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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. 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cells are cells specialized cell, capable of renewing themselves through cell division and can differentiate into multi-lineage cells. These cells are categorized as embryonic stem cells (ESCs), induced pluripotent stem cells (iPSCs) and adult stem cells. Mesenchymal stem cells (MSCs) are adult stem cells which can be isolated from human and animal sources. Human MSCs (hMSCs) are the non-haematopoietic, multipotent stem cells with the capacity to differentiate into mesodermal lineage such as osteocytes, adipocytes and chondrocytes as well ectodermal (neurocytes) and endodermal lineages (hepatocytes). MSCs express cell surface markers like cluster of differentiation (CD)29, CD44, CD73, CD90, CD105 and lack the expression of CD14, CD34, CD45 and HLA (human leucocyte antigen)-DR. hMSCs for the first time were reported in the bone marrow and till now they have been isolated from various tissues, including adipose tissue, amniotic fluid, endometrium, dental tissues, umbilical cord and Wharton's jelly which harbours potential MSCs. hMSCs have been cultured long-term in specific media without any severe abnormalities. Furthermore, MSCs have immunomodulatory features, secrete cytokines and immune-receptors which regulate the microenvironment in the host tissue. Multilineage potential, immunomodulation and secretion of anti-inflammatory molecules makes MSCs an effective tool in the treatment of chronic diseases. In the present review, we have highlighted recent research findings in the area of hMSCs sources, expression of cell surface markers, long-term in vitro culturing, in vitro differentiation potential, immunomodulatory features, its homing capacity, banking and cryopreservation, its application in the treatment of chronic diseases and its use in clinical trials.\u003C\u002Fjats:p>",{"EN":839},"Human mesenchymal stem cells - current trends and future prospective",{"VOID":841},"25797907",{"VOID":843},"10.1042\u002Fbsr20150025","PUBLICATION","Auto 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Biotechnol., 26, 101, 10.1038\u002Fnbt1374",{"doi":987},"10.1038\u002Fnbt1374",{"id":26,"text":989,"url":26,"identifiers":990},"Friedenstein, 1976, Fibroblast precursors in normal and irradiated mouse hematopoietic organs, Exp. Hematol., 4, 267",{},{"id":26,"text":992,"url":26,"identifiers":993},"Horwitz, 2005, Clarification of the nomenclature for MSC: The International Society for Cellular Therapy position statement, Cytotherapy, 7, 393, 10.1080\u002F14653240500319234",{"doi":994},"10.1080\u002F14653240500319234",{"id":26,"text":996,"url":26,"identifiers":997},"Pittenger, 1999, Multilineage potential of adult human mesenchymal stem cells, Science, 284, 143, 10.1126\u002Fscience.284.5411.143",{"doi":998},"10.1126\u002Fscience.284.5411.143",{"id":26,"text":1000,"url":26,"identifiers":1001},"Crisan, 2008, A perivascular origin for mesenchymal stem cells in multiple human organs, Cell Stem Cell, 3, 301, 10.1016\u002Fj.stem.2008.07.003",{"doi":1002},"10.1016\u002Fj.stem.2008.07.003",{"id":26,"text":1004,"url":26,"identifiers":1005},"Dominici, 2006, Minimal criteria for defining multipotent mesenchymal stromal cells. 