Pedersen (2004) ArticleTitleThe IL-6−174G>C polymorphism is associated with cardiovascular disease and mortality in 80-year-old humans Exp Gerontol 39 255–261 Occurrence Handle10.1016\u002Fj.exger.2003.10.012 Occurrence Handle1:CAS:528:DC%2BD2cXptFCjtw%3D%3D Occurrence Handle15036420\nC Capurso V Solfrizzi A D’Introno AM Colacicco SA Capurso C Semeraro A Capurso F Panza (2004) ArticleTitleInterleukin-6−174 G\u002FC promoter gene polymorphism in centenarians: no evidence of association with human longevity or interaction with apolipoprotein E alleles Exp Gerontol 39 1109–1114 Occurrence Handle1:CAS:528:DC%2BD2cXltl2gu7o%3D Occurrence Handle15236771\nME Charlson P Pompei KL Ales CR MacKenzie (1987) ArticleTitleA new method of classifying prognostic comorbidity in longitudinal studies: development and validation J Chron Dis 40 373–383 Occurrence Handle1:STN:280:BiiC28nlsVc%3D Occurrence Handle3558716\nL Christiansen L Bathum K Andersen-Ranberg B Jeune K Christensen (2004) ArticleTitleModest implication of interleukin-6 promoter polymorphisms in longevity Mech Ageing Dev 125 391–395 Occurrence Handle10.1016\u002Fj.mad.2004.03.004 Occurrence Handle1:CAS:528:DC%2BD2cXjvVeqsbc%3D Occurrence Handle15130757\nWB Ershler ET Keller (2000) ArticleTitleAge-associated increased interleukin-6 gene expression, late-life diseases, and frailty Annu Rev Med 51 245–270 Occurrence Handle10.1146\u002Fannurev.med.51.1.245 Occurrence Handle1:CAS:528:DC%2BD3cXisVelsbY%3D Occurrence Handle10774463\nD Fishman G Faulds R Jeffery V Mohamed-Ali JS Yudkin S Humphries P Woo (1998) ArticleTitleThe effect of novel polymorphisms in the interleukin-6 (IL-6) gene on IL-6 transcription and plasma IL-6 levels, and an association with systemic-onset juvenile chronic arthritis J Clin Invest 102 1369–1376 Occurrence Handle1:CAS:528:DyaK1cXmsFOrsrY%3D Occurrence Handle9769329\nR Giacconi C Cipriano F Albanese G Boccoli V Saba F Olivieri C Franceschi E Mocchegiani (2004) ArticleTitleThe −174G\u002FC polymorphism of IL-6 is useful to screen old subjects at risk for atherosclerosis or to reach successful ageing Exp Gerontol 39 621–628 Occurrence Handle10.1016\u002Fj.exger.2003.12.013 Occurrence Handle1:CAS:528:DC%2BD2cXisF2nu7o%3D Occurrence Handle15050298\nKG Jones DJ Brull LC Brown M Sian RM Greenhalgh SE Humphries JT Powel (2001) ArticleTitleInterleukin-6 (IL-6) and the prognosis of abdominal aortic aneurysms Circulation 8 2222–2224\nS Kilpinen J Hulkkonen XY Wang M Hurme (2001) ArticleTitleThe promoter polymorphism of the interleukin-6 gene regulated interleukin-6 production in neonates but not in adults Eur Cytokine Netw 12 62–68 Occurrence Handle1:CAS:528:DC%2BD3MXivFGltLg%3D Occurrence Handle11282548\nKS Krabbe M Pedersen H Bruunsgaard (2004) ArticleTitleInflammatory mediators in the elderly Exp Gerontol 39 687–699 Occurrence Handle10.1016\u002Fj.exger.2004.01.009 Occurrence Handle1:CAS:528:DC%2BD2cXjvVahtbg%3D Occurrence Handle15130663\nF Licastro LME Grimaldi M Bonafè M Chiappelli F Olivieri L Cavallone S Giovanietti E Masliah C Franceschi (2003) ArticleTitleInterleukin-6 genes alleles affect the risk of Alzheimer’s disease and levels of the cytokine in blood and brain Neurobiol Aging 24 921–926 Occurrence Handle10.1016\u002FS0197-4580(03)00013-7 Occurrence Handle1:CAS:528:DC%2BD3sXmsVeis7c%3D Occurrence Handle12928051\nJE Morley RN Baumgartner (2004) ArticleTitleCytokine-related aging process J Gerontol Med Sci 59A 924–929 Occurrence Handle1:CAS:528:DC%2BD2cXpslGhsb8%3D\nM Nauck BR Winkelmann MM Hoffman BO Bohm H Wieland W Marz (2002) ArticleTitleThe interleukin-6 G(-174) C promoter polymorphism in the LURIC cohort: no association with plasma interleukin-6, coronary artery disease, and myocardial infarction J Mol Med 80 507–513 Occurrence Handle10.1007\u002Fs00109-002-0354-2 Occurrence Handle1:CAS:528:DC%2BD38Xns1ags7g%3D Occurrence Handle12185451\nF Olivieri M Bonafè L Cavallone S Giovagnetti F Marchegiani M Cardelli E Mugianesi C Giampieri R Moresi R Stecconi R Lisa C Franceschi (2002) ArticleTitleThe –174 C\u002FG locus affects in vitro\u002Fin vivo IL-6 production during aging Exp Gerontol 37 309–314 Occurrence Handle10.1016\u002FS0531-5565(01)00197-8 Occurrence Handle1:CAS:528:DC%2BD38XitlGm Occurrence Handle11772517\nGM Pes D Lio C Carru L Deiana G Baggio C Franceschi L Ferrucci F Oliveri L Scola A Crivello G Candare G Colonna-Romano C Caruso (2004) ArticleTitleAssociations between longevity and cytokine gene polymorphisms. A study in Sardinian centenarians Aging Clin Exp Res 16 244–248 Occurrence Handle1:CAS:528:DC%2BD2cXptVegsrs%3D Occurrence Handle15462469\nR Rauramaa SB Vaisanen LA Luong A Schmidt-Trucksass IM Penttila C Bouchard J Toyry SE Humphries (2000) ArticleTitleStromelysin-1 and interleukin-6 gene promoter polymorphisms are determinants of asymptomatic carotid artery atherosclerosis Arterioscler Thromb Vasc Biol 20 2657–2662 Occurrence Handle1:CAS:528:DC%2BD3MXitlWhsA%3D%3D Occurrence Handle11116068\nG Ravaglia P Forti F Maioli L Sacchetti E Mariani V Nativio T Talerico C Vettori PL Macini (2002) ArticleTitleEducation, occupation, and prevalence of dementia: findings from the Conselice study Dement Geriatr Cogn Disord 14 90–100 Occurrence Handle10.1159\u002F000064930 Occurrence Handle12145456\nIM Rea OA Ross M Armstrong S McNerlan DH Alexander MD Curran D Middleton (2003) ArticleTitleInterleukin-6-gene C\u002FG 174 polymorphism in nonagenarian and octogenarian subjects in the BELFAST study. Reciprocal effects on IL-6, soluble IL-6 receptor and for IL-10 in serum and monocyte supernants Mech Ageing Dev 124 555–561 Occurrence Handle10.1016\u002FS0047-6374(03)00036-8 Occurrence Handle1:CAS:528:DC%2BD3sXjtVCqt7c%3D Occurrence Handle12714267\nOA Ross MD Curran A Meenagh F Williams YA Barnett D Middleton IM Rea (2003) ArticleTitleStudy of age-association with cytokine gene polymorphisms in an aged Irish population Mech Ageing Dev 124 199–206 Occurrence Handle1:CAS:528:DC%2BD3sXhvFWqsLo%3D Occurrence Handle12633940\nXY Wang M Hurme M Jylha A Hervonen (2001) ArticleTitleLack of association between human longevity and polymorphisms of IL-1 cluster, IL-6, IL-10 and TNF-alpha genes in Finnish nonagenarians Mech Ageing Dev 123 29–38 Occurrence Handle10.1016\u002FS0047-6374(01)00338-4 Occurrence Handle1:CAS:528:DC%2BD3MXnsF2hurY%3D Occurrence Handle11640949\nZ Xing J Gauldie G Cox H Baumann M Jordana XF Lei MK Achong (1998) ArticleTitleIL-6 is an antiinflammatory cytokine required for controlling local or systemic acute inflammatory responses J Clin Invest 101 311–320 Occurrence Handle1:CAS:528:DyaK1cXmtF2jug%3D%3D Occurrence Handle9435302",{"VOID":1336},"10.1007\u002Fs10522-005-4908-x","http:\u002F\u002Flink.springer.com\u002F10.1007\u002Fs10522-005-4908-x",[1339,1354,1367,1380,1395,1410,1423,1438,1451,1466],{"id":1340,"sortIndex":32,"researcher":28,"roles":1341,"affiliations":1342,"properties":1351,"displayName":1353,"givenName":28,"familyName":28},"573154c4-eb4e-4926-bd27-ab13bcadb856",[1016],[1343],{"id":1344,"sortIndex":32,"affiliation":1345,"properties":28},"a7f16308-99a9-4769-a797-96597ce09606",{"id":1344,"createTime":28,"updateTime":28,"relativeEntities":1346,"slug":28,"properties":1347,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1350,"statistic":28},[],{"title":1348},{"VI":1349},"Department of Internal Medicine, Cardioangiology and Hepatology, University Hospital S. Orsola-Malpighi, Bologna, Italy",[],{"title":1352},{"VI":1353},"Giovanni Ravaglia",{"id":1355,"sortIndex":40,"researcher":28,"roles":1356,"affiliations":1357,"properties":1364,"displayName":1366,"givenName":28,"familyName":28},"a9e4d0e0-6af9-44fe-9899-f707e068eff5",[1016],[1358],{"id":1344,"sortIndex":32,"affiliation":1359,"properties":28},{"id":1344,"createTime":28,"updateTime":28,"relativeEntities":1360,"slug":28,"properties":1361,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1363,"statistic":28},[],{"title":1362},{"VI":1349},[],{"title":1365},{"VI":1366},"Paola 