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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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Elsevier",{"EN":738,"VI":740},"Cơ sở dữ liệu Scopus thuộc Elsevier","scopus",[743],"SCOPUS","https:\u002F\u002Fwww.scopus.com\u002Fsourceid\u002F24004","1945-2025",[747,748,749,750],"0404956d-7818-4510-b67a-db80799a6ec0","e89cebf4-fecf-4b74-8ab4-88fca891e4c2","f845e4fe-178d-4593-b013-715b3c1cc81c","6265d46a-80a6-48ce-b79a-f3a34594a0bd","SCOPUS__Q1",{"id":753,"indexDatabase":754,"url":768,"indexYears":26,"academicFieldIds":769,"indexDatabaseRanking":26},"ec0e5632-0882-4f93-b85d-ef279bbda997",{"id":755,"createTime":756,"updateTime":757,"relativeEntities":758,"label":759,"description":761,"key":764,"publicationTags":765,"standard":26},"a4921856-b128-4d9f-8f1f-e80813d3bbd4","2023-05-22T09:59:31.026+00:00","2025-11-21T10:07:52.153+00:00",[],{"EN":760,"VI":760},"ISI\u002FSCIE - Science Citation Index Expanded",{"VI":762,"EN":763},"Cơ sở dữ liệu SCIE","SCIE database","scie",[766,767],"SCIE","ISI","https:\u002F\u002Fmjl.clarivate.com\u002Fsearch-results?issn=0031-9333",[770],"08b1efac-a7b2-46c7-9e79-ef24d3d9025d","https:\u002F\u002Fjournals.physiology.org\u002Fjournal\u002Fphysrev",{"meta":773,"data":775},{"total":774},"390",[776,2872,5998,8926,9021,13667,15412,16707,16799,18019],{"id":777,"createTime":778,"updateTime":779,"relativeEntities":780,"slug":781,"properties":782,"entityType":799,"verifyStatus":25,"verifyTime":800,"verifyNote":801,"syncStatus":28,"languages":802,"translateLanguages":803,"viewCount":36,"primaryUrl":804,"fullTextUrl":26,"authors":805,"publicationType":826,"publisherRelationship":827,"citationCount":860,"citationInfo":861,"publishDate":874,"publishYear":875,"citationAnalyzeStatus":28,"lastCitationAnalyze":26,"indexDatabases":26,"openAccess":26,"references":876,"isForceReanalyzing":2871},"cb11d03c-ee10-4bb9-b23b-7fdc913adb32","2024-09-18T07:39:07.999+00:00","2025-02-08T00:02:26.926+00:00",[],"Free-Radicals-in-the-Physiological-Control-of-Cell-Function",{"mag":783,"keywords":785,"openalex":787,"abstract":789,"title":792,"pm":795,"doi":797},{"VOID":784},"2147993424",{"VI":786},"",{"VOID":788},"W2147993424",{"EN":790,"VI":791},"\u003Cjats:p>At high concentrations, free radicals and radical-derived, nonradical reactive species are hazardous for living organisms and damage all major cellular constituents. At moderate concentrations, however, nitric oxide (NO), superoxide anion, and related reactive oxygen species (ROS) play an important role as regulatory mediators in signaling processes. Many of the ROS-mediated responses actually protect the cells against oxidative stress and reestablish “redox homeostasis.” Higher organisms, however, have evolved the use of NO and ROS also as signaling molecules for other physiological functions. These include regulation of vascular tone, monitoring of oxygen tension in the control of ventilation and erythropoietin production, and signal transduction from membrane receptors in various physiological processes. NO and ROS are typically generated in these cases by tightly regulated enzymes such as NO synthase (NOS) and NAD(P)H oxidase isoforms, respectively. In a given signaling protein, oxidative attack induces either a loss of function, a gain of function, or a switch to a different function. Excessive amounts of ROS may arise either from excessive stimulation of NAD(P)H oxidases or from less well-regulated sources such as the mitochondrial electron-transport chain. In mitochondria, ROS are generated as undesirable side products of the oxidative energy metabolism. An excessive and\u002For sustained increase in ROS production has been implicated in the pathogenesis of cancer, diabetes mellitus, atherosclerosis, neurodegenerative diseases, rheumatoid arthritis, ischemia\u002Freperfusion injury, obstructive sleep apnea, and other diseases. In addition, free radicals have been implicated in the mechanism of senescence. That the process of aging may result, at least in part, from radical-mediated oxidative damage was proposed more than 40 years ago by Harman ( J Gerontol 11: 298–300, 1956). There is growing evidence that aging involves, in addition, progressive changes in free radical-mediated regulatory processes that result in altered gene expression.