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Journal of Medicine and Pharmacy","Tạp chí Y Dược học Cần Thơ",{"EN":571,"VI":572},"\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":574},"wcQ1uqwAAAAJ","2023-05-30T08:17:21.868+00:00",[],[578],{"id":579,"createTime":20,"updateTime":20,"relativeEntities":580,"slug":20,"properties":581,"entityType":20,"verifyStatus":20,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":20,"url":591,"parentIds":592,"statistic":20},"6413896b-eca9-442b-a73f-182a58a0ce40",[],{"title":582,"address":585,"country":588,"abbreviation":589},{"EN":583,"VI":584},"Can Tho University of Medicine and Pharmacy","Trường Đại học Y Dược Cần Thơ",{"EN":586,"VI":587},"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":118},{"VOID":590},"ctump","http:\u002F\u002Fwww.ctump.edu.vn\u002F",[],[],"https:\u002F\u002Ftapchi.ctump.edu.vn\u002Findex.php\u002Fctump",{"impactFactor":21,"impactFactorByYear":596,"i10Index":21,"i10IndexLast5Year":21,"totalPublication":598,"totalPublicationByYear":599,"totalCitation":604,"totalCitationByYear":605,"totalCitationPerPublication":204,"totalCitationPerPublicationByYear":607,"hindexLast5Year":144,"hindex":144},{"2022":597,"2023":81,"2024":202},0.01,1556,{"2020":146,"2021":600,"2022":601,"2023":602,"2024":603,"2025":215},57,306,801,358,161,{"2021":235,"2022":368,"2023":606},99,{"2021":608,"2022":82,"2023":85},0.23,{"impactFactor":20,"impactFactorByYear":20,"i10Index":216,"i10IndexLast5Year":216,"totalPublication":610,"totalPublicationByYear":611,"totalCitation":610,"totalCitationByYear":612,"totalCitationPerPublication":104,"totalCitationPerPublicationByYear":615,"hindexLast5Year":105,"hindex":105},476,{"0":293,"2019":216,"2021":229,"2022":543,"2023":535,"2024":441,"2025":105,"2026":86},{"2021":141,"2022":216,"2023":249,"2024":613,"2025":444,"2026":614},136,83,{"2021":201,"2022":597,"2023":616,"2024":220,"2025":617,"2026":618},0.62,25.43,13.83,{"id":620,"createTime":621,"updateTime":466,"relativeEntities":622,"slug":623,"properties":624,"entityType":18,"verifyStatus":128,"verifyTime":20,"verifyNote":20,"languages":636,"translateLanguages":20,"viewCount":89,"subjectFields":637,"manageAffiliations":638,"indexDatabases":639,"url":640,"thumbnailPath":641,"statistic":642,"gsStatistic":678,"type":152,"analyzePriority":20},"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":625,"issn":626,"title":628,"introduce":631,"gsId":634},{"VOID":118},{"VOID":627},"25252445",{"EN":629,"VI":630},"VNU Journal of Foreign Studies","Tạp chí Nghiên cứu nước ngoài",{"EN":632,"VI":633},"{\"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. Since then, the journal has grown in quality, size and scope and now comprises a dozen of serials spanning academic research. 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Although, the main text structure may vary based on the review subtopics, the articles should be formatted according to suitable Templates as research articles.\"},{\"attributes\":{\"align\":\"justify\"},\"insert\":\"\\n\"},{\"insert\":\"\\n\"}]}","{\"ops\":[{\"insert\":\"Tạp chí Khoa học Trường ĐHSP Hà Nội 2 nhằm mục đích cung cấp một nền tảng liên ngành của sự phổ biến những tiến bộ của khoa học và công nghệ. Tạp chí xuất bản các bài báo gốc có giá trị khoa học hoặc công nghệ trong tất cả các lĩnh vực khoa học tự nhiên, xã hội hoặc giáo dục.\\n\"},{\"attributes\":{\"bold\":true},\"insert\":\"Chuyên san Khoa học tự nhiên và công nghệ:\"},{\"insert\":\" Là các bài báo mô tả những phát hiện có giá trị trong vật lý, toán học, hóa học, sinh học; giải quyết các vấn đề kỹ thuật hoặc công nghệ.\"},{\"attributes\":{\"list\":\"bullet\"},\"insert\":\"\\n\"},{\"attributes\":{\"bold\":true},\"insert\":\"Chuyên san Khoa học Xã hội và Nhân văn:\"},{\"insert\":\" là các bài báo xuất bản chất lượng cao trong các lĩnh vực khác nhau của khoa học xã hội và nghiên cứu phát triển con người.\"},{\"attributes\":{\"list\":\"bullet\"},\"insert\":\"\\n\"},{\"attributes\":{\"bold\":true},\"insert\":\"Chuyên san Khoa học giáo dục:\"},{\"insert\":\" là các bài báo xuất bản trong lĩnh vực khoa học giáo dục và các ứng dụng của tiến bộ vào giáo dục để cải thiện và nâng cao giáo dục khoa học ở tất cả các cấp.\"},{\"attributes\":{\"list\":\"bullet\"},\"insert\":\"\\n\"},{\"insert\":\"Tạp chí trường ĐHSP Hà Nội 2 xuất bản được phản biện kín, xét duyệt bởi ít nhất 02 chuyên gia, và được đánh giá, chọn lựa từ ban biên tập và Tổng biên tập.\\n\"},{\"attributes\":{\"bold\":true},\"insert\":\"Các loại bài báo\"},{\"insert\":\":\\nBài báo nghiên cứu:\"},{\"attributes\":{\"list\":\"ordered\"},\"insert\":\"\\n\"},{\"insert\":\"Báo cáo học thuật về nghiên cứu ban đầu chưa từng được xuất bản ở bất kỳ nơi nào, hay bằng bất kỳ ngôn ngữ nào khác. Bản thảo thích hợp, nên chứa các phần sau theo thứ tự: Tiêu đề, Tác giả, Liên kết tác giả, Địa chỉ email của tác giả tương ứng, Tóm tắt, Từ khóa, Danh pháp (nếu có), Giới thiệu, Thử nghiệm, Lý thuyết, Kết quả và thảo luận, Kết luận, Xung đột quan tâm, Lời cảm ơn (nếu có), Tài liệu tham khảo, Phụ lục (nếu có). Bản xuất bản trước phải được định dạng theo Mẫu (phiên bản MS-Word).\\n2. Bài báo tổng quan:\\nNgoài các bài phê bình được mời, các bài phê bình tài liệu, bài phê bình có hệ thống và bài phê bình sẽ được chấp nhận để xem xét. Bản thảo cần được soạn thảo và sắp xếp theo trình tự yêu cầu: Tên sách, Tên tác giả, Liên kết, Địa chỉ email, Tóm tắt, Từ khóa, Nội dung chính, Kết luận, Xung đột lợi ích, Lời cảm ơn (nếu có), Tài liệu tham khảo. Mặc dù, cấu trúc văn bản chính có thể thay đổi dựa trên các chủ đề phụ của bài đánh giá, các bài báo nên được định dạng theo các Mẫu phù hợp như các bài báo nghiên cứu.\\n\"}]}",{"VOID":809},"YPoBvsIAAAAJ",[],[],[],"https:\u002F\u002Fsj.hpu2.edu.vn\u002Findex.php\u002Fjournal","\u002Fapi\u002Fpublic\u002Ffile\u002Fpublisher\u002F954132b5-ca74-461c-b819-45ad6e49a404\u002F2790ef1d0a7d7a40a504c2fc1647f670.jpg",{"impactFactor":21,"impactFactorByYear":816,"i10Index":21,"i10IndexLast5Year":21,"totalPublication":416,"totalPublicationByYear":818,"totalCitation":225,"totalCitationByYear":819,"totalCitationPerPublication":608,"totalCitationPerPublicationByYear":820,"hindexLast5Year":216,"hindex":216},{"2024":817},0.17,{"2022":227,"2023":366,"2024":231},{"2022":441,"2023":219,"2024":216},{"2022":257,"2023":312,"2024":253},{"impactFactor":20,"impactFactorByYear":20,"i10Index":144,"i10IndexLast5Year":144,"totalPublication":417,"totalPublicationByYear":822,"totalCitation":242,"totalCitationByYear":823,"totalCitationPerPublication":824,"totalCitationPerPublicationByYear":825,"hindexLast5Year":145,"hindex":145},{"0":216,"2022":225,"2023":227,"2024":166,"2025":234},{"2023":145,"2024":227,"2025":289,"2026":366},1.22,{"2023":83,"2024":425,"2025":826},4.56,{"id":828,"createTime":829,"updateTime":830,"relativeEntities":831,"slug":832,"properties":833,"entityType":18,"verifyStatus":128,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":166,"subjectFields":845,"manageAffiliations":846,"indexDatabases":854,"url":894,"thumbnailPath":20,"statistic":895,"gsStatistic":927,"type":152,"analyzePriority":20},"21ccdb34-414d-420f-8a60-a592a2fa848e","2023-05-29T10:42:53.358+00:00","2026-08-27T01:57:29.560+00:00",[],"Vietnam-Journal-of-Earth-Sciences",{"country":834,"eissn":835,"issn":837,"title":839,"introduce":841,"gsId":843},{"VOID":118},{"VOID":836},"26159783",{"VOID":838},"08667187",{"EN":840},"Vietnam Journal of Earth Sciences",{"EN":842},"Science of the Earth, formerly Vietnam Journal of Earth Sciences, is a peer-reviewed journal to publish high-quality articles on the entire range of earth sciences and the environment, focused on the Asia Pacific region and their correlations and connections to the globe. The journal publishes fundamental and applied research in earth sciences and the environment, including geology, geophysics, geography, soil science, hydrology, meteorology, oceanography, petroleum, geohazards, environmental sciences, environmental engineering, sustainable development, geoinformatics, geodesy, GIS, and remote sensing.",{"VOID":844},"5htfr3YAAAAJ",[],[847],{"id":170,"createTime":20,"updateTime":20,"relativeEntities":848,"slug":20,"properties":849,"entityType":20,"verifyStatus":20,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":20,"url":179,"parentIds":853,"statistic":20},[],{"title":850,"country":851,"abbreviation":852},{"EN":174,"VI":175},{"VOID":118},{"VOID":178},[],[855,866,878],{"id":856,"indexDatabase":857,"url":862,"indexYears":863,"academicFieldIds":864,"indexDatabaseRanking":20},"dadb15a8-ee22-41c2-a287-49e969d9a998",{"id":185,"createTime":20,"updateTime":20,"relativeEntities":858,"label":859,"description":860,"key":191,"publicationTags":861,"standard":20},[],{"EN":188,"VI":188},{"EN":190,"VI":190},[193],"https:\u002F\u002Fasean-cites.org\u002Fjournal_info?jid=10629","2016-2022",[865],"e04f14cf-280b-4aa8-b711-b77ddd79cbaf",{"id":867,"indexDatabase":868,"url":873,"indexYears":874,"academicFieldIds":875,"indexDatabaseRanking":877},"6ace2085-a177-4a27-b309-8813b832111e",{"id":48,"createTime":20,"updateTime":20,"relativeEntities":869,"label":870,"description":871,"key":54,"publicationTags":872,"standard":20},[],{"EN":51,"VI":51},{"EN":51,"VI":53},[56],"https:\u002F\u002Fwww.scopus.com\u002Fsourceid\u002F21101039869","2018-2024",[876],"1689391c-5702-4349-aaa7-d720ee4321fc","NONE",{"id":879,"indexDatabase":880,"url":891,"indexYears":20,"academicFieldIds":892,"indexDatabaseRanking":20},"06f278ee-37b9-41eb-a9b0-3d2d77fa502b",{"id":881,"createTime":20,"updateTime":20,"relativeEntities":882,"label":883,"description":885,"key":888,"publicationTags":889,"standard":20},"88bab0f7-443b-476c-a72a-7fa5222da393",[],{"EN":884,"VI":884},"ISI\u002FESCI  - 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This mechanism is named “developmental phenotypic plasticity”. Experimental evidences from rodents show that early experiences influence long-term development of behavioral, neuroendocrine and cognitive functions. While some neonatal conditions lead to positive outcomes, offspring might also display neurological dysfunctions in adulthood in case of adverse conditions during the early development. Different factors have been suggested to mediate the effects of neonatal conditions on offspring development but their exact contribution as well as their interaction still needs to be clarified. Studies based on rodents have been developed to model the long-term effects of early environmental conditions on the developing brain. These studies highlight importance of maternal behavior in mediating the effects of early environmental conditions on the offspring. However, other studies suggest that aside from the level of maternal care, other factors (gender, neonatal glucocorticoid levels) contribute to the adjustment of offspring phenotype to early environmental cues. Altogether, rodents-based evidence suggests that developmental plasticity is a very complex phenomenon mediated by multiple factors that interact one to each other. Ultimately, the goal is to understand how early life events can lead to advantageous phenotype in adult life, or, on the contrary, can predispose individuals to psychopathologies such as depression or anxiety.",{"EN":954},"Rodent models of early environment effects on offspring development and susceptibility to neurological diseases in adulthood",{"VOID":956},"Tollrian R., Predator-induced morphological defenses — costs, life history shifts, and maternal effects in Daphnia pulex, Ecology, 1995, 76, 1691–1705\nAgrawal A. 