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I (GLOI) is the first enzyme of the glyoxalase system that catalyzes the metabolism of reactive dicarbonyls, such as methylglyoxal (MGO). During aging and cataract development, human lens proteins are chemically modified by MGO, which is likely due to inadequate metabolism of MGO by the glyoxalase system. In this study, we have determined the effect of aging on GLOI activity and the immunoreactivity and morphological distribution of GLOI in the human lens. A monoclonal antibody was developed against human GLOI. GLOI immunoreactivity was strongest in the anterior epithelial cells and weaker in rest of the lens. Cultured human lens epithelial cells showed immunostaining throughout the cytoplasm. In the human lens, GLOI activity and immunoreactivity both decreased with age. We believe that this would lead to promotion of MGO-modification in aging lens proteins.",{"EN":1546},"Glyoxalase I activity and immunoreactivity in the aging human lens",{"VOID":1548},"Ahmed N, Thornalley PJ (2002) Chromatographic assay of glycation adducts in human serum albumin glycated in vitro by derivatization with 6-aminoquinolyl-N-hydroxysuccinimidyl-carbamate and intrinsic fluorescence. Biochem J 364:15–24\nAhmed N, Thornalley PJ, Dawczynski J, Franke S, Strobel J, Stein G, Haik GM (2003) Methylglyoxal-derived hydroimidazolone advanced glycation end-products of human lens proteins. Invest Ophthalmol Vis Sci 44:5287–5292. doi:10.1167\u002Fiovs.03-0573\nAhmed U, Dobler D, Larkin SJ, Rabbani N, Thornalley PJ (2008) Reversal of hyperglycemia-induced angiogenesis deficit of human endothelial cells by overexpression of glyoxalase 1 in vitro. Ann N Y Acad Sci 1126:262–264. doi:10.1196\u002Fannals.1433.035\nBhat SP (2001) The ocular lens epithelium. Biosci Rep 21:537–563. doi:10.1023\u002FA:1017952128502\nBiemel KM, Friedl DA, Lederer MO (2002) Identification and quantification of major maillard cross-links in human serum albumin and lens protein. Evidence for glucosepane as the dominant compound. J Biol Chem 277:24907–24915. doi:10.1074\u002Fjbc.M202681200\nChellan P, Nagaraj RH (1999) Protein crosslinking by the maillard reaction: dicarbonyl-derived imidazolium crosslinks in aging and diabetes. Arch Biochem Biophys 368:98–104. doi:10.1006\u002Fabbi.1999.1291\nDavid LL, Shearer TR (1989) Role of proteolysis in lenses: a review. Lens Eye Toxic Res 6:725–747\nDegenhardt TP, Thorpe SR, Baynes JW (1998) Chemical modification of proteins by methylglyoxal. Cell Mol Biol Noisy-le-grand 44:1139–1145\nde Hemptinne V, Rondas D, Vandekerckhove J, Vancompernolle K (2007) Tumour necrosis factor induces phosphorylation primarily of the nitric-oxide-responsive form of glyoxalase I. Biochem J 407:121–128. doi:10.1042\u002FBJ20070379\nFujiwara H, Takigawa Y, Suzuki T, Nakata K (1992) Superoxide dismutase activity in cataractous lenses. Jpn J Ophthalmol 36:273–280\nHaik GM Jr, Lo TW, Thornalley PJ (1994) Methylglyoxal concentration and glyoxalase activities in the human lens. Exp Eye Res 59:497–500. doi:10.1006\u002Fexer.1994.1135\nHovatta I, Tennant RS, Helton R, Marr RA, Singer O, Redwine JM, Ellison JA, Schadt EE, Verma IM, Lockhart DJ, Barlow C (2005) Glyoxalase 1 and glutathione reductase 1 regulate anxiety in mice. Nature 438:662–666. doi:10.1038\u002Fnature04250\nJedziniak JA, Arredondo LM, Meys M (1986) Human lens enzyme alterations with age and cataract: glyceraldehyde-3-P dehydrogenase and triose phosphate isomerase. Curr Eye Res 5:119–126. doi:10.3109\u002F02713688609015100\nJunaid MA, Kowal D, Barua M, Pullarkat PS, Sklower Brooks S, Pullarkat RK (2004) Proteomic studies identified a single nucleotide polymorphism in glyoxalase I as autism susceptibility factor. Am J Med Genet A 131:11–17. doi:10.1002\u002Fajmg.a.30349\nKawatani M, Okumura H, Honda K, Kanoh N, Muroi M, Dohmae N, Takami M, Kitagawa M, Futamura Y, Imoto M, Osada H (2008) The identification of an osteoclastogenesis inhibitor through the inhibition of glyoxalase I. Proc Natl Acad Sci USA 105:11691–11696. doi:10.1073\u002Fpnas.0712239105\nKuhla B, Boeck K, Schmidt A, Ogunlade V, Arendt T, Munch G, Luth HJ (2007) Age- and stage-dependent glyoxalase I expression and its activity in normal and Alzheimer’s disease brains. Neurobiol Aging 28:29–41. doi:10.1016\u002Fj.neurobiolaging.2005.11.007\nKumar MS, Reddy PY, Kumar PA, Surolia I, Reddy GB (2004) Effect of dicarbonyl-induced browning on alpha-crystallin chaperone-like activity: physiological significance and caveats of in vitro aggregation assays. Biochem J 379:273–282. doi:10.1042\u002FBJ20031633\nLou MF (2000) Thiol regulation in the lens. J Ocul Pharmacol Ther 16:137–148. doi:10.1089\u002Fjop.2000.16.137\nMancini MA, Unakar NJ, Giblin FJ, Reddan JR (1989) Histochemical localization of catalase in cultured lens epithelial cells. Ophthalmic Res 21:369–373\nMannervik B (2008) Molecular enzymology of the glyoxalase system. Drug Metabol Drug Interact 23:13–27\nMiller AG, Smith DG, Bhat M, Nagaraj RH (2006) Glyoxalase I is critical for human retinal capillary pericyte survival under hyperglycemic conditions. J Biol Chem 281:11864–11871. doi:10.1074\u002Fjbc.M513813200\nMitsumoto A, Kim KR, Oshima G, Kunimoto M, Okawa K, Iwamatsu A, Nakagawa Y (2000) Nitric oxide inactivates glyoxalase I in cooperation with glutathione. J Biochem 128:647–654\nMorcos M, Du X, Pfisterer F, Hutter H, Sayed AA, Thornalley P, Ahmed N, Baynes J, Thorpe S, Kukudov G, Schlotterer A, Bozorgmehr F, El Baki RA, Stern D, Moehrlen F, Ibrahim Y, Oikonomou D, Hamann A, Becker C, Zeier M, Schwenger V, Miftari N, Humpert P, Hammes HP, Buechler M, Bierhaus A, Brownlee M, Nawroth PP (2008) Glyoxalase-1 prevents mitochondrial protein modification and enhances lifespan in Caenorhabditis elegans. Aging Cell 7:260–269. doi:10.1111\u002Fj.1474-9726.2008.00371.x\nNagaraj RH, Oya-Ito T, Padayatti PS, Kumar R, Mehta S, West K, Levison B, Sun J, Crabb JW, Padival AK (2003) Enhancement of chaperone function of alpha-crystallin by methylglyoxal modification. Biochemistry 42:10746–10755. doi:10.1021\u002Fbi034541n\nOrnek K, Karel F, Buyukbingol Z (2003) May nitric oxide molecule have a role in the pathogenesis of human cataract? Exp Eye Res 76:23–27. doi:10.1016\u002FS0014-4835(02)00268-3\nOya T, Hattori N, Mizuno Y, Miyata S, Maeda S, Osawa T, Uchida K (1999) Methylglyoxal modification of protein. Chemical and immunochemical characterization of methylglyoxal-arginine adducts. J Biol Chem 274:18492–18502. doi:10.1074\u002Fjbc.274.26.18492\nPadayatti PS, Jiang C, Glomb MA, Uchida K, Nagaraj RH (2001a) High concentrations of glucose induce synthesis of argpyrimidine in retinal endothelial cells. Curr Eye Res 23:106–115. doi:10.1076\u002Fceyr.23.2.106.5472\nPadayatti PS, Ng AS, Uchida K, Glomb MA, Nagaraj RH (2001b) Argpyrimidine, a blue fluorophore in human lens proteins: high levels in brunescent cataractous lenses. Invest Ophthalmol Vis Sci 42:1299–1304\nPiec I, Listrat A, Alliot J, Chambon C, Taylor RG, Bechet D (2005) Differential proteome analysis of aging in rat skeletal muscle. FASEB J 19:1143–1145\nRathbun WB, Bovis MG (1986) Activity of glutathione peroxidase and glutathione reductase in the human lens related to age. Curr Eye Res 5:381–385. doi:10.3109\u002F02713688609025177\nReddan JR, Steiger CA, Dziedzic DC, Gordon SR (1996) Regional differences in the distribution of catalase in the epithelium of the ocular lens. Cell Mol Biol Noisy-le-grand 42:209–219\nRehnstrom K, Ylisaukko-Oja T, Vanhala R, von Wendt L, Peltonen L, Hovatta I (2008) No association