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Commun., 341, 1135, 10.1016\u002Fj.bbrc.2006.01.072",{"doi":1643},"10.1016\u002Fj.bbrc.2006.01.072",{"id":26,"text":1645,"url":26,"identifiers":1646},"Anzalone, 2010, New emerging potentials for human Wharton's jelly mesenchymal stem cells: immunological features and hepatocyte-like differentiative capacity, Stem Cells Dev., 19, 423, 10.1089\u002Fscd.2009.0299",{"doi":1647},"10.1089\u002Fscd.2009.0299",{"id":26,"text":1649,"url":26,"identifiers":1650},"Mitchell, 2003, Matrix cells from Wharton's jelly form neurons and glia, Stem Cells, 21, 50, 10.1634\u002Fstemcells.21-1-50",{"doi":1651},"10.1634\u002Fstemcells.21-1-50",false,{"id":1654,"createTime":1655,"updateTime":1655,"relativeEntities":1656,"slug":1657,"properties":1658,"entityType":844,"verifyStatus":25,"verifyTime":1674,"verifyNote":845,"syncStatus":28,"languages":1675,"translateLanguages":26,"viewCount":36,"primaryUrl":1676,"fullTextUrl":26,"authors":1677,"publicationType":914,"publisherRelationship":1752,"citationCount":1786,"citationInfo":1787,"publishDate":1792,"publishYear":1793,"citationAnalyzeStatus":28,"lastCitationAnalyze":26,"indexDatabases":26,"openAccess":26,"references":1794,"isForceReanalyzing":1652},"61b28353-7350-4c52-ad0b-234e86241942","2024-10-16T19:16:21.343+00:00",[],"Apoptosis-and-apoptotic-body-disease-message-and-therapeutic-target-potentials",{"mag":1659,"keywords":1661,"pmc":1662,"openalex":1664,"abstract":1666,"title":1668,"pm":1670,"doi":1672},{"VOID":1660},"2905039795",{},{"VOID":1663},"6340950",{"VOID":1665},"W2905039795",{"EN":1667},"\u003Cjats:title>Abstract\u003C\u002Fjats:title>\u003Cjats:p>Apoptosis is widely known as programmed cell death eliciting no inflammatory responses. The intricacy of apoptosis has been a focus of an array of researches, accumulating a wealth of knowledge which led to not only a better understanding of the fundamental process, but also potent therapies of diseases. The classic intrinsic and extrinsic signaling pathways of apoptosis, along with regulatory factors have been well delineated. Drugs and therapeutic measures designed based on current understanding of apoptosis have long been employed. Small-molecule apoptosis inducers have been clinically used for eliminating morbid cells and therefore treating diseases, such as cancer. Biologics with improved apoptotic efficacy and selectivity, such as recombinant proteins and antibodies, are being extensively researched and some have been approved by the FDA. Apoptosis also produces membrane-bound vesicles derived from disassembly of apoptotic cells, now known as apoptotic bodies (ApoBDs). These little sealed sacs containing information as well as substances from dying cells were previously regarded as garbage bags until they were discovered to be capable of delivering useful materials to healthy recipient cells (e.g., autoantigens). In this review, current understandings and knowledge of apoptosis were summarized and discussed with a focus on apoptosis-related therapeutic applications and ApoBDs.\u003C\u002Fjats:p>",{"EN":1669},"Apoptosis and apoptotic body: disease message and therapeutic target 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U.S.A., 108, 20684, 10.1073\u002Fpnas.1116848108",{"doi":2257},"10.1073\u002Fpnas.1116848108",{"id":26,"text":2259,"url":26,"identifiers":2260},"Rubartelli, 1997, The selective engulfment of apoptotic bodies by dendritic cells is mediated by the alpha(v)beta3 integrin and requires intracellular and extracellular calcium, Eur. J. Immunol., 27, 1893, 10.1002\u002Feji.1830270812",{"doi":2261},"10.1002\u002Feji.1830270812",{"id":26,"text":2263,"url":26,"identifiers":2264},"Albert, 1998, Dendritic cells acquire antigen from apoptotic cells and induce class I-restricted CTLs, Nature, 392, 86, 10.1038\u002F32183",{"doi":2265},"10.1038\u002F32183",{"id":26,"text":2267,"url":26,"identifiers":2268},"Li, 2014, Anti-inflammatory response following uptake of apoptotic bodies by meningothelial cells, J. Neuroinflammation, 11, 35, 10.1186\u002F1742-2094-11-35",{"doi":2269},"10.1186\u002F1742-2094-11-35",{"id":26,"text":2271,"url":26,"identifiers":2272},"Kogianni, 2008, Apoptotic bodies convey activity capable of initiating osteoclastogenesis