\u003C\u002Fjats:p>","\u003Cjats:p>Tại nồng độ cao, các gốc tự do và các species phản ứng không gốc xuất phát từ gốc tự do có thể gây nguy hiểm cho sinh vật sống và làm tổn thương tất cả các thành phần chính của tế bào. Tuy nhiên, tại nồng độ trung bình, nitric oxide (NO), anion siêu ôxy và các species oxy phản ứng liên quan (ROS) đóng vai trò quan trọng như các chất trung gian điều tiết trong các quá trình tín hiệu. Nhiều phản ứng trung gian ROS thực sự bảo vệ tế bào khỏi stress oxy hóa và tái thiết lập “cân bằng redox”. Tuy nhiên, các sinh vật bậc cao đã tiến hóa để sử dụng NO và ROS như là các phân tử tín hiệu cho các chức năng sinh lý khác. Các chức năng này bao gồm điều chỉnh trương lực mạch máu, giám sát áp lực oxy trong kiểm soát thông khí và sản xuất erythropoietin, cũng như truyền tín hiệu từ các thụ thể màng trong nhiều quá trình sinh lý. Trong những trường hợp này, NO và ROS thường được sinh ra bởi các enzyme được điều tiết chặt chẽ như NO synthase (NOS) và các dạng isozyme NAD(P)H oxidase, tương ứng. Trong một protein tín hiệu nhất định, sự tấn công oxy hóa có thể gây ra mất chức năng, tăng chức năng, hoặc chuyển đổi sang một chức năng khác. Lượng ROS dư thừa có thể xuất phát từ sự kích thích quá mức của NAD(P)H oxidase hoặc từ các nguồn ít được điều tiết hơn như chuỗi vận chuyển electron ti thể. Trong ti thể, ROS được sinh ra như là sản phẩm phụ không mong muốn của quá trình chuyển hóa năng lượng oxy hóa. Việc sản xuất ROS gia tăng quá mức và\u002Fhoặc kéo dài đã được gán cho sự khởi phát của ung thư, bệnh tiểu đường, xơ vữa động mạch, các bệnh thoái hóa thần kinh, viêm khớp dạng thấp, chấn thương thiếu máu\u002Ftái tưới máu, ngưng thở khi ngủ tắc nghẽn, và các căn bệnh khác. Ngoài ra, các gốc tự do cũng đã được gán cho cơ chế lão hóa. Quá trình lão hóa có thể xảy ra, ít nhất một phần, do tổn thương oxy hóa do gốc tự do gây ra như đã được đề xuất hơn 40 năm trước bởi Harman (J Gerontol 11: 298–300, 1956). Có bằng chứng ngày càng tăng rằng quá trình lão hóa liên quan đến những thay đổi tiến triển trong các quá trình điều tiết do gốc tự do trung gian, dẫn đến sự thay đổi biểu hiện gen.\u003C\u002Fjats:p>",{"EN":793,"VI":794},"Free Radicals in the Physiological Control of Cell Function","Các gốc tự do trong việc kiểm soát sinh lý chức năng tế bào",{"VOID":796},"11773609",{"VOID":798},"10.1152\u002Fphysrev.00018.2001","PUBLICATION","2024-09-18T07:39:07.998+00:00","Auto 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Dröge","ARTICLE",{"url":26,"publisher":828,"properties":853},{"id":659,"createTime":660,"updateTime":661,"relativeEntities":829,"slug":663,"properties":830,"entityType":24,"verifyStatus":28,"verifyTime":26,"verifyNote":26,"syncStatus":28,"languages":26,"translateLanguages":26,"viewCount":36,"subjectFields":836,"manageAffiliations":837,"indexDatabases":838,"url":771,"thumbnailPath":26,"statistic":26,"gsStatistic":26,"type":26,"analyzePriority":26},[],{"country":831,"issn":832,"introduce":833,"eissn":834,"title":835},{"VOID":666},{"VOID":668},{"EN":670},{"VOID":672},{"EN":674},[],[],[839,846],{"id":731,"indexDatabase":840,"url":744,"indexYears":745,"academicFieldIds":845,"indexDatabaseRanking":751},{"id":733,"createTime":734,"updateTime":735,"relativeEntities":841,"label":842,"description":843,"key":741,"publicationTags":844,"standard":26},[],{"EN":738,"VI":738},{"EN":738,"VI":740},[743],[747,748,749,750],{"id":753,"indexDatabase":847,"url":768,"indexYears":26,"academicFieldIds":852,"indexDatabaseRanking":26},{"id":755,"createTime":756,"updateTime":757,"relativeEntities":848,"label":849,"description":850,"key":764,"publicationTags":851,"standard":26},[],{"EN":760,"VI":760},{"VI":762,"EN":763},[766,767],[770],{"volume":854,"pages":856,"issue":858},{"VOID":855},"82",{"VOID":857},"47-95",{"VOID":859},"1",9429,{"total":860,"publishYear":26,"statisticByYear":862},{"2012":863,"2013":864,"2014":865,"2015":866,"2016":867,"2017":868,"2018":869,"2019":868,"2020":467,"2021":870,"2022":871,"2023":872,"2024":873},529,564,569,545,473,449,401,512,495,393,195,"2002-01-01",2002,[877,880,883,886,889,892,895,898,901,904,907,910,913,916,919,922,925,928,931,934,937,940,943,946,949,952,955,958,961,965,968,970,973,976,979,982,985,988,991,994,997,1001,1004,1007,1010,1013,1017,1020,1023,1026,1029,1032,1036,1039,1042,1045,1048,1051,1054,1057,1060,1064,1067,1070,1073,1076,1079,1082,1085,1088,1091,1094,1097,1100,1103,1106,1109,1112,1115,1118,1121,1124,1128,1131,1134,1137,1140,1143,1147,1150,1153,1156,1159,1162,1165,1169,1173,1177,1180,1183,1186,1189,1192,1195,1198,1201,1204,1207,1210,1213,1216,1219,1222,1225,1228,1231,1234