between common variants in glyoxalase 1 and autism spectrum disorders. Am J Med Genet B Neuropsychiatr Genet 147:124–127. doi:10.1002\u002Fajmg.b.30582\nRulli A, Carli L, Romani R, Baroni T, Giovannini E, Rosi G, Talesa V (2001) Expression of glyoxalase I and II in normal and breast cancer tissues. Breast Cancer Res Treat 66:67–72. doi:10.1023\u002FA:1010632919129\nShamsi FA, Lin K, Sady C, Nagaraj RH (1998) Methylglyoxal-derived modifications in lens aging and cataract formation. Invest Ophthalmol Vis Sci 39:2355–2364\nShamsi FA, Sharkey E, Creighton D, Nagaraj RH (2000) Maillard reactions in lens proteins: methylglyoxal-mediated modifications in the rat lens. Exp Eye Res 70:369–380. doi:10.1006\u002Fexer.1999.0800\nShang F, Gong X, Palmer HJ, Nowell TR Jr, Taylor A (1997) Age-related decline in ubiquitin conjugation in response to oxidative stress in the lens. Exp Eye Res 64:21–30. doi:10.1006\u002Fexer.1996.0176\nShinohara M, Thornalley PJ, Giardino I, Beisswenger P, Thorpe SR, Onorato J, Brownlee M (1998) Overexpression of glyoxalase-I in bovine endothelial cells inhibits intracellular advanced glycation endproduct formation and prevents hyperglycemia-induced increases in macromolecular endocytosis. J Clin Invest 101:1142–1147. doi:10.1172\u002FJCI119885\nSilva MS, Barata L, Ferreira AE, Romao S, Tomas AM, Freire AP, Cordeiro C (2008) Catalysis and structural properties of leishmania infantum glyoxalase II: trypanothione specificity and phylogeny. Biochemistry 47:195–204. doi:10.1021\u002Fbi700989m\nSpector A (1995) Oxidative stress-induced cataract: mechanism of action. FASEB J 9:1173–1182\nThornalley PJ (2003) Glyoxalase I–structure, function and a critical role in the enzymatic defence against glycation. Biochem Soc Trans 31:1343–1348. doi:10.1042\u002FBST0311343\nThornalley PJ (2007) Endogenous alpha-oxoaldehydes and formation of protein and nucleotide advanced glycation endproducts in tissue damage. Novartis Found Symp 285:229–243. doi:10.1002\u002F9780470511848.ch17 (discussion 243-226)\nWilker SC, Chellan P, Arnold BM, Nagaraj RH (2001) Chromatographic quantification of argpyrimidine, a methylglyoxal-derived product in tissue proteins: comparison with pentosidine. Anal Biochem 290:353–358. doi:10.1006\u002Fabio.2001.4992",{"VOID":1550},"10.1007\u002Fs10522-009-9218-2","https:\u002F\u002Flink.springer.com\u002Farticle\u002F10.1007\u002Fs10522-009-9218-2",[1553,1568,1581,1594,1609,1622],{"id":1554,"sortIndex":32,"researcher":28,"roles":1555,"affiliations":1556,"properties":1565,"displayName":1567,"givenName":28,"familyName":28},"d9277e8f-d1c1-4e58-8c14-5e80790c9450",[1016],[1557],{"id":1558,"sortIndex":32,"affiliation":1559,"properties":28},"62e8feb7-4177-43cd-ba34-485091f31342",{"id":1558,"createTime":28,"updateTime":28,"relativeEntities":1560,"slug":28,"properties":1561,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1564,"statistic":28},[],{"title":1562},{"VI":1563},"Department of Ophthalmology and Visual Sciences, Case Western Reserve University, Cleveland, USA",[],{"title":1566},{"VI":1567},"Maneesh Mailankot",{"id":1569,"sortIndex":40,"researcher":28,"roles":1570,"affiliations":1571,"properties":1578,"displayName":1580,"givenName":28,"familyName":28},"30f65de7-9c95-457d-a975-1e2c545b6ec7",[1016],[1572],{"id":1558,"sortIndex":32,"affiliation":1573,"properties":28},{"id":1558,"createTime":28,"updateTime":28,"relativeEntities":1574,"slug":28,"properties":1575,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1577,"statistic":28},[],{"title":1576},{"VI":1563},[],{"title":1579},{"VI":1580},"Smitha Padmanabha",{"id":1582,"sortIndex":123,"researcher":28,"roles":1583,"affiliations":1584,"properties":1591,"displayName":1593,"givenName":28,"familyName":28},"e749e377-d918-44e0-86d0-e2289abfc68c",[1016],[1585],{"id":1558,"sortIndex":32,"affiliation":1586,"properties":28},{"id":1558,"createTime":28,"updateTime":28,"relativeEntities":1587,"slug":28,"properties":1588,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1590,"statistic":28},[],{"title":1589},{"VI":1563},[],{"title":1592},{"VI":1593},"NagaRekha Pasupuleti",{"id":1595,"sortIndex":42,"researcher":28,"roles":1596,"affiliations":1597,"properties":1606,"displayName":1608,"givenName":28,"familyName":28},"27f0220d-ad7a-459b-999b-7c6f2cb6e93c",[1016],[1598],{"id":1599,"sortIndex":32,"affiliation":1600,"properties":28},"240b835a-2834-472d-8ee8-8c3252754890",{"id":1599,"createTime":28,"updateTime":28,"relativeEntities":1601,"slug":28,"properties":1602,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1605,"statistic":28},[],{"title":1603},{"VI":1604},"Visual Sciences Research Center, Case Western Reserve University, Cleveland, USA",[],{"title":1607},{"VI":1608},"Denice Major",{"id":1610,"sortIndex":45,"researcher":28,"roles":1611,"affiliations":1612,"properties":1619,"displayName":1621,"givenName":28,"familyName":28},"ebdcdbf4-213b-481d-9cfc-9164f29a16cc",[1016],[1613],{"id":1599,"sortIndex":32,"affiliation":1614,"properties":28},{"id":1599,"createTime":28,"updateTime":28,"relativeEntities":1615,"slug":28,"properties":1616,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1618,"statistic":28},[],{"title":1617},{"VI":1604},[],{"title":1620},{"VI":1621},"Scott Howell",{"id":1623,"sortIndex":46,"researcher":28,"roles":1624,"affiliations":1625,"properties":1632,"displayName":1634,"givenName":28,"familyName":28},"927f9351-1bc0-4d5b-8e57-a0c2be073959",[1016],[1626],{"id":1558,"sortIndex":32,"affiliation":1627,"properties":28},{"id":1558,"createTime":28,"updateTime":28,"relativeEntities":1628,"slug":28,"properties":1629,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1631,"statistic":28},[],{"title":1630},{"VI":1563},[],{"title":1633},{"VI":1634},"Ram H. 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These programmed cell fate decisions include true cell death (apoptosis-necroptosis) and therapy-induced cellular senescence (TIS), a permanent “proliferative arrest” commonly portrayed as premature cellular aging. Despite a permanent loss of proliferative potential, senescent cells remain viable and are highly bioactive at the microenvironment level, resulting in a prolonged impact on tissue architecture and functions. Cellular senescence is primarily documented as a tumor suppression mechanism that prevents cellular transformation. In the context of normal tissues, cellular senescence also plays important roles in tissue repair, but contributes to age-associated tissue dysfunction when senescent cells accumulate. Theoretically, in multi-step cancer progression models, cancer cells have already bypassed cellular senescence during their immortalization step (see hallmarks of cancer). It is then perhaps surprising to find that cancer cells often retain the ability to undergo TIS, or premature aging. This occurs because cellular senescence results from multiple signalling pathways, some retained in cancer cells, aiming to prevent cell cycle progression in damaged cells. Since senescent cancer cells persist after therapy and secrete an array of cytokines and growth factors that can modulate the tumor microenvironment, these cells may have beneficial and detrimental effects regarding immune modulation and survival of remaining proliferation-competent cancer cells. Similarly, while normal cells undergoing senescence are believed to remain indefinitely growth arrested, whether this is true for senescent cancer cells remains unclear, raising the possibility that these cells may represent a reservoir for cancer recurrence after treatment. This review discusses our current knowledge on cancer cell senescence and highlight questions that must be addressed to fully understand the beneficial and detrimental impacts of cellular senescence during cancer therapy.",{"EN":1704},"Premature aging\u002Fsenescence in cancer cells facing therapy: good or bad?",{"VOID":1706},"Acosta JC, Gil J (2012) Senescence: a new weapon for cancer therapy. Trends Cell Biol 22:211–219\nAcosta JC, O’Loghlen A, Banito A, Guijarro MV, Augert A, Raguz S, Fumagalli M, Da Costa M, Brown C, Popov N, Takatsu Y, Melamed J, d’Adda di Fagagna F, Bernard D, Hernando E, Gil J (2008) Chemokine signaling via the CXCR2 receptor reinforces senescence. Cell 133:1006–1018\nAird KM, Zhang R (2013) Detection of senescence-associated heterochromatin foci (SAHF). 