and localized bone destruction, J. Bone Miner. Res., 23, 915, 10.1359\u002Fjbmr.080207",{"doi":2273},"10.1359\u002Fjbmr.080207",{"id":26,"text":2275,"url":26,"identifiers":2276},"Schiller, 2008, Autoantigens are translocated into small apoptotic bodies during early stages of apoptosis, Cell Death Differ., 15, 183, 10.1038\u002Fsj.cdd.4402239",{"doi":2277},"10.1038\u002Fsj.cdd.4402239",{"id":26,"text":2279,"url":26,"identifiers":2280},"Jiang, 2009, Apoptotic body engulfment by hepatic stellate cells promotes their survival by the JAK\u002FSTAT and Akt\u002FNF-kappa B-dependent pathways, J. Hepatol., 51, 139, 10.1016\u002Fj.jhep.2009.03.024",{"doi":2281},"10.1016\u002Fj.jhep.2009.03.024",{"id":26,"text":2283,"url":26,"identifiers":2284},"Marin-Gallen, 2010, Dendritic cells pulsed with antigen-specific apoptotic bodies prevent experimental type 1 diabetes, Clin. Exp. Immunol., 160, 207, 10.1111\u002Fj.1365-2249.2009.04082.x",{"doi":2285},"10.1111\u002Fj.1365-2249.2009.04082.x",{"id":26,"text":2287,"url":26,"identifiers":2288},"Singh, 2012, Tubular cell HIV-entry through apoptosed CD4 T cells: a novel pathway, Virology, 434, 68, 10.1016\u002Fj.virol.2012.09.009",{"doi":2289},"10.1016\u002Fj.virol.2012.09.009",{"id":26,"text":2291,"url":26,"identifiers":2292},"Kranich, 2010, Engulfment of cerebral apoptotic bodies controls the course of prion disease in a mouse strain-dependent manner, J. Exp. Med., 207, 2271, 10.1084\u002Fjem.20092401",{"doi":2293},"10.1084\u002Fjem.20092401",{"id":26,"text":2295,"url":26,"identifiers":2296},"Samos, 2006, Circulating nucleic acids in plasma\u002Fserum and tumor progression – are apoptotic bodies involved? An experimental study in a rat cancer model, Ann. N. Y. Acad. Sci., 1075, 165, 10.1196\u002Fannals.1368.022",{"doi":2297},"10.1196\u002Fannals.1368.022",{"id":26,"text":2227,"url":26,"identifiers":2299},{"doi":2229},{"id":26,"text":2301,"url":26,"identifiers":2302},"Wiley, 2006, Immature dendritic cell-derived exosomes can mediate HIV-1 trans infection, Proc. Natl. Acad. Sci. U.S.A., 103, 738, 10.1073\u002Fpnas.0507995103",{"doi":2303},"10.1073\u002Fpnas.0507995103",{"id":26,"text":2305,"url":26,"identifiers":2306},"Izquierdo-Useros, 2010, HIV and mature dendritic cells: Trojan exosomes riding the Trojan horse?, PLoS Pathog., 6, 10.1371\u002Fjournal.ppat.1000740",{"doi":2307},"10.1371\u002Fjournal.ppat.1000740",{"id":26,"text":2309,"url":26,"identifiers":2310},"Poon, 2014, Unexpected link between an antibiotic, pannexin channels and apoptosis, Nature, 507, 329, 10.1038\u002Fnature13147",{"doi":2311},"10.1038\u002Fnature13147",{"id":26,"text":2313,"url":26,"identifiers":2314},"Poon, 2014, Apoptotic cell clearance: basic biology and therapeutic potential, Nat. Rev. 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Na+, K+-ATPase is responsible for generating andmaintaining transmembrane ionic gradients that are of vital importance forcellular function and subservient activities such as volume regulation, pHmaintenance, and generation of action potentials and secondary activetransport. The diversity of Na+, K+-ATPase subunit isoforms andtheir complex spatial and temporal patterns of cellular expression suggestthat Na+, K+-ATPase isozymes perform specialized physiologicalfunctions. Recent studies have shown that the α subunit isoformspossess considerably different kinetic properties and modes of regulationand the β subunit isoforms modulate the activity, expression and plasmamembrane targeting of Na+, K+-ATPase isozymes. This review focuseson recent developments in Na+, K+-ATPase research, and in particular reportsof expression of isoforms in various tissues and experiments aimed atelucidating the intrinsic structural features of isoforms important forNa+, K+-ATPase function.