,1237,1240,1243,1246,1249,1253,1256,1260,1264,1268,1271,1274,1277,1280,1283,1286,1289,1292,1295,1298,1301,1304,1307,1310,1313,1316,1319,1322,1326,1329,1332,1335,1338,1341,1344,1347,1350,1353,1356,1359,1362,1365,1368,1371,1374,1377,1380,1383,1386,1389,1392,1395,1398,1401,1404,1407,1411,1414,1417,1420,1424,1427,1430,1433,1437,1440,1443,1446,1449,1452,1455,1458,1461,1464,1467,1470,1473,1476,1479,1482,1485,1488,1491,1494,1497,1500,1503,1506,1510,1513,1516,1519,1522,1525,1529,1532,1535,1538,1541,1544,1547,1550,1553,1557,1560,1563,1566,1570,1573,1576,1579,1582,1585,1588,1591,1594,1598,1602,1605,1608,1611,1614,1617,1620,1623,1627,1630,1633,1636,1639,1643,1646,1649,1652,1655,1658,1661,1664,1667,1671,1674,1677,1680,1683,1686,1689,1692,1695,1698,1701,1704,1707,1710,1713,1716,1719,1722,1725,1728,1731,1734,1737,1740,1743,1747,1750,1753,1756,1759,1762,1765,1768,1771,1774,1777,1780,1783,1786,1789,1792,1795,1798,1801,1804,1807,1810,1814,1817,1820,1823,1826,1829,1832,1835,1838,1841,1844,1847,1850,1853,1856,1859,1862,1865,1868,1871,1874,1877,1880,1883,1886,1889,1892,1895,1898,1902,1905,1908,1911,1914,1917,1920,1923,1926,1929,1932,1935,1938,1941,1944,1947,1950,1953,1956,1959,1962,1965,1968,1971,1974,1977,1980,1983,1986,1989,1992,1995,1998,2001,2004,2007,2010,2013,2017,2021,2024,2027,2030,2033,2036,2040,2043,2046,2049,2052,2055,2058,2061,2064,2067,2070,2073,2076,2079,2082,2086,2089,2092,2095,2098,2101,2104,2107,2110,2113,2117,2120,2123,2126,2129,2132,2135,2138,2141,2144,2147,2150,2153,2156,2159,2162,2165,2168,2171,2174,2177,2180,2184,2187,2190,2193,2196,2199,2202,2205,2208,2211,2214,2217,2220,2223,2226,2229,2232,2235,2238,2241,2244,2247,2251,2254,2257,2260,2263,2266,2269,2272,2275,2279,2282,2285,2288,2291,2294,2297,2300,2303,2306,2309,2312,2315,2318,2321,2324,2327,2330,2333,2336,2339,2342,2345,2348,2352,2356,2360,2363,2366,2369,2372,2375,2378,2381,2384,2387,2390,2394,2397,2400,2403,2406,2410,2413,2416,2419,2422,2425,2429,2432,2435,2438,2442,2445,2448,2452,2455,2458,2461,2464,2467,2470,2473,2476,2479,2482,2485,2488,2491,2494,2497,2500,2503,2506,2509,2512,2515,2518,2521,2524,2527,2530,2534,2537,2540,2543,2546,2549,2552,2555,2558,2561,2564,2567,2570,2573,2576,2580,2583,2586,2589,2592,2595,2598,2601,2604,2607,2610,2613,2616,2619,2622,2625,2628,2631,2634,2637,2640,2643,2646,2649,2653,2656,2659,2662,2666,2669,2672,2675,2678,2681,2684,2687,2690,2693,2696,2699,2702,2705,2708,2711,2714,2717,2720,2723,2725,2728,2732,2736,2739,2742,2745,2748,2751,2754,2758,2761,2764,2767,2770,2773,2776,2779,2782,2785,2788,2791,2794,2797,2800,2803,2806,2809,2812,2815,2818,2821,2825,2828,2831,2834,2837,2840,2843,2846,2849,2852,2855,2858,2861,2864,2867],{"id":26,"text":878,"url":26,"identifiers":879},"10.1126\u002Fscience.2118682",{"doi":878},{"id":26,"text":881,"url":26,"identifiers":882},"10.1074\u002Fjbc.271.28.16586",{"doi":881},{"id":26,"text":884,"url":26,"ident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10.1016\u002FS0021-9258(18)69163-X",{"doi":2735},"10.1016\u002FS0021-9258(18)69163-X",{"id":26,"text":2737,"url":26,"identifiers":2738},"10.1016\u002F0042-6822(79)90019-9",{"doi":2737},{"id":26,"text":2740,"url":26,"identifiers":2741},"10.1096\u002Ffasebj.11.13.9367355",{"doi":2740},{"id":26,"text":2743,"url":26,"identifiers":2744},"10.1016\u002F0167-5699(95)80067-0",{"doi":2743},{"id":26,"text":2746,"url":26,"identifiers":2747},"10.1042\u002Fbj2450325",{"doi":2746},{"id":26,"text":2749,"url":26,"identifiers":2750},"10.1128\u002FMCB.17.8.4792",{"doi":2749},{"id":26,"text":2752,"url":26,"identifiers":2753},"10.1006\u002Fjmbi.1997.1426",{"doi":2752},{"id":26,"text":2755,"url":26,"identifiers":2756},"Williams MS, 1996, J Immunol, 157, 2395, 10.4049\u002Fjimmunol.157.6.2395",{"doi":2757},"10.4049\u002Fjimmunol.157.6.2395",{"id":26,"text":2759,"url":26,"identifiers":2760},"10.1023\u002FA:1005804508902",{"doi":2759},{"id":26,"text":2762,"url":26,"identifiers":2763},"10.1016\u002F0531-5565(87)90002-7",{"doi":2762},{"id":26,"text":2765,"url":26,"identifiers":2766},"10.2337\u002Fdiab.36.9.1014",{"doi":2765},{"id":26,"text":2768,"url":26,"identifiers":2769},"10.1084\u002Fjem.42.6.753",{"doi":2768},{"id":26,"text":2771,"url":26,"identifiers":2772},"10.1016\u002F0891-5849(91)90040-A",{"doi":2771},{"id":26,"text":2774,"url":26,"identifiers":2775},"10.1093\u002Foxfordjournals.bmb.a072637",{"doi":2774},{"id":26,"text":2777,"url":26,"identifiers":2778},"10.1007\u002FBF01947562",{"doi":2777},{"id":26,"text":2780,"url":26,"identifiers