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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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of new quinolones in the treatment and prophylaxis of infectious diseases: Introductory remarks",{"VOID":983},"Neu, H. C. Clinical uses of the quinolones. Lancet 1987, ii: 1319–1322.\nPaton, J. H., Reeves, D. S. Fluoroquinolone antibiotics. Microbiology, pharmacokinetics and clinical use. Drugs 1988, 36: 193–228.\nRubinstein, E., Adams, D., Moellering, R., Waldvogel, F. (ed.): International symposium on new quinolones. Reviews of Infectious Diseases 1988, 10, Supplement 1: 1–271.\nWolfson, J. S., Hooper, D. C. (ed.): Quinolone antimicrobial agents. American Society for Microbiology, Washington, DC, 1989.\nWolfson, J. S., Hooper, D. C., Swartz, M. N. Mechanisms of action of and resistance to quinolone antimicrobial agents. In: Wolfson, J. S., Hooper, D. C. (ed.): Quinolone antimicrobial agents. American Society for Microbiology, Washington, DC, 1989, p. 5–34.\nDomagala, J. M., Hanna, L. D., Heifetz, C. L., Hutt, M. P., Mich, T. F., Sanchez, J. P., Solomon, M. New structure-activity relationships of quinolone anti-bacterials using the target enzyme. The development and application of a DNA gyrase assay. Journal of Medicinal Chemistry 1986, 29: 394–404.\nMitscher, L. A., Sharma, P. N., Chu, D. T. W., Shen, L. L., Pernet, A. G. Chiral DNA gyrase inhibitors. I. Synthesis and antimicrobial activity of the enantiomers of 6-fluoro-7-(1-piperazinyl)-1-12′-trans-phenyl-1′-cyclopropyl)-1,4-dihydro-4-oxoquinolone-3-carboxylic acid. Journal of Medicinal Chemistry 1986, 29: 2044–2047.\nCrumplin, G. C. Aspects of chemistry in the development of the 4-quinolone antibacterial agents. Reviews of Infectious Diseases 1988, 10, Supplement 1: 2–9.\nHooper, D. C., Wolfson, J. S. Mode of action of the quinolone antimicrobial agents. Reviews of Infectious Diseases 1988, 10, Supplement 1: 14–21.\nChu, D. T. W., Fernandes, P. B. Structure-activity relationships of the fluoroquinolones. Antimicrobial Agents and Chemotherapy 1989, 33: 131–135.\nFernandes, P. B., Chu, D. T. W., Swanson, R. N., Ramer, N. R., Hanson, C. W., Bower, R. R., Stamm, J. M., Hardy, D. J. A-61827 (A-60969), a new fluoronaphthyridine with activity against both aerobic and anaerobic bacteria. Antimicrobial Agents and Chemotherapy 1988, 32: 27–32.\nEspinoza, A. M., Chin, N.-C., Novelli, A., Neu, H. C. Comparative in vitro activity of a new fluorinated 4-quinolone T-3262 (A-60969). Antimicrobial Agents and Chemotherapy 1988, 32: 663–670.\nFujimaki, K., Noumi, T., Saikawa, I., Inoue, M., Mitsuhashi, S. In vitro and in vivo antibacterial activities of T-3262, a new fluoroquinolone. Antimicrobial Agents and Chemotherapy 1988, 32: 827–833.\nWise, R., Ashby, J. P., Andrews, J. M. In vitro activity of PD 127,391, an enhanced-spectrum quinolone. Antimicrobial Agents and Chemotherapy 1988, 32: 1251–1256.\nNorrby, S. R., Jonsson, M. Comparative in vitro activity of PD 127,391, a new fluorinated 4-quinolone derivative. Antimicrobial Agents and Chemotherapy 1988, 32: 1278–1281.\nMontay, G., Goueffon, Y., Roquet, F. Absorption, distribution, metabolic fate, and elimination of pefloxacin mesylate in mice, rats, dogs, monkeys, and humans. Antimicrobial Agents and Chemotherapy 1984, 25: 463–472.\nGranneman, G. R., Snyder, K. M., Shu, V. S. Difloxacin metabolism and pharmacokinetics in humans after single oral doses. Antimicrobial Agents and Chemotherapy 1986, 30: 689–693.\nWise, R., Kirkpatrick, B., Ashby, J., Griggs, D. J. Pharmacokinetics and tissue penetration of Ro 23-6240, a new trifluoroquinolone. Antimicrobial Agents and Chemotherapy 1987, 31: 161–163.\nCozzarelli, N. R. DNA gyrase and the supercoiling of DNA. Science 1980, 207: 953–960.\nGellert, M. DNA topoisomerases. Annual Review of Biochemistry 1981, 50: 879–910.\nWang, J. C. DNA topoisomerases. Annual Review of Biochemistry 1985, 54: 655–697.\nGellert, M., Mizuuchi, K., O'Dea, M. H., Nash, H. A. DNA gyrase: an enzyme that introduces superhelical turns into DNA. Proceedings of the National Academy of Sciences USA 1976, 73: 3872–3876.\nSugino, A., Peebles, C. L., Kreuzer, K. N., Cozzarelli, N. R. Mechanism of action of nalidixic acid: purification ofEscherichia coli nalA gene product and its relationship to DNA gyrase and a novel nicking-closing enzyme. Proceedings of the National Academy of Sciences USA 1977, 74: 4767–4771.\nGellert, M., Mizuuchi, K., O'Dea, M. H., Itoh, T., Tomizawa, J. Nalidixic acid resistance: a second genetic character involved in DNA gyrase activity. Proceedings of the National Academy of Sciences USA 1977, 74: 4772–4776.\nShen, L. L., Pernet, A. G. Mechanism of inhibition of DNA gyrase by analogues of nalidixic acid: the target of the drugs is DNA. Proceedings of the National Academy of Sciences USA 1985, 82: 307–311.\nShen, L. L., Kohlbrenner, W. E., Weigl, D., Baranowski, J. Mechanism of quinolone inhibition of DNA gyrase. Journal of Biological Chemistry 1989, 264: 2973–2978.\nMitsuhashi, S. Comparative antibacterial activity of new quinolone-carboxyclic acid derivatives. Reviews of Infectious Diseases 1988, 10, Supplement 1: 27–31.\nEliopoulos, G. M., Eliopoulos, C. T. Quinolone antimicrobial agents: activity in vitro. In: Wolfson, J. S., Hooper, D. C. (ed.): Quinolone antimicrobial agents. American Society for Microbiology, Washington, DC, 1989, p. 35–70.",{"VOID":985},"10.1007\u002FBF01975173","PUBLICATION","Auto Verify","https:\u002F\u002Flink.springer.com\u002Farticle\u002F10.1007\u002FBF01975173",[990,1006],{"id":991,"sortIndex":32,"researcher":28,"roles":992,"affiliations":994,"properties":1003,"displayName":1005,"givenName":28,"familyName":28},"79fdbb62-9ccd-49ba-bfda-5e58dcef6448",[993],"AUTHOR",[995],{"id":996,"sortIndex":32,"affiliation":997,"properties":28},"aef476bd-ed2e-448b-b14e-1c235f61ba90",{"id":996,"createTime":28,"updateTime":28,"relativeEntities":998,"slug":28,"properties":999,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1002,"statistic":28},[],{"title":1000},{"VI":1001},"Infectious Disease Unit, Medical Services, Massachusetts General Hospital, Boston, USA",[],{"title":1004},{"VI":1005},"J. S. 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Bacteroides ureolyticus was isolat-ed from 45 (34.9 %) of the controls and from 31 (26.3 %) of the urethritis patients; there was no significant difference between these rates (p=0.1). There was no association between the density ofBacteroides ureolyticus on primary isolation plates in either group.",{"EN":1092},"Isolation ofBacteroides ureolyticus from the genital tract of men with and without non-conococcal urethritis",{"VOID":1094},"Taylor-Robinson D, Thomas BJ: The role ofChlamydia trachomatis in genital tract and associated diseases. Journal of Clinical Pathology 1980, 33: 205–233.\nTjiam KH, van Heijst YM, van Zuuren A, Wagenvoort JHT, van Joost T, Michel MF: Evaluation of an enzyme immunoassay for the diagnosis of chlamydial infection in urogenital specimens. Journal of Clinical Microbiology 1986, 23: 752–754.\nWoolley PD, Kinghorn GR, Talbot MD, Duerden BI: Microbial flora in men with non-gonococcal urethritis with particular reference to anaerobic bacteria. International Journal of STD and AIDS 1990, 1: 122–125.\nHawkins DA, Taylor-Robinson D: Non-gonococcal urethritis in the male. In: Asscher AW, Brumfitt W (ed): Microbiological diseases in nephrology. John Wiley, Chichester, 1986, p. 47–67.\nFontaine EA, Taylor-Robinson D, Hanna NF, Coufalik D: Anaerobes in men with urethritis. British Journal of Venereal Diseases 1982, 58: 321–326.\nTaylor AJ, Dawson CA, Owen RJ: The identification ofBacteroides ureolyticus from patients with non-gonococcal urethritis by conventional biochemical tests and DNA and protein analysis. Journal of Medical Microbiology 1986, 21: 109–116.\nAkhtar N, Eley A, Kinghorn GR: Simple transport medium forBacteroides ureolyticus. European Journal of Clinical Microbiology and Infectious Diseases 1989, 8: 321–322.\nEley A, Clarry T, Bennett KW: Selective and differential medium for isolation ofBacteroides ureolyticus from clinical specimens. European Journal of Clinical Microbiology and Infectious Diseases 1989, 8: 83–85.