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Baseline telomere length (TL) is determined by rare and common germline genetic variants but shortens with age and is susceptible to certain environmental exposures. Cellular senescence or apoptosis are normally triggered when telomeres reach a critically short length, but cancer cells overcome these protective mechanisms and continue to divide despite chromosomal instability. Rare germline variants in telomere maintenance genes cause exceedingly short telomeres for age (\u003C 1st percentile) and the telomere biology disorders, which are associated with elevated risks of bone marrow failure, myelodysplastic syndrome, acute myeloid leukemia, and squamous cell carcinoma of the head\u002Fneck and anogenital regions. Long telomeres due to rare germline variants in the same or different telomere maintenance genes are associated with elevated risks of other cancers, such as chronic lymphocytic leukemia or sarcoma. Early epidemiology studies of TL in the general population lacked reproducibility but new methods, including creation of a TL polygenic score using common variants, have found longer telomeres associated with excess risks of renal cell carcinoma, glioma, lung cancer, and others. It has become clear that when it comes to TL and cancer etiology, not too short, not too long, but “just right” telomeres are important in minimizing cancer risk.",{"EN":1932},"Telomere length and cancer risk: finding Goldilocks",{"VOID":1934},"Alder JK, Hanumanthu VS, Strong MA, DeZern AE, Stanley SE, Takemoto CM, Danilova L, Applegate CD, Bolton SG, Mohr DW, Brodsky RA, Casella JF, Greider CW, Jackson JB, Armanios M (2018) Diagnostic utility of telomere length testing in a hospital-based setting. Proc Natl Acad Sci USA 115(10):E2358–E2365. https:\u002F\u002Fdoi.org\u002F10.1073\u002Fpnas.1720427115\nAllaire P, He J, Mayer J, Moat L, Gerstenberger P, Wilhorn R, Strutz S, Kim DSL, Zeng C, Cox N, Shay JW, Denny J, Bastarache L, Hebbring S (2023) Genetic and clinical determinants of telomere length. HGG Adv 4(3):100201. https:\u002F\u002Fdoi.org\u002F10.1016\u002Fj.xhgg.2023.100201\nAlter BP, Baerlocher G, Savage SA, Chanock SJ, Weksler BB, Willner JP, Peters JA, Lansdorp PM (2006) Telomere length measurement by flow-FISH distinguishes dyskeratosis congenita from other bone marrow failure syndromes. Blood 108(11):58A–59A\nAlter BP, Giri N, Savage SA, Rosenberg PS (2018) Cancer in the National Cancer Institute inherited bone marrow failure syndrome cohort after fifteen years of follow-up. 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Ageing Res Rev 85:101854. https:\u002F\u002Fdoi.org\u002F10.1016\u002Fj.arr.2023.101854\nAubert G, Hills M, Lansdorp PM (2012) Telomere length measurement—Caveats and a critical assessment of the available technologies and tools. Mutat Res 730(1):59–67\nAviv A, Shay JW (2018) Reflections on telomere dynamics and ageing-related diseases in humans. Philos Trans R Soc Lond B Biol Sci 373(1741):20160436. https:\u002F\u002Fdoi.org\u002F10.1098\u002Frstb.2016.0436\nAviv A, Hunt SC, Lin J, Cao X, Kimura M, Blackburn E (2011) Impartial comparative analysis of measurement of leukocyte telomere length\u002FDNA content by Southern blots and qPCR. Nucleic Acids Res 39(20):e134. https:\u002F\u002Fdoi.org\u002F10.1093\u002Fnar\u002Fgkr634\nAviv A, Anderson JJ, Shay JW (2017) Mutations, cancer and the telomere length paradox. Trends Cancer 3(4):253–258. https:\u002F\u002Fdoi.org\u002F10.1016\u002Fj.trecan.2017.02.005\nBallinger ML, Pattnaik S, Mundra PA, Zaheed M, Rath E, Priestley P, Baber J, Ray-Coquard I, Isambert N, Causeret S, van der Graaf WTA, Puri A, Duffaud F, Le Cesne A, Seddon B, Chandrasekar C, Schiffman JD, Brohl AS, James PA, Kurtz JE, Penel N, Myklebost O, Meza-Zepeda LA, Pickett H, Kansara M, Waddell N, Kondrashova O, Pearson JV, Barbour AP, Li S, Nguyen TL, Fatkin D, Graham RM, Giannoulatou E, Green MJ, Kaplan W, Ravishankar S, Copty J, Powell JE, Cuppen E, van Eijk K, Veldink J, Ahn JH, Kim JE, Randall RL, Tucker K, Judson I, Sarin R, Ludwig T, Genin E, Deleuze JF, French Exome Project Consortium, Haber M, Marshall G, Cairns MJ, Blay JY, International Sarcoma Kindred Study, Thomas DM, Tattersall M, Neuhaus S, Lewis C, Tucker K, Carey-Smith R, Wood D, Porceddu S, Dickinson I, Thorne H, James P, Ray-Coquard I, Blay JY, Cassier P, Le Cesne A, Duffaud F, Penel N, Isambert N, Kurtz JE, Puri A, Sarin R, Ahn JH, Kim JE, Ward I, Judson I, van der Graaf W, Seddon B, Chandrasekar C, Rickar R, Hennig I, Schiffman J, Randall RL, Silvestri A, Zaratzian A, Tayao M, Walwyn K, Niedermayr E, Mang D, Clark R, Thorpe T, MacDonald J, Riddell K, Mar J, Fennelly V, Wicht A, Zielony B, Galligan E, Glavich G, Stoeckert J, Williams L, Djandjgava L, Buettner I, Osinki C, Stephens S, Rogasik M, Bouclier L, Girodet M, Charreton A, Fayet Y, Crasto S, Sandupatla B, Yoon Y, Je N, Thompson L, Fowler T, Johnson B, Petrikova G, Hambridge T, Hutchins A, Bottero D, Scanlon D, Stokes-Denson J, Génin E, Campion D, Dartigues JF, Deleuze JF, Lambert JC, Redon R, Ludwig T, Grenier-Boley B, Letort S, Lindenbaum P, Meyer V, Quenez O, Dina C, Bellenguez C, Le Clézio CC, Giemza J, Chatel S, Férec C, Le Marec H, Letenneur L, Nicolas G, Rouault K (2023) Heritable defects in telomere and mitotic function selectively predispose to sarcomas. Science 379(6629):253–260. https:\u002F\u002Fdoi.org\u002F10.1126\u002Fscience.abj4784\nBarragan R, Ortega-Azorin C, Sorli JV, Asensio EM, Coltell O, St-Onge MP, Portoles O, Corella D (2021) Effect of physical activity, smoking, and sleep on telomere length: a systematic review of observational and intervention studies. J Clin Med 11(1):76. https:\u002F\u002Fdoi.org\u002F10.3390\u002Fjcm11010076\nBarthel FP, Wei W, Tang M, Martinez-Ledesma E, Hu X, Amin SB, Akdemir KC, Seth S, Song X, Wang Q, Lichtenberg T, Hu J, Zhang J, Zheng S, Verhaak RG (2017) Systematic analysis of telomere length and somatic alterations in 31 cancer types. Nat Genet 49(3):349–357. https:\u002F\u002Fdoi.org\u002F10.1038\u002Fng.3781\nBodelon C, Savage SA, Gadalla SM (2014) Telomeres in molecular epidemiology studies. Prog Mol Biol Transl Sci 125:113–131. https:\u002F\u002Fdoi.org\u002F10.1016\u002FB978-0-12-397898-1.00005-0\nBonnell E, Pasquier E, Wellinger RJ (2021) Telomere replication: solving multiple end replication problems. Front Cell Dev Biol 9:668171. https:\u002F\u002Fdoi.org\u002F10.3389\u002Ffcell.2021.668171\nBrown DW, Zhou W, Wang Y, Jones K, Luo W, Dagnall C, Teshome K, Klein A, Zhang T, Lin SH, Lee OW, Khan S, Vo JB, Hutchinson A, Liu J, Wang J, Zhu B, Hicks B, Martin AS, Spellman SR, Wang T, Deeg HJ, Gupta V, Lee SJ, Freedman ND, Yeager M, Chanock SJ, Savage SA, Saber W, Gadalla SM, Machiela MJ (2022) Germline-somatic JAK2 interactions are associated with clonal expansion in myelofibrosis. Nat Commun 13(1):5284. https:\u002F\u002Fdoi.org\u002F10.1038\u002Fs41467-022-32986-7\nCalvete O, Martinez P, Garcia-Pavia P, Benitez-Buelga C, Paumard-Hernandez B, Fernandez V, Dominguez F, Salas C, Romero-Laorden N, Garcia-Donas J, Carrillo J, Perona R, Trivino JC, Andres R, Cano JM, Rivera B, Alonso-Pulpon L, Setien F, Esteller M, Rodriguez-Perales