":2781},"10.1016\u002F0968-0004(86)90228-8",{"doi":2780},{"id":26,"text":2783,"url":26,"identifiers":2784},"10.1016\u002FS0034-5687(99)00023-7",{"doi":2783},{"id":26,"text":2786,"url":26,"identifiers":2787},"10.1104\u002Fpp.115.2.427",{"doi":2786},{"id":26,"text":2789,"url":26,"identifiers":2790},"10.1074\u002Fjbc.270.17.10323",{"doi":2789},{"id":26,"text":2792,"url":26,"identifiers":2793},"10.1002\u002Fj.1460-2075.1996.tb00845.x",{"doi":2792},{"id":26,"text":2795,"url":26,"identifiers":2796},"10.1016\u002FS0074-7696(08)62312-8",{"doi":2795},{"id":26,"text":2798,"url":26,"identifiers":2799},"10.1002\u002Fj.1460-2075.1992.tb05097.x",{"doi":2798},{"id":26,"text":2801,"url":26,"identifiers":2802},"10.1002\u002Fj.1460-2075.1992.tb05411.x",{"doi":2801},{"id":26,"text":2804,"url":26,"identifiers":2805},"10.1126\u002Fscience.1373522",{"doi":2804},{"id":26,"text":2807,"url":26,"identifiers":2808},"10.1038\u002F366701a0",{"doi":2807},{"id":26,"text":2810,"url":26,"identifiers":2811},"10.1172\u002FJCI116508",{"doi":2810},{"id":26,"text":2813,"url":26,"identifiers":2814},"10.1038\u002F385595a0",{"doi":2813},{"id":26,"text":2816,"url":26,"identifiers":2817},"10.1038\u002F384484a0",{"doi":2816},{"id":26,"text":2819,"url":26,"identifiers":2820},"10.1016\u002F0005-2760(92)90297-9",{"doi":2819},{"id":26,"text":2822,"url":26,"identifiers":2823},"Yan SD, 1994, J Biol Chem, 269, 9889, 10.1016\u002FS0021-9258(17)36966-1",{"doi":2824},"10.1016\u002FS0021-9258(17)36966-1",{"id":26,"text":2826,"url":26,"identifiers":2827},"10.1016\u002F0022-510X(86)90152-8",{"doi":2826},{"id":26,"text":2829,"url":26,"identifiers":2830},"10.1016\u002F0022-510X(87)90238-3",{"doi":2829},{"id":26,"text":2832,"url":26,"identifiers":2833},"10.1016\u002F0022-510X(88)90204-3",{"doi":2832},{"id":26,"text":2835,"url":26,"identifiers":2836},"Yashpe-Purer Henis Y, 1977, J Microbiol, 23, 84",{},{"id":26,"text":2838,"url":26,"identifiers":2839},"10.1172\u002FJCI113011",{"doi":2838},{"id":26,"text":2841,"url":26,"identifiers":2842},"10.1074\u002Fjbc.275.16.11706",{"doi":2841},{"id":26,"text":2844,"url":26,"identifiers":2845},"10.1056\u002FNEJM199304293281704",{"doi":2844},{"id":26,"text":2847,"url":26,"identifiers":2848},"10.1161\u002F01.HYP.32.3.488",{"doi":2847},{"id":26,"text":2850,"url":26,"identifiers":2851},"10.1096\u002Ffj.99-0881com",{"doi":2850},{"id":26,"text":2853,"url":26,"identifiers":2854},"10.1084\u002Fjem.182.2.367",{"doi":2853},{"id":26,"text":2856,"url":26,"identifiers":2857},"10.1002\u002Fpro.5560021003",{"doi":2856},{"id":26,"text":2859,"url":26,"identifiers":2860},"10.1126\u002Fscience.279.5357.1718",{"doi":2859},{"id":26,"text":2862,"url":26,"identifiers":2863},"10.1016\u002FS0006-2952(99)00289-0",{"doi":2862},{"id":26,"text":2865,"url":26,"identifiers":2866},"10.1016\u002FS0034-5687(99)00024-9",{"doi":2865},{"id":26,"text":2868,"url":26,"identifiers":2869},"Zweier JL, 1994, J Biol Chem, 269, 24156, 10.1016\u002FS0021-9258(19)51062-6",{"doi":2870},"10.1016\u002FS0021-9258(19)51062-6",false,{"id":2873,"createTime":2874,"updateTime":2875,"relativeEntities":2876,"slug":2877,"properties":2878,"entityType":799,"verifyStatus":28,"verifyTime":2874,"verifyNote":2894,"syncStatus":28,"languages":2895,"translateLanguages":2896,"viewCount":36,"primaryUrl":2897,"fullTextUrl":26,"authors":2898,"publicationType":826,"publisherRelationship":2931,"citationCount":2963,"citationInfo":2964,"publishDate":2977,"publishYear":2978,"citationAnalyzeStatus":28,"lastCitationAnalyze":26,"indexDatabases":26,"openAccess":26,"references":2979,"isForceReanalyzing":2871},"f86e91b5-1849-4741-81bf-44b0d0ada434","2024-09-01T17:12:10.853+00:00","2025-02-08T00:03:23.379+00:00",[],"The-NOX-Family-of-ROS-Generating-NADPH-Oxidases-Physiology-and-Pathophysiology",{"mag":2879,"keywords":2881,"openalex":2882,"abstract":2884,"title":2887,"pm":2890,"doi":2892},{"VOID":2880},"2085128107",{"VI":786},{"VOID":2883},"W2085128107",{"EN":2885,"VI":2886},"\u003Cjats:p>For a long time, superoxide generation by an NADPH oxidase was considered as an oddity only found in professional phagocytes. Over the last years, six homologs of the cytochrome subunit of the phagocyte NADPH oxidase were found: NOX1, NOX3, NOX4, NOX5, DUOX1, and DUOX2. Together with the phagocyte NADPH oxidase itself (NOX2\u002Fgp91\u003Cjats:sup>phox\u003C\u002Fjats:sup>), the homologs are now referred to as the NOX family of NADPH oxidases. These enzymes share the capacity to transport electrons across