\nHolst E, Mardh PA, Thelin I: Recovery of anaerobic curved rods andGardnerella vaginalis from the urethrea of men, including male heterosexual contacts of female carriers. In: Mardh PA, Taylor-Robinson D (ed): Bacterial vaginosis. Almquist and Wiksell, Stockholm, Sweden, 1984, p. 173–177.",{"VOID":1096},"10.1007\u002FBF01967383","http:\u002F\u002Flink.springer.com\u002F10.1007\u002FBF01967383",[1099,1114,1129,1144],{"id":1100,"sortIndex":32,"researcher":28,"roles":1101,"affiliations":1102,"properties":1111,"displayName":1113,"givenName":28,"familyName":28},"a37e5bb5-bc98-444a-b0e1-4d5e486dbbce",[993],[1103],{"id":1104,"sortIndex":32,"affiliation":1105,"properties":28},"216f371d-f01a-474c-943f-c58ac9c4ed42",{"id":1104,"createTime":28,"updateTime":28,"relativeEntities":1106,"slug":28,"properties":1107,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1110,"statistic":28},[],{"title":1108},{"VI":1109},"Department of Bacteriology, Royal Hallamshire Hospital, Sheffield, UK",[],{"title":1112},{"VI":1113},"K. W. 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We aimed to assess these three points in a retrospective analysis of a 10-year experience in our tertiary hospital. All episodes of significant anaerobic bacteremia diagnosed from 2003 to 2012 were included. Risk factors for mortality and clinical predictability of anaerobic bacteremia were evaluated in 113 randomly selected episodes. Overall incidence of anaerobic bacteremia was 1.2 episodes\u002F1000 admissions, with no significant changes during the 10-year study period. B. fragilis group (38.1 %) and Clostridium spp. (13.7 %) were the most frequent isolated microorganisms. As for the clinical study, 43.4 % of the patients had a comorbidity classified as ultimately fatal or rapidly fatal according to the McCabe and Jackson scale. Clinical manifestations suggestive of anaerobic involvement were present in only 55 % of the patients. Twenty-eight patients (24.8 %) died during the hospitalization. Independent predictive factors of mortality were a high Charlson’s comorbidity index and presentation with septic shock, whereas, an adequate source control of the infection was associated with a better outcome. In our centre, incidence of anaerobic bacteremia remained stable during the last decade. The routine use of anaerobic BCs seems to be adequate, since in about half of the cases anaerobes could not be suspected on clinical bases. Moreover, prompt source control of infection is essential in order to reduce mortality of patients with anaerobic bacteremia.",{"EN":1224},"Are incidence and epidemiology of anaerobic bacteremia really changing?",{"VOID":1226},"Lombardi DP, Engleberg NC (1992) Anaerobic bacteremia: incidence, patient characteristics, and clinical significance. Am J Med 92(1):53–60\nGoldstein EJ (1993) Patterns of susceptibility to fluoroquinolones among anaerobic bacterial isolates in the United States. Clin Infect Dis 16(Suppl 4):S377–S381\nDorsher CW, Rosenblatt JE, Wilson WR, Ilstrup DM (1991) Anaerobic bacteremia: decreasing rate over a 15-year period. Rev Infect Dis 13(4):633–636\nBrook I (2002) Anaerobic infections in children. Microbes Infect 4(12):1271–1280\nBlairon L, De Gheldre Y, Delaere B, Sonet A, Bosly A, Glupczynski Y (2006) A 62-month retrospective epidemiological survey of anaerobic bacteraemia in a university hospital. Clin Microbiol Infect 12(6):527–532\nLassmann B, Gustafson DR, Wood CM, Rosenblatt JE (2007) Reemergence of anaerobic bacteremia. Clin Infect Dis 44(7):895–900\nGrohs P, Mainardi JL, Podglajen I, Hanras X, Eckert C, Buu-Hoi A, Varon E, Gutmann L (2007) Relevance of routine use of the anaerobic blood culture bottle. J Clin Microbiol 45(8):2711–2715\nFenner L, Widmer AF, Straub C, Frei R (2008) Is the incidence of anaerobic bacteremia decreasing? Analysis of 114,000 blood cultures over a ten-year period. J Clin Microbiol 46(7):2432–2434\nZahar JR, Farhat H, Chachaty E, Meshaka P, Antoun S, Nitenberg G (2005) Incidence and clinical significance of anaerobic bacteraemia in cancer patients: a 6-year retrospective study. Clin Microbiol Infect 11(9):724–729\nBengualid V, Singh H, Singh V, Berger J (2008) An increase in the incidence of anaerobic bacteremia: true for tertiary care referral centers but not for community hospitals? Clin Infect Dis 46(2):323–324\nLazarovitch T, Freimann S, Shapira G, Blank H (2010) Decrease in anaerobe-related bacteraemias and increase in Bacteroides species isolation rate from 1998 to 2007: a retrospective study. Anaerobe 16(3):201–205\nNgo JT, Parkins MD, Gregson DB, Pitout JD, Ross T, Church DL, Laupland KB (2013) Population-based assessment of the incidence, risk factors, and outcomes of anaerobic bloodstream infections. Infection 41(1):41–48\nFriedman ND, Kaye KS, Stout JE, McGarry SA, Trivette SL, Briggs JP, Lamm W, Clark C, MacFarquhar J, Walton AL, Reller LB, Sexton DJ (2002) Health care-associated bloodstream infections in adults: a reason to change the accepted definition of community-acquired infections. Ann Intern Med 137(10):791–797\nDellinger RP, Levy MM, Carlet JM, Bion J, Parker MM, Jaeschke R, Reinhart K, Angus DC, Brun-Buisson C, Beale R, Calandra T, Dhainaut JF, Gerlach H, Harvey M, Marini JJ, Marshall J, Ranieri M, Ramsay G, Sevransky J, Thompson BT, Townsend S, Vender JS, Zimmerman JL, Vincent JL (2008) Surviving Sepsis Campaign: international guidelines for management of severe sepsis and septic shock: 2008. Crit Care Med 36(1):296–327\nGransden WR, Eykyn SJ, Phillips I (1991) Anaerobic bacteremia: declining rate over a 15-year period. Rev Infect Dis 13 (6):1255–1256\nPeraino VA, Cross SA, Goldstein EJ (1993) Incidence and clinical significance of anaerobic bacteremia in a community hospital. Clin Infect Dis 16(Suppl 4):S288–S291\nGomez J, Banos V, Ruiz J, Herrero F, Perez M, Pretel L, Canteras M, Valdes M (1993) Clinical significance of anaerobic bacteremias in a general hospital. A prospective study from 1988 to 1992. Clin Investig 71(8):595–599\nRiley TV, Aravena MA (1995) Anaerobic bacteraemia in an Australian teaching hospital. Eur J Clin Microbiol Infect Dis 14 (1):73–75\nArzese A, Trevisan R, Menozzi MG (1995) Anaerobe-induced bacteremia in Italy: a nationwide survey. The Italian Anaerobe Study Group. Clin Infect Dis 20 Suppl 2:S230–232\nSalonen JH, Eerola E, Meurman O (1998) Clinical significance and outcome of anaerobic bacteremia. Clin Infect Dis 26 (6):1413–1417\nHecht DW (2007) Routine anaerobic blood cultures: back where we started? Clin Infect Dis 44(7):901–903\nLiu CY, Huang YT, Liao CH, Yen LC, Lin HY, Hsueh PR (2008) Increasing trends in antimicrobial resistance among clinically important anaerobes and Bacteroides fragilis isolates causing nosocomial infections: emerging resistance to carbapenems. Antimicrob Agents Chemother 52(9):3161–3168\nSnydman DR, Jacobus NV, McDermott LA, Golan Y, Hecht DW, Goldstein EJ, Harrell L, Jenkins S, Newton D, Pierson C, Rihs JD, Yu VL, Venezia R, Finegold SM, Rosenblatt JE, Gorbach SL (2010) Lessons learned from the anaerobe survey: historical perspective and review of the most recent data (2005–2007). Clin Infect Dis 50(Suppl 1):S26–S33\nCLSI Institute (2012) Methods for antimicrobial susceptibility testing of anaerobic bacteria; approved standard. 8th ed. CLSI document M11-A8. CLSI, Wayne PA\nMorris AJ, Wilson ML, Mirrett S, Reller LB (1993) Rationale for selective use of anaerobic blood cultures. J Clin Microbiol 31(8):2110–2113\nBrook I (1989) Anaerobic bacterial bacteremia: 12-year experience in two military hospitals. J Infect Dis 160(6):1071–1075\nBrook I (2010) The role of anaerobic bacteria in bacteremia. Anaerobe 16(3):183–189\nBouza E, Reig M, Garcia de la Torre M, Rodriguez-Creixems M, Romero J, Cercenado E, Baquero F (1985) Retrospective analysis of two hundred and twelve cases of bacteremia due to anaerobic microorganisms. Eur J Clin Microbiol 4(3):262–267\nNguyen MH, Yu VL, Morris AJ, McDermott L, Wagener MW, Harrell L, Snydman DR (2000) Antimicrobial resistance and clinical outcome of Bacteroides bacteremia: findings of a multicenter prospective observational trial. 