S, Bougeard G, Frebourg T, Urioste M, Blasco MA, Benitez J (2015) A mutation in the POT1 gene is responsible for cardiac angiosarcoma in TP53-negative Li-Fraumeni-like families. Nat Commun 6:8383. https:\u002F\u002Fdoi.org\u002F10.1038\u002Fncomms9383\nCawthon RM (2002) Telomere measurement by quantitative PCR. Nucleic Acids Res 30(10):e47\nChakravarti D, LaBella KA, DePinho RA (2021) Telomeres: history, health, and hallmarks of aging. Cell 184(2):306–322. https:\u002F\u002Fdoi.org\u002F10.1016\u002Fj.cell.2020.12.028\nChen B, Yan Y, Wang H, Xu J (2023) Association between genetically determined telomere length and health-related outcomes: A systematic review and meta-analysis of Mendelian randomization studies. Aging Cell 22(7):e13874. https:\u002F\u002Fdoi.org\u002F10.1111\u002Facel.13874\nClaude E, Decottignies A (2020) Telomere maintenance mechanisms in cancer: telomerase, ALT or lack thereof. Curr Opin Genet Dev 60:1–8. https:\u002F\u002Fdoi.org\u002F10.1016\u002Fj.gde.2020.01.002\nCodd V, Mangino M, van der Harst P, Braund PS, Kaiser M, Beveridge AJ, Rafelt S, Moore J, Nelson C, Soranzo N, Zhai G, Valdes AM, Blackburn H, Mateo Leach I, de Boer RA, Kimura M, Aviv A, Wellcome Trust Case Control Consortium, Goodall AH, Ouwehand W, van Veldhuisen DJ, van Gilst WH, Navis G, Burton PR, Tobin MD, Hall AS, Thompson JR, Spector T, Samani NJ (2010) Common variants near TERC are associated with mean telomere length. 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J Cell Physiol 238(6):1237–1255. https:\u002F\u002Fdoi.org\u002F10.1002\u002Fjcp.31034",{"VOID":1936},"10.1007\u002Fs10522-023-10080-9","2025-01-15T00:10:11.073+00:00","https:\u002F\u002Flink.springer.com\u002Farticle\u002F10.1007\u002Fs10522-023-10080-9",[1940],{"id":1941,"sortIndex":32,"researcher":28,"roles":1942,"affiliations":1943,"properties":1952,"displayName":1954,"givenName":28,"familyName":28},"9aab13cd-1426-445f-8f1e-b77ebfcf2acc",[1016],[1944],{"id":1945,"sortIndex":32,"affiliation":1946,"properties":28},"342ed8a1-0d58-40ae-8502-5ec4fd884262",{"id":1945,"createTime":28,"updateTime":28,"relativeEntities":1947,"slug":28,"properties":1948,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1951,"statistic":28},[],{"title":1949},{"EN":1950},"Clinical Genetics Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, USA",[],{"title":1953},{"VI":1954},"Sharon A. Savage",{"url":1938,"publisher":1956,"properties":2006},{"id":868,"createTime":869,"updateTime":870,"relativeEntities":1957,"slug":872,"properties":1958,"entityType":25,"verifyStatus":881,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":32,"subjectFields":1962,"manageAffiliations":1975,"indexDatabases":1986,"url":28,"thumbnailPath":28,"statistic":2001,"gsStatistic":28,"type":55,"analyzePriority":28},[],{"issn":1959,"title":1960,"eissn":1961},{"VOID":877},{"EN":872},{"VOID":875},[1963,1967,1971],{"id":884,"createTime":28,"updateTime":28,"relativeEntities":1964,"label":1965,"description":1966,"parentId":28,"standard":28,"scholarHubFieldId":28},[],{"EN":887},{},{"id":890,"createTime":28,"updateTime":28,"relativeEntities":1968,"label":1969,"description":1970,"parentId":28,"standard":28,"scholarHubFieldId":28},[],{"EN":893},{},{"id":896,"createTime":28,"updateTime":28,"relativeEntities":1972,"label":1973,"description":1974,"parentId":28,"standard":28,"scholarHubFieldId":28},[],{"EN":899},{},[1976,1981],{"id":903,"createTime":28,"updateTime":28,"relativeEntities":1977,"slug":28,"properties":1978,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1980,"statistic":28},[],{"title":1979},{"EN":907},[909],{"id":911,"createTime":28,"updateTime":28,"relativeEntities":1982,"slug":28,"properties":1983,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1985,"statistic":28},[],{"title":1984},{"EN":915},[],[1987,1994],{"id":919,"indexDatabase":1988,"url":925,"indexYears":926,"academicFieldIds":1993,"indexDatabaseRanking":931},{"id":775,"createTime":28,"updateTime":28,"relativeEntities":1989,"label":1990,"description":1991,"key":781,"publicationTags":1992,"standard":28},[],{"EN":778,"VI":778},{"EN":778,"VI":780},[783],[928,929,930],{"id":933,"indexDatabase":1995,"url":945,"indexYears":28,"academicFieldIds":2000,"indexDatabaseRanking":28},{"id":935,"createTime":28,"updateTime":28,"relativeEntities":1996,"label":1997,"description":1998,"key":942,"publicationTags":1999,"standard":28},[],{"EN":938,"VI":938},{"EN":940,"VI":941},[944,813],[947],{"impactFactor":32,"impactFactorByYear":2002,"i10Index":955,"i10IndexLast5Year":127,"totalPublication":956,"totalPublicationByYear":2003,"totalCitation":958,"totalCitationByYear":2004,"totalCitationPerPublication":970,"totalCitationPerPublicationByYear":2005,"hindexLast5Year":150,"hindex":150},{"2012":173,"2013":363,"2014":369,"2015":170,"2016":950,"2017":348,"2018":951,"2019":368,"2020":952,"2021":166,"2022":953,"2023":954},{"2000":147,"2001":136,"2002":149,"2003":201,"2004":139,"2005":142,"2006":688,"2007":202,"2008":436,"2009":150,"2010":196,"2011":202,"2012":69,"2013":689,"2014":139,"2015":325,"2016":142,"2017":280,"2018":147,"2019":436,"2020":201,"2021":131,"2022":352,"2023":325,"2024":126},{"2003":47,"2004":599,"2005":689,"2006":960,"2007":856,"2008":276,"2009":961,"2010":41,"2011":962,"2012":963,"2013":964,"2014":577,"2015":965,"2016":966,"2017":217,"2018":332,"2019":967,"2020":968,"2021":969,"2022":434,"2023":47,"2024":42},{"2003":121,"2004":972,"2005":973,"2006":974,"2007":975,"2008":976,"2009":977,"2010":978,"2011":979,"2012":980,"2013":981,"2014":982,"2015":983,"2016":984,"2017":985,"2018":986,"2019":987,"2020":988,"2021":989,"2022":707,"2023":194,"2024":168},{"pages":2007},{"VOID":2008},"1-14","2023-12-18",[944,931],{"id":2012,"createTime":2013,"updateTime":2014,"relativeEntities":2015,"slug":2016,"properties":2017,"entityType":1009,"verifyStatus":26,"verifyTime":2014,"verifyNote":1010,"languages":28,"translateLanguages":28,"viewCount":32,"primaryUrl":2026,"fullTextUrl":28,"authors":2027,"publicationType":1064,"publisherRelationship":2193,"citationCount":28,"citationInfo":28,"publishDate":2249,"publishYear":2250,"citationAnalyzeStatus":881,"lastCitationAnalyze":28,"indexDatabases":2251,"openAccess":28,"references":28,"isForceReanalyzing":1124},"0288af34-6d63-4757-97e7-f5c2096d5384","2024-01-10T23:40:48.228+00:00","2025-01-08T23:01:42.860+00:00",[],"Cell-proliferation-arrest-and-redox-state-status-as-part-of-different-stages-during-senescence-establishment-in-mouse-fibroblasts",{"abstract":2018,"title":2020,"references":2022,"doi":2024},{"EN":2019},"Senescence phenotype can be achieved by multiple pathways. Most of them involve the activation of negative cell cycle regulators as well as a shift to an oxidative status. However, the exact participation of these events in senescence establishment and maintenance is not completely understood. In this study we investigated the content of three final cell cycle regulators, as well as the redox state in some critical points during the pre-senescent and the full-senescent states. Our results highlight the existence of a critical pre-phase in senescent phenotype establishment, in which cell proliferation stops with the participation of the cell cycle inhibitors, and a second maintenance stage where the exacerbated pro-oxidant state inside the cell induces the physiological decline characteristic in senescent cells.",{"EN":2021},"Cell proliferation arrest and redox state status as part of different stages during senescence establishment in mouse fibroblasts",{"VOID":2023},"Ahmed EK, Rogowska-Wrzesinska A, Roepstorff P, Bulteau AL, Friguet B (2010) Protein modification and replicative senescence of WI-38 human embryonic fibroblasts. Aging Cell 9:252–272. doi:10.1111\u002Fj.1474-9726.2010.00555.x\nAlarcón-Aguilar A, González-Puertos VY, Luna–López A, Morán J, Santamaría A, Königsberg M (2013) Comparing the effects of two neurotoxins in cortical astrocytes from newborn and adult rats: involvement of oxidative damage. 