the plasma membrane and to generate superoxide and other downstream reactive oxygen species (ROS). Activation mechanisms and tissue distribution of the different members of the family are markedly different. The physiological functions of NOX family enzymes include host defense, posttranlational processing of proteins, cellular signaling, regulation of gene expression, and cell differentiation. NOX enzymes also contribute to a wide range of pathological processes. NOX deficiency may lead to immunosuppresion, lack of otoconogenesis, or hypothyroidism. Increased NOX actvity also contributes to a large number or pathologies, in particular cardiovascular diseases and neurodegeneration. This review summarizes the current state of knowledge of the functions of NOX enzymes in physiology and pathology.\u003C\u002Fjats:p>","\u003Cjats:p>Trong một thời gian dài, việc sinh ra siêu oxit bởi một NADPH oxidase được coi là một hiện tượng kỳ lạ chỉ xuất hiện ở các tế bào thực bào chuyên nghiệp. Trong những năm gần đây, sáu đồng yếu tố của tiểu đơn vị cytochrome của NADPH oxidase ở tế bào thực bào đã được phát hiện: NOX1, NOX3, NOX4, NOX5, DUOX1 và DUOX2. Cùng với NADPH oxidase ở tế bào thực bào (NOX2\u002Fgp91\u003Cjats:sup>phox\u003C\u002Fjats:sup>), các đồng yếu tố này giờ đây được gọi chung là gia đình NOX của các NADPH oxidase. Những enzyme này có khả năng truyền điện tử qua màng tế bào và sinh ra siêu oxit cũng như các loại oxy phản ứng (ROS) khác. Cơ chế kích hoạt và phân bố mô của các thành viên khác nhau trong gia đình có sự khác biệt rõ rệt. Chức năng sinh lý của các enzyme NOX bao gồm phòng thủ chống lại tác nhân gây bệnh, xử lý hậu chuyển gải của protein, tín hiệu tế bào, điều hòa biểu hiện gen và sự biệt hóa tế bào. Các enzyme NOX cũng góp phần vào một loạt các quá trình bệnh lý. Suy giảm NOX có thể dẫn đến tình trạng ức chế miễn dịch, thiếu otoconogenesis, hoặc suy giáp. Hoạt động tăng cường NOX cũng đóng góp vào một số lượng lớn các bệnh lý, đặc biệt là các bệnh tim mạch và thoái hóa thần kinh. Bài tổng quan này tóm tắt trạng thái hiện tại của kiến thức về chức năng của các enzyme NOX trong sinh lý học và bệnh học.\u003C\u002Fjats:p>",{"EN":2888,"VI":2889},"The NOX Family of ROS-Generating NADPH Oxidases: Physiology and Pathophysiology","Gia đình NOX của các NADPH Oxidase sinh ra ROS: Sinh lý và Bệnh lý",{"VOID":2891},"17237347",{"VOID":2893},"10.1152\u002Fphysrev.00044.2005","Author affiliation is blank",[102],[101],"https:\u002F\u002Fwww.physiology.org\u002Fdoi\u002F10.1152\u002Fphysrev.00044.2005",[2899,2920],{"id":2900,"sortIndex":36,"researcher":26,"roles":2901,"affiliations":2902,"properties":2913},"c64d5b91-fe91-4dfa-8927-5908142e3e3b",[],[2903],{"id":2904,"sortIndex":36,"affiliation":2905,"properties":26},"4e67183a-ec52-4cb5-8639-0ba683258983",{"id":2906,"createTime":2907,"updateTime":2907,"relativeEntities":2908,"slug":2909,"properties":2910,"entityType":98,"verifyStatus":28,"verifyTime":26,"verifyNote":26,"syncStatus":28,"languages":26,"translateLanguages":26,"viewCount":36},"380e5cae-9906-431e-bf08-22da3d058654","2024-09-01T17:12:10.871+00:00",[],"Biology-of-Ageing-Laboratories-University-of-Geneva-Geneva-Switzerland-",{"title":2911},{"EN":2912},"Biology of Ageing Laboratories, University of Geneva, Geneva, 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RH, Marti HH, Schuerer-Maly CC, Kvietikova I, Bauer C, Gassmann M, Maly FE.Hypoxic induction of gene expression in chronic granulomatous disease-derived B-cell lines: oxygen sensing is independent of the cytochromeb558-containing nicotinamide adenine dinucleotide phosphate oxidase.Blood87: 756–761, 1996.",{},{"id":26,"text":5851,"url":26,"identifiers":5852},"10.1096\u002Ffj.00-0827fje",{"doi":5851},{"id":26,"text":5854,"url":26,"identifiers":5855},"10.1083\u002Fjcb.200111028",{"doi":5854},{"id":26,"text":5857,"url":26,"identifiers":5858},"10.1074\u002Fjbc.M212076200",{"doi":5857},{"id":26,"text":5860,"url":26,"identifiers":5861},"10.1046\u002Fj.1365-2605.1999.00173.x",{"doi":5860},{"id":26,"text":5863,"url":26,"identifiers":5864},"10.1042\u002Fbj2960557",{"doi":5863},{"id":26,"text":5866,"url":26,"identifiers":5867},"10.1046\u002Fj.0001-6772.2003.01205.x",{"doi":5866},{"id":26,"text":5869,"url":26,"identifiers":5870},"Wilkinson B, Koenigsknecht-Talboo J, Grommes C, Lee CY, Landreth G.Fibrillar beta-amyloid stimulated intracellular signaling cascades require Vav for induction of respiratory burst and phagocytosis in