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G., Sexually dimorphic effects of maternal separation stress on corticotrophinreleasing factor and vasopressin systems in the adult rat brain, Int. J. Dev. Neurosci., 2008, 26, 259–268\nGross C. M., Flubacher A., Tinnes S., Heyer A., Scheller M., Herpfer I., et al., Early life stress stimulated hippocampal reelin gene expression in a sex-specific manner: evidence for corticosterone-mediated action, Hippocampus, 2010, 22, 409–420\nHeim C., Nemeroff C. B., The role of childhood trauma in the neurobiology of mood and anxiety disorders: preclinical and clinical studies, Biol. Psychiatry, 2001, 49, 1023–1039\nHarlow H. F., Dodsworth R. O., Harlow M. K., Total social isolation in monkeys, Proc. Natl. Acad. Sci. USA, 1965, 54, 90–97\nHarlow H. F., Harlow M. K., Suomi S. J., From thought to therapy: lessons from a primate laboratory, Am. Sci., 1971, 59, 538–549\nDaniels W. M. U., Pietersen C. Y., Carsten M. E., Stein D. J., Maternal separation in rats leads to anxiety-like behavior and an ACTH blunted response and altered neurotransmitter levels in response to a subsequent stressor, Metabol. Brain. Dis., 2004, 19, 3–14\nMillstein R. A., Holmes A., Effects of repeated maternal separation on anxiety- and depression-related phenotypes in different mouse strains, Neurosci. Biobehav. Rev., 2007, 31, 3–17",{"VOID":958},"10.2478\u002Fs13380-012-0034-9","PUBLICATION","https:\u002F\u002Fwww.degruyter.com\u002Fdocument\u002Fdoi\u002F10.2478\u002Fs13380-012-0034-9\u002Fhtml",[962],{"id":963,"sortIndex":21,"researcher":20,"roles":964,"affiliations":966,"properties":975,"displayName":977,"givenName":20,"familyName":20},"2bc25e4c-5610-4fe6-b104-a59405e15e90",[965],"AUTHOR",[967],{"id":968,"sortIndex":21,"affiliation":969,"properties":20},"a09bc662-338a-4648-bc05-5b987a56c833",{"id":968,"createTime":20,"updateTime":20,"relativeEntities":970,"slug":20,"properties":971,"entityType":20,"verifyStatus":20,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":20,"url":20,"parentIds":974,"statistic":20},[],{"title":972},{"VI":973},"Behavioral and Functional Neuroscience Laboratory; School of Medicine, Stanford University, Palo Alto, USA",[],{"title":976},{"VI":977},"Laurence Coutellier","ARTICLE",{"url":960,"publisher":980,"properties":1022},{"id":6,"createTime":7,"updateTime":8,"relativeEntities":981,"slug":10,"properties":982,"entityType":18,"verifyStatus":19,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":21,"subjectFields":986,"manageAffiliations":991,"indexDatabases":1002,"url":20,"thumbnailPath":20,"statistic":1017,"gsStatistic":20,"type":20,"analyzePriority":20},[],{"issn":983,"title":984,"eissn":985},{"VOID":13},{"EN":15},{"VOID":17},[987],{"id":24,"createTime":20,"updateTime":20,"relativeEntities":988,"label":989,"description":990,"parentId":20,"standard":20,"scholarHubFieldId":20},[],{"EN":27},{},[992,997],{"id":31,"createTime":20,"updateTime":20,"relativeEntities":993,"slug":20,"properties":994,"entityType":20,"verifyStatus":20,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":20,"url":20,"parentIds":996,"statistic":20},[],{"title":995},{"EN":35},[],{"id":38,"createTime":20,"updateTime":20,"relativeEntities":998,"slug":20,"properties":999,"entityType":20,"verifyStatus":20,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":20,"url":20,"parentIds":1001,"statistic":20},[],{"title":1000},{"EN":42},[],[1003,1010],{"id":46,"indexDatabase":1004,"url":57,"indexYears":58,"academicFieldIds":1009,"indexDatabaseRanking":61},{"id":48,"createTime":20,"updateTime":20,"relativeEntities":1005,"label":1006,"description":1007,"key":54,"publicationTags":1008,"standard":20},[],{"EN":51,"VI":51},{"EN":51,"VI":53},[56],[60],{"id":63,"indexDatabase":1011,"url":76,"indexYears":20,"academicFieldIds":1016,"indexDatabaseRanking":20},{"id":65,"createTime":20,"updateTime":20,"relativeEntities":1012,"label":1013,"description":1014,"key":72,"publicationTags":1015,"standard":20},[],{"EN":68,"VI":68},{"EN":70,"VI":71},[74,75],[78],{"impactFactor":21,"impactFactorByYear":1018,"i10Index":86,"i10IndexLast5Year":21,"totalPublication":87,"totalPublicationByYear":1019,"totalCitation":93,"totalCitationByYear":1020,"totalCitationPerPublication":98,"totalCitationPerPublicationByYear":1021,"hindexLast5Year":105,"hindex":105},{"2012":81,"2013":82,"2014":83,"2015":84,"2016":85},{"2010":89,"2011":90,"2012":90,"2013":91,"2014":92},{"2010":92,"2011":95,"2012":96,"2013":97,"2014":92},{"2010":100,"2011":101,"2012":102,"2013":103,"2014":104},{"pages":1023,"volume":1025},{"VOID":1024},"258-262",{"VOID":1026},"3","2012-08-28",2012,[61,74],false,{"id":1032,"createTime":1033,"updateTime":1033,"relativeEntities":1034,"slug":20,"properties":1035,"entityType":959,"verifyStatus":19,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":21,"primaryUrl":1044,"fullTextUrl":20,"authors":1045,"publicationType":978,"publisherRelationship":1076,"citationCount":20,"citationInfo":20,"publishDate":1123,"publishYear":1028,"citationAnalyzeStatus":19,"lastCitationAnalyze":20,"indexDatabases":1124,"openAccess":20,"references":20,"isForceReanalyzing":1030},"0bd1a6e3-3529-4975-bd6f-b1677185fc08","2024-02-06T18:36:02.948+00:00",[],{"abstract":1036,"title":1038,"references":1040,"doi":1042},{"EN":1037},"Lithium is one of the most widely used drugs in neuropsychopharmacology. Preclinical scientists have made several advances in ascertaining the molecular mechanisms of action of this cation; such as its ability to stabilize monoamine levels, to interact with second messengers, and its neuroprotective effects, possibly over suicidal behaviors. Nevertheless, there remains a gap of knowledge between the pharmacological advances and the number of reliable clinical trials, creating a lack of evidence-based medicine to support medical prescriptions. In this review we examine lithium’s molecular mechanisms of action and evaluate their relevance in clinical applications.",{"EN":1039},"Lithium: Molecular interactions, clinical actions",{"VOID":1041},"Machado-Vieira R., Manji H. K., Zarate C.A. Jr., The role of lithium in the treatment of bipolar disorder: convergent evidence for neurotrophic effects as a unifying hypothesis, Bipolar Disord., 2009, 11(Suppl. 2), 92–109\nGrof P., Müller-Oerlinghausen B., A critical appraisal of lithium’s efficacy and effectiveness: the last 60 years, Bipolar Disord., 2009, 11(Suppl. 2), 10–19\nFiekers J. F., The contributions of plasma membrane Na+-Ca2+-exchange and the Ca2+-ATPase to the regulation of cytosolic calcium ([Ca2+]i) in a clonal pituitary cell line (AtT-20) of mouse corticotropes, Life Sci., 2001, 70, 681–698\nShaw D. M., Mineral metabolism, mania, and melancholia, Br. Med. J., 1966, 2, 262–267\nWood A. J., Smith C. E., Clarke E. E., Cowen P. J., Aronson J. K., Grahame-Smith D. G., Altered in vivo adaptive responses of lymphocyte Na+, K+-ATPase in patients with manic-depressive psychosis, J. Affect. Disord., 1991, 21, 199–206\nEl-Mallakh R. S., Ion homeostasis and the mechanism of action of lithium, Clin. Neurosci. Res., 2004, 4, 227–231\nSilva H., Litio y Psiquiatría: Uso Clínico, Mitos y Realidades, Santiago, Chile, Ed. Mediterráneo, 2011\nEl-Mallakh R. S., Lithium actions and mechanisms, Washington DC, American Psychiatric Association, 1996\nLenox R. H., Frazer A., Mechanism of action of antidepressants and mood stabilizers, In: Davis D. L., Charney D., Coyle J. T. (eds.), Neuropsychopharmacology: the fifth generation of progress, Nashville, American College of Neuropharmacology, 2002, 1139–1163\nDubovsky S. L., Murphy J., Thomas M., Rademacher J., Abnormal intracellular calcium ion concentrations in platelets and lymphocytes of bipolar patients, Am. J. Psychiatry, 1992, 149, 118–120\nYoon I. S., Li P. P., Siu K. P., Kennedy J. L., Macciardi F., Cooke R.G., et al., Altered TRPC7 gene expression in bipolar-I disorder, Biol. Psychiatry, 2001, 50, 620–626\nDubovsky S. L., Christiano J., Daniell L. C., Franks R. D., Murphy J., Adler L., et al., Increased platelet intracellular calcium concentrations in patients with bipolar affective disorders, Arch. Gen. Psychiatry, 1989, 46, 632–638\nEl-Mallakh R. S., Wyatt R. J., The Na,K-ATPase hypothesis for bipolar illness, Biol. Psychiatry, 1995, 37, 235–244\nEl-Mallakh R. S., Li R., Is the Na(+),K(+)-ATPase the link between phosphoinositide metabolism and bipolar disorder?, J. Neuropsychiatry Clin. Neurosci., 1993, 5, 361–368\nSourial-Bassillious N., Rydelius P. A., Aperia A., Aizman O., Glutamatemediated calcium signaling: a potential target for lithium action, Neuroscience, 2009, 161, 1126–1134\nShaw D. M., Mineral metabolism, mania, and melancholia, Br. Med. J., 1966, 2, 262–267\nKabakov A. Y., Karkanias N.B., Lenox R.H., Papke R. L., Synapse-specific accumulation of lithium in intracellular microdomains: a model for uncoupling coincidence detection in the brain, Synapse, 1998, 28, 271–279\nHuang X., Lei Z., El-Mallakh R. S., Lithium normalizes elevated intracellular sodium, Bipolar Disord., 2007, 9, 298–300\nBerridge M. J., Downes C. P., Hanley M. R., Neural and developmental actions of lithium: a unifying hypothesis, Cell, 1989, 59, 411–419\nGould T. D., Quiroz J. A., Singh J., Zarate C. A., Manji H. K., Emerging experimental therapeutics for bipolar disorder: insights from the molecular and cellular actions of current mood stabilizers, Mol. Psychiatry, 2004, 9, 734–755\nWilliams R. S., Cheng L., Mudge A. W., Harwood A. J., A common mechanism of action for three mood-stabilizing drugs, Nature, 2002, 417, 292–295\nBeurel E., Michalek S. M., Jope R. S., Innate and adaptive immune responses regulated by glycogen synthase kinase-3 (GSK3), Trends Immunol., 2010, 31, 24–31\nHøyer-Hansen M., Bastholm L., Szyniarowski P., Campanella M., Szabadkai G., Farkas T., et al., Control of macroautophagy by calcium, calmodulin-dependent kinase kinase-beta, and Bcl-2, Mol. Cell., 2007, 25, 193–205\nPigino G., Morfini G., Pelsman A., Mattson M. P., Brady S. T., Busciglio J., Alzheimer’s presenilin 1 mutations impair kinesin-based axonal transport, J. Neurosci., 2003, 23, 4499–4508\nSang H., Lu Z., Li Y., Ru B., Wang W., Chen J., Phosphorylation of tau by glycogen synthase kinase 3beta in intact mammalian cells influences the stability of microtubules, Neurosci. Lett., 2001, 312, 141–144\nRyves W. J., Harwood A. J., Lithium inhibits glycogen synthase kinase-3 by competition for magnesium, Biochem. Biophys. Res. Commun., 2001, 280, 720–725\nJope R. S., Lithium and GSK-3: one inhibitor, two inhibitory actions, multiple outcomes, Trends Pharmacol. Sci., 2003, 24, 441–443\nMoon R. T., Kohn A. D., De Ferrari G. V., Kaykas A., WNT and b-catenin signalling: diseases and therapies, Nat. Rev. Genet., 2004, 5, 691–701\nZhang Z., Hartmann H., Do V. M., Abramowski D., Sturchler-Pierrat C., Staufenbiel M., et al., Destabilization of b-catenin by mutations in presenilin-1 potentiates neuronal apoptosis, Nature, 1998, 395, 698–702\nToledo E. M., Inestrosa N. C., Activation of Wnt signaling by lithium and rosiglitazone reduced spatial memory impairment and neurodegeneration in brains of an APPswe\u002FPSEN1DeltaE9 mouse model of Alzheimer’s disease, Mol. Psychiatry, 2010, 15, 272–285\nSchechter R., Yen S. H., Terry R. D., Fibrous astrocytes in senile dementia of the Alzheimer type, J. Neuropathol. Exp. Neurol., 1981, 40, 95–101\nDuman R. S., Nestler E. J., Signal transduction pathways for catecholamine receptors, In: Bloom F. E., Kupfer D. J. (eds.), Psychopharmacology: the fourth generation of progress, New York: Raven Press, 1995, 303–320\nDuman R. S., Heninger G. R., Nestler E. J., A molecular and cellular theory of depression, Arch. Gen. Psychiatry, 1997, 54, 597–606\nFields A., Li P. P., Kish S. J., Warsh J. J., Increased cyclic AMP-dependent protein kinase activity in post-mortem brain from patients with bipolar affective disorder, J. Neurochem., 1999, 73, 1704–1710\nHashimoto R., Hough C., Nakazawa T., Yamamoto T., Chuang D.