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Exp Cell Res 212:167–175. doi:10.1006\u002Fexcr 1994.1132\nMoyzis RK, Buckingham JM, Cram LS, Dani M, Deaven LL, Jones MD, Meyne J, Ratliff RL, Wu J-R (1988) A highly conserved repetitive DNA sequence, (TTAGGG), present at the telomeres of human chromosomes. Proc Natl Acad Sci USA 85:6622–6626\nMuller M (2006) Premature cellular senescence induced by pyocyanin, a redox-active Pseudomonas aeruginosa toxin. Free Radic Biol Med 41:1670–1677. doi:10.1016\u002Fjfreeradbiomed.2006.09.004\nMuller M (2009) Cellular senescence: molecular mechanisms, in vivo significance, and redox considerations. Antiox Redox Signal 11:60–98. doi:10.1089\u002Fars 2008.2104\nNakayama K, Hatakeyama S, Nakayama K (2001) Regulation of the cell cycle at the G1–S transition by proteolysis of cyclin E and p27Kip1. 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Exp Gerontol 42:1039–1042. doi:10.1016\u002Fj.exger.2007.08.005\nRodier F, Campisi J (2011) Four faces of cellular senescence. J Cell Biol 192:547–556. doi:10.1083\u002Fjcb.201009094\nRodier F, Muñoz DP, Teachenor R, Chu V, Le O, Bhaumik D, Coppé JF, Campeau E, Beauséjour CM, Kim SH, Davalos AR, Campisi J (2011) DNA-SCARS: distinct nuclear structures that sustain damage-induced senescence growth arrest and inflammatory cytokine secretion. J Cell Sci 124:68–81. doi:10.1242\u002Fjcs.071340\nShay JW, Pereira-Smith OM, Wright WE (1991) A role for both RB and p53 in the regulation of human cellular senescence. Exp Cell Res 196:33–39. doi:10.1016\u002F0014-4827(91)90453-2\nSikora E, Arendt T, Bennettc M, Narita M (2011) Impact of cellular senescence signature on ageing research. Age Res Rev 10:146–152. doi:10.1016\u002Fj.arr.2010.10.002\nStein GH, Beeson M, Gordon L (1990) Failure to phosphorylate the retinoblastoma gene product in senescent human fibroblasts. Science 249:666–669. doi:10.1126\u002Fscience.216634\nStein GH, Drullinger LF, Robetorye RS, Pereira-Smith OM, Smith JR (1991) Senescent cells fail to express cdc2, cycA, and cycB in response to mitogen stimulation. Proc Natl Acad Sci USA 88:11012–11016\nTorres C, Lewis L, Cristofalo VJ (2006) Proteasome inhibitors shorten replicative life span and induce a senescent-like phenotype of human fibroblasts. J Cell Physiol 207:845–853. doi:10.1002\u002Fjcp.20630\nToussaint O, Medrano E, von Zglinicki T (2000) Cellular and molecular mechanisms of stress-induced premature senescence (SIPS) of human diploid fibroblasts and melanocytes. Exp Gerontol 35:927–945. doi:10.1016\u002FS0531-5565(00)00180-7\nVijg J, Campisi J (2008) Puzzles, promises and a cure for ageing. Nature 28:1065–1071. doi:10.1038\u002Fnature07216\nvon Zglinicki T (2002) Oxidative stress shortens telomeres. Trends Biochem Sci 27:339–344. doi:10.1016\u002FS0968-0004(02)02110-2\nvon Zglinicki T, Saretzki G, Döcke W, Lotze C (1995) Mild hypoxia shortens telomeres and inhibits proliferation of fibroblasts: a model for senescence? Exp Cell Res 220:186–193. doi:10.1006\u002Fexcr1995.1305\nvon Zglinicki T, Serra V, Lorenz M, Saretzki G, Lenzen- Grossimlighaus R, Gessner R, Risch A, Steinhagen-Thiessen E (2000) Short telomeres in patients with vascular dementia: an indicator of low antioxidative capacity and a possible risk factor? 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HSP27 is a small heat shock protein that modulates the ability of cells to respond to heat shock and oxidative stress, and also functions as a chaperone independent of ATP, participating in the proteasomal degradation of proteins. The expression of HSP27 is associated with survival in mammalian cells. In cancer cells, it confers resistance to chemotherapy; in neurons, HSP27 has a positive effect on neuronal viability in models of Alzheimerʼs and Parkinsonʼs diseases. To better understand the mechanism by which HSP27 expression contributes to cell survival, we expressed human HSP27 in the budding yeast Saccharomyces cerevisiae under control of different mutant TEF promoters, that conferred nine levels of graded basal expression, and showed that replicative lifespan and proteasomal activity increase as well as the resistance to oxidative and thermal stresses. The profile of these phenotypes display a dose–response effect characteristic of hormesis, an adaptive phenomenon that is observed when cells are exposed to increasing amounts of stress or toxic substances. The hormetic response correlates with changes in expression levels of HSP27 and also with its oligomeric states when correlated to survival assays. Our results indicate that fine tuning of HSP27 concentration could be used as a strategy for cancer therapy, and also for improving neuronal survival in neurodegenerative diseases.",{"EN":2262},"Expression of human HSP27 in yeast extends replicative lifespan and uncovers a hormetic response",{"VOID":2264},"Alper H, Fischer C, Nevoigt E, Stephanopoulos G (2005) Tuning genetic control through promoter engineering. Proc Natl Acad Sci USA 102:12678–12683. https:\u002F\u002Fdoi.org\u002F10.1073\u002Fpnas.0504604102\nAquilina JA, Shrestha S, Morris AM, Ecroyd H (2013) Structural and functional aspects of hetero-oligomers formed by the small heat shock proteins alphaB-crystallin and HSP27. J Biol Chem 288:13602–13609. https:\u002F\u002Fdoi.org\u002F10.1074\u002Fjbc.M112.443812\nArrigo AP (1998) Small stress proteins: chaperones that act as regulators of intracellular redox state and programmed cell death. Biol Chem 379:19–26\nArrigo AP (2001) Hsp27: novel regulator of intracellular redox state. IUBMB Life 52:303–307. https:\u002F\u002Fdoi.org\u002F10.1080\u002F152165401317291165\nArrigo AP (2011) Structure-functions of HspB1 (Hsp27). Methods Mol Biol 787:105–119. https:\u002F\u002Fdoi.org\u002F10.1007\u002F978-1-61779-295-3_9\nArrigo AP (2017) Mammalian HspB1 (Hsp27) is a molecular sensor linked to the physiology and environment of the cell. Cell Stress Chaperones 22:517–529. https:\u002F\u002Fdoi.org\u002F10.1007\u002Fs12192-017-0765-1\nArrigo AP, Suhan JP, Welch WJ (1988) Dynamic changes in the structure and intracellular locale of the mammalian low-molecular-weight heat shock protein. Mol Cell Biol 8:5059–5071. https:\u002F\u002Fdoi.org\u002F10.1128\u002Fmcb.8.12.5059\nArrigo AP, Virot S, Chaufour S, Firdaus W, Kretz-Remy C, Diaz-Latoud C (2005) Hsp27 consolidates intracellular redox homeostasis by upholding glutathione in its reduced form and by decreasing iron intracellular levels. Antioxid Redox Signal 7:414–422. https:\u002F\u002Fdoi.org\u002F10.1089\u002Fars.2005.7.414\nAwasthi N, Wagner BJ (2005) Upregulation of heat shock protein expression by proteasome inhibition: an antiapoptotic mechanism in the lens. Invest Ophthalmol Vis Sci 46:2082–2091. https:\u002F\u002Fdoi.org\u002F10.1167\u002Fiovs.05-0002\nBenesch JL et al (2010) The quaternary organization and dynamics of the molecular chaperone HSP26 are thermally regulated. Chem Biol 17:1008–1017. https:\u002F\u002Fdoi.org\u002F10.1016\u002Fj.chembiol.2010.06.016\nCalabrese EJ, Dhawan G, Kapoor R, Iavicoli I, Calabrese V (2015) What is hormesis and its relevance to healthy aging and longevity? Biogerontology 16:693–707. https:\u002F\u002Fdoi.org\u002F10.1007\u002Fs10522-015-9601-0\nCalderwood SK, Gong J (2016) Heat shock proteins promote cancer: it's a protection racket. Trends Biochem Sci 41:311–323. https:\u002F\u002Fdoi.org\u002F10.1016\u002Fj.tibs.2016.01.003\nCarper SW, Rocheleau TA, Storm FK (1990) cDNA sequence of a human heat shock protein HSP27. Nucleic Acids Res 18:6457. https:\u002F\u002Fdoi.org\u002F10.1093\u002Fnar\u002F18.21.6457\nCashikar