monocytes and microglia.J Biol Chem.In press.",{},{"id":26,"text":5872,"url":26,"identifiers":5873},"10.1016\u002Fj.freeradbiomed.2004.05.029",{"doi":5872},{"id":26,"text":5875,"url":26,"identifiers":5876},"10.1016\u002FS0891-5849(01)00727-4",{"doi":5875},{"id":26,"text":5878,"url":26,"identifiers":5879},"10.1097\u002F00005792-200005000-00003",{"doi":5878},{"id":26,"text":5881,"url":26,"identifiers":5882},"10.1016\u002Fj.devcel.2004.10.014",{"doi":5881},{"id":26,"text":5884,"url":26,"identifiers":5885},"Wood KC, Hebbel RP, Granger DN.Endothelial cell NADPH oxidase mediates the cerebral microvascular dysfunction in sickle cell transgenic mice.FASEB J19: 989–991, 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Y, Chaiswing L, Bakthavatchalu V, Oberley TD, St Clair DK.Ras mutation promotes p53 activation and apoptosis of skin keratinocytes.Carcinogenesis.In press.",{},{"id":26,"text":5978,"url":26,"identifiers":5979},"Zhou C, Ziegler C, Birder LA, Stewart AF, Levitan ES.Angiotensin II and stretch activate NADPH oxidase to destabilize cardiac Kv4.3 channel mRNA.Circ Res.In press.",{},{"id":26,"text":5981,"url":26,"identifiers":5982},"10.1182\u002Fblood-2005-04-1612",{"doi":5981},{"id":26,"text":5984,"url":26,"identifiers":5985},"Zhukov AIngelman-Sundberg M.Relationship between cytochromeP450 catalytic cycling and stability: fast degradation of ethanol-inducible cytochromeP450 2E1 (CYP2E1) in hepatoma cells is abolished by inactivation of its electron donor NADPH-cytochromeP450 reductase.Biochem J340: 453–458, 1999.",{},{"id":26,"text":5987,"url":26,"identifiers":5988},"10.1161\u002F01.RES.0000139957.22530.b9",{"doi":5987},{"id":26,"text":5990,"url":26,"identifiers":5991},"10.1161\u002F01.RES.0000043501.47934.FA",{"doi":5990},{"id":26,"text":5993,"url":26,"identifiers":5994},"10.1161\u002F01.HYP.0000153463.22621.5e",{"doi":5993},{"id":26,"text":5996,"url":26,"identifiers":5997},"10.1089\u002F152308603770310347",{"doi":5996},{"id":5999,"createTime":6000,"updateTime":6001,"relativeEntities":6002,"slug":6003,"properties":6004,"entityType":799,"verifyStatus":25,"verifyTime":6000,"verifyNote":801,"syncStatus":28,"languages":6021,"translateLanguages":6022,"viewCount":36,"primaryUrl":6023,"fullTextUrl":26,"authors":6024,"publicationType":826,"publisherRelationship":6064,"citationCount":6096,"citationInfo":6097,"publishDate":6110,"publishYear":6111,"citationAnalyzeStatus":28,"lastCitationAnalyze":26,"indexDatabases":26,"openAccess":26,"references":6112,"isForceReanalyzing":2871},"a64e099a-601e-4cde-849c-77790cea5421","2024-10-03T19:37:02.541+00:00","2025-02-08T00:04:22.189+00:00",[],"Brown-Adipose-Tissue-Function-and-Physiological-Significance",{"mag":6005,"keywords":6007,"openalex":6009,"abstract":6011,"title":6014,"pm":6017,"doi":6019},{"VOID":6006},"2132358997",{"VI":6008},"mô béo nâu, sinh nhiệt, norepinephrine, vùng dưới đồi, sự thích nghi với lạnh",{"VOID":6010},"W2132358997",{"EN":6012,"VI":6013},"\u003Cjats:p>Cannon, Barbara, and Jan Nedergaard. Brown Adipose Tissue: Function and Physiological Significance. Physiol Rev 84: 277–359, 2004; 10.1152\u002Fphysrev.00015.2003.—The function of brown adipose tissue is to transfer energy from food into heat; physiologically, both the heat produced and the resulting decrease in metabolic efficiency can be of significance. Both the acute activity of the tissue, i.e., the heat production, and the recruitment process in the tissue (that results in a higher thermogenic capacity) are under the control of norepinephrine released from sympathetic nerves. In thermoregulatory thermogenesis, brown adipose tissue is essential for classical nonshivering thermogen-esis (this phenomenon does not exist in the absence of functional brown adipose tissue), as well as for the cold acclimation-recruited norepinephrine-induced thermogenesis. Heat production from brown adipose tissue is activated whenever the organism is in need of extra heat, e.g., postnatally, during entry into a febrile state, and during arousal from hibernation, and the rate of thermogenesis is centrally controlled via a pathway initiated in the hypothalamus. Feeding as such also results in activation of brown adipose tissue; a series of diets, apparently all characterized by being low in protein, result in a leptin-dependent recruitment of the tissue; this metaboloregulatory thermogenesis is also under hypothalamic control. When the tissue is active, high amounts of lipids and glucose are combusted in the tissue. The development of brown adipose tissue with its characteristic protein, uncoupling protein-1 (UCP1), was probably determinative for the evolutionary success of mammals, as its thermogenesis enhances neonatal survival and allows for active life even in cold surroundings.