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A rapid and accurate diagnostic test for the detection of leptospirosis is essential to prevent disease progression from acute non-severe illness to potentially fatal infection. Rapid diagnostic tests (RDTs) recognized as point-of-care (PoC) tests may support clinical decision-making in resource-poor settings. We aimed to assess the accuracy of PoC (Leptocheck-WB) for the detection of acute leptospirosis by meta-analysis of data from eligible studies. This study adhered to the Preferred Reporting Items for Systematic Reviews and Meta-Analysis for Diagnostic Test Accuracy (PRISMA-DTA) guideline. The pooling of data was done only when there were two or more studies that used a particular type of reference test. A total of ten studies (n = 5369) were identified. The majority (70%) were from the Asian region. Using microscopic agglutination test (MAT) as reference test, the pooled sensitivity (0.75, 95% CI: 0.64 to 0.84, 10 studies, I2: 85.9%) and specificity (0.87, 95% CI: 0.77 to 0.94, 10 studies, I2: 97.37%) of Leptocheck-WB in the detection of leptospirosis were moderate. With the use of enzyme-linked immunosorbent assay (ELISA) reference test, the pooled sensitivity 0.85 (95% CI: 0.79 to 0.9, 4 studies, I2: 27.49%) and specificity 0.79 (95% CI: 0.71 to 0.85, 4 studies, I2: 58.9%) of Leptocheck-WB were also moderate. Diagnostic odds ratio of Leptocheck-WB with MAT (21, 95% CI: 10–44) or with ELISA as reference test (21, 95% CI: 9–46) showed an acceptable level of accuracy. Meta-regression analysis showed methodological quality of studies (p: 0.06) and study design (p: 0.09) were potential factors that affected the accuracy of Leptocheck-WB test. Findings suggest that Leptocheck-WB has a moderate level of acceptance for detection of acute leptospirosis. Further confirmation with large-sampled, prospectively designed studies using the same samples for evaluating test accuracy is recommended.",{"EN":1457},"Rapid diagnostic test (Leptocheck-WB) for detection of acute leptospirosis: a meta-analysis of diagnostic accuracy",{"VOID":1459},"Levett PN (2001) Leptospirosis. Clin Microbiol Rev 14(2):296–326\nCosta F, Hagan JE, Calcagno J, Kane M, Torgerson P, Martinez-Silveira MS et al (2015) Global morbidity and mortality of leptospirosis: a systematic review. PLoS Negl Trop Dis 9(9):e0003898\nVictoriano AF, Smythe LD, Gloriani-Barzaga N, Cavinta LL, Kasai T, Limpakarnjanarat K et al (2009) Leptospirosis in the Asia Pacific region. BMC Infect Dis 4(9):147\nSoo ZMP, Khan NA, Siddiqui R (2020) Leptospirosis: increasing importance in developing countries. Acta Trop. 201:105183\nMcBride AJ, Athanazio DA, Reis MG, Ko AI (2005) Leptospirosis. Curr Opin Infect Dis 18(5):376–386\nBudihal SV, Perwez K (2014) Leptospirosis diagnosis: competancy of various laboratory tests. J Clin Diagn Res 8(1):199–202\nNiloofa R, Fernando N, de Silva NL, Karunanayake L, Wickramasinghe H, Dikmadugoda N et al (2015) Diagnosis of leptospirosis: comparison between microscopic agglutination test, IgM-ELISA and IgM rapid immunochromatography test. PLoS One. 10(6):e0129236\nWHO. (2003) Human leptospirosis: guidance for diagnosis, surveillance and control. WHO\nChirathaworn C, Inwattana R, Poovorawan Y, Suwancharoen D (2014) Interpretation of microscopic agglutination test for leptospirosis diagnosis and seroprevalence. Asian Pac J Trop Biomed 4(Suppl 1):S162–S164\nRosa MI, Reis MFD, Simon C, Dondossola E, Alexandre MC, Colonetti T et al (2017) IgM ELISA for leptospirosis diagnosis: a systematic review and meta-analysis. Cien Saude Colet 22(12):4001–4012\nLam J-Y, Low GK-K, Chee H-Y (2020) Diagnostic accuracy of genetic markers and nucleicacid techniques for the detection of Leptospira in clinical samples: a meta-analysis. PLoS Negl Trop Dis 14(2):e0008074\nLee JW, Park S, Kim SH, Christova I, Jacob P, Vanasco NB et al (2016) Clinical evaluation of rapid diagnostic test kit using the polysaccharide as a genus-specific diagnostic antigen for leptospirosis in Korea, Bulgaria, and Argentina. J Korean Med Sci 31(2):183–189\nBharti AR, Nally JE, Ricaldi JN, Matthias MA, Diaz MM, Lovett MA et al (2003) Peru-United States Leptospirosis Consortium. Leptospirosis: a zoonotic disease of global importance. Lancet Infect Dis 3(12):757–771\nPicardeau M (2013) Diagnosis and epidemiology of leptospirosis. Med Mal Infect 43(1):1–9\nRao M, Amran F, Aquilla N. (2019) Evaluation of a rapid kit for detection of IgM against Leptospira in human. Can J Infect Dis Med Microbiol. 5763595\nMcInnes MDF, Moher D, Thombs BD, McGrath TA, Bossuyt PM, The PRISMA-DTA Group et al (2018) Preferred Reporting Items for a Systematic Review and Meta-analysis of Diagnostic Test Accuracy studies: The PRISMA-DTA statement. JAMA 319(4):388–396\nBossuyt P, Davenport C, Deeks J, Hyde C, Leeflang M, Scholten R. (2013) Chapter 11: Interpreting results and drawing conclusions. In: Deeks JJ, Bossuyt PM, Gatsonis C (editors), Cochrane Handbook for Systematic Reviews of Diagnostic Test Accuracy Version 0.9. The Cochrane Collaboration, http:\u002F\u002Fsrdta.cochrane.org\u002F. Accessed 24 October 2021.\nLeeflang MM (2014) Systematic reviews and meta-analyses of diagnostic test accuracy. Clin Microbiol Infect 20(2):105–113\nDeshmukh H, Way SS (2019) Immunological basis for recurrent fetal loss and pregnancy complications. Annu Rev Pathol 14:185–210\nWhiting PF, Rutjes AW, Westwood ME, Mallett S, Deeks JJ, Reitsma JB et al (2011) QUADAS-2: a revised tool for the quality assessment of diagnostic accuracy studies. Ann Intern Med 155(8):529–536\nSchueler S, Schuetz GM, Dewey M (2012) The revised QUADAS-2 tool. Ann Intern Med 156(4):323\nJones C, Athanasiou T (2005) Summary receiver operating characteristic curve analysis techniques in the evaluation of diagnostic tests. Ann Thorac Surg 79(1):16–20\nPanwala T, Mulla S, Patel P (2011) Seroprevalence of leptospirosis in south Gujarat region by evaluating the two rapid commercial diagnostic kits against the mat test for detection of antibodies to Leptospira Interrogans. National J Comm Med 2(1):64–70\nGoris MG, Leeflang MM, Loden M, Wagenaar JF, Klatser PR, Hartskeerl RA et al (2013) Prospective evaluation of three rapid diagnostic tests for diagnosis of human leptospirosis. PLoS Negl Trop Dis. 7(7):e2290\nBhatia M, Umapathy BL, Navaneeth BV (2015) An evaluation of dark field microscopy, culture and commercial serological kits in the diagnosis of leptospirosis. Indian J Med Microbiol 33(3):416–421\nEugene EJ, Handunnetti SM, Wickramasinghe SA, Kalugalage TL, Rodrigo C, Wickremesinghe H et al (2015) Evaluation of two immunodiagnostic tests for early rapid diagnosis of leptospirosis in Sri Lanka: a preliminary study. BMC Infect Dis 15:319\nGoarant C, Bourhy P, D’Ortenzio E, Dartevelle S, Mauron C, Soupe-Gilbert ME et al (2013) Sensitivity and specificity of a new vertical flow rapid diagnostic test for the serodiagnosis of human leptospirosis. PLoS Negl Trop Dis. 7(6):e2289\nPanwala T, Rajdev S, Mulla S (2015) To evaluate the different rapid screening tests for diagnosis of leptospirosis. J Clin Diagn Res 9(2):DC21-24\nPodgorsek D, Cerar T, Logar M, Lesnicar G, Remec T, Baklan Z et al (2015) Evaluation of the immunochromatographic (Leptocheck) test for detection of specific antibodies against leptospires. Wien Klin Wochenschr 127(23–24):948–953\nAlia SN, Joseph N, Philip N, Azhari NN, Garba B, Masri SN et al (2019) Diagnostic accuracy of rapid diagnostic tests for the early detection of leptospirosis. J Infect Public Health 12(2):263–269\nTDR Diagnostics Evaluation Expert Panel, Banoo S, Bell D, Bossuyt P, Herring A, Mabey D et al (2010) Evaluation of diagnostic tests for infectious diseases: general principles. Nat Rev Microbiol 8(12 Suppl):S17-29\nLimmathurotsakul D, Turner EL, Wuthiekanun V, Thaipadungpanit J, Suputtamongkol Y, Chierakul W et al (2012) Fool’s gold: why imperfect reference tests are undermining the evaluation of novel diagnostics: a reevaluation of 5 diagnostic tests for leptospirosis. Clin Infect Dis 55(3):322–331\nVerma V, Kala D, Gupta S, Kumar H, Kaushal A, Kuča K et al (2021) Leptospira interrogans outer membrane protein-based nanohybrid sensor for the diagnosis of leptospirosis. 