AG, Duennwald M, Lindquist SL (2005) A chaperone pathway in protein disaggregation. Hsp26 alters the nature of protein aggregates to facilitate reactivation by Hsp104. J Biol Chem 280:23869–23875. https:\u002F\u002Fdoi.org\u002F10.1074\u002Fjbc.M502854200\nChen H, Zheng C, Zhang Y, Chang YZ, Qian ZM, Shen X (2006) Heat shock protein 27 downregulates the transferrin receptor 1-mediated iron uptake. Int J Biochem Cell Biol 38:1402–1416. https:\u002F\u002Fdoi.org\u002F10.1016\u002Fj.biocel.2006.02.006\nChen SF et al (2012) Autophagy-related gene 7 is downstream of heat shock protein 27 in the regulation of eye morphology, polyglutamine toxicity, and lifespan in Drosophila. J Biomed Sci 19:52. https:\u002F\u002Fdoi.org\u002F10.1186\u002F1423-0127-19-52\nChondrogianni N et al (2015) Proteasome activation: an innovative promising approach for delaying aging and retarding age-related diseases. Ageing Res Rev 23:37–55. https:\u002F\u002Fdoi.org\u002F10.1016\u002Fj.arr.2014.12.003\nConti B et al (2006) Transgenic mice with a reduced core body temperature have an increased life span. Science 314:825–828. https:\u002F\u002Fdoi.org\u002F10.1126\u002Fscience.1132191\nCriddle DN et al (2006) Menadione-induced reactive oxygen species generation via redox cycling promotes apoptosis of murine pancreatic acinar cells. J Biol Chem 281:40485–40492. https:\u002F\u002Fdoi.org\u002F10.1074\u002Fjbc.M607704200\nda Cunha FM, Demasi M, Kowaltowski AJ (2011) Aging and calorie restriction modulate yeast redox state, oxidized protein removal, and the ubiquitin-proteasome system. Free Radic Biol Med 51:664–670. https:\u002F\u002Fdoi.org\u002F10.1016\u002Fj.freeradbiomed.2011.05.035\nDayalan Naidu S, Dinkova-Kostova AT (2017) Regulation of the mammalian heat shock factor 1. FEBS J 284:1606–1627. https:\u002F\u002Fdoi.org\u002F10.1111\u002Ffebs.13999\nDegasperi A, Birtwistle MR, Volinsky N, Rauch J, Kolch W, Kholodenko BN (2014) Evaluating strategies to normalise biological replicates of Western blot data. PLoS ONE 9:e87293. https:\u002F\u002Fdoi.org\u002F10.1371\u002Fjournal.pone.0087293\nErjavec N, Larsson L, Grantham J, Nystrom T (2007) Accelerated aging and failure to segregate damaged proteins in Sir2 mutants can be suppressed by overproducing the protein aggregation-remodeling factor Hsp104p. 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               Rosa damascena, or Damask rose, is a rose hybrid commonly harvested for rose oil used in perfumery and for rose water used to flavor food. The petal extract of R. damascena was recently found to decrease Drosophila melanogaster mortality without impairing reproductive fitness or metabolic rate. Here, we report that R. damascena extended both mean and maximum lifespan of the fly. The extract also protected against oxidative stress in flies, predominantly in females. However, it did not alter mitochondrial respiration or content, superoxide production, or the major antioxidant defenses, superoxide dismutase and catalase. The extract increased survival in both sexes when exposed to reduced iron, though surprisingly, it sensitized both sexes to heat stress (survival at 37°C), and appeared to down-regulate the major heat shock protein HSP70 and the small mitochondrial heat shock protein HSP22, at 25°C and after heat shock (4 h at 37°C). We hypothesize that R. damascena extends lifespan by protecting against iron, which concomitantly leads to decreased HSP expression and compromising heat tolerance.",{"EN":2477},"Extension of Drosophila lifespan by Rosa damascena associated with an increased sensitivity to heat",{"VOID":2479},"Awai M, Narasaki M, Yamanoi Y, Seno S (1979) Induction of diabetes in animals by parenteral administration of ferric nitrilotriacetate. A model of experimental hemochromatosis. Am J Pathol 95(3):663–673\nAwale S, Tohda C, Tezuka Y, Miyazaki M, Kadota S (2009) Protective Effects of Rosa damascena and its active constituent on A{beta}(25-35)-induced neuritic atrophy. Evidence Based Complement Altern Med. doi:10.1093\u002Fecam\u002Fnep149\nBallinger SW (2005) Mitochondrial dysfunction in cardiovascular disease. Free Radic Biol Med 38(10):1278–1295. doi:10.1016\u002Fj.freeradbiomed.2005.02.014\nBaron M, Kudin AP, Kunz WS (2007) Mitochondrial dysfunction in neurodegenerative disorders. Biochem Soc Trans 35(Pt 5):1228–1231. doi:10.1042\u002FBST0351228\nBartke A (2011) Single-gene mutations and healthy ageing in mammals. Philos Trans Roy Soc Lond B 366(1561):28–34. doi:10.1098\u002Frstb.2010.0281\nBasim E, Basim H (2003) Antibacterial activity of Rosa damascena essential oil. Fitoterapia 74(4):394–396\nBaur JA, Pearson KJ, Price NL, Jamieson HA, Lerin C, Kalra A, Prabhu VV, Allard JS, Lopez-Lluch G, Lewis K, Pistell PJ, Poosala S, Becker KG, Boss O, Gwinn D, Wang M, Ramaswamy S, Fishbein KW, Spencer RG, Lakatta EG, Le Couteur D, Shaw RJ, Navas P, Puigserver P, Ingram DK, de Cabo R, Sinclair DA (2006) Resveratrol improves health and survival of mice on a high-calorie diet. Nature 444(7117):337–342. doi:10.1038\u002Fnature05354\nBeckman KB, Ames BN (1998) The free radical theory of aging matures. Physiol Rev 78(2):547–581\nBeers RF Jr, Sizer IW (1952) A spectrophotometric method for measuring the breakdown of hydrogen peroxide by catalase. J Biol Chem 195(1):133–140\nBhole D, Allikian MJ, Tower J (2004) Doxycycline-regulated over-expression of hsp22 has negative effects on stress resistance and life span in adult Drosophila melanogaster. Mech Ageing Dev 125(9):651–663. doi:10.1016\u002Fj.mad.2004.08.010\nBjedov I, Toivonen JM, Kerr F, Slack C, Jacobson J, Foley A, Partridge L (2010) Mechanisms of life span extension by rapamycin in the fruit fly Drosophila melanogaster. Cell Metab 11(1):35–46. doi:10.1016\u002Fj.cmet.2009.11.010\nChen H, Zheng C, Zhang Y, Chang YZ, Qian ZM, Shen X (2006) Heat shock protein 27 downregulates the transferrin receptor 1-mediated iron uptake. Int J Biochem Cell Biol 38(8):1402–1416. doi:10.1016\u002Fj.biocel.2006.02.006\nChoi J, Rees HD, Weintraub ST, Levey AI, Chin LS, Li L (2005) Oxidative modifications and aggregation of Cu,Zn-superoxide dismutase associated with Alzheimer and Parkinson diseases. J Biol Chem 280(12):11648–11655. doi:10.1074\u002Fjbc.M414327200\nDavis JM, Murphy EA, Carmichael MD, Davis B (2009) Quercetin increases brain and muscle mitochondrial biogenesis and exercise tolerance. Am J Physiol Regul Integr Comp Physiol 296(4):R1071–R1077. doi:10.1152\u002Fajpregu.90925.2008\nDunkov B, Georgieva T (2006) Insect iron binding proteins: insights from the genomes. Insect Biochem Mol Biol 36(4):300–309. doi:10.1016\u002Fj.ibmb.2006.01.007\nFearon IM, Faux SP (2009) Oxidative stress and cardiovascular disease: novel tools give (free) radical insight. J Mol Cell Cardiol 47(3):372–381. doi:10.1016\u002Fj.yjmcc.2009.05.013\nFriedman DB, Johnson TE (1988) A mutation in the age-1 gene in Caenorhabditis elegans lengthens life and reduces hermaphrodite fertility. Genetics 118(1):75–86\nGiannakou ME, Partridge L (2007) Role of insulin-like signalling in Drosophila lifespan. Trends Biochem Sci 32(4):180–188. doi:10.1016\u002Fj.tibs.2007.02.007\nHarman D (1956) Aging: a theory based on free radical and radiation chemistry. J Gerontol 11(3):298–300\nHarrison DE, Strong R, Sharp ZD, Nelson JF, Astle CM, Flurkey K, Nadon NL, Wilkinson JE, Frenkel K, Carter CS, Pahor M, Javors MA, Fernandez E, Miller RA (2009) Rapamycin fed late in life extends lifespan in genetically heterogeneous mice. Nature 460(7253):392–395. doi:10.1038\u002Fnature08221\nHausladen A, Fridovich I (1996) Measuring nitric oxide and superoxide: rate constants for aconitase reactivity. Methods Enzymol 269:37–41\nHenchcliffe C, Beal MF (2008) Mitochondrial biology and oxidative stress in Parkinson disease pathogenesis. Nat Clin Pract Neurol 4(11):600–609. doi:10.1038\u002Fncpneuro0924\nJafari M, Zarban A, Pham S, Wang T (2008) Rosa damascena decreased mortality in adult Drosophila. J Med Food 11(1):9–13. doi:10.1089\u002Fjmf.2007.546\nJohannsen DL, Ravussin E (2009) The role of mitochondria in health and disease. Curr Opin Pharmacol 9(6):780–786. doi:10.1016\u002Fj.coph.2009.09.002\nKampkotter A, Timpel C, Zurawski RF, Ruhl S, Chovolou Y, Proksch P, Watjen W (2008) Increase of stress resistance and lifespan of Caenorhabditis elegans by quercetin. Comp Biochem Physiol B 149(2):314–323. doi:10.1016\u002Fj.cbpb.2007.10.004\nKenyon CJ (2010) The genetics of ageing. Nature 464(7288):504–512. doi:10.1038\u002Fnature08980\nKing V, Tower J (1999) Aging-specific expression of Drosophila hsp22. Dev Biol 207(1):107–118. doi:10.1006\u002Fdbio.1998.9147\nKirkwood TB, Austad SN (2000) Why do we age? Nature 408(6809):233–238. doi:10.1038\u002F35041682\nKondapalli KC, Kok NM, Dancis A, Stemmler TL (2008) Drosophila frataxin: an iron chaperone during cellular Fe-S cluster bioassembly. Biochemistry 47(26):6917–6927. doi:10.1021\u002Fbi800366d\nKumar N, Bhandari P, Singh B, Gupta AP, Kaul VK (2008) Reversed phase-HPLC for rapid determination of polyphenols in flowers of rose species. J Sep Sci 31(2):262–267. doi:10.1002\u002Fjssc.200700372\nKurapati R, Passananti HB, Rose MR, Tower J (2000) Increased hsp22 RNA levels in Drosophila lines genetically selected for increased longevity. J Gerontol A Biol Sci Med Sci 55(11):B552–B559\nLagouge M, Argmann C, Gerhart-Hines Z, Meziane H, Lerin C, Daussin F, Messadeq N, Milne J, Lambert P, Elliott P, Geny B, Laakso M, Puigserver P, Auwerx J (2006) Resveratrol improves mitochondrial function and protects against metabolic disease by activating SIRT1 and PGC-1alpha. Cell 127(6):1109–1122. doi:10.1016\u002Fj.cell.2006.11.013\nLapointe J, Hekimi S (2010) When a theory of aging ages badly. Cell Mol Life Sci 67(1):1–8. doi:10.1007\u002Fs00018-009-0138-8\nLoghmani-Khouzani H, Sabzi Fini O, Safari J (2007) Essential oil composition of Rosa damascena mill cultivated in central Iran. Sci Iran 14(4):316–319\nMagwere T, Goodall S, Skepper J, Mair W, Brand MD, Partridge L (2006) The effect of dietary restriction on mitochondrial protein density and flight muscle mitochondrial morphology in Drosophila. J Gerontol A Biol Sci Med Sci 61(1):36–47\nMartin LJ (2006) Mitochondriopathy in Parkinson disease and amyotrophic lateral sclerosis. J Neuropathol Exp Neurol 65(12):1103–1110. doi:10.1097\u002F01.jnen.0000248541.05552.c4\nMassie HR, Aiello VR, Williams TR (1993) Inhibition of iron absorption prolongs the life span of Drosophila. Mech Ageing Dev 67(3):227–237\nMiller RA, Harrison DE, Astle CM, Baur JA, Boyd AR, de Cabo R, Fernandez E, Flurkey K, Javors MA, Nelson JF, Orihuela CJ, Pletcher S, Sharp ZD, Sinclair D, Starnes JW, Wilkinson JE, Nadon NL, Strong R (2011) Rapamycin, but not resveratrol or simvastatin, extends life span of genetically heterogeneous mice. J Gerontol A Biol Sci Med Sci 66(2):191–201. doi:10.1093\u002Fgerona\u002Fglq178\nMorrow G, Samson M, Michaud S, Tanguay RM (2004) Overexpression of the small mitochondrial Hsp22 extends Drosophila life span and increases resistance to oxidative stress. FASEB J 18(3):598–599. doi:10.1096\u002Ffj.03-0860fje\nNisoli E, Tonello C, Cardile A, Cozzi V, Bracale R, Tedesco L, Falcone S, Valerio A, Cantoni O, Clementi E, Moncada S, Carruba MO (2005) Calorie restriction promotes mitochondrial biogenesis by inducing the expression of eNOS. Science 310(5746):314–317. doi:10.1126\u002Fscience.1117728\nRamezani R, Moghimi A, Rakhshandeh H, Ejtehadi H, Kheirabadi M (2008) The effect of Rosa damascena essential oil on the amygdala electrical kindling seizures in rat. Pak J Biol Sci 11(5):746–751\nRobinson KM, Janes MS, Pehar M, Monette JS, Ross MF, Hagen TM, Murphy MP, Beckman JS (2006) Selective fluorescent imaging of superoxide in vivo using ethidium-based probes. Proc Natl Acad Sci USA 103(41):15038–15043. doi:10.1073\u002Fpnas.0601945103\nRose MR, Charlesworth B (1981) Genetics of life history in Drosophila melanogaster. I. Sib analysis of adult females. Genetics 97(1):173–186\nRose MR, Drapeau MD, Yazdi PG, Shah KH, Moise DB, Thakar RR, Rauser CL, Mueller LD (2002) Evolution of late-life mortality in Drosophila melanogaster. Evolution 56(10):1982–1991\nSalmon AB, Richardson A, Perez VI (2010) Update on the oxidative stress theory of aging: does oxidative stress play a role in aging or healthy aging? Free Radic Biol Med 48(5):642–655. doi:10.1016\u002Fj.freeradbiomed.2009.12.015\nShokouhinejad N, Emaneini M, Aligholi M, Jabalameli F (2010) Antimicrobial effect of Rosa damascena extract on selected endodontic pathogens. J Calif Dent Assoc 38(2):123–126\nSpeakman JR, Selman C (2011) The free-radical damage theory: accumulating evidence against a simple link of oxidative stress to ageing and lifespan. Bioessays 33(4):255–259. doi:10.1002\u002Fbies.201000132\nTower J (2011) Heat shock proteins and Drosophila aging. Exp Gerontol 46(5):355–362. doi:10.1016\u002Fj.exger.2010.09.002\nVermeulen CJ, Loeschcke V (2007) Longevity and the stress response in Drosophila. Exp Gerontol 42(3):153–159. doi:10.1016\u002Fj.exger.2006.09.014\nWallace DC (2005) A mitochondrial paradigm of metabolic and degenerative diseases, aging, and cancer: a dawn for evolutionary medicine. Annu Rev Genet 39:359–407. doi:10.1146\u002Fannurev.genet.39.110304.095751\nWallace DC, Brown MD, Melov S, Graham B, Lott M (1998) Mitochondrial biology, degenerative diseases and aging. Biofactors 7(3):187–190\nWang X, Su B, Perry G, Smith MA, Zhu X (2007) Insights into amyloid-beta-induced mitochondrial dysfunction in Alzheimer disease. Free Radic Biol Med 43(12):1569–1573. doi:10.1016\u002Fj.freeradbiomed.2007.09.007\nWilliams AJ, Coakley J, Christodoulou J (1998) Automated analysis of mitochondrial enzymes in cultured skin fibroblasts. Anal Biochem 259(2):176–180. doi:10.1006\u002Fabio.1998.2624\nWinterbourn CC, Hawkins RE, Brian M, Carrell RW (1975) The estimation of red cell superoxide dismutase activity. J Lab Clin Med 85(2):337–341\nXu J, Marzetti E, Seo AY, Kim JS, Prolla TA, Leeuwenburgh C (2010) The emerging role of iron dyshomeostasis in the mitochondrial decay of aging. Mech Ageing Dev 131(7–8):487–493. doi:10.1016\u002Fj.mad.2010.04.007\nYang J, Tower J (2009) Expression of hsp22 and hsp70 transgenes is partially predictive of Drosophila survival under normal and stress conditions. J Gerontol A Biol Sci Med Sci 64(8):828–838. doi:10.1093\u002Fgerona\u002Fglp054\nZhang X, Min X, Li C, Benjamin IJ, Qian B, Ding Z, Gao X, Yao Y, Ma Y, Cheng Y, Liu L (2010) Involvement of reductive stress in the cardiomyopathy in transgenic mice with cardiac-specific overexpression of heat shock protein 27. Hypertension 55(6):1412–1417. doi:10.1161\u002FHYPERTENSIONAHA.109.147066",{"VOID":2481},"10.1007\u002Fs10522-011-9357-0","http:\u002F\u002Flink.springer.com\u002F10.1007\u002Fs10522-011-9357-0",[2484,2499,2512,2525,2538,2553],{"id":2485,"sortIndex":32,"researcher":28,"roles":2486,"affiliations":2487,"properties":2496,"displayName":2498,"givenName":28,"familyName":28},"5ed4163a-3c67-489a-9080-82f945a55231",[1016],[2488],{"id":2489,"sortIndex":32,"affiliation":2490,"properties":28},"21cd6815-d5c8-47c6-9049-7cfe68d17c41",{"id":2489,"createTime":28,"updateTime":28,"relativeEntities":2491,"slug":28,"properties":2492,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":2495,"statistic":28},[],{"title":2493},{"VI":2494},"Department of Pharmaceutical Sciences, University of California, Irvine, USA",[],{"title":2497},{"VI":2498},"Samuel E. 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