\u003C\u002Fjats:p>",{"EN":2330},"Na+, K+-ATPase Isozyme Diversity; Comparative Biochemistry and Physiological Implications of Novel Functional Interactions",{"VOID":2332},"10965965",{"VOID":2334},"10.1023\u002Fa:1005580332144",[102],"https:\u002F\u002Fportlandpress.com\u002Fbioscirep\u002Farticle\u002F20\u002F2\u002F51\u002F54290\u002FNa-K-ATPase-Isozyme-Diversity-Comparative",[2338,2357,2374,2395,2417,2434,2454,2469],{"id":2339,"sortIndex":111,"researcher":26,"roles":2340,"affiliations":2341,"properties":2352},"4bf656c9-979a-417f-9dc8-0c256e380433",[],[2342],{"id":2343,"sortIndex":36,"affiliation":2344,"properties":26},"db6aacce-4dce-404e-9b24-0e442060c178",{"id":2345,"createTime":2346,"updateTime":2346,"relativeEntities":2347,"slug":2348,"properties":2349,"entityType":98,"verifyStatus":28,"verifyTime":26,"verifyNote":26,"syncStatus":28,"languages":26,"translateLanguages":26,"viewCount":36},"7b7ec5c3-bf58-4c1f-8912-2983a27e150e","2024-10-12T08:50:22.639+00:00",[],"Dept-of-Veterinary-Preclinical-Sciences-University-of-Liverpool-Brownlow-Hill-and-Crown-Street-Liverpool-L69-3BX",{"title":2350},{"EN":2351},"Dept of Veterinary Preclinical Sciences, University of Liverpool, Brownlow Hill and Crown Street, Liverpool L69 3BX",{"openalex":2353,"title":2355},{"VOID":2354},"A5073502851",{"EN":2356},"M. 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this review, chemical and biological parameters are discussed thatstrongly influence the speciation of heavy metals, their availability tobiological systems and, consequently, the possibilities to usebioremediation as a cleanup tool for heavy metal polluted sites. In orderto assess heavy metal availability, a need exists for rapid, cost-effectivesystems that reliably predict this parameter and, based on this, thefeasibility of using biological remediation techniques for site managementand restoration. Special attention is paid to phytoremediation as anemerging technology for stabilization and remediation of heavy metalpollution. In order to improve phytoremediation of heavy metal pollutedsites, several important points relevant to the process have to beelucidated. These include the speciation and bioavailability of the heavymetals in the soil determined by many chemical and biological parameters, the role of plant-associated soil microorganisms and fungi inphytoremediation, and the plants. 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The absence of a defined pathway to excrete excess iron makes it essential for the body to regulate the amount of iron absorbed; a deficiency could lead to iron deficiency and an excess to iron overload and associated disorders such as anaemia and haemochromatosis respectively. This regulation is mediated by the iron-regulatory hormone hepcidin. Hepcidin binds to the only known iron export protein, ferroportin (FPN), inducing its internalization and degradation, thus limiting the amount of iron released into the blood. The major factors that are implicated in hepcidin regulation include iron stores, hypoxia, inflammation and erythropoiesis. 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Chem., 286, 4090, 10.1074\u002Fjbc.M110.173096",{"doi":3980},"10.1074\u002Fjbc.M110.173096",{"id":26,"text":3982,"url":26,"identifiers":3983},"Mastrogiannaki, 2012, Hepatic hypoxia-inducible factor-2 down-regulates hepcidin expression in mice through an erythropoietin-mediated increase in erythropoiesis, Haematologica, 97, 827, 10.3324\u002Fhaematol.2011.056119",{"doi":3984},"10.3324\u002Fhaematol.2011.056119",{"id":26,"text":3986,"url":26,"identifiers":3987},"Sonnweber, 2014, Hypoxia induced downregulation of hepcidin is mediated by platelet derived growth factor BB, Gut, 63, 1951, 10.1136\u002Fgutjnl-2013-305317",{"doi":3988},"10.1136\u002Fgutjnl-2013-305317",{"id":26,"text":3990,"url":26,"identifiers":3991},"Vecchi, 