-M., Lithium protection against glutamate excitotoxicity in rat cerebral cortical neurons: involvement of NMDA receptor inhibition possibly by decreasing NR2B tyrosine phosphorylation, J. Neurochem., 2002, 80, 589–597\nNonaka S., Chuang D.-M., Neuroprotective effects of chronic lithium on focal cerebral ischemia in rats, Neuroreport, 1998, 9, 2081–2084\nRen M., Chen R.-W., Senatorov V. V., Chuang D.-M., Acute lithium protects against brain injury in an ischemia\u002Freperfusion model of rats, Society for Neuroscience Annual Meeting Abstract, 2000, 285.17\nLipton P., Ischemic cell death in brain neurons, Physiol. Rev., 1999, 79, 1431–1568\nWei H., Qin Z.-H., Senatorov V. V., Wei W., Wang Y., Qian Y., et al., Lithium suppresses excitotoxicity-induced striatal lesions in rats, an animal model of Huntington’s disease, Neuroscience, 2001, 106, 603–612\nChuang D. M., Chen R. W., Chalecka-Franaszek E., Ren M., Hashimoto R., Senatorov V., et al., Neuroprotective effects of lithium in cultured cells and animal models of diseases, Bipolar Disord., 2002, 4, 129–136\nBeaulieu J. M., A role for Akt and glycogen synthase kinase-3 as integrators of dopamine and serotonin neurotransmission in mental health, J. Psychiatry Neurosci., 2012, 37, 7–16\nPrice L. H., Charney D. S., Delgado P. L., Heninger G. R., Lithium and serotonin function: implications for the serotonin hypothesis of depression, Psychopharmacology (Berl), 1990, 100, 3–12\nJones R. M., Arlidge J., Gillham R., Reagu S., van den Bree M., Taylor P. J., Efficacy of mood stabilisers in the treatment of impulsive or repetitive aggression: systematic review and meta-analysis, Br. J. Psychiatry, 2011, 198, 93–98\nSheard M. H., Marini J. L., Bridges C. I., Wagner E., The effect of lithium on impulsive aggressive behavior in man, Am. J. Psychiatry, 1976, 133, 1409–1413\nLenox R. H., Hahn C. G., Overview of the mechanism of action of lithium in the brain: fifty-year update, J. Clin. Psychiatry, 2000, 61(Suppl. 9), 5–15\nTakahashi A., Quadros I. M., de Almeida R.M., Miczek K. A., Behavioral and pharmacogenetics of aggressive behavior, Curr. Top. Behav. Neurosci., 2012 (epub ahead of print)\nLeucht S., Kissling W., McGrath J., Lithium for schizophrenia, Cochrane Database Syst. Rev., 2007, CD003834\nCipriani A., Smith K., Burgess S., Carney S., Goodwin G., Geddes J., Lithium versus antidepressants in the long-term treatment of unipolar affective disorder, Cochrane Database Syst. Rev., 2006, CD003492\nChiu C. T., Chuang D. M., Molecular actions and therapeutic potential of lithium in preclinical and clinical studies of CNS disorders, Pharmacol. Ther., 2010, 128, 281–304\nZhou R., Yuan P., Wang Y., Hunsberger J. G., Elkahloun A., Wei Y., Damschroder-Williams P., Du J., Chen G., Manji H. K., Evidence for selective microRNAs and their effectors as common long-term targets for the actions of mood stabilizers, Neuropsychopharmacology, 2009, 34, 1395–1405\nRyves W. J., Harwood A. J., Lithium inhibits glycogen synthase kinase-3 by competition for magnesium, Biochem. Biophys. Res. Commun., 2001, 280, 720–725\nSerretti A., Lilli R., Mandelli L., Lorenzi C., Smeraldi E., Serotonin transporter gene associated with lithium prophylaxis in mood disorders, Pharmacogenomics J., 2001, 1, 71–77\nJensen J. B., Mørk A., Altered protein phosphorylation in the rat brain following chronic lithium and carbamazepine treatments, Eur. Neuropharmacol., 1997, 7, 173–179\nLin J. Y., Chung S. Y., Lin M. C., Cheng F.C., Effects of magnesium sulfate on energy metabolites and glutamate in the cortex during focal cerebral ischemia and reperfusion in the gerbil monitored by a dual-probe microdialysis technique, Life Sci., 2002, 71, 803–811\nMuir K. W., Magnesium in stroke treatment, Postgrad. Med. J., 2002, 78, 641–645\nHuang C. Y., Liou Y. F., Chung S. Y., Lin W. Y., Jong G. P., Kuo C. H., et al., Role of ERK signaling in the neuroprotective efficacy of magnesium sulfate treatment during focal cerebral ischemia in the gerbil cortex, Chin. J. Physiol., 2010, 53, 299–309",{"VOID":1043},"10.2478\u002Fs13380-012-0011-3","https:\u002F\u002Fwww.degruyter.com\u002Fdocument\u002Fdoi\u002F10.2478\u002Fs13380-012-0011-3\u002Fhtml",[1046,1061],{"id":1047,"sortIndex":21,"researcher":20,"roles":1048,"affiliations":1049,"properties":1058,"displayName":1060,"givenName":20,"familyName":20},"16d3c132-4486-4472-9889-8dbc1d66befa",[965],[1050],{"id":1051,"sortIndex":21,"affiliation":1052,"properties":20},"794bb217-5373-4c82-b756-8d44ca7330c5",{"id":1051,"createTime":20,"updateTime":20,"relativeEntities":1053,"slug":20,"properties":1054,"entityType":20,"verifyStatus":20,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":20,"url":20,"parentIds":1057,"statistic":20},[],{"title":1055},{"VI":1056},"MD Sci. Millenium Institute of Biomedical Neuroscience, Cellular and Molecular Neurobiology. Pharmacology Ph.D. Program. Faculty of Medicine, University of Chile, Santiago, Chile",[],{"title":1059},{"VI":1060},"Johanna F. Catalán",{"id":1062,"sortIndex":104,"researcher":20,"roles":1063,"affiliations":1064,"properties":1073,"displayName":1075,"givenName":20,"familyName":20},"05d4bc8f-6a2d-4dd0-b136-b6684a188514",[965],[1065],{"id":1066,"sortIndex":21,"affiliation":1067,"properties":20},"25e190b2-ae51-4120-b66d-943d11580542",{"id":1066,"createTime":20,"updateTime":20,"relativeEntities":1068,"slug":20,"properties":1069,"entityType":20,"verifyStatus":20,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":20,"url":20,"parentIds":1072,"statistic":20},[],{"title":1070},{"VI":1071},"MD. Pontifical Catholic University of Chile, Santiago, Chile",[],{"title":1074},{"VI":1075},"María Paz Quezada",{"url":1044,"publisher":1077,"properties":1119},{"id":6,"createTime":7,"updateTime":8,"relativeEntities":1078,"slug":10,"properties":1079,"entityType":18,"verifyStatus":19,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":21,"subjectFields":1083,"manageAffiliations":1088,"indexDatabases":1099,"url":20,"thumbnailPath":20,"statistic":1114,"gsStatistic":20,"type":20,"analyzePriority":20},[],{"issn":1080,"title":1081,"eissn":1082},{"VOID":13},{"EN":15},{"VOID":17},[1084],{"id":24,"createTime":20,"updateTime":20,"relativeEntities":1085,"label":1086,"description":1087,"parentId":20,"standard":20,"scholarHubFieldId":20},[],{"EN":27},{},[1089,1094],{"id":31,"createTime":20,"updateTime":20,"relativeEntities":1090,"slug":20,"properties":1091,"entityType":20,"verifyStatus":20,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":20,"url":20,"parentIds":1093,"statistic":20},[],{"title":1092},{"EN":35},[],{"id":38,"createTime":20,"updateTime":20,"relativeEntities":1095,"slug":20,"properties":1096,"entityType":20,"verifyStatus":20,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":20,"url":20,"parentIds":1098,"statistic":20},[],{"title":1097},{"EN":42},[],[1100,1107],{"id":46,"indexDatabase":1101,"url":57,"indexYears":58,"academicFieldIds":1106,"indexDatabaseRanking":61},{"id":48,"createTime":20,"updateTime":20,"relativeEntities":1102,"label":1103,"description":1104,"key":54,"publicationTags":1105,"standard":20},[],{"EN":51,"VI":51},{"EN":51,"VI":53},[56],[60],{"id":63,"indexDatabase":1108,"url":76,"indexYears":20,"academicFieldIds":1113,"indexDatabaseRanking":20},{"id":65,"createTime":20,"updateTime":20,"relativeEntities":1109,"label":1110,"description":1111,"key":72,"publicationTags":1112,"standard":20},[],{"EN":68,"VI":68},{"EN":70,"VI":71},[74,75],[78],{"impactFactor":21,"impactFactorByYear":1115,"i10Index":86,"i10IndexLast5Year":21,"totalPublication":87,"totalPublicationByYear":1116,"totalCitation":93,"totalCitationByYear":1117,"totalCitationPerPublication":98,"totalCitationPerPublicationByYear":1118,"hindexLast5Year":105,"hindex":105},{"2012":81,"2013":82,"2014":83,"2015":84,"2016":85},{"2010":89,"2011":90,"2012":90,"2013":91,"2014":92},{"2010":92,"2011":95,"2012":96,"2013":97,"2014":92},{"2010":100,"2011":101,"2012":102,"2013":103,"2014":104},{"pages":1120,"volume":1122},{"VOID":1121},"61-66",{"VOID":1026},"2012-03-14",[61,74],{"id":1126,"createTime":1127,"updateTime":1128,"relativeEntities":1129,"slug":1130,"properties":1131,"entityType":959,"verifyStatus":128,"verifyTime":1128,"verifyNote":1140,"languages":20,"translateLanguages":20,"viewCount":104,"primaryUrl":1141,"fullTextUrl":20,"authors":1142,"publicationType":978,"publisherRelationship":1158,"citationCount":20,"citationInfo":20,"publishDate":1206,"publishYear":1207,"citationAnalyzeStatus":19,"lastCitationAnalyze":20,"indexDatabases":1208,"openAccess":20,"references":20,"isForceReanalyzing":1030},"0c53c924-3340-4b2d-b361-ca26c084fc3d","2024-01-27T00:26:03.672+00:00","2025-02-23T19:08:33.905+00:00",[],"F-K-Studni%C4%8Dka-1894-Fishes-and-amphibians-also-have-the-cerebral-cortex",{"abstract":1132,"title":1134,"references":1136,"doi":1138},{"EN":1133},"The aim of this paper is to provide translation of probably the first report (Studnička 1894) demonstrating that the telencephalon of all vertebrate taxa (including fishes and amphibians) is characterized by the presence of the cerebral cortex (pallium). This report was one of those initiating a century-long and still not fully resolved discussion concerning homologies of various pallial subdivisions in different vertebrate taxa and probably the first to draw attention to the importance of careful study of the pallium in representatives of agnathans (Cyclostomes) such as lampreys (Petromyzonts) and hagfishes (Myxinoids). This article also briefly reviews the current status of comparative research on vertebrate telencephalon, and provides historical notes which position Studnička’s report in its historical context.",{"EN":1135},"F. K. Studnička (1894): Fishes and amphibians also have the cerebral cortex",{"VOID":1137},"Butler A. B., Hodos W., Comparative Vertebrate Neuroanatomy. Evolution and Adaptation, 2nd Edition, Hoboken, New Jersey: Wiley-Interscience, 2005\nKaas J. H., Bullock T. H., Evolution of Nervous Systems. A Comprehensive Reference, Volume 2: Non-Mammalian Vertebrates, Oxford — San Diego: Academic Press, 2007\nStriedter G., Principles of Brain Evolution, Sinauer Associates, 2005\nFurlong R. F., Holland P. W. H., Bayesian phylogenetic analysis supports monophyly of Ambulacraria and of cyclostomes, Zoological Science 2002, 19, 593–599\nMallat J., Sullivan J., 28S and 18S rDNA sequences support the monophyly of lampreys and hagfishes, Mol Biol Evol, 1998, 15, 1706–1718\nBruce L.L., Evolution of the nervous system in Reptiles, In: Kaas J.H., Bullock T.H. (Eds) Evolution of Nervous Systems Vol. 2, Oxford-San Diego: Academic Press, 2007, 125–156\nWullimann M. F., Vernier P., Evolution of the nervous system in fishes, In: Kaas J.H., Bullock T.H. (Eds) Evolution of Nervous Systems Vol. 2, Oxford-San Diego: Academic Press, 2007, 39–60\nPuelles L., Brain segmentation and forebrain development in amniotes, Brain Res Bull, 2007, 55, 695–710\nBruce L.L., Neary T.J., The limbic system of tetrapods: A comparative analysis of cortical and amygdalar populations, Brain Behav Evol, 1995, 46, 224–234\nWullimann M.F., Mueller T., Teleostean and mammalian forebrains contrasted: Evidence from genes to behavior, J Comp Neurol 2004, 475, 143–162\nBraun C.B., The sensory biology of lampreys and hagfishes: A phylogenetic assessment, Brain Behav Evol 1996, 48, 262–276\nWicht H., The brains of lampreys and hagfishes: Characteristics, characters, and comparisons, Brain Behav Evol 1996, 48, 248–261\nWicht H., Northcutt R.G., The forebrain of the pacific hagfish: A cladistic reconstruction of the ancestral craniate forebrain, Brain Behav Evol, 1992, 40, 25–64\nWicht H., Northcutt R.G., Telencephalic connections in the Pacific hagfish (Eptatretus stouti), with special reference to the thalamopallial system, J Comp Neurol 1998, 395, 245–260\nPolenova O. A., Vesselkin N. P., Olfactory and non-olfactory projections in the river lamprey (Lampetra fluviatilis) telencephalon, J Hirnforsch, 1993, 34, 261–279\nMurakami Y., Uchida K., Rijli F. M., Kuratani S., Evolution of the brain developmental plan: Insights from agnathans, Dev Biol, 2005, 280, 249–259\nDicke U., Roth G., Evolution of the Amphibian nervous system, In: Kaas JH, Bullock TH (Eds) Evolution of Nervous Systems Vol. 2, Oxford-San Diego: Academic Press, 2007, 61–124\nBrinkmann H., Denk A., Zitzler J., Joss J. J., Meyer A., Complete mitochondrial genome sequences of the South American and the Australian lungfish: Testing of the phylogenetic performance of mitochondrial data sets for phylogenetic problems in tetrapod relationships, J Mol Evol, 2004, 59, 834–848\nKuhlenbeck H., Zur Morphologie des Gymnophionengehirns, Jenaische Zeitschrift für Naturwissenschaften, 1922, 58, 453–484\nHerrick C. J., The Brain of the Tiger Salamander Ambystoma tigrinum, Chicago: University of Chicago Press, 1948\nGregory T. R., Genome size and developmental complexity, Genetica, 2002, 115, 131–146\nGregory T. R., Variation across amphibian species in the size of the nuclear genome supports a pluralistic, hierarchical approach to the C-value enigma, Biol J Linn Soc 2002, 79, 329–339\nNorthcutt R. G., Evolution of the telencephalon in nonmammals, Ann Rev Neurosci 1981, 4, 301–350\nWesthoff G., Roth G., Morphology and projection pattern of medial and dorsal pallial neurons in the frog Discoglossus pictus and the salamander Plethodon jordani, J Comp Neurol, 2002, 445, 97–121\nReiner A., Perkel D. J., Bruce L. L., Butler A. B., Csillag A., Kuenzel W., et al., Revised nomenclature for avian telencephalon and some related brainstem nuclei, J Comp Neurol, 2004, 473, 377–414\nShepherd GM (1991) Foundations of the Neuron Doctrine. New York — Oxford: Oxford University Press.\nJacobson M., Developmental Neurobiology, Third Edition, New York — London: Plenum Press, 1991",{"VOID":1139},"10.2478\u002Fs13380-011-0010-9","Auto Verify","https:\u002F\u002Fwww.degruyter.com\u002Fdocument\u002Fdoi\u002F10.2478\u002Fs13380-011-0010-9\u002Fhtml",[1143],{"id":1144,"sortIndex":21,"researcher":20,"roles":1145,"affiliations":1146,"properties":1155,"displayName":1157,"givenName":20,"familyName":20},"0f6968e2-3df0-459c-aa50-90d3fc354d64",[965],[1147],{"id":1148,"sortIndex":21,"affiliation":1149,"properties":20},"4ce2bdd2-3402-4eb7-ac16-c6b64d5de0ef",{"id":1148,"createTime":20,"updateTime":20,"relativeEntities":1150,"slug":20,"properties":1151,"entityType":20,"verifyStatus":20,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":20,"url":20,"parentIds":1154,"statistic":20},[],{"title":1152},{"EN":1153},"Croatian Institute for Brain Research, University of Zagreb School of Medicine, Zagreb, Croatia",[],{"title":1156},{"VI":1157},"Miloš Judaš",{"url":1141,"publisher":1159,"properties":1201},{"id":6,"createTime":7,"updateTime":8,"relativeEntities":1160,"slug":10,"properties":1161,"entityType":18,"verifyStatus":19,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":21,"subjectFields":1165,"manageAffiliations":1170,"indexDatabases":1181,"url":20,"thumbnailPath":20,"statistic":1196,"gsStatistic":20,"type":20,"analyzePriority":20},[],{"issn":1162,"title":1163,"eissn":1164},{"VOID":13},{"EN":15},{"VOID":17},[1166],{"id":24,"createTime":20,"updateTime":20,"relativeEntities":1167,"label":1168,"description":1169,"parentId":20,"standard":20,"scholarHubFieldId":20},[],{"EN":27},{},[1171,1176],{"id":31,"createTime":20,"updateTime":20,"relativeEntities":1172,"slug":20,"properties":1173,"entityType":20,"verifyStatus":20,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":20,"url":20,"parentIds":1175,"statistic":20},[],{"title":1174},{"EN":35},[],{"id":38,"createTime":20,"updateTime":20,"relativeEntities":1177,"slug":20,"properties":1178,"entityType":20,"verifyStatus":20,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":20,"url":20,"parentIds":1180,"statistic":20},[],{"title":1179},{"EN":42},[],[1182,1189],{"id":46,"indexDatabase":1183,"url":57,"indexYears":58,"academicFieldIds":1188,"indexDatabaseRanking":61},{"id":48,"createTime":20,"updateTime":20,"relativeEntities":1184,"label":1185,"description":1186,"key":54,"publicationTags":1187,"standard":20},[],{"EN":51,"VI":51},{"EN":51,"VI":53},[56],[60],{"id":63,"indexDatabase":1190,"url":76,"indexYears":20,"academicFieldIds":1195,"indexDatabaseRanking":20},{"id":65,"createTime":20,"updateTime":20,"relativeEntities":1191,"label":1192,"description":1193,"key":72,"publicationTags":1194,"standard":20},[],{"EN":68,"VI":68},{"EN":70,"VI":71},[74,75],[78],{"impactFactor":21,"impactFactorByYear":1197,"i10Index":86,"i10IndexLast5Year":21,"totalPublication":87,"totalPublicationByYear":1198,"totalCitation":93,"totalCitationByYear":1199,"totalCitationPerPublication":98,"totalCitationPerPublicationByYear":1200,"hindexLast5Year":105,"hindex":105},{"2012":81,"2013":82,"2014":83,"2015":84,"2016":85},{"2010":89,"2011":90,"2012":90,"2013":91,"2014":92},{"2010":92,"2011":95,"2012":96,"2013":97,"2014":92},{"2010":100,"2011":101,"2012":102,"2013":103,"2014":104},{"pages":1202,"volume":1204},{"VOID":1203},"79-89",{"VOID":1205},"2","2011-03-26",2011,[61,74],{"id":1210,"createTime":1211,"updateTime":1212,"relativeEntities":1213,"slug":1214,"properties":1215,"entityType":959,"verifyStatus":128,"verifyTime":1212,"verifyNote":1140,"languages":20,"translateLanguages":20,"viewCount":21,"primaryUrl":1224,"fullTextUrl":20,"authors":1225,"publicationType":978,"publisherRelationship":1274,"citationCount":20,"citationInfo":20,"publishDate":1321,"publishYear":1207,"citationAnalyzeStatus":19,"lastCitationAnalyze":20,"indexDatabases":1322,"openAccess":20,"references":20,"isForceReanalyzing":1030},"0c6d0b55-4ba9-47f3-8f5d-52415b07c577","2024-02-17T11:15:42.787+00:00","2024-12-25T19:25:34.205+00:00",[],"Pathology-of-acute-disseminated-encephalomyelitis",{"abstract":1216,"title":1218,"references":1220,"doi":1222},{"EN":1217},"Acute disseminated encephalomyelitis (ADEM) is an acute, monophasic neurologic syndrome that occurs after vaccination against various viruses and after many viral infections and rarely occurs again in the same patient. Weston Hurst disease or acute hemorrhagic encephalomyelitis (AHE) is a hyperacute ADEM variant that shares many pathological similarities with ADEM. ADEM clinically and neuropathologically faithfully reflects the animal model of experimental allergic encephalomyelitis (EAE), and animal studies have provided us with new insights into pathogenesis of this disorder. Although there is much controversy whether ADEM is a separate disease or just one of possible manifestations of multiple sclerosis, there are clear histopathological characteristics that support ADEM as a separate disease This mini review will focus on pathological characteristics of ADEM emphasizing differences from other types of idiopathic demyelinating diseases.",{"EN":1219},"Pathology of acute disseminated encephalomyelitis",{"VOID":1221},"Poser C., The epidemiology of multiple sclerosis: a general overview, Ann. Neurol.,1994, 36, S231–S243\nBrinar V. V., Habek M., Diagnostic imaging in acute disseminated encephalomyelitis, Expert Rev. Neurother., 2010, 10, 459–467\nHart M. N., Earle K. M., Haemorrhagic and perivenous encephalitis: a clinical-pathological review of 38 cases, J. Neurol. Neurosurg. Psychiatry, 1975, 38, 585–591\nGold R., Linington C., Lassmann H., Understanding pathogenesis and therapy of multiple sclerosis via animal models: 70 years of merits and culprits in experimental autoimmune encephalomyelitis research, Brain, 2006, 129:1953–1971\nKadlubowski M., Highes R., The neuritogenecity and encephalogenecity of P2 in in the rat, guinea pig and rabbit, J. Neurol. Sci., 1980, 48, 171–178\nvan Bogaert L., Post-infectious encephalomyelitis and multiple sclerosis. The significance of perivenous encephalomyelitis, J. Neuropathol. Exp. Neurol., 1950, 9, 219–249\nWegner C., Pathological differences in acute inflammatory demyelinating diseases of the central nervous system, Int. MS J., 2005, 12, 12–19\nLassmann H., Acute disseminated encephalomyelitis and multiple sclerosis, Brain, 2010, 133, 317–319\nYoung N. P., Weinshenker B. G., Parisi J. E., Scheithauer B., Giannini C., Roemer S. F. et al., Perivenous demyelination: association with clinically defined acute disseminated encephalomyelitis and comparison with pathologically confirmed multiple sclerosis, Brain, 2010, 133, 333–348\nGarg R.K., Acute disseminated encephalomyelitis, Postgrad. Med. J., 2003, 79, 11–17\nRossi A., Imaging of acute disseminated encephalomyelitis, Neuroimaging Clin. N. Am., 2008, 18, 149e61\nWingerchuk D. M., Lucchinetti C. F., Comparative immunopathogenesis of acute disseminated encephalomyelitis, neuromyelitis optica, and multiple sclerosis, Curr. Opin. Neurol., 2007, 20, 343–350\nMarchioni E., Ravaglia S., Piccolo G., Furione M., Zardini E., Franciotta D. et al., Postinfectious inflammatory disorders: subgroups based on prospective follow-up, Neurology, 2005, 65, 1057–1065\nCohen O., Steiner-Birmanns B., Biran I., Abramsky O., Honigman S., Steiner I., Recurrence of acute disseminated encephalomyelitis at the previously affected brain site, Arch. Neurol., 2001, 58, 797–801\nMar S., Lenox J., Benzinger T., Brown S., Noetzel M., Long-term prognosis of pediatric patients with relapsing acute disseminated encephalomyelitis, J. Child Neurol., 2010, 25, 681–688\nKuperan S., Ostrow P., Landi M. K., Bakshi R., Acute hemorrhagic leukoencephalitis vs ADEM: FLAIR MRI and neuropathology findings, Neurology, 2003, 60, 721–722\nFontoura P., Leucoencefalitis aguda hemorragica de Weston Hurst. Estudio neuropatologico de un caso, Rev. Neurol., 2002, 35, 328–331\nLumsden C., The clinical immunology of multiple sclerosis. In: McAlpine D., Lumsden C., Acheson E., editors. Multiple sclerosis a reaprraisal: 2nd ed. Baltimore, MD: Williams & Wilkins, 1972. p 519\nLassmann H., Comparative neuropathology of chronic relapsing experimental allergic encephalomyelitis and multiple sclerosis, Schriftr. Neurol., 1983, 25, 1–135\nLipton H. L., Theiler’s virus infection in mice: an unusual biphasic disease process leading to demyelination, Infect. Immun., 1975, 11, 1147–1155\nJarousse N., Viktorova E. G., Pilipenko E. V., Agol V. I., Brahic M., An attenuated variant of the GDVII strain of Theiler’s virus does not persist and does not infect the white matter of the central nervous system, J. Virol., 1999, 73, 801–804\nClark G., Bogdanove L. H., The induction of the lesions of allergic meningoencephalomyelitis in a predetermined location, J. Neuropathol. Exp. Neurol., 1955, 14, 433–437\nBogdanove L. H., Clark G., The induction of exacerbations of allergic meningoencephalomyelitis, J. Neuropathol. Exp. Neurol., 1957, 16, 57–60\nCabre P., Smadja D., Merle H., Vernant J. C., Poser C., Multiphasic disseminated encephalomyelitis, Neurol. Infect. Epidemiol., 1997, 2, 135–139\nJahnke U., Fischer E., Alvord E., Sequence homology between certain viral proteins and proteins related to encephalomyelitis and neuritis, Science, 1985, 229, 282–284\nPirko I., Suidan G. L., Rodriguez M., Johnson A.J., Acute hemorrhagic demyelination in a murine model of multiple sclerosis, J. Neuroinflammation., 2008, 5, 31",{"VOID":1223},"10.2478\u002Fs13380-011-0030-5","https:\u002F\u002Fwww.degruyter.com\u002Fdocument\u002Fdoi\u002F10.2478\u002Fs13380-011-0030-5\u002Fhtml",[1226,1250],{"id":1227,"sortIndex":21,"researcher":20,"roles":1228,"affiliations":1229,"properties":1247,"displayName":1249,"givenName":20,"familyName":20},"c2ae0d90-8b19-46e7-84cc-9cb61f1f7aae",[965],[1230,1238],{"id":1231,"sortIndex":21,"affiliation":1232,"properties":20},"c8a93e3f-5a28-44b4-b8a7-44660be19e34",{"id":1231,"createTime":20,"updateTime":20,"relativeEntities":1233,"slug":20,"properties":1234,"entityType":20,"verifyStatus":20,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":20,"url":20,"parentIds":1237,"statistic":20},[],{"title":1235},{"EN":1236},"Department of Neurology, School of Medicine, University of Zagreb, Zagreb, Croatia",[],{"id":1239,"sortIndex":104,"affiliation":1240,"properties":1246},"012f12e6-0f59-4723-a3c3-2d21ccae8003",{"id":1239,"createTime":20,"updateTime":20,"relativeEntities":1241,"slug":20,"properties":1242,"entityType":20,"verifyStatus":20,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":20,"url":20,"parentIds":1245,"statistic":20},[],{"title":1243},{"VI":1244},"Department of Neurology, Refferal Center for Demyelinating Diseases of the Central Nervous System, University Hospital Center Zagreb, Zagreb, Croatia",[],{},{"title":1248},{"VI":1249},"Mario Habek",{"id":1251,"sortIndex":104,"researcher":20,"roles":1252,"affiliations":1253,"properties":1271,"displayName":1273,"givenName":20,"familyName":20},"afcaaffa-9dc5-4d33-b25d-fa020fe06a90",[965],[1254,1262],{"id":1255,"sortIndex":21,"affiliation":1256,"properties":20},"311cefc8-e2f7-458a-8605-1bac1cc0b65a",{"id":1255,"createTime":20,"updateTime":20,"relativeEntities":1257,"slug":20,"properties":1258,"entityType":20,"verifyStatus":20,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":20,"url":20,"parentIds":1261,"statistic":20},[],{"title":1259},{"VI":1260},"Department of Pathology, School of Medicine, University of Zagreb, Zagreb, Croatia",[],{"id":1263,"sortIndex":104,"affiliation":1264,"properties":1270},"5afb15df-e079-4a2d-84e1-392b70669fa6",{"id":1263,"createTime":20,"updateTime":20,"relativeEntities":1265,"slug":20,"properties":1266,"entityType":20,"verifyStatus":20,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":20,"url":20,"parentIds":1269,"statistic":20},[],{"title":1267},{"VI":1268},"Department of Pathology, Division for Neuropathology, University Hospital Center Zagreb, Zagreb, Croatia",[],{},{"title":1272},{"VI":1273},"Kamelija Žarković",{"url":1224,"publisher":1275,"properties":1317},{"id":6,"createTime":7,"updateTime":8,"relativeEntities":1276,"slug":10,"properties":1277,"entityType":18,"verifyStatus":19,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":21,"subjectFields":1281,"manageAffiliations":1286,"indexDatabases":1297,"url":20,"thumbnailPath":20,"statistic":1312,"gsStatistic":20,"type":20,"analyzePriority":20},[],{"issn":1278,"title":1279,"eissn":1280},{"VOID":13},{"EN":15},{"VOID":17},[1282],{"id":24,"createTime":20,"updateTime":20,"relativeEntities":1283,"label":1284,"description":1285,"parentId":20,"standard":20,"scholarHubFieldId":20},[],{"EN":27},{},[1287,1292],{"id":31,"createTime":20,"updateTime":20,"relativeEntities":1288,"slug":20,"properties":1289,"entityType":20,"verifyStatus":20,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":20,"url":20,"parentIds":1291,"statistic":20},[],{"title":1290},{"EN":35},[],{"id":38,"createTime":20,"updateTime":20,"relativeEntities":1293,"slug":20,"properties":1294,"entityType":20,"verifyStatus":20,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":20,"url":20,"parentIds":1296,"statistic":20},[],{"title":1295},{"EN":42},[],[1298,1305],{"id":46,"indexDatabase":1299,"url":57,"indexYears":58,"academicFieldIds":1304,"indexDatabaseRanking":61},{"id":48,"createTime":20,"updateTime":20,"relativeEntities":1300,"label":1301,"description":1302,"key":54,"publicationTags":1303,"standard":20},[],{"EN":51,"VI":51},{"EN":51,"VI":53},[56],[60],{"id":63,"indexDatabase":1306,"url":76,"indexYears":20,"academicFieldIds":1311,"indexDatabaseRanking":20},{"id":65,"createTime":20,"updateTime":20,"relativeEntities":1307,"label":1308,"description":1309,"key":72,"publicationTags":1310,"standard":20},[],{"EN":68,"VI":68},{"EN":70,"VI":71},[74,75],[78],{"impactFactor":21,"impactFactorByYear":1313,"i10Index":86,"i10IndexLast5Year":21,"totalPublication":87,"totalPublicationByYear":1314,"totalCitation":93,"totalCitationByYear":1315,"totalCitationPerPublication":98,"totalCitationPerPublicationByYear":1316,"hindexLast5Year":105,"hindex":105},{"2012":81,"2013":82,"2014":83,"2015":84,"2016":85},{"2010":89,"2011":90,"2012":90,"2013":91,"2014":92},{"2010":92,"2011":95,"2012":96,"2013":97,"2014":92},{"2010":100,"2011":101,"2012":102,"2013":103,"2014":104},{"pages":1318,"volume":1320},{"VOID":1319},"252-255",{"VOID":1205},"2011-09-24",[61,74],{"id":1324,"createTime":1325,"updateTime":1326,"relativeEntities":1327,"slug":1328,"properties":1329,"entityType":959,"verifyStatus":128,"verifyTime":1326,"verifyNote":1140,"languages":20,"translateLanguages":20,"viewCount":21,"primaryUrl":1338,"fullTextUrl":20,"authors":1339,"publicationType":978,"publisherRelationship":1418,"citationCount":20,"citationInfo":20,"publishDate":1206,"publishYear":1207,"citationAnalyzeStatus":19,"lastCitationAnalyze":20,"indexDatabases":1465,"openAccess":20,"references":20,"isForceReanalyzing":1030},"0d510e1b-f568-46d6-95f7-e5c641945141","2024-02-18T10:43:35.694+00:00","2025-01-04T12:46:18.023+00:00",[],"Quest-for-new-genomic-and-proteomic-biomarkers-in-neurology",{"abstract":1330,"title":1332,"references":1334,"doi":1336},{"EN":1331},"The possibility of identifying novel biomarkers for neurodegenerative diseases has been greatly enhanced with recent advances in genomics and proteomics. Novel technologies have the potential to hasten the development of new biomarkers useful as predictors of disease etiology and outcome, as well as responsiveness to therapy. Disease-modifying new therapies are very much needed in modern approaches to treatment of neurodegenerative diseases. Current progress in the field encounters a degree of skepticism about the reliability of genomic and proteomic data and its relevance for clinical applications. Standard operating procedures covering sample collection, methodology and statistical analysis need to be fully developed and strictly adhered to in order to assure reproducible and clinically relevant results. Previous studies involving patients with neurodegenerative diseases show promise in using genomic and proteomic approaches for development of new biomarkers. Confirmation of any novel biomarker in multiple independent patient cohorts and correlation of the improvement in biomarker endpoint with clinical improvement in longitudinal patient studies remains crucial for future successful application. We propose that a combination of approaches in biomarker discovery may in the end lead to identification of promising candidates at DNA, RNA, protein and small molecule level.",{"EN":1333},"Quest for new genomic and proteomic biomarkers in neurology",{"VOID":1335},"Atkinson A.J., Colburn W.A., DeGruttola V.G., Demets D.L., Downing G.J., Hoth D.F., et al., Biomarkers and surrogate endpoints: preferred definitions and conceptual framework, Clin. Pharmacol. Ther., 2001, 69, 89–95\nManolio T., Novel risk markers and clinical practice, N. Engl. J. Med., 2003, 349, 1587–1589\nScherzer C.R., Chipping away at diagnostics for neurodegenerative diseases, Neurobiol. Dis., 2009, 35, 148–156\nAlonso A., Molenberghs G., Geys H., Buyse M., Vangeneugden T., A unifying approach for surrogate marker validation based on Prentice’s criteria, Stat. Med., 2006, 25, 205–221\nManolio T.A., Collins F.S., The HapMap and genome-wide association studies in diagnosis and therapy, Annu. Rev. Med., 2009, 60, 443–456\nNess S.A., Microarray analysis: basic strategies for successful experiments, Mol. Biotechnol., 2007, 36, 205–219\nPhan J.H., Quo C.F., Wang M.D., Functional genomics and proteomics in the clinical neurosciences: data mining and bioinformatics, Prog. Brain Res., 2006, 158, 83–108\nLiew C.C., Ma J., Tang H.C., Zheng R., Dempsey A.A., The peripheral blood transcriptome dynamically reflects system wide biology: a potential diagnostic tool, J. Lab. Clin. Med., 2006, 147, 126–132\nBurczynski M.E., Dorner A.J., Transcriptional profiling of peripheral blood cells in clinical pharmacogenomic studies, Pharmacogenomics, 2006, 7, 187–202\nIbarreta D., Urcelay E., Parrilla R., Ayuso M.S., Distinct pH homeostatic features in lymphoblasts from Alzheimer’s disease patients, Ann. Neurol., 1998, 44, 216–222\nStieler J.T., Lederer C., Bruckner M.K., Wolf H., Holzer M., Gertz H.J., et al., Impairment of mitogenic activation of peripheral blood lymphocytes in Alzheimer’s disease, NeuroReport, 2001, 12, 3969–3972\nBlandini F., Sinforiani E., Pacchetti C., Samuele A., Bazzini E., Zangaglia R., et al., Peripheral proteasome and caspase activity in Parkinson disease and Alzheimer disease, Neurology, 2006, 66, 529–534\nKerlero de Rosbo N., Milo R., Lees M.B., Burger D., Bernard C.C., Ben-Nun A., Reactivity to myelin antigens in multiple sclerosis. Peripheral blood lymphocytes respond predominantly to myelin oligodendrocyte glycoprotein, J. Clin. Invest., 1993, 92, 2602–2608\nMahad D.J., Lawry J., Howell S.J., Woodroofe M.N., Longitudinal study of chemokine receptor expression on peripheral lymphocytes in multiple sclerosis: CXCR3 upregulation is associated with relapse, Mult. Scler., 2003, 9, 189–198\nVallittu A.M., Saraste M., Airas L., CCR7 expression on peripheral blood lymphocytes is up-regulated following treatment of multiple sclerosis with interferon-beta, Neurol. Res., 2007, 29, 763–766\nAchiron A., Gurevich M., Friedman N., Kaminski N., Mandel M., Blood transcriptional signatures of multiple sclerosis: unique gene expression of disease activity, Ann. Neurol., 2004, 55, 410–417\nBorovecki F., Lovrecic L., Zhou J., Jeong H., Then F., Rosas H.D., et al., Genome-wide expression profiling of human blood reveals biomarkers for Huntington’s disease, Proc. Natl. Acad. Sci. USA, 2005, 102, 11023–11028\nScherzer C.R., Eklund A.C., Morse L.J., Liao Z., Locascio J.J., Fefer D., et al., Molecular markers of early Parkinson’s disease based on gene expression in blood, Proc. Natl. Acad. Sci. USA, 2007, 104, 955–960\nDunckley T., Huentelman M.J., Craig D.W., Pearson J.V., Szelinger S., Joshipura K., et al., Whole-genome analysis of sporadic amyotrophic lateral sclerosis, N. Engl. J. Med., 2007, 357, 775–788\nMaraganore D.M., de Andrade M., Lesnick T.G., Strain K.J., Farrer M.J., Rocca W.A., et al., High-resolution whole-genome association study of Parkinson disease, Am. J. Hum. Genet., 2005, 77, 685–693\nPapapetropoulos S., Shehadeh L., McCorquodale D., Optimizing human post-mortem brain tissue gene expression profiling in Parkinson’s disease and other neurodegenerative disorders: From target “fishing” to translational breakthroughs, J. Neurosci, Res., 2007, 85, 3013–3024\nPapasssotiropoulos A., Fountoulakis M., Dunckley T., Stephan D.A., Reiman E.M., Genetics, transcriptomics, and proteomics of Alzheimer’s disease, J. Clin. Psychiatry, 2006, 67, 652–670\nTang Y., Gilbert D.L., Glauser T.A., Hershey A.D., Sharp F.R., Blood gene expression profiling of neurological diseases: a pilot microarray study, Arch. Neurol., 2005, 62, 210–215\nVan Es M.A., Van Vught P.W., Blauw H.M., Franke L., Saris C.G., Andersen P.M., et al., ITPR 2 as a susceptibility gene in sporadic amyotrophic lateral sclerosis: a genomewide association study, Lancet Neurol., 2007, 6, 869–877\nWhitney L.W., Ludwin S.K., McFarland H.F., Biddison W.E., Microarray analysis of gene expression in multiple sclerosis and EAE identifies 5-lipoxygenase as a component of inflammatory lesions, J. 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U S A, 2004, 101, 10804–10809\nBotella-Lopez A., Burgaya F., Gavin R., Garcia-Ayllon M.S., Gomez-Tortosa E., Pena-Casanova J., et al., Reelin expression and glycosylation patterns are altered in Alzheimer’s disease, Proc. Natl. Acad. Sci. U S A, 2006, 103, 5573–5578",{"VOID":1337},"10.2478\u002Fs13380-011-0005-6","https:\u002F\u002Fwww.degruyter.com\u002Fdocument\u002Fdoi\u002F10.2478\u002Fs13380-011-0005-6\u002Fhtml",[1340,1355,1370,1385,1398],{"id":1341,"sortIndex":21,"researcher":20,"roles":1342,"affiliations":1343,"properties":1352,"displayName":1354,"givenName":20,"familyName":20},"8ab34b83-96e2-4342-9d99-8f033d1ba80b",[965],[1344],{"id":1345,"sortIndex":21,"affiliation":1346,"properties":20},"aaefb850-04a9-4a07-a925-c77ef7ed5660",{"id":1345,"createTime":20,"updateTime":20,"relativeEntities":1347,"slug":20,"properties":1348,"entityType":20,"verifyStatus":20,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":20,"url":20,"parentIds":1351,"statistic":20},[],{"title":1349},{"VI":1350},"Department for Functional Genomics, Center for Translational and Clinical Research, University of Zagreb School of Medicine, University Hospital Center Zagreb, Zagreb, 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disease (AD) is a progressive neurodegenerative disorder characterized by the extracellular deposits of β amyloid peptides (Aβ) in senile plaques, and intracellular aggregates of hyperphosphorylated tau in neurofibrillary tangles (NFT). Although accumulation of Aβ has been long considered a leading hypothesis in the disease pathology, it is increasingly evident that the role hyperphosphorylation of tau in destabilization of microtubule assembly and disturbance of axonal transport is equally detrimental in the neurodegenerative process. The main kinase involved in phosphorylation of tau is glycogen-synthase kinase 3-beta (GSK-3β). Intracellular accumulation of Aβ also likely induces increase in hyperphosphorylated tau by a mechanism dependent on GSK-3β. In addition, Aβ affects production of ceramides, the major sphingolipids in mammalian cells, by acting on sphingomyelinases, enzymes responsible for the catabolic formation of ceramides from the sphingomyelin. Generated ceramides in turn increase production of Aβ by acting on β-secretase, a key enzyme in the proteolytic processing of the amyloid precursor protein (APP), altogether leading to a ceramide-Aβ-hyperphosphorylated tau cascade that ends in neuronal death. Modulators and inhibitors acting on members of this devastating cascade are considered as potential targets for AD therapy. There is still no adequate treatment for AD patients. Novel therapeutic strategies increasingly consider the combination of multiple targets and interactions among the key members of implicated molecular pathways. This review summarizes recent findings and therapeutic perspectives in the pathology and treatment of AD, with the emphasis on the interplay between hyperphosphorylated tau, amyloid β, and sphingolipid mediators.",{"EN":1476},"Hyperphosphorylation of tau by GSK-3β in Alzheimer’s disease: The interaction of Aβ and sphingolipid mediators as a therapeutic target",{"VOID":1478},"Hanger D.P., Anderton B.H., Noble W., Tau phosphorylation: the therapeutic challenge for neurodegenerative disease, Trends Mol. 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Hof",{"id":1552,"sortIndex":144,"researcher":20,"roles":1553,"affiliations":1554,"properties":1561,"displayName":1563,"givenName":20,"familyName":20},"6e1bbdc6-1a3b-4e3a-8a99-53886180a2c2",[965],[1555],{"id":1512,"sortIndex":21,"affiliation":1556,"properties":20},{"id":1512,"createTime":20,"updateTime":20,"relativeEntities":1557,"slug":20,"properties":1558,"entityType":20,"verifyStatus":20,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":20,"url":20,"parentIds":1560,"statistic":20},[],{"title":1559},{"VI":1517},[],{"title":1562},{"VI":1563},"Goran Šimić",{"url":1481,"publisher":1565,"properties":1607},{"id":6,"createTime":7,"updateTime":8,"relativeEntities":1566,"slug":10,"properties":1567,"entityType":18,"verifyStatus":19,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":21,"subjectFields":1571,"manageAffiliations":1576,"indexDatabases":1587,"url":20,"thumbnailPath":20,"statistic":1602,"gsStatistic":20,"type":20,"analyzePriority":20},[],{"issn":1568,"title":1569,"eissn":1570},{"VOID":13},{"EN":15},{"VOID":17},[1572],{"id":24,"createTime":20,"updateTime":20,"relativeEntities":1573,"label":1574,"description":1575,"parentId":20,"standard":20,"scholarHubFieldId":20},[],{"EN":27},{},[1577,1582],{"id":31,"createTime":20,"updateTime":20,"relativeEntities":1578,"slug":20,"properties":1579,"entityType":20,"verifyStatus":20,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":20,"url":20,"parentIds":1581,"statistic":20},[],{"title":1580},{"EN":35},[],{"id":38,"createTime":20,"updateTime":20,"relativeEntities":1583,"slug":20,"properties":1584,"entityType":20,"verifyStatus":20,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":20,"url":20,"parentIds":1586,"statistic":20},[],{"title":1585},{"EN":42},[],[1588,1595],{"id":46,"indexDatabase":1589,"url":57,"indexYears":58,"academicFieldIds":1594,"indexDatabaseRanking":61},{"id":48,"createTime":20,"updateTime":20,"relativeEntities":1590,"label":1591,"description":1592,"key":54,"publicationTags":1593,"standard":20},[],{"EN":51,"VI":51},{"EN":51,"VI":53},[56],[60],{"id":63,"indexDatabase":1596,"url":76,"indexYears":20,"academicFieldIds":1601,"indexDatabaseRanking":20},{"id":65,"createTime":20,"updateTime":20,"relativeEntities":1597,"label":1598,"description":1599,"key":72,"publicationTags":1600,"standard":20},[],{"EN":68,"VI":68},{"EN":70,"VI":71},[74,75],[78],{"impactFactor":21,"impactFactorByYear":1603,"i10Index":86,"i10IndexLast5Year":21,"totalPublication":87,"totalPublicationByYear":1604,"totalCitation":93,"totalCitationByYear":1605,"totalCitationPerPublication":98,"totalCitationPerPublicationByYear":1606,"hindexLast5Year":105,"hindex":105},{"2012":81,"2013":82,"2014":83,"2015":84,"2016":85},{"2010":89,"2011":90,"2012":90,"2013":91,"2014":92},{"2010":92,"2011":95,"2012":96,"2013":97,"2014":92},{"2010":100,"2011":101,"2012":102,"2013":103,"2014":104},{"pages":1608,"volume":1610},{"VOID":1609},"466-476",{"VOID":1611},"4","2013-12-20",2013,[61,74],{"id":1616,"createTime":1617,"updateTime":1618,"relativeEntities":1619,"slug":1620,"properties":1621,"entityType":959,"verifyStatus":128,"verifyTime":1618,"verifyNote":1140,"languages":20,"translateLanguages":20,"viewCount":21,"primaryUrl":1630,"fullTextUrl":20,"authors":1631,"publicationType":978,"publisherRelationship":1647,"citationCount":20,"citationInfo":20,"publishDate":1694,"publishYear":1028,"citationAnalyzeStatus":19,"lastCitationAnalyze":20,"indexDatabases":1695,"openAccess":20,"references":20,"isForceReanalyzing":1030},"0eeddce7-7a69-4517-a0cc-b47c791ef85b","2023-12-25T20:19:28.537+00:00","2025-01-23T15:19:57.778+00:00",[],"The-role-of-%CE%B1-synuclein-in-neurodegeneration-An-update",{"abstract":1622,"title":1624,"references":1626,"doi":1628},{"EN":1623},"Genetic, neuropathological and biochemical evidence implicates α-synuclein, a 140 amino acid presynaptic neuronal protein, in the pathogenesis of Parkinson’s disease and other neurodegenerative disorders. The aggregated protein inclusions mainly containing aberrant α-synuclein are widely accepted as morphological hallmarks of α-synucleinopathies, but their composition and location vary between disorders along with neuronal networks affected. α-Synuclein exists physiologically in both soluble and membran-bound states, in unstructured and α-helical conformations, respectively, while posttranslational modifications due to proteostatic deficits are involved in β-pleated aggregation resulting in formation of typical inclusions. The physiological function of α-synuclein and its role linked to neurodegeneration, however, are incompletely understood. Soluble oligomeric, not fully fibrillar α-synuclein is thought to be neurotoxic, main targets might be the synapse, axons and glia. The effects of aberrant α-synuclein include alterations of calcium homeostasis, mitochondrial dysfunction, oxidative and nitric injuries, cytoskeletal effects, and neuroinflammation. Proteasomal dysfunction might be a common mechanism in the pathogenesis of neuronal degeneration in α-synucleinopathies. However, how α-synuclein induces neurodegeneration remains elusive as its physiological function. Genome wide association studies demonstrated the important role for genetic variants of the SNCA gene encoding α-synuclein in the etiology of Parkinson’s disease, possibly through effects on oxidation, mitochondria, autophagy, and lysosomal function. The neuropathology of synucleinopathies and the role of α-synuclein as a potential biomarker are briefly summarized. Although animal models provided new insights into the pathogenesis of Parkinson disease and multiple system atrophy, most of them do not adequately reproduce the cardinal features of these disorders. Emerging evidence, in addition to synergistic interactions of α-synuclein with various pathogenic proteins, suggests that prionlike induction and seeding of α-synuclein could lead to the spread of the pathology and disease progression. Intervention in the early aggregation pathway, aberrant cellular effects, or secretion of α-synuclein might be targets for neuroprotection and disease-modifying therapy.",{"EN":1625},"The role of α-synuclein in neurodegeneration — An update",{"VOID":1627},"Vekrellis K., Xilouri M., Emmanouilidou E., Rideout H.J., Stefanis L., Pathological roles of α-synuclein in neurological disorders, Lancet Neurol., 2011, 10, 1015–1025\nFarrer M.J., Genetics of Parkinson disease: paradigm shifts and future prospects, Nat. Rev. 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Olfactory involvement is present in several degenerative disorders, especially in Alzheimer’s disease (AD). The peripheral and central parts of the olfactory system are damaged even in the early stages of AD, manifesting in profound olfactory deficits. Besides the early pathology, the olfactory system may be involved in the pathogenesis of AD by providing a route of entry for pathological agents still unknown. In contrast to this olfactory vector hypothesis, the olfactory system can be used to deliver therapeutic agents in AD, such as nerve growth factor and insulin, by decreasing the side-effects of the therapy or providing a non-invasive method of delivery.",{"EN":1706},"The olfactory system in Alzheimer’s disease: Pathology, pathophysiology and pathway for therapy",{"VOID":1708},"Querfurth H.W., LaFerla F.M., Alzheimer’s disease, N. Engl. J. Med., 2010, 362, 329–344\nKovács T., Mechanism of olfactory dysfunction in aging and neurodegenerative disorders, Ageing Res. 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Aging, 2006, 27, 402–412",{"VOID":1710},"10.2478\u002Fs13380-013-0108-3","https:\u002F\u002Fwww.degruyter.com\u002Fdocument\u002Fdoi\u002F10.2478\u002Fs13380-013-0108-3\u002Fhtml",[1713],{"id":1714,"sortIndex":21,"researcher":20,"roles":1715,"affiliations":1716,"properties":1725,"displayName":1727,"givenName":20,"familyName":20},"6de24641-fc63-4cfe-8533-e4c9833c3829",[965],[1717],{"id":1718,"sortIndex":21,"affiliation":1719,"properties":20},"d4f41247-f7d8-4ea4-88c0-4747d789acc0",{"id":1718,"createTime":20,"updateTime":20,"relativeEntities":1720,"slug":20,"properties":1721,"entityType":20,"verifyStatus":20,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":20,"url":20,"parentIds":1724,"statistic":20},[],{"title":1722},{"VI":1723},"Department of Neurology, Semmelweis University, Budapest, Hungary",[],{"title":1726},{"VI":1727},"Tibor Kovács",{"url":1711,"publisher":1729,"properties":1771},{"id":6,"createTime":7,"updateTime":8,"relativeEntities":1730,"slug":10,"properties":1731,"entityType":18,"verifyStatus":19,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":21,"subjectFields":1735,"manageAffiliations":1740,"indexDatabases":1751,"url":20,"thumbnailPath":20,"statistic":1766,"gsStatistic":20,"type":20,"analyzePriority":20},[],{"issn":1732,"title":1733,"eissn":1734},{"VOID":13},{"EN":15},{"VOID":17},[1736],{"id":24,"createTime":20,"updateTime":20,"relativeEntities":1737,"label":1738,"description":1739,"parentId":20,"standard":20,"scholarHubFieldId":20},[],{"EN":27},{},[1741,1746],{"id":31,"createTime":20,"updateTime":20,"relativeEntities":1742,"slug":20,"properties":1743,"entityType":20,"verifyStatus":20,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":20,"url":20,"parentIds":1745,"statistic":20},[],{"title":1744},{"EN":35},[],{"id":38,"createTime":20,"updateTime":20,"relativeEntities":1747,"slug":20,"properties":1748,"entityType":20,"verifyStatus":20,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":20,"url":20,"parentIds":1750,"statistic":20},[],{"title":1749},{"EN":42},[],[1752,1759],{"id":46,"indexDatabase":1753,"url":57,"indexYears":58,"academicFieldIds":1758,"indexDatabaseRanking":61},{"id":48,"createTime":20,"updateTime":20,"relativeEntities":1754,"label":1755,"description":1756,"key":54,"publicationTags":1757,"standard":20},[],{"EN":51,"VI":51},{"EN":51,"VI":53},[56],[60],{"id":63,"indexDatabase":1760,"url":76,"indexYears":20,"academicFieldIds":1765,"indexDatabaseRanking":20},{"id":65,"createTime":20,"updateTime":20,"relativeEntities":1761,"label":1762,"description":1763,"key":72,"publicationTags":1764,"standard":20},[],{"EN":68,"VI":68},{"EN":70,"VI":71},[74,75],[78],{"impactFactor":21,"impactFactorByYear":1767,"i10Index":86,"i10IndexLast5Year":21,"totalPublication":87,"totalPublicationByYear":1768,"totalCitation":93,"totalCitationByYear":1769,"totalCitationPerPublication":98,"totalCitationPerPublicationByYear":1770,"hindexLast5Year":105,"hindex":105},{"2012":81,"2013":82,"2014":83,"2015":84,"2016":85},{"2010":89,"2011":90,"2012":90,"2013":91,"2014":92},{"2010":92,"2011":95,"2012":96,"2013":97,"2014":92},{"2010":100,"2011":101,"2012":102,"2013":103,"2014":104},{"pages":1772,"volume":1774},{"VOID":1773},"34-45",{"VOID":1611},"2013-03-07",[61,74],{"id":1778,"createTime":1779,"updateTime":1780,"relativeEntities":1781,"slug":1782,"properties":1783,"entityType":959,"verifyStatus":128,"verifyTime":1780,"verifyNote":1140,"languages":20,"translateLanguages":20,"viewCount":21,"primaryUrl":1792,"fullTextUrl":20,"authors":1793,"publicationType":978,"publisherRelationship":1835,"citationCount":20,"citationInfo":20,"publishDate":1882,"publishYear":1207,"citationAnalyzeStatus":19,"lastCitationAnalyze":20,"indexDatabases":1883,"openAccess":20,"references":20,"isForceReanalyzing":1030},"13059424-81a3-4148-9473-777f22dd8327","2023-12-06T22:20:49.759+00:00","2025-01-03T05:16:42.495+00:00",[],"Tau-gene-promoter-rs242557-and-allele-specific-protein-binding",{"abstract":1784,"title":1786,"references":1788,"doi":1790},{"EN":1785},"The H1 haplotype clade of the tau gene (MAPT) is associated with increased risk of the sporadic disorders, progressive supranuclear palsy (PSP) and corticobasal degeneration (CBD) and to a lesser extent, Parkinson’s disease (PD). The H1c sub-haplotype drives this association in PSP and CBD, and is also weakly associated with Alzheimer’s disease (AD), suggesting involvement in common pathogenic pathway(s). The rs242557 single-nucleotide polymorphism (SNP) that defines H1c resides in a highly conserved repressor domain in the MAPT promoter. Previously, in cellular reporter assays, we showed significant rs242557 allele-specific differences in transcriptional repression, with the H1c-specific rs242557\u002FA allele contributing a significantly higher MAPT promoter activity compared to the non-H1c rs242557\u002FG allele. With evidence of allele-specific differences in protein binding to this repressor domain, we set out to identify those proteins that bind to this region. Electrophoretic mobility shift assay (EMSA) analysis strongly suggested allele-specific differences in protein affinities. In order to identify nuclear proteins that differentially bind to this repressor domain, we carried out a promoter-trap assay and analysed the bound proteins by SDS-PAGE and HPLC ESI-QTOF mass spectrometry. We identified 37 proteins and used bioinformatic tools such as STRING and Reactome to analyse and stratify the results. These included U2AF65, hnRNPU, PTBP1, hnRNPD0, U5 snRNP 116, ALY, HMGB2, H1 and actin and provide the basis for further studies of the role of the MAPT repressor domain and the binding proteins in regulating MAPT gene transcription and splicing.",{"EN":1787},"Tau gene promoter rs242557 and allele-specific protein binding",{"VOID":1789},"Pittman, A.M., Fung, H.C., and de Silva, R., Untangling the tau gene association with neurodegenerative disorders, Hum Mol Genet, 2006, 15 Spec No 2, R188–195\nBaker, M., Litvan, I., Houlden, H., Adamson, J., Dickson, D., Perez-Tur, J., et al., Association of an extended haplotype in the tau gene with progressive supranuclear palsy, Hum Mol Genet, 1999, 8, 711–715\nHoulden, H., Baker, M., Morris, H.R., MacDonald, N., Pickering-Brown, S., Adamson, J., et al., Corticobasal degeneration and progressive supranuclear palsy share a common tau haplotype, Neurology, 2001, 56, 1702–1706\nSimon-Sanchez, J., Schulte, C., Bras, J.M., Sharma, M., Gibbs, J.R., Berg, D., et al., Genome-wide association study reveals genetic risk underlying Parkinson’s disease, Nat Genet, 2009, 41, 1308–1312\nPittman, A.M., Myers, A.J., Abou-Sleiman, P., Fung, H.C., Kaleem, M., Marlowe, L., et al., Linkage disequilibrium fine mapping and haplotype association analysis of the tau gene in progressive supranuclear palsy and corticobasal degeneration, J Med Genet, 2005, 42, 837–846\nPittman, A.M., Myers, A.J., Duckworth, J., Bryden, L., Hanson, M., Abou-Sleiman, P., et al., The structure of the tau haplotype in controls and in progressive supranuclear palsy, Hum Mol Genet, 2004, 13, 1267–1274\nMyers, A.J., Kaleem, M., Marlowe, L., Pittman, A.M., Lees, A.J., Fung, H.C., et al., The H1c haplotype at the MAPT locus is associated with Alzheimer’s disease, Hum Mol Genet, 2005, 14, 2399–2404\nVandrovcova, J., Anaya, F., Kay, V., Lees, A., Hardy, J., and de Silva, R., Disentangling the Role of the tau Gene Locus in Sporadic Tauopathies, Curr Alzheimer Res, 2010, 7, 726–734\nHöglinger, G., Melhem, N.M., Dickson, D., Sleiman, P.M.A., Wang, L.S., Klei, L., et al., Common variants affect risk for the tauopathy progressive supranuclear palsy, Nature Genet, 2011, doi: 0.1038\u002Fng.859\nCaffrey, T.M., Joachim, C., Paracchini, S., Esiri, M.M., and Wade-Martins, R., Haplotype-specific expression of exon 10 at the human MAPT locus, Hum Mol Genet, 2006, 15, 3529–3537\nCaffrey, T.M., Joachim, C., and Wade-Martins, R., Haplotype-specific expression of the N-terminal exons 2 and 3 at the human MAPT locus, Neurobiol Aging, 2008, 29, 1923–1929\nMyers, A.J., Pittman, A.M., Zhao, A.S., Rohrer, K., Kaleem, M., Marlowe, L., et al., The MAPT H1c risk haplotype is associated with increased expression of tau and especially of 4 repeat containing transcripts, Neurobiol Dis, 2007, 25, 561–570\nAndreadis, A., Wagner, B.K., Broderick, J.A., and Kosik, K.S., A tau promoter region without neuronal specificity, J Neurochem, 1996, 66, 2257–2263\nKerr, L.D., Electrophoretic mobility shift assay, Methods Enzymol, 1995, 254, 619–632\nLudwig, L.B., Hughes, B.J., and Schwartz, S.A., Biotinylated probes in the electrophoretic mobility shift assay to examine specific dsDNA, ssDNA or RNA-protein interactions, Nucleic Acids Res, 1995, 23, 3792–3793\nBannister, A.J. and Kouzarides, T., Basic peptides enhance protein\u002FDNA interaction in vitro, Nucleic Acids Res, 1992, 20, 3523\nJensen, L.J., Kuhn, M., Stark, M., Chaffron, S., Creevey, C., Muller, J., et al., STRING 8—a global view on proteins and their functional interactions in 630 organisms, Nucleic Acids Res, 2009, 37, D412–416\nvon Mering, C., Jensen, L.J., Snel, B., Hooper, S.D., Krupp, M., Foglierini, M., Jouffre, N., Huynen, M.A., and Bork, P., STRING: known and predicted protein-protein associations, integrated and transferred across organisms, Nucleic Acids Res, 2005, 33, D433–437\nVastrik, I., D’Eustachio, P., Schmidt, E., Gopinath, G., Croft, D., de Bono, B., et al., Reactome: a knowledge base of biologic pathways and processes, Genome Biol, 2007, 8, R39\nMatthews, L., Gopinath, G., Gillespie, M., Caudy, M., Croft, D., de Bono, B., et al., Reactome knowledgebase of human biological pathways and processes, Nucleic Acids Res, 2009, 37, D619–622\nKornblihtt, A.R., Promoter usage and alternative splicing, Curr Opin Cell Biol, 2005, 17, 262–268\nChambers, C.B., Lee, J.M., Troncoso, J.C., Reich, S., and Muma, N.A., Overexpression of four-repeat tau mRNA isoforms in progressive supranuclear palsy but not in Alzheimer’s disease, Ann Neurol, 1999, 46, 325–332\nLuk, C., Vandrovcova, J., Malzer, E., Lees, A., and de Silva, R., Brain tau isoform mRNA and protein correlation in PSP brain, Transl Neurosci, 2010, 1, 30–36\nRademakers, R., Melquist, S., Cruts, M., Theuns, J., Del-Favero, J., Poorkaj, P., et al., High-density SNP haplotyping suggests altered regulation of tau gene expression in progressive supranuclear palsy, Hum Mol Genet, 2005, 14, 3281–3292\nMisteli, T. and Spector, D.L., RNA polymerase II targets pre-mRNA splicing factors to transcription sites in vivo, Mol Cell, 1999, 3, 697–705\nBird, G., Zorio, D.A., and Bentley, D.L., RNA polymerase II carboxyterminal domain phosphorylation is required for cotranscriptional pre-mRNA splicing and 3′-end formation, Mol Cell Biol, 2004, 24, 8963–8969\nDas, R., Yu, J., Zhang, Z., Gygi, M.P., Krainer, A.R., Gygi, S.P., and Reed, R., SR proteins function in coupling RNAP II transcription to pre-mRNA splicing, Mol Cell, 2007, 26, 867–881\nCramer, P., Caceres, J.F., Cazalla, D., Kadener, S., Muro, A.F., Baralle, F.E., and Kornblihtt, A.R., Coupling of transcription with alternative splicing: RNA pol II promoters modulate SF2\u002FASF and 9G8 effects on an exonic splicing enhancer, Mol Cell, 1999, 4, 251–258\nCramer, P., Pesce, C.G., Baralle, F.E., and Kornblihtt, A.R., Functional association between promoter structure and transcript alternative splicing, Proc Natl Acad Sci U S A, 1997, 94, 11456–11460\nPagani, F., Stuani, C., Zuccato, E., Kornblihtt, A.R., and Baralle, F.E., Promoter architecture modulates CFTR exon 9 skipping, J Biol Chem, 2003, 278, 1511–1517\nKornblihtt, A.R., Coupling transcription and alternative splicing, Adv Exp Med Biol, 2007, 623, 175–189\nDawson, H.N., Cantillana, V., Chen, L., and Vitek, M.P., The tau N279K exon 10 splicing mutation recapitulates frontotemporal dementia and parkinsonism linked to chromosome 17 tauopathy in a mouse model, J Neurosci, 2007, 27, 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angiomatosis is defined as a benign vascular proliferation affecting the medullar cavity of the bone and at least one other type of tissue, including skin, subcutaneous tissue, viscera, muscle, or synovium, and which does not spread to avascular tissue such as cartilage. Primary hemangiomas\u002Fcavernous hemangiomas (cavernomas) are exceedingly rare in the skull, accounting for 0.2% of all osseous neoplasms and are usually located in frontal and parietal bones. The authors present the case of a 66-year-old man who was admitted with right-side hemiparesis. MRI revealed a destructive bone lesion of the left frontal bone. Digital subtraction angiography of the brain did not reveal pathological vascularization, but a minor submucous hemangioma was seen in the nasal airway. Urine test for Bence-Jones proteins was positive for IgG λ light chain. Bone marrow aspiration and CSF analysis revealed no evidence of systemic myelomatosis suggesting a monoclonal gammopathy of undetermined significance. A highly vascular tumor was surgically removed. The histopathology verified cavernous hemangioma of the skull and the nasal submucous hemangioma. We discuss the diagnostic procedure, possible pathophysiological mechanisms and treatment implementation. It is possible that immunoglobulins from monoclonal gammopathies have an etiologic role in the development of the bone and skin changes in older patients, as an acquired condition, by producing a vascular injury that could lead to the multiple hemangiomas in skeletal-extraskeletal angiomatosis. To prevent misdiagnosis with lesions of other origins, multiple lesions of the head must be resected and histopathologically verified. In conclusion, to the best of our knowledge, this is the first case of giant cavernous hemangioma of the skull associated with paraproteinemia and skeletalextraskeletal angiomatosis limited to the head.",{"EN":1894},"Giant cavernoma of the skull and skeletal-extraskeletal angiomatosis associated with paraproteinemia",{"VOID":1896},"Devaney K., Vinh T.N., Sweet D. E., Skeletal-extraskeletal angiomatosis. A clinicopathological study of fourtheen patients and nosologic considerations, J. Bone Joint Surg. Am., 1994, 76A, 878–891\nAlexanian R., Weber D., Liu F., Differential diagnosis of monoclonal gammopathies, Arch. Pathol. Lab. Med., 1999, 123, 108–113\nHeckl S., Aschoff A., Kunze S., Cavernomas of the skull: review of the literature 1975–2000, Neurosurg. Rev., 2002, 25, 56–62\nKhanam H., Lipper M. H., Wolff C. L., Lopes, M. B., Calvarial hemangiomas: report of two cases and review of the literature, Surg. Neurol., 2001, 55, 63–67\nMaroon J. C., Haines S. J., Philips J. G., Calvarial hemangioendothelioma with intracranial hemorrhage: case report, Neurosurgery, 1979, 4, 178–180\nWyke B. D., Primary hemangioma of the skull, a rare cranial tumor, Am. J. Roentgenol., 1949, 61, 302–316\nSalama S., Jenkin P., Angiomatosis of skin with local intravascular immunoglobulin deposits, associated with monoclonal gammopathy. A potential cutaneous marker for B-chronic lymphocytic leukemia, J. Cutan. Pathol., 1999, 26, 206–212\nChang J., Most D., Bresnick S., Mehrara B., Steinbrech D. S., Reinich J. et al., Proliferative hemangiomas: analysis of cytokine gene expression and angiogenesis, Plast. Reconstr. Surg., 1999, 103, 1–9\nGodanich I. F., Campanacci M., Vascular hamartomata and infantile angioectatic osteohyperplasia of the extremities, J. Bone Joint Surg., 1962, 44A, 815\nMuliken J. B., Cutaneous vascular anomalies. In: McCarthy J. G., May J. W. Jr., Littler J. W, Plastic Surgery: Tumors of the head & neck and skin, Philadelphia: WB Saunders Co., 1990\nDurie B. G., Salmon S. E., A clinical staging system for multiple myeloma, Cancer, 1975, 36, 842–854\nClayer M., Skeletal angiomatosis in association with gastro-intestinal angiodysplasia and paraproteinemia: a case report, J. Orthop. Surg., 2002, 10, 85–88\nKumar A., Loughran T., Alsina M, Durie B. G., Djulbegovic B., Management of multiple myeloma: a systematic review and critical appraisal of published studies, Lancet Oncol., 2003, 4, 293–304\nResnick D., Kyriakos M., Greenway G. D., Tumors and tumor-like lesions of soft tissues. In: Resnick D., Kransdorf N. J., eds., Bone and joint imaging, 3rd ed. USA, Elsevier Saunders, 2005, 1219–1220\nKyle R. A., Rajkumar S. V., Monoclonal gammopathies of undetermined significance, Hematol. Oncol. Clin. North Am., 1999, 13, 1181–1202\nGottfried O. N., Gluf W. M., Schmidt H. M., Cavernous hemangioma of the skull presenting with subdural hematoma. Case report., Neurosurg. Focus, 2004, 17, ECP1\nFornasier V., Protzner K., Radiation-induced tibial sarcoma in a treated case of hind foot angiomatosis, Skel. Radiol., 1998, 27, 164–168",{"VOID":1898},"10.2478\u002Fs13380-011-0032-3","2024-12-26T01:51:40.731+00:00","https:\u002F\u002Fwww.degruyter.com\u002Fdocument\u002Fdoi\u002F10.2478\u002Fs13380-011-0032-3\u002Fhtml",[1902,1917,1931,1946,1959,1974,1989,2004,2017,2031,2045],{"id":1903,"sortIndex":21,"researcher":20,"roles":1904,"affiliations":1905,"properties":1914,"displayName":1916,"givenName":20,"familyName":20},"0bbea34d-2fb1-4433-ae27-a33ce7b86618",[965],[1906],{"id":1907,"sortIndex":21,"affiliation":1908,"properties":20},"963421ac-3d01-4b32-aa80-8c6368ea987e",{"id":1907,"createTime":20,"updateTime":20,"relativeEntities":1909,"slug":20,"properties":1910,"entityType":20,"verifyStatus":20,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":20,"url":20,"parentIds":1913,"statistic":20},[],{"title":1911},{"VI":1912},"School of Medicine, University Hospital Centre Zagreb, Department of Neurology and Croatian Institute for Brain Research, Diagnostic Centre „Neuron“, Department of Neurology, School of Medicine, University of Zagreb, University of Zagreb, Zagreb, Croatia",[],{"title":1915},{"VI":1916},"Helena Šarac",{"id":1918,"sortIndex":104,"researcher":20,"roles":1919,"affiliations":1920,"properties":1929,"displayName":1384,"givenName":20,"familyName":20},"0d6e7a64-3418-445a-8ac9-7bd7b8b9912b",[965],[1921],{"id":1922,"sortIndex":21,"affiliation":1923,"properties":20},"a92d790b-551e-43ec-81c6-fa6de79a4c38",{"id":1922,"createTime":20,"updateTime":20,"relativeEntities":1924,"slug":20,"properties":1925,"entityType":20,"verifyStatus":20,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":20,"url":20,"parentIds":1928,"statistic":20},[],{"title":1926},{"VI":1927},"School of Medicine, University Hospital Centre Zagreb, Department of Neurology, University of Zagreb, Zagreb, 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