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aim was to evaluate the utility of the neonatal early-onset sepsis risk calculator (NEOSC) to the utility of C-reactive protein (CRP) for diagnosing neonatal EOS. This retrospective study reviewed the records of neonates who underwent sepsis workups due to equivocal symptoms and compared their CRP values to the calculator’s recommendations and their cultures. A total of 382 newborns who underwent sepsis work-up due to equivocal symptoms were included in our study. The calculator’s recommendations would have reduced the number of newborns who underwent sepsis workups by 82.5% and antibiotic treatment by 83.4% (n = 315). Considering that 373 of 382 (97.6%) ultimately had no sepsis, the calculator’s specificity was higher than that of CRP (83.9% versus 76.1%). When comparing the maximal CRP value with the risk according to the neonatal sepsis calculator, a significant correlation was found between them (P \u003C 0.01), but the relationship was not strong (Pearson’s correlation = 0.27). We found a significant correlation between the risk of sepsis according to the NEOSC and the CRP values, although the correlation was not strong. The calculator’s high specificity enables safe avoidance of multiple blood tests and antibiotic treatments for suspected neonates who are not infected. CRP tests can reduce the number of infected newborns the calculator may miss, at the cost of unnecessary blood tests and antibiotic therapy to many newborns.",{"EN":1600},"C-reactive protein and the neonatal early-onset sepsis calculator for the diagnosis of neonatal sepsis",{"VOID":1602},"Escobar GJ, Puopolo KM, Wi S, Turk BJ, Kuzniewicz MW, Walsh EM, Newman TB, Zupancic J, LiebermanE DD (2014) Stratification of risk of early-onset sepsis in newborns ≥ 34 weeks’ gestation. Pediatrics 133(1):30–36\nWeston EJ, Pondo T, Lewis MM, Martell-Cleary P, Morin C, Jewell B, Daily P, Apostol M, Petit S, Farley M, Lynfield R, Reingold A, Hansen IN, Stoll BJ, Shane AL, Zell E, Schrag SJ (2011) The burden of invasive early-onset neonatal sepsis in the United States, 2005–2008. Pediatr Infect Dis J 30(11):937–941\nVan Herk W, Stocker M, van Rossum AM (2016) Recognising early onset neonatal sepsis: an essential step in appropriate antimicrobial use. J Infect 5(72):S77–S82\nKumar V, Shearer JC, Kumar A, Darmstadt GL (2009) Neonatal hypothermia in low resource settings: a review. J Perinatol 29(6):401–412\nDoctor BA, O’Riordan MA, Kirchner HL, Shah D, Hack M (2001) Perinatal correlates and neonatal outcomes of small for gestational age infants born at term gestation. Am J Obstet Gynecol 185(3):652–659\nVoora S, Srinivasan G, Lilien LD, Yeh TF, Pildes RS (1982) Fever in full-term newborns in the first four days of life. Pediatrics 69(1):40–44\nBoyle RJ, Chandler BD, Stonestreet BS, Oh W (1978) Early identification of sepsis in infants with respiratory distress. Pediatrics 62(5):744–750\nChan DK, Ho LY (1997) Usefulness of C-reactive protein in the diagnosis of neonatal sepsis. Singap Med J 38(6):252–255\nKuzniewicz MW, Puopolo KM, FischerA WEM, Li S, Newman TB, Kipnis P, Escobar G (2017) A quantitative, risk-based approach to the management of neonatal early-onset sepsis. JAMA Pediatr 171(4):365–371\nDhudasia MB, Mukhopadhyay S, Puopolo KM (2018) Implementation of the sepsis risk calculator at an academic birth hospital. Hosp Pediatr 8(5):243–250\nAchtenN B, Dorigo-Zetsma JW, van der Linden PD, van Brakel M, Plötz FB (2018) Sepsis calculator implementation reduces empiric antibiotics for suspected early-onset sepsis. Eur J Pediatr 177(5):741–746\nStrunk T, Buchiboyina A, Sharp M, Nathan E, Doherty D, Patole S (2018) Implementation of the neonatal sepsis calculator in an Australian tertiary perinatal centre. Neonatology 113(4):379–382\nHofer N, Zacharias E, Müller W, Resch B (2012) An update on the use of C-reactive protein in early-onset neonatal sepsis: current insights and new tasks. Neonatology 102(1):25–36\nLai MY, Tsai MH, Lee CW, Chiang MC, Lien R, Fu RH, Huang HR, Chu SM, Hsu JF (2015) Characteristics of neonates with culture-proven bloodstream infection who have low levels of C-reactive protein (≤10 mg\u002FL). BMC Infect Dis 15:320\nSundarapandian S, Chinnakkannan S, Ahmed M, Das R (2017) Utility of serial serum C-reactive protein in the diagnosis of neonatal infection. Indian J Child Health 4:374–378\nBenitz WE, Han MY, Madan A, Ramachandra P (1998) Serial serum C-reactive protein levels in the diagnosis of neonatal infection. Pediatrics 102(4):e41–e41\nBenitz WE, Gould JB, Druzin ML (1999) Risk factors for early-onset group B streptococcal sepsis: estimation of odds ratios by critical literature review. Pediatrics 103(6):e77–e77\nKlingenberg CA, Kornelisse R, Buonocore G, Maier RF, Stocker M (2018) Culture-negative neonatal sepsis–at the crossroad between efficient sepsis care and antimicrobial stewardship. Front Pediatr 9(6):285\nCantey JB, Wozniak PS, Pruszynski JE, Sánchez PJ (2016) Reducing unnecessary antibiotic use in the neonatal intensive care unit (SCOUT): a prospective interrupted time-series study. Lancet Infect Dis 16(10):1178–1184\nGoel N, Shrestha S, Smith R, Mehta A, Ketty M, Muxworthy H, Abelian A, Kirupaalar V, Saeed S, Jain S, Asokkumar A, Natti M, Barnard I, Pitchaikani PK, Banerjee S (2020) Screening for early onset neonatal sepsis: NICE guidance-based practice versus projected application of the Kaiser Permanente sepsis risk calculator in the UK population. Arch Dis Child Fetal Neonatal Ed 105(2):F118–F122\nMurkW RKR, Bracken MB (2011) Prenatal or early-life exposure to antibiotics and risk of childhood asthma: a systematic review. Pediatrics 127(6):1125–1138\nSaari A, Virta LJ, SankilampiU DL, Saxen H (2015) Antibiotic exposure in infancy and risk of being overweight in the first 24 months of life. Pediatrics 135(4):617–626\nCorvaglia L, Tonti G, Martini S, Aceti A, Mazzola G, Aloisio I, Gioia DD, Faldella G (2016) Influence of intrapartum antibiotic prophylaxis for group B streptococcus on gut microbiota in the first month of life. J Pediatr Gastroenterol Nutr 62(2):304–308\nCantey JB, Baird SD (2017) Ending the culture of culture-negative sepsis in the neonatal ICU. Pediatrics 140(4):e20170044\nSchelonka RL, Chai MK, Yoder BA, Hensley D, Brockett RM, Ascher DP (1996) Volume of blood required to detect common neonatal pathogens. J Pediatr 129(2):275–278",{"VOID":1604},"10.1007\u002Fs10096-021-04156-y","https:\u002F\u002Flink.springer.com\u002Farticle\u002F10.1007\u002Fs10096-021-04156-y",[1607,1622,1635,1648,1661],{"id":1608,"sortIndex":32,"researcher":28,"roles":1609,"affiliations":1610,"properties":1619,"displayName":1621,"givenName":28,"familyName":28},"dd2a7d85-66ea-4b3b-b027-978d6f0ede9d",[993],[1611],{"id":1612,"sortIndex":32,"affiliation":1613,"properties":28},"3118058e-ae1f-4ec0-a3ee-e940e05a8db6",{"id":1612,"createTime":28,"updateTime":28,"relativeEntities":1614,"slug":28,"properties":1615,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1618,"statistic":28},[],{"title":1616},{"VI":1617},"Department of Neonatology, Dana Dwek Children’s Hospital, Tel Aviv Sourasky Medical Center, Tel Aviv, Israel, affiliated to the Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel",[],{"title":1620},{"VI":1621},"Nati Friedman",{"id":1623,"sortIndex":40,"researcher":28,"roles":1624,"affiliations":1625,"properties":1632,"displayName":1634,"givenName":28,"familyName":28},"89e32fb1-fd5e-456d-9c82-25a15ee06545",[993],[1626],{"id":1612,"sortIndex":32,"affiliation":1627,"properties":28},{"id":1612,"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":1617},[],{"title":1633},{"VI":1634},"Sivan 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Children’s Hospital, Tel Aviv Sourasky Medical Center, Tel Aviv, Israel",[],{},{"title":1681},{"VI":1682},"Ronella 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culture is probably the most significant specimen used for the diagnosis of bacterial infections, especially for bloodstream infections. In the present study, we compared the resin-containing BD BACTEC™ Plus-Aerobic (Becton Dickinson), non-charcoal-containing BacT\u002FAlert® SA (bioMérieux), and charcoal-containing BacT\u002FAlert® FA (bioMérieux) blood culture bottles with direct identification by matrix-assisted laser desorption ionization time-of-flight mass spectrometry (MALDI-TOF MS). A total of 103 bacterial isolates, from clinical blood cultures, representing the most frequent 13 genera and 24 species were examined. Bacteria were extracted from positive blood culture broth by density centrifugation and then subjected to identification by MALDI-TOF MS using two different volumes and chemical treatments. Overall, correct identification by MALDI-TOF MS was obtained for the BD BACTEC™ Plus-Aerobic, BacT\u002FAlert® SA, and BacT\u002FAlert® FA blood culture bottles in 72%, 45.6%, and 23%, respectively, for Gram-negative bacteria in 86.6%, 69.2%, and 47.1%, respectively, and for Gram-positive bacteria in 60.0%, 28.8%, and 5.4%, respectively. The lack of identification was observed mainly with viridans streptococci. Depending on the blood culture bottles used in routine diagnostic procedures and the protocol for bacterial preparation, the applied MALDI-TOF MS represents an efficient and rapid method for direct bacterial identification.",{"EN":1752},"Rapid identification of bacteria in positive blood culture by matrix-assisted laser desorption ionization time-of-flight mass spectrometry",{"VOID":1754},"Bizzini A, Durussel C, Bille J, Greub G, Prod’hom G (2010) Performance of matrix-assisted laser desorption ionization-time of flight mass spectrometry for identification of bacterial strains routinely isolated in a clinical microbiology laboratory. J Clin Microbiol 48(5):1549–1554\nFerroni A, Suarez S, Beretti JL, Dauphin B, Bille E, Meyer J et al (2010) Real-time identification of bacteria and Candida species in positive blood culture broths by matrix-assisted laser desorption ionization-time of flight mass spectrometry. J Clin Microbiol 48(5):1542–1548\nChristner M, Rohde H, Wolters M, Sobottka I, Wegscheider K, Aepfelbacher M (2010) Rapid identification of bacteria from positive blood culture bottles by use of matrix-assisted laser desorption-ionization time of flight mass spectrometry fingerprinting. J Clin Microbiol 48(5):1584–1591\nFerreira L, Sánchez-Juanes F, Porras-Guerra I, García-García MI, García-Sánchez JE, González-Buitrago JM et al (2011) Microorganisms direct identification from blood culture by matrix-assisted laser desorption\u002Fionization time-of-flight mass spectrometry. Clin Microbiol Infect 17(4):546–551\nMoussaoui W, Jaulhac B, Hoffmann A-M, Ludes B, Kostrzewa M, Riegel P et al (2010) Matrix-assisted laser desorption ionization time-of-flight mass spectrometry identifies 90% of bacteria directly from blood culture vials. Clin Microbiol Infect 16:1631–1638\nLa Scola B, Raoult D (2009) Direct identification of bacteria in positive blood culture bottles by matrix-assisted laser desorption ionisation time-of-flight mass spectrometry. PLoS One 4(11):e8041\nProd’hom G, Bizzini A, Durussel C, Bille J, Greub G (2010) Matrix-assisted laser desorption ionization-time of flight mass spectrometry for direct bacterial identification from positive blood culture pellets. J Clin Microbiol 48(4):1481–1483\nStevenson LG, Drake SK, Murray PR (2010) Rapid identification of bacteria in positive blood culture broths by matrix-assisted laser desorption ionization-time of flight mass spectrometry. J Clin Microbiol 48(2):444–447\nSzabados F, Michels M, Kaase M, Gatermann S (2011) The sensitivity of direct identification from positive BacT\u002FALERT™ (bioMérieux) blood culture bottles by matrix-assisted laser desorption ionization time-of-flight mass spectrometry is low. Clin Microbiol Infect 17(2):192–195\nRomero-Gómez MP, Mingorance J (2011) The effect of the blood culture bottle type in the rate of direct identification from positive cultures by matrix-assisted laser desorption\u002Fionisation time-of-flight (MALDI-TOF) mass spectrometry. J Infect 62(3):251–253\nCherkaoui A, Hibbs J, Emonet S, Tangomo M, Girard M, Francois P et al (2010) Comparison of two matrix-assisted laser desorption ionization-time of flight mass spectrometry methods with conventional phenotypic identification for routine identification of bacteria to the species level. J Clin Microbiol 48(4):1169–1175",{"VOID":1756},"10.1007\u002Fs10096-011-1312-0","https:\u002F\u002Flink.springer.com\u002Farticle\u002F10.1007\u002Fs10096-011-1312-0",[1759,1774,1789,1802,1815,1828],{"id":1760,"sortIndex":32,"researcher":28,"roles":1761,"affiliations":1762,"properties":1771,"displayName":1773,"givenName":28,"familyName":28},"c3e1bace-a709-4b1f-ab22-ee61681ae119",[993],[1763],{"id":1764,"sortIndex":32,"affiliation":1765,"properties":28},"ebd0e9d6-2de0-44c0-8dbe-ed4815eeeba8",{"id":1764,"createTime":28,"updateTime":28,"relativeEntities":1766,"slug":28,"properties":1767,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1770,"statistic":28},[],{"title":1768},{"VI":1769},"Medical Faculty, University of Cologne Medical Center, Cologne, Germany",[],{"title":1772},{"VI":1773},"V. 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These novel signaling pathways, in concert with or independent of Th1\u002FTh2 responses, have potentially important implications for yielding valuable insights into the pathogenesis of immune reconstitution syndrome (IRS) in transplant recipients, for aiding the diagnosis of this entity, and for achieving a balance of immune responses that enhance host immunity while curbing unfettered inflammation in IRS.",{"EN":1917},"Novel immune regulatory pathways and their role in immune reconstitution syndrome in organ transplant recipients with invasive mycoses",{"VOID":1919},"Singh N, Perfect JR (2007) Immune reconstitution syndrome associated with opportunistic mycoses. Lancet Infect Dis 7:395–401\nLortholary O, Fontanet A, Memain N et al (2005) Incidence and risk factors of immune reconstitution inflammatory syndrome complicating HIV-associated cryptococcosis in France. AIDS 19:1043–1049\nShelburne SA, Hamill RJ, Rodriguez-Barradas MC et al (2002) Immune reconstitution inflammatory syndrome, emergence of a unique syndrome during highly active antiretroviral therapy. Medicine 81:213–227\nCasadevall A, Pirofski LA (2003) The damage-response framework of microbial pathogenesis. Nat Rev Microbiol 1:17–24\nShelburne SA, Darcourt J, White C Jr et al (2005) The role of immune reconstitution inflammatory syndrome in AIDS-related Cryptococcus neoformans disease in the era of highly active antiretroviral therapy. Clin Infect Dis 40:1045–1052\nHirsch HH, Kaufmann G, Sendi P et al (2004) Immune reconstitution in HIV-infected patients. Clin Infect Dis 38:1159–1166\nCheng VCC, Yuen KY, Wong SSY et al (2001) Immunorestitution disease in patients not infected with HIV. Eur J Clin Microbiol Infect Dis 20:402–406\nEinsiedel L, Gordon DL, Dyer JR (2004) Paradoxical inflammatory reaction during treatment of Cryptococcus neoformans var. gattii meningitis in an HIV seronegative woman. Clin Infect Dis 39:e78–e82\nClemons KV, Stevens DA (2001) Overview of host defense mechanisms in systemic mycoses and the basis for immunotherapy. Semin Respir Infect 16:60–66\nRomani L, Pucetti P (2007) Controlling pathogenic inflammation to fungi. Expert Rev Anti Infect Ther 5:1007–1017\nCenci E, Perito S, Enssle KH et al (1997) Th1 and Th2 cytokines in mice with invasive aspergillosis. Infect Immun 65:564–570\nParkin J, Cohen B (2001) An overview of the immune system. Lancet 357:1777–1789\nGoriely S, Goldman M (2007) The interleukin-12 family: new players in transplantation immunity? Am J Transplant 7:278–284\nNelms K, Keegan A, Zamorano J et al (1999) The IL-4 receptor: signaling mechanisms and biologic functions. Ann Rev Immunol 17:701–738\nAfzali B, Lombardi G, Lechler R, Lord G (2007) The role of T helper (TH17) and regulatory T cells (Treg) in human organ transplantation and autoimmune disease. Clin Exp Immunol 148:32–46\nMangan P, Harrington L, O’Quinn D et al (2006) Transforming growth factor-beta induces development of the T (H) 17 lineage. Nature 441:231–234\nCooke A (2006) Th17 cells in inflammatory conditions. Rev Diabetic Stud 372–375\nBi Y, Guangwei L, Yang R (2007) Th17 cell induction and immune regulatory effects. J Cell Physiol 211:273–278\nSchmidt-Weber C, Akdis M, Akdis C (2007) TH17 cells in the big picture of immunology. J Allergy Clin Immunol 120:247–254\nStockinger B, Veldhoen M (2007) Differentiation and function of Th17 T cells. Curr Opin Immunol 3:281–286\nBettelli E, Carrier Y, Gao W et al (2006) Reciprocal developmental pathways for the generation of pathogenic effector TH17 and regulatory T cells. Nature 441:235–238\nVeldhoen M, Hocking R, Atkins C et al (2006) TGFbeta in the context of an inflammatory cytokine milieu supports de nova differentiation of IL-17-producing T cells. Immunity 24:179–189\nPyzik M, Piccirillo C (2007) TGF-beta 1 modulates FoxP3 expression and regulatory activity in distinct CD4+ T cell subsets. J Leukov Biol 82:335–346\nChen W, Jin W, Hardegen N et al (2003) Conversion of peripheral TGF-beta CD4+CD5-naive T cells to CD4+CD25+ regulatory T cells by TGF-beta induction of transcription factor Foxp3. J Exp Med 1875–1886\nYagi H, Normura T, Nakamura K et al (2004) Crucial role of FoxP3 in the development and function of human CD25+CD4+ regulatory T cells. Int Immunol 11:1643–1656\nSakaguchi S (2005) Naturally arising FoxP3-expressing CD25+ CD4+ regulatory T cells in immunological tolerance to self and non-self. Nature Immun 6:345–354\nFontenot J, Gavin M, Rudensky A (2003) FoxP3 programs the development and function of CD4+CD25+ regulatory T cells. Nature Immun 4:330–336\nWaldmann H, Graca L, Cobbold S et al (2004) Regulatory T cells and organ transplantation. Semin Immunol 16:119–126\nde Kleer I, Wedderburn L, Taams L et al (2004) CD4+CD25bright regulatory T cells activity regulate inflammation in the joints of patients with the remitting form of juvenile idiopathic arthritis. J Immunol 10:6423–6435\nMatthys P, Vermeire K, Mitera T et al (1998) Anti-IL-12 antibody prevents the development and progression of collagen-induced arthritis in IFN-gamma receptor-deficient mice. Eur J Immunol 28:2143–2151\nTang Q, Henriksen K, Bi M et al (2004) In vitro-expanded antigen-specific regulatory T cells suppress autoimmune diabetes. J Exp Med 199:1455–1465\nLong E, Wood K (2007) Understanding FOXP3: progress towards achieving transplantation tolerance. Transplantation 84:459–461\nGras J, Cornet A, Latinne D et al (2004) Evidence that Th1\u002FTh2 immune deviation impacts on early graft acceptance after pediatric liver transplantation: results of immunological monitoring in 40 children. Am J Transplant 4:444\nSaggi B, Fisher R, Naar J et al (1999) Intragraft cytokine expression in tolerant rat renal allografts with rapamycin and cyclosporin immunosuppression. Clin Transplant 13:90–97\nSalama A, Najafian N, Clarkson M et al (2003) Regulatory CD25+ T cells in human kidney transplant recipients. J Am Soc Nephrol 6:1643–1651\nGraca L, Cobbold S, Waldmann H (2002) Identification of regulatory T cells in tolerated allografts. J Exp Med 195:1641\nBloom DD, Brahmbhatt R, Knechtle S (2007) Flow cytometric characterization regulatory T lymphocyte populations in renal transplant patients treated with Campath and tacrolimus. Presented at the American Transplant Congress, May 5–7, San Francisco, CA\nLopez M, Clarkson M, Sayegh A et al (2006) A novel mechanism of action for anti-thymocyte globulin induction of CD4+CD25+FoxP3+ regulatory T cells. J Am Soc Nephrol 10:2644–2646\nWatanabe T, Masuyama J, Sohma Y et al (2006) CD52 is a novel costimulatory molecule for induction of CD4+ regulatory T cells. Clin Immunol 3:247–259\nKaragiannidis C, Akdis M, Holopainen P et al (2004) Glucocorticoids up-regulate CAP3 expression and regulatory T cells in asthma. J Allergy Clin Immunol 114:1425–1433\nSegundo D, Ruiz J, Izquierdo M et al (2006) Calcineurin inhibitors, but no rapamycin, reduce percentages of CD4+CD25+FoxP3+ Regulatory T cells in renal transplant recipients. Transplantation 82:550–557\nBaan C, van der Mast B, Klepper M et al (2005) Differential effect of calcineurin inhibitors, anti-CD25 antibodies and rapamycin of the induction of FoxP3 in human T Cells. Transplantation 80:110–117\nBensinger S, Walsh P, Zhang J (2004) Distinct IL-2 receptor signaling pattern in CD4+CD25+regulatory T cells. J Immunol 172:5287\nFontenot J, Rasmussen J, Gavin M et al (2005) A function for interleukin 2 in FoxP3-expressing regulatory T cells. Nat Immunol 6:1142\nBattaglia M, Stabilini A, Roncarolo M (2005) Rapamycin selectively expands CD4+CD25+FoxP3+ regulatory T cells. Blood 105:4743–4748\nNagai H, Guo J, Choi H et al (1995) Interferon-gamma and tumor necrosis factor-alpha protect mice from invasive aspergillosis. J Infect Dis 172:1554–1560\nKawakami K (2004) Regulation by innate immune T lymphocytes in the host defense against pulmonary infection with Cryptococcus neoformans. Jpn J Infect Dis 57:137–145\nDecken K, Kohler G, Palmer-Lehmann K et al (1998) Interleukin-12 is essential for protective Th1 response in mice infected with Cryptococcus neoformans. Infect Immun 66:4994–5000\nAguirre K, Havell EA, Gibson GW (1995) Role of tumor necrosis factor and gamma interferon in acquired resistance to Cryptococcus neoformans in the central nervous system of mice. Infect Immun 63:1725–1731\nVecchiarelli A, Retini C, Monari C et al (1996) Purified capsular polysaccharide of Cryptococcus neoformans induces interleukin-10 secretion by human monocytes. Infect Immun 64:2846–2849\nVecchiarelli A, Retini C, Pietrella D et al (1995) Downregulation by cryptococcal polysaccharide of tumor necrosis factor alpha and interleukin-1β secretion from human monocytes. Infect Immun 63:2919–2923\nRudner X, Happel K, Young E et al (2007) Interleukin-23 (IL-23)-IL-17 cytokine axis in murine Pneumocystis carinii infection. Infect Immun 75:3055–3061\nZelante T, De Luca A, Bonifazi P et al (2007) IL-23 and the Th17 pathway promote inflammation and impair antifungal immune resistance. Eur J Immunol 37:2695–2706\nRogers PD, Pearson MM, Cleary JD et al (2002) Differential expression of genes encoding immunomodulatory proteins in response to amphotericin B in human mononuclear cells identified by cDNA microarray analysis. J Antimicrob Chemotherap 50:811–817\nRazonable RR, Henault M, Lee LN et al (2005) Secretion of proinflammatory cytokines and chemokines during amphotericin B exposure is mediated by coactivation of toll-like receptors 1 and 2. Antimicrob Ag Chemother 4:1617–1621\nShadkchan Y, Keisari Y, Segal E (2004) Cytokines in mice treated with amphotericin B-intralipid. Med Mycol 42:123–128\nHohl T, Feldmesser M, Perlin D et al (2007) Caspofungin modulates inflammatory responses to Aspergillus fumgiatus through stage-specific effects on fungal β-glucan exposure. Annual meeting of the Infectious Diseases Society of America, 4–7 October, San Diego, CA\nWheeler RT, Fink GR (2006) A drug-sensitive genetic network masks fungi from the immune system. PLOS Pathogens 2:328–339\nLortholary O, Sitbon K, Dromer F et al (2005) Evidence for HIV and Cryptococcus neoformans interactions on the pro- and antiinflammatory responses in blood during AIDS-associated cryptococcosis. Clin Microbiol Infect 11:296–300\nSingh N, Lortholary O, Alexander BD et al (2005) An “immune reconstitution syndrome”-like entity associated with Cryptococcus neoformans infections in organ transplant recipients. Clin Infect Dis 40:1756–1761\nBreton G, Adle-Biassette H, Therby A et al (2006) Immune reconstitution inflammatory syndrome in HIV-infected patients with disseminated histoplasmosis. AIDS 20:119–121\nCheng VCC, Yuen KY, Chan WM et al (2000) Immunorestitution disease involving the innate and adaptive response. Clin Infect Dis 30:882–892\nMiceli M, Maertens J, Buve K et al (2007) Immune reconstitution inflammatory syndrome in cancer patients with pulmonary aspergillosis recovering from neutropenia: proof of principle, description, and clinical and research implications. Cancer 110:112–120\nTang Q, Bluestone J (2006) Regulatory T-cell physiology and application to treat autoimmunity. Immunol Rev 212:217–237\nTarbell K, Petit L, Zuo X et al (2007) Dendritic cell-expanded, islet-specific CD4+CD25+CD62L+regulatory T cells restore normoglycemia in diabetic NOD mice. J Exp Med 204:191–201\nTarbell K, Yamazaki S, Olson K et al (2004) CD25+CD4+ T cells, expanded with dendritic cells presenting a single autoantigenic peptide, suppress autoimmune diabetes. J Exp Med 199:1467–1477\nIngram P, Howman R, Leahy M et al (2007) Cryptococcal immune reconstitution inflammatory syndrome following alemtuzumab therapy. Clin Infect Dis 12:115–117",{"VOID":1921},"10.1007\u002Fs10096-008-0461-2","https:\u002F\u002Flink.springer.com\u002Farticle\u002F10.1007\u002Fs10096-008-0461-2",[1924],{"id":1925,"sortIndex":32,"researcher":28,"roles":1926,"affiliations":1927,"properties":1936,"displayName":1938,"givenName":28,"familyName":28},"7a101f29-399a-4f68-94c7-7dac2e64f307",[993],[1928],{"id":1929,"sortIndex":32,"affiliation":1930,"properties":28},"095352ec-d361-46b1-8c09-83cfae2741ba",{"id":1929,"createTime":28,"updateTime":28,"relativeEntities":1931,"slug":28,"properties":1932,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1935,"statistic":28},[],{"title":1933},{"VI":1934},"Infectious Diseases Section, VA Medical Center, Pittsburgh, USA",[],{"title":1937},{"VI":1938},"N. 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Some experts consider infection with influenza B as milder than that with influenza A. The objective of this study is to evaluate the outcomes of hospitalized patients with laboratory-confirmed influenza A or B in 2017–2018 influenza season. All hospitalized patients between October 2017 and April 2018 with laboratory-confirmed influenza A and B were included. The primary composite outcomes were pneumonia\u002Fmyocarditis\u002Fencephalitis, mechanical ventilation, ICU admission, and 30-day mortality. Secondary outcomes were 30-\u002F90-day mortality, length of hospital stay, and readmission rates. The study included 201 influenza A and 325 influenza B. For the primary composite outcome, no significant difference was demonstrated between influenza A and B. Rates of mortality were similar at 30 and 90 days. Influenza A had higher pneumonia rates and mechanical ventilation. On multivariate analysis, higher Charlson’s score, hypoalbuminemia, and vasopressor use were associated with 30-day mortality, while infection with either influenza A or B was not. Influenza A was associated with higher pneumonia and mechanical ventilation rates. However, influenza B resulted with similar 30-day mortality rate as influenza A.",{"EN":2008},"Comparison of clinical outcomes of influenza A and B at the 2017–2018 influenza season: a cohort study",{"VOID":2010},"Centers for Disease C, Prevention (2010) Estimates of deaths associated with seasonal influenza --- United States, 1976–2007. MMWR Morb Mortal Wkly Rep 59(33):1057–1062\nSimonsen L, Clarke MJ, Williamson GD, Stroup DF, Arden NH, Schonberger LB (1997) The impact of influenza epidemics on mortality: introducing a severity index. Am J Public Health 87(12):1944–1950\nVan Kerkhove MD, Vandemaele KA, Shinde V, Jaramillo-Gutierrez G, Koukounari A, Donnelly CA et al (2011) Risk factors for severe outcomes following 2009 influenza A (H1N1) infection: a global pooled analysis. PLoS Med 8(7):e1001053\nBennett JE, Dolin R, Blaser MJ (2019) Principles and Practice of Infectious Diseases, Elsevier\nMcBean AM, Hebert PL (2004) New estimates of influenza-related pneumonia and influenza hospitalizations among the elderly. Int J Infect Dis 8(4):227–235\nThompson WW, Shay DK, Weintraub E, Brammer L, Bridges CB, Cox NJ et al (2004) Influenza-associated hospitalizations in the United States. Jama. 292(11):1333–1340\nIrving SA, Patel DC, Kieke BA, Donahue JG, Vandermause MF, Shay DK et al (2012) Comparison of clinical features and outcomes of medically attended influenza A and influenza B in a defined population over four seasons: 2004-2005 through 2007-2008. Influenza Other Respir Viruses 6(1):37–43\nKorem M, Orenbuch-Harroch E, Ben-Chetrit E, Israel S, Cohen MJ, Sviri S, et al. (2019) Intensive Care Admissions and Associated Severity of Influenza B Versus A During Influenza B Vaccine-mismatched Seasons. Clin Infect Dis 30;69(6):1049–1052\nSurveillance of influenza-like illness in Israel. Weekly update report 2019. Available from: https:\u002F\u002Fwww.health.gov.il\u002FPublicationsFiles\u002FFlu2017_2018.pdf\nTran D, Vaudry W, Moore D, Bettinger JA, Halperin SA, Scheifele DW et al (2016) Hospitalization for influenza A versus B. Pediatrics 138(3)\nHinds AM, Bozat-Emre S, Van Caeseele P, Mahmud SM (2015) Comparison of the epidemiology of laboratory-confirmed influenza A and influenza B cases in Manitoba, Canada. BMC Public Health 15:35. https:\u002F\u002Fdoi.org\u002F10.1186\u002Fs12889-015-1351-z\nChaves SS, Aragon D, Bennett N, Cooper T, D’Mello T, Farley M et al (2013) Patients hospitalized with laboratory-confirmed influenza during the 2010-2011 influenza season: exploring disease severity by virus type and subtype. 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FK-037 inhibited 90 % ofEnterobacteriaceae isolates at ≤ 0.25 µg\u002Fml, with the exception ofEnterobacter aerogenes (MIC90 1 µg\u002Fml),Enterobacter cloacae andCitrobacter freundii (MIC90 8 µg\u002Fml). In cefotaxime-and ceftazidime-resistantKlebsiella pneumoniae strains producing SHV-2 and SHV-6 β-lactamases, the activity of FK-037, cefpirome and cefepime was similar (MIC range 0.25–32 µg\u002Fml). InEnterobacteriaceae strains hyperproducing chromosomally inducible β-lactamases, FK-037 (MIC90 range, 0.25–8 µg\u002Fml) was 8- to 16-fold more active than cefotaxime and ceftazidime but two- to eightfold less active than cefpirome and cefepime. FK-037 and cefpirome were twofold more active than ceftazidime and cefepime againstPseudomonas aeruginosa isolates, with MIC90 values of 16 µg\u002Fml. The activity of FK-037, cefpirome and cefepime was two- to eightfold lower in ceftazidime-resistant derepressedPseudomonas aeruginosa mutants. FK-037 (MIC range, 0.12–2 µg\u002Fml) and the other β-lactam agents tested were active against methicillin-susceptible staphylococci; however, only cefpirome and, particularly, FK-037 (MIC90 of 32 µg\u002Fml) displayed some activity against methicillin-resistant strains. In penicillin-susceptible,-intermediate and -resistantStreptococcus pneumoniae isolates, the MIC90s of FK-037 were 0.03, 0.5 and 1 µg\u002Fml, respectively. The corresponding values forStreptococcus viridans isolates were 0.12, 1 and 8 µg\u002Fml, respectively. In bothStreptococcus pneumoniae andStreptococcus viridans isolates, FK-037 displayed activity similar to that of cefotaxime and cefpirome and slightly higher than that of cefepime.",{"EN":2258},"Multicentre comparative study on the antibacterial activity of FK-037, a new parenteral cephalosporin",{"VOID":2260},"King A, Boothman C, Phillips I: Comparative in vitro activity of cefpirome and cefepime, two new cephalosporins. European Journal of Clinical Microbiology & Infectious Diseases 1990, 9: 677–685.\nJones RN, Pfaller MA, Allen SD, Gerlach EH, Fuchs PC, Aldridge KE: Antimicrobial activity of cefpirome. An update compared to five third-generation cephalosporins against nearly 6,000 recent clinical isolates from five medical centers. Diagnostic Microbiology and Infectious Disease 1991, 14: 361–364.\nThornsberry C, Brown SD, Yee YC, Bouchillon SK, Marler JK, Rich T: In vitro activity of cefepime and other antimicrobials: survey of European isolates. Journal of Antimicrobial Chemotherapy 1993, 32, Supplement B: 31–53.\nJones RN, Fuchs PC: Activity of cefepime (BMY 28142) and cefpirome (HR 810) against gram negative bacilli resistant to cefotaxime or ceftazidime. Journal of Antimicrobial Chemotherapy 1989, 33: 163–165.\nFung-Tomc J, Dougherty TJ, DeOrio FJ, Simich-Jacobson V, Kessler RE: Activity of cefepime against ceftazidime- and cefotaxime-resistant gram-negative bacteria and its relationship to β-lactamase levels. Antimicrobial Agents and Chemotherapy 1989, 33: 498–502.\nMine Y, Watanabe Y, Sakamoto H, Hatano K, Kuno K, Higashi Y, Kamimura T, Matsumoto Y, Tawara S, Matsumoto F: In vitro antibacterial activity of FK-037, a novel parenteral broad-cephalosporin. Journal of Antibiotics 1993, 46: 71–87.\nFu KP, Foleno BD, Lafredo SC, LoCoco JM, Isaacson DM: In vitro and in vivo antibacterial activities of FK-037, a novel parenteral broad-spectrum cephalosporin. Antimicrobial Agents and Chemotherapy 1993, 37: 301–307.\nNeu HC, Chin NX, Huang HB: In vitro activity and β-lactamase stability of FK-037, a parenteral cephalosporin. Antimicrobial Agents and Chemotherapy 1993, 37: 566–573.\nWashington JA, Jones RN, Gerlach EH, Murray PR, Allen SD, Knapp CC: Multicenter comparison of in vitro activities of FK-037, cefepime, ceftriaxone, ceftazidime, and cefuroxime. Antimicrobial Agents and Chemotherapy 1993, 37: 1696–1700.\nSanchez ML, Jones RN, and the United States Consortium for Antimicrobial and Surveillance Trials: Antimicrobial activity of FK-037 against class I β-lactamase producing species resistant to ceftazidime: a multi-laboratory clinical isolate sample. Journal of Antimicrobial Chemotherapy 1993, 32: 654–656.\nJones RN, Barrett MS, Erwin ME: In-vitro activity of FK-037, a new cephalosporin. Journal of Antimicrobial Chemotherapy 1994, 33: 137–144.\nNational Committee for Clinical Laboratory Standards: Methods for dilution antimicrobial susceptibility tests for bacteria that grow aerobically. Approved standard M7-A3. NCCLS, Villanova, PA, 1993.\nHancock REW, Bellido F: Factors involved in the enhanced efficacy against gram-negative bacteria of fourth generation cephalosporins. Journal of Antimicrobial Chemotherapy 1992, 29, Supplement A: 1–6.\nErhardt AF, Sanders CC: β-lactam resistance amongstEnterobacter species. Journal of Antimicrobial Chemotherapy 1993, 32, Supplement B: 1–11.\nChen HY, Livermore DM: Effects of β-lactamase inducibility and derepression on the activity of cefepime and cefpirome against gram-negative bacteria. Journal of Antimicrobial Chemotherapy 1993, 32: 651–652.\nSpangler SK, Jacobs MR, Applebaum PC: Susceptibility of 177 penicillin-susceptible and -resistant pneumococci to FK-037, cefpirome, cefepime, ceftriaxone, cefotaxime, ceftazidime, imipenem, biapenem, meropenem, and vancomycin. 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We present complement levels in Staphylococcus aureus bacteremia (SAB) and Gram-negative bacteremia (GNB) and describe observed associations of complement levels with clinical outcomes. Complement and cytokine levels were measured in serum samples from 20 hospitalized patients with SAB, 20 hospitalized patients with GNB, 10 non-infected hospitalized patients, and 10 community controls. C5a levels were significantly higher in patients with SAB as compared to patients with GNB. Low C4 and C3 levels were associated with septic shock and 30-day mortality in patients with GNB, and elevated C3 was associated with a desirable outcome defined as absence of (1) septic shock, (2) acute renal failure, and (3) death within 30 days of bacteremia. Low levels of C9 were associated with septic shock in patients with GNB but not SAB. Elevated IL-10 was associated with increased 30-day mortality in patients with SAB. Complement profiles differ in patients with SAB and those with GNB. Measurement of IL-10 in patients with SAB and of C4, C3, and C9 in patients with GNB may help to identify those at higher risk for poor outcomes.",{"EN":2438},"Complement levels in patients with bloodstream infection due to Staphylococcus aureus or Gram-negative bacteria",{"VOID":2440},"Pliakos EE, Andreatos N, Shehadeh F, Ziakas PD, Mylonakis E (2018) The cost-effectiveness of rapid diagnostic testing for the diagnosis of bloodstream infections with or without antimicrobial stewardship. Clin Microbiol Rev 31(3):e00095–17\nGoto M, Al-Hasan MN (2013) Overall burden of bloodstream infection and nosocomial bloodstream infection in North America and Europe. Clin Microbiol Infect 19:501–509\nvan Hal SJ, Jensen SO, Vaska VL, Espedido BA, Paterson DL, Gosbell IB (2012) Predictors of mortality in Staphylococcus aureus bacteremia. Clin Microbiol Rev 25:362–386\nAmmerlaan H, Seifert H, Harbarth S, Brun-Buisson C, Torres A, Antonelli M, Kluytmans J, Bonten M (2009) Adequacy of antimicrobial treatment and outcome of Staphylococcus aureus bacteremia in 9 Western European countries. Clin Infect Dis 49:997–1005\nAckerman AL, Parameshwar PS, Anger JT (2018) Diagnosis and treatment of patients with prostatic abscess in the post-antibiotic era. Int J Urol 25:103–110\nFlierl MA, Rittirsch D, Nadeau BA, Day DE, Zetoune FS, Sarma JV, Huber-Lang MS, Ward PA (2008) Functions of the complement components C3 and C5 during sepsis. FASEB J 22:3483–3490\nWard PA, Gao H (2009) Sepsis, complement and the dysregulated inflammatory response. J Cell Mol Med 13:4154–4160\nCharchaflieh J, Wei J, Labaze G, Hou YJ, Babarsh B, Stutz H, Lee H, Worah S, Zhang M (2012) The role of complement system in septic shock. Clin Dev Immunol 2012:407324\nChousterman BG, Swirski FK, Weber GF (2017) Cytokine storm and sepsis disease pathogenesis. Semin Immunopathol 39:517–528\nAnonymous (1992) American College of Chest Physicians\u002FSociety of Critical Care Medicine Consensus Conference: definitions for sepsis and organ failure and guidelines for the use of innovative therapies in sepsis. Crit Care Med 20:864–874\nKellum JA, Lameire N (2013) Diagnosis, evaluation, and management of acute kidney injury: a KDIGO summary (Part 1). Crit Care 17:204\nSouli M, Ruffin F, Choi SH, Park LP, Gao S, Lent NC, Sharma-Kuinkel BK, Thaden JT, Maskarinec SA, Wanda L, Hill-Rorie J, Warren B, Hansen B, Fowler VG (2019) Changing characteristics of Staphylococcus aureus bacteremia: results from a 21-year, prospective, Longitudinal Study. Clin Infect Dis. https:\u002F\u002Fdoi.org\u002F10.1093\u002Fcid\u002Fciz112\nHarris JA, Cobbs CG (1973) Persistent gram-negative bacteremia. Observations in twenty patients. Am J Surg 125:705–717\nCLSI (2010) Defining, establishing, and verifying reference intervals in the clinical laboratory; approved guideline—third edition. Clinical Lab Standards Institute, Wayne\nVarela JC, Tomlinson S (2015) Complement: an overview for the clinician. Hematol Oncol Clin North Am 29:409–427\nXu R, Lin F, Bao C, Wang FS (2017) Mechanism of C5a-induced immunologic derangement in sepsis. Cell Mol Immunol 14:792–793\nHuber-Lang M, Sarma VJ, Lu KT, McGuire SR, Padgaonkar VA, Guo RF, Younkin EM, Kunkel RG, Ding J, Erickson R, Curnutte JT, Ward PA (2001) Role of C5a in multiorgan failure during sepsis. J Immunol 166:1193–1199\nHack CE, Nuijens JH, Felt-Bersma RJ, Schreuder WO, Eerenberg-Belmer AJ, Paardekooper J, Bronsveld W, Thijs LG (1989) Elevated plasma levels of the anaphylatoxins C3a and C4a are associated with a fatal outcome in sepsis. Am J Med 86:20–26\nGroeneveld AB, Tacx AN, Bossink AW, van Mierlo GJ, Hack CE (2003) Circulating inflammatory mediators predict shock and mortality in febrile patients with microbial infection. Clin Immunol 106:106–115\nGuo RF, Ward PA (2005) Role of C5a in inflammatory responses. Annu Rev Immunol 23:821–852\nRooijakkers SH, Ruyken M, van Roon J, van Kessel KP, van Strijp JA, van Wamel WJ (2006) Early expression of SCIN and CHIPS drives instant immune evasion by Staphylococcus aureus. Cell Microbiol 8:1282–1293\nWard PA (2004) The dark side of C5a in sepsis. Nat Rev Immunol 4:133–142\nvon Kockritz-Blickwede M, Konrad S, Foster S, Gessner JE, Medina E (2010) Protective role of complement C5a in an experimental model of Staphylococcus aureus bacteremia. J Innate Immun 2:87–92\nGeorgoutsou-Spyridonos M, Ricklin D, Pratsinis H, Perivolioti E, Pirmettis I, Garcia BL, Geisbrecht BV, Foukas PG, Lambris JD, Mastellos DC, Sfyroera G (2015) Attenuation of Staphylococcus aureus-induced bacteremia by human mini-antibodies targeting the complement inhibitory protein Efb. J Immunol 195:3946–3958\nCzermak BJ, Sarma V, Pierson CL, Warner RL, Huber-Lang M, Bless NM, Schmal H, Friedl HP, Ward PA (1999) Protective effects of C5a blockade in sepsis. Nat Med 5:788–792\nRen J, Zhao Y, Yuan Y, Han G, Li W, Huang Q, Tong Z, Li J (2012) Complement depletion deteriorates clinical outcomes of severe abdominal sepsis: a conspirator of infection and coagulopathy in crime? PLoS One 7:e47095\nYounger JG, Bracho DO, Chung-Esaki HM, Lee M, Rana GK, Sen A, Jones AE (2010) Complement activation in emergency department patients with severe sepsis. Acad Emerg Med 17:353–359\nModi S, Rashid M, Malik A, Shahid M (2014) Study of complement activation, C3 and interleukin-6 levels in burn patients and their role as prognostic markers. Indian J Med Microbiol 32:137–142\nFischer MB, Prodeus AP, Nicholson-Weller A, Ma M, Murrow J, Reid RR, Warren HB, Lage AL, Moore FD Jr, Rosen FS, Carroll MC (1997) Increased susceptibility to endotoxin shock in complement C3- and C4-deficient mice is corrected by C1 inhibitor replacement. J Immunol 159:976–982\nLassiter HA, Wilson JL, Feldhoff RC, Hoffpauir JM, Klueber KM (1994) Supplemental complement component C9 enhances the capacity of neonatal serum to kill multiple isolates of pathogenic Escherichia coli. Pediatr Res 35:389–396\nCoonrod JD, Rylko-Bauer B (1977) Complement levels in pneumococcal pneumonia. Infect Immun 18:14–22\nGaya da Costa M, Poppelaars F, van Kooten C, Mollnes TE, Tedesco F, Würzner R, Trouw LA, Truedsson L, Daha MR, Roos A, Seelen MA (2018) Age and sex-associated changes of complement activity and complement levels in a healthy Caucasian population. Front Immunol 9:2664\nMcCullough JW, Renner B, Thurman JM (2013) The role of the complement system in acute kidney injury. Semin Nephrol 33:543–556\nSchuerholz T, Leuwer M, Cobas-Meyer M, Vangerow B, Kube F, Kirschfink M, Marx G (2005) Terminal complement complex in septic shock with capillary leakage: marker of complement activation? Eur J Anaesthesiol 22:541–547\nFrodermann V, Chau TA, Sayedyahossein S, Toth JM, Heinrichs DE, Madrenas J (2011) A modulatory interleukin-10 response to staphylococcal peptidoglycan prevents Th1\u002FTh17 adaptive immunity to Staphylococcus aureus. J Infect Dis 204:253–262\nRose WE, Eickhoff JC, Shukla SK, Pantrangi M, Rooijakkers S, Cosgrove SE, Nizet V, Sakoulas G (2012) Elevated serum interleukin-10 at time of hospital admission is predictive of mortality in patients with Staphylococcus aureus bacteremia. J Infect Dis 206:1604–1611\nChau TA, McCully ML, Brintnell W, An G, Kasper KJ, Vines ED, Kubes P, Haeryfar SM, McCormick JK, Cairns E, Heinrichs DE, Madrenas J (2009) Toll-like receptor 2 ligands on the staphylococcal cell wall downregulate superantigen-induced T cell activation and prevent toxic shock syndrome. Nat Med 15:641–648\nGabay C, Kushner I (1999) Acute-phase proteins and other systemic responses to inflammation. N Engl J Med 340:448–454\nDaef EA, Elsherbiny NM, Agban MN, Riad KF, Mohammed LF (2018) Bloodstream infections in febrile neutropenic pediatric Cancer patients: microbiological and sepsis biomarkers insight. Egypt J Immunol 25:21–34\nMiedema KG, Vermont CL, Ball LM, de Bont ES, Kamps WA, van Tol MJ, Jol-van der Zijde CM, Tissing WJ (2014) The diagnostic value of interleukin-8 for the detection of bacteremia in pediatric hematopoietic stem cell recipients with febrile neutropenia. Transplantation 98:e80–e81\nSpooner CE, Markowitz NP, Saravolatz LD (1992) The role of tumor necrosis factor in sepsis. Clin Immunol Immunopathol 62:S11–S17\nWiseman AC (2016) Immunosuppressive medications. 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