2009, ER stress controls iron metabolism through induction of hepcidin, Science, 325, 877, 10.1126\u002Fscience.1176639",{"doi":3992},"10.1126\u002Fscience.1176639",{"id":26,"text":3994,"url":26,"identifiers":3995},"Patel, 2014, The transcription factor ATOH8 is regulated by erythropoietic activity and regulates HAMP transcription and cellular pSMAD1,5,8 levels, Br. J. Haematol., 164, 586, 10.1111\u002Fbjh.12649",{"doi":3996},"10.1111\u002Fbjh.12649",{"id":26,"text":3998,"url":26,"identifiers":3999},"Goodnough, 2012, Inhibition of hepcidin transcription by growth factors, Hepatology, 56, 291, 10.1002\u002Fhep.25615",{"doi":4000},"10.1002\u002Fhep.25615",{"id":26,"text":4002,"url":26,"identifiers":4003},"Yang, 2012, 17β-Estradiol inhibits iron hormone hepcidin through an estrogen responsive element half-site, Endocrinology, 153, 3170, 10.1210\u002Fen.2011-2045",{"doi":4004},"10.1210\u002Fen.2011-2045",{"id":26,"text":4006,"url":26,"identifiers":4007},"Bachman, 2010, Testosterone suppresses hepcidin in men: a potential mechanism for testosterone-induced erythrocytosis, J. Clin. Endocrinol. Metab., 95, 4743, 10.1210\u002Fjc.2010-0864",{"doi":4008},"10.1210\u002Fjc.2010-0864",{"id":26,"text":4010,"url":26,"identifiers":4011},"Guo, 2013, Testosterone administration inhibits hepcidin transcription and is associated with increased iron incorporation into red blood cells, Aging Cell, 12, 280, 10.1111\u002Facel.12052",{"doi":4012},"10.1111\u002Facel.12052",{"id":26,"text":4014,"url":26,"identifiers":4015},"Bachman, 2013, Testosterone induces erythrocytosis via increased erythropoietin and suppressed hepcidin: evidence for a new erythropoietin\u002Fhemoglobin set point, J. Gerontol. A Biol. Sci. Med. Sci., 69, 725, 10.1093\u002Fgerona\u002Fglt154",{"doi":4016},"10.1093\u002Fgerona\u002Fglt154",{"id":26,"text":4018,"url":26,"identifiers":4019},"Latour, 2013, Testosterone perturbs systemic iron balance through activation of EGFR signaling in the liver and repression of hepcidin, Hepatology, 59, 683, 10.1002\u002Fhep.26648",{"doi":4020},"10.1002\u002Fhep.26648",{"id":26,"text":4022,"url":26,"identifiers":4023},"Latour, 2014, Testosterone perturbs systemic iron balance through activation of epidermal growth factor receptor signaling in the liver and repression of hepcidin, Hepatology, 59, 683, 10.1002\u002Fhep.26648",{"doi":4020},{"id":26,"text":4025,"url":26,"identifiers":4026},"Ikeda, 2012, Estrogen regulates hepcidin expression via GPR30-BMP6-dependent signaling in hepatocytes, PLoS One, 7, e40465, 10.1371\u002Fjournal.pone.0040465",{"doi":4027},"10.1371\u002Fjournal.pone.0040465",{"id":26,"text":4029,"url":26,"identifiers":4030},"Mleczko-Sanecka, 2014, Unbiased RNAi screen for hepcidin regulators links hepcidin suppression to the proliferative Ras\u002FRAF and the nutrient-dependent mTOR signaling pathways, Blood, 123, 1574, 10.1182\u002Fblood-2013-07-515957",{"doi":4031},"10.1182\u002Fblood-2013-07-515957",{"id":4033,"createTime":4034,"updateTime":4034,"relativeEntities":4035,"slug":4036,"properties":4037,"entityType":844,"verifyStatus":25,"verifyTime":4034,"verifyNote":845,"syncStatus":28,"languages":4053,"translateLanguages":26,"viewCount":36,"primaryUrl":4054,"fullTextUrl":26,"authors":4055,"publicationType":914,"publisherRelationship":4321,"citationCount":350,"citationInfo":4355,"publishDate":4357,"publishYear":4358,"citationAnalyzeStatus":28,"lastCitationAnalyze":26,"indexDatabases":26,"openAccess":26,"references":4359,"isForceReanalyzing":1652},"07af6ba9-eeb4-4f8e-81e3-e5cecf74b43f","2024-10-12T10:37:10.481+00:00",[],"Abdominal-obesity-and-colorectal-cancer-risk-systematic-review-and-meta-analysis-of-prospective-studies",{"mag":4038,"keywords":4040,"pmc":4041,"openalex":4043,"abstract":4045,"title":4047,"pm":4049,"doi":4051},{"VOID":4039},"2761480915",{},{"VOID":4042},"5725611",{"VOID":4044},"W2761480915",{"EN":4046},"\u003Cjats:p>The association between abdominal obesity (as measured by waist circumference (WC) and waist-to-hip ratio (WHR)) and colorectal cancer (CRC) has not been fully quantified, and the magnitude of CRC risk associated with abdominal obesity is still unclear. A meta-analysis of prospective studies was performed to elucidate the CRC risk associated with abdominal obesity. Pubmed and Embase were searched for studies assessing the association between abdominal obesity and CRC risk. Relative risks (RRs) with 95% confidence intervals (95% CIs) were pooled using random-effects model of meta-analysis. Nineteen prospective cohort studies from eighteen publications were included in this meta-analysis. A total of 12,837 CRC cases were identified among 1,343,560 participants. Greater WC and WHR were significantly associated with increased risk of total colorectal cancer (WC: RR 1.42, 95% CI 1.30, 1.55; WHR: RR 1.39, 95% CI 1.25, 1.53), colon cancer (WC: RR 1.53, 95% CI 1.36, 1.72; WHR: 1.39, 95% CI 1.18, 1.63), and rectal cancer (WC: RR 1.20, 95% CI 1.03, 1.39; WHR: RR 1.22, 95% CI 1.05, 1.42). Subgroup analyses further identified the robustness of the association above. No obvious risk of publication bias was observed. In summary, abdominal obesity may play an important role in the development of CRC.\u003C\u002Fjats:p>",{"EN":4048},"Abdominal obesity and colorectal cancer risk: systematic review and meta-analysis of prospective 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of Orthopedic Surgery, The People’s Hospital of Yuxi City, The 6th Affiliated Hospital of Kunming Medical University, Yuxi 653100, China",{"openalex":4071,"title":4073},{"VOID":4072},"A5102206330",{"EN":4074},"Li-Fen Xu",{"id":4076,"sortIndex":53,"researcher":26,"roles":4077,"affiliations":4078,"properties":4089},"8aea26f9-fec6-4bd8-9771-bc2be36df549",[],[4079],{"id":4080,"sortIndex":36,"affiliation":4081,"properties":26},"40118bbe-9025-4e07-9de7-e937f856b63b",{"id":4082,"createTime":4083,"updateTime":4083,"relativeEntities":4084,"slug":4085,"properties":4086,"entityType":98,"verifyStatus":28,"verifyTime":26,"verifyNote":26,"syncStatus":28,"languages":26,"translateLanguages":26,"viewCount":36},"482441fc-aaaa-4cd6-988c-25ebec704545","2024-10-12T10:37:10.644+00:00",[],"Department-of-Science-and-Education-The-People-s-Hospital-of-Yuxi-City-The-6th-Affiliated-Hospital-of-Kunming-Medical-University-Yuxi-653100-China",{"title":4087},{"EN":4088},"Department of Science and Education, The People’s Hospital of Yuxi City, The 6th Affiliated Hospital of Kunming Medical University, Yuxi 653100, China",{"openalex":4090,"orcid":4092,"title":4094},{"VOID":4091},"A5100317669",{"VOID":4093},"https:\u002F\u002Forcid.org\u002F0000-0002-0320-061X",{"EN":4095},"Jianping 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Metab., 89, 1879, 10.1210\u002Fjc.2003-031349",{"doi":4545},"10.1210\u002Fjc.2003-031349",{"id":26,"text":4547,"url":26,"identifiers":4548},"Sandhu, 2002, Insulin, insulin-like growth factor-I (IGF-I), IGF binding proteins, their biologic interactions, and colorectal cancer, J. Natl. Cancer Inst., 94, 972, 10.1093\u002Fjnci\u002F94.13.972",{"doi":4549},"10.1093\u002Fjnci\u002F94.13.972",{"id":26,"text":4551,"url":26,"identifiers":4552},"Clayton, 2011, Growth hormone, the insulin-like growth factor axis, insulin and cancer risk, Nat. Rev. Endocrinol., 7, 11, 10.1038\u002Fnrendo.2010.171",{"doi":4553},"10.1038\u002Fnrendo.2010.171",{"id":26,"text":4417,"url":26,"identifiers":4555},{"doi":4419},{"id":26,"text":4425,"url":26,"identifiers":4557},{"doi":4427},{"id":26,"text":4559,"url":26,"identifiers":4560},"Pischon, 2006, Body size and risk of colon and rectal cancer in the European Prospective Investigation Into Cancer and Nutrition (EPIC)., J. Natl. Cancer Inst., 98, 920, 10.1093\u002Fjnci\u002Fdjj246",{"doi":4431},{"id":26,"text":4421,"url":26,"identifiers":4562},{"doi":4423},{"id":4564,"createTime":4565,"updateTime":4565,"relativeEntities":4566,"slug":4567,"properties":4568,"entityType":844,"verifyStatus":25,"verifyTime":4565,"verifyNote":845,"syncStatus":28,"languages":4584,"translateLanguages":26,"viewCount":36,"primaryUrl":4585,"fullTextUrl":26,"authors":4586,"publicationType":914,"publisherRelationship":4682,"citationCount":4715,"citationInfo":4716,"publishDate":4719,"publishYear":4720,"citationAnalyzeStatus":28,"lastCitationAnalyze":26,"indexDatabases":26,"openAccess":26,"references":4721,"isForceReanalyzing":1652},"95deaede-8922-4d8d-9175-a47f9c73f829","2024-09-24T09:52:33.063+00:00",[],"Gene-editing-and-CRISPR-in-the-clinic-current-and-future-perspectives",{"mag":4569,"keywords":4571,"pmc":4572,"openalex":4574,"abstract":4576,"title":4578,"pm":4580,"doi":4582},{"VOID":4570},"3012901598",{},{"VOID":4573},"7146048",{"VOID":4575},"W3012901598",{"EN":4577},"\u003Cjats:title>Abstract\u003C\u002Fjats:title>\u003Cjats:p>Genome editing technologies, particularly those based on zinc-finger nucleases (ZFNs), transcription activator-like effector nucleases (TALENs), and CRISPR (clustered regularly interspaced short palindromic repeat DNA sequences)\u002FCas9 are rapidly progressing into clinical trials. Most clinical use of CRISPR to date has focused on ex vivo gene editing of cells followed by their re-introduction back into the patient. The ex vivo editing approach is highly effective for many disease states, including cancers and sickle cell disease, but ideally genome editing would also be applied to diseases which require cell modification in vivo. However, in vivo use of CRISPR technologies can be confounded by problems such as off-target editing, inefficient or off-target delivery, and stimulation of counterproductive immune responses. Current research addressing these issues may provide new opportunities for use of CRISPR in the clinical space. In this review, we examine the current status and scientific basis of clinical trials featuring ZFNs, TALENs, and CRISPR-based genome editing, the known limitations of CRISPR use in humans, and the rapidly developing CRISPR engineering space that should lay the groundwork for further translation to clinical application.\u003C\u002Fjats:p>",{"EN":4579},"Gene editing and CRISPR in the clinic: current and future perspectives",{"VOID":4581},"32207531",{"VOID":4583},"10.1042\u002Fbsr20200127",[102],"https:\u002F\u002Fportlandpress.com\u002Fbioscirep\u002Farticle\u002F40\u002F4\u002FBSR20200127\u002F222452\u002FGene-editing-and-CRISPR-in-the-clinic-current-and",[4587,4606,4627,4644,4665],{"id":4588,"sortIndex":59,"researcher":26,"roles":4589,"affiliations":4590,"properties":4601},"780afa27-9f0d-4fbe-b73a-446de5978a0c",[],[4591],{"id":4592,"sortIndex":36,"affiliation":4593,"properties":26},"f5fdb79b-b188-4096-9daa-982af0bfe1af",{"id":4594,"createTime":4595,"updateTime":4595,"relativeEntities":4596,"slug":4597,"properties":4598,"entityType":98,"verifyStatus":28,"verifyTime":26,"verifyNote":26,"syncStatus":28,"languages":26,"translateLanguages":26,"viewCount":36},"332fad16-291c-419b-afe2-b976d18135a5","2024-09-24T09:52:33.136+00:00",[],"Advanced-Materials-Laboratory-Sandia-National-Laboratories-Albuquerque-NM-87185-U-S-A-",{"title":4599},{"EN":4600},"Advanced Materials Laboratory, Sandia National Laboratories, Albuquerque, NM 87185, U.S.A.",{"openalex":4602,"title":4604},{"VOID":4603},"A5106037649",{"EN":4605},"James P. 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