\u003C\u002Fjats:p>","\u003Cjats:p>Cannon, Barbara, và Jan Nedergaard. Mô Béo Nâu: Chức Năng và Ý Nghĩa Sinh Lý. Physiol Rev 84: 277–359, 2004; 10.1152\u002Fphysrev.00015.2003.—Chức năng của mô béo nâu là chuyển hóa năng lượng từ thực phẩm thành nhiệt; về mặt sinh lý, cả nhiệt lượng được sản xuất cũng như sự giảm hiệu suất chuyển hóa sau đó có thể có ý nghĩa quan trọng. Cả hoạt động cấp tính của mô, tức là quá trình sản xuất nhiệt, và quá trình thu nhận trong mô (dẫn đến khả năng sinh nhiệt cao hơn) đều dưới sự kiểm soát của norepinephrine được tiết ra từ các dây thần kinh giao cảm. Trong sinh nhiệt điều hòa thân nhiệt, mô béo nâu rất quan trọng cho sinh nhiệt không run cổ điển (hiện tượng này không tồn tại trong trường hợp mô béo nâu không hoạt động), cũng như cho sinh nhiệt được kích thích bởi norepinephrine trong quá trình thích nghi với lạnh. Việc sản xuất nhiệt từ mô béo nâu được kích hoạt bất cứ khi nào cơ thể cần thêm nhiệt, chẳng hạn như sau sinh, khi bước vào trạng thái sốt, và khi tỉnh dậy sau thời gian ngủ đông, và tốc độ sinh nhiệt được kiểm soát chính xác qua một con đường bắt đầu từ vùng dưới đồi. Việc ăn uống cũng dẫn đến việc kích hoạt mô béo nâu; một loạt các chế độ ăn, rõ ràng là đặc trưng bởi lượng protein thấp, dẫn đến việc thu nhận mô phụ thuộc vào leptin; sinh nhiệt điều hòa theo chuyển hóa này cũng dưới sự kiểm soát của vùng dưới đồi. Khi mô hoạt động, một lượng lớn lipid và glucose được đốt cháy trong mô. Sự phát triển của mô béo nâu với protein đặc trưng của nó, protein không kết hợp-1 (UCP1), có thể là yếu tố quyết định cho sự thành công tiến hóa của động vật có vú, vì sinh nhiệt của nó tăng cường sự sống sót ở sơ sinh và cho phép hoạt động tích cực ngay cả trong điều kiện lạnh.\u003C\u002Fjats:p>",{"EN":6015,"VI":6016},"Brown Adipose Tissue: Function and Physiological Significance","Mô Tả Chức Năng và Ý Nghĩa Sinh Lý Của Mô Béo 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hypothalamic paraventricular nucleus and norepinephrine turnover in rats.Endocrinology36: 187–194, 1989.",{"doi":8873},"10.1507\u002Fendocrj1954.36.187",{"id":26,"text":8875,"url":26,"identifiers":8876},"10.1016\u002F0006-8993(92)91486-X",{"doi":8875},{"id":26,"text":8878,"url":26,"identifiers":8879},"10.1016\u002F0006-8993(93)91702-T",{"doi":8878},{"id":26,"text":8881,"url":26,"identifiers":8882},"10.2170\u002Fjjphysiol.39.957",{"doi":8881},{"id":26,"text":8884,"url":26,"identifiers":8885},"Yoshioka K, Yoshida T, and Kondo M.Reduced brown adipose tissue thermogenesis and metabolic rate in pre-obese mice treated with monosodium-l-glutamate.Endocrinology38: 75–79, 1991.",{"doi":8886},"10.1507\u002Fendocrj1954.38.75",{"id":26,"text":8888,"url":26,"identifiers":8889},"10.1172\u002FJCI110541",{"doi":8888},{"id":26,"text":8891,"url":26,"identifiers":8892},"Young JB, Saville NE, and Landsberg L.Effect of thyroid state on norepinephrine (NE) turnover in rat brown adipose tissue (BAT): 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discovery that mammalian cells have the ability to synthesize the free radical nitric oxide (NO) has stimulated an extraordinary impetus for scientific research in all the fields of biology and medicine. Since its early description as an endothelial-derived relaxing factor, NO has emerged as a fundamental signaling device regulating virtually every critical cellular function, as well as a potent mediator of cellular damage in a wide range of conditions. Recent evidence indicates that most of the cytotoxicity attributed to NO is rather due to peroxynitrite, produced from the diffusion-controlled reaction between NO and another free radical, the superoxide anion. Peroxynitrite interacts with lipids, DNA, and proteins via direct oxidative reactions or via indirect, radical-mediated mechanisms. These reactions trigger cellular responses ranging from subtle modulations of cell signaling to overwhelming oxidative injury, committing cells to necrosis or apoptosis. In vivo, peroxynitrite generation represents a crucial pathogenic mechanism in conditions such as stroke, myocardial infarction, chronic heart failure, diabetes, circulatory shock, chronic inflammatory diseases, cancer, and neurodegenerative disorders. Hence, novel pharmacological strategies aimed at removing peroxynitrite might represent powerful therapeutic tools in the future. Evidence supporting these novel roles of NO and peroxynitrite is presented in detail in this review.\u003C\u002Fjats:p>","\u003Cjats:p>Sự phát hiện rằng tế bào động vật có vú có khả năng tổng hợp nitric oxide (NO) dạng tự do đã tạo ra một động lực phi thường cho nghiên cứu khoa học trong tất cả các lĩnh vực sinh học và y học. Kể từ khi được mô tả lần đầu tiên như một yếu tố thư giãn có nguồn gốc từ nội mô, NO đã phát triển thành một thiết bị tín hiệu cơ bản điều chỉnh hầu như mọi chức năng tế bào quan trọng, cũng như là một chất trung gian mạnh mẽ gây tổn thương tế bào trong một loạt các điều kiện khác nhau. Bằng chứng gần đây cho thấy hầu hết độc tính tế bào được quy cho NO thực chất là do peroxynitrite, được sản xuất từ phản ứng kiểm soát khuếch tán giữa NO và một gốc tự do khác, ion superoxide. Peroxynitrite tương tác với lipid, DNA và protein thông qua các phản ứng oxy hóa trực tiếp hoặc thông qua các cơ chế gián tiếp do gốc tự do điều khiển. Những phản ứng này kích thích các phản ứng tế bào dao động từ những điều chỉnh tinh tế trong tín hiệu tế bào đến tổn thương oxy hóa mạnh mẽ, khiến tế bào bị chết theo cách hoại tử hoặc apoptosis. Trong cơ thể, sự hình thành peroxynitrite đại diện cho một cơ chế bệnh lý quan trọng trong các tình trạng như đột quỵ, nhồi máu cơ tim, suy tim mãn tính, tiểu đường, sốc tuần hoàn, các bệnh viêm mãn tính, ung thư và rối loạn thoái hóa thần kinh. Do đó, các chiến lược dược lý mới nhằm loại bỏ peroxynitrite có thể đại diện cho các công cụ điều trị mạnh mẽ trong tương lai. 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C, Jozsef L, Ouellet S, Paquette Y, Filep JG.Peroxynitrite mediates cytokine-induced IL-8 gene expression and production by human leukocytes.J Leukoc Biol69: 815–824, 2001.",{"doi":13660},"10.1189\u002Fjlb.69.5.815",{"id":26,"text":13662,"url":26,"identifiers":13663},"10.1096\u002Ffj.00-0521fje",{"doi":13662},{"id":26,"text":13665,"url":26,"identifiers":13666},"10.1089\u002F152308601750100443",{"doi":13665},{"id":13668,"createTime":13669,"updateTime":13670,"relativeEntities":13671,"slug":13672,"properties":13673,"entityType":799,"verifyStatus":25,"verifyTime":13669,"verifyNote":801,"syncStatus":28,"languages":13689,"translateLanguages":13690,"viewCount":36,"primaryUrl":13691,"fullTextUrl":26,"authors":13692,"publicationType":826,"publisherRelationship":13731,"citationCount":13763,"citationInfo":13764,"publishDate":13773,"publishYear":875,"citationAnalyzeStatus":28,"lastCitationAnalyze":26,"indexDatabases":26,"openAccess":26,"references":13774,"isForceReanalyzing":2871},"cea68bdf-deda-4543-9676-703798326545","2024-09-25T19:03:13.629+00:00","2025-02-08T00:06:19.580+00:00",[],"The-Ubiquitin-Proteasome-Proteolytic-Pathway-Destruction-for-the-Sake-of-Construction",{"mag":13674,"keywords":13676,"openalex":13677,"abstract":13679,"title":13682,"pm":13685,"doi":13687},{"VOID":13675},"2150123812",{"VI":786},{"VOID":13678},"W2150123812",{"EN":13680,"VI":13681},"\u003Cjats:p>Between the 1960s and 1980s, most life scientists focused their attention on studies of nucleic acids and the translation of the coded information. Protein degradation was a neglected area, considered to be a nonspecific, dead-end process. Although it was known that proteins do turn over, the large extent and high specificity of the process, whereby distinct proteins have half-lives that range from a few minutes to several days, was not appreciated. The discovery of the lysosome by Christian de Duve did not significantly change this view, because it became clear that this organelle is involved mostly in the degradation of extracellular proteins, and their proteases cannot be substrate specific. The discovery of the complex cascade of the ubiquitin pathway revolutionized the field. It is clear now that degradation of cellular proteins is a highly complex, temporally controlled, and tightly regulated process that plays major roles in a variety of basic pathways during cell life and death as well as in health and disease. With the multitude of substrates targeted and the myriad processes involved, it is not surprising that aberrations in the pathway are implicated in the pathogenesis of many diseases, certain malignancies, and neurodegeneration among them. Degradation of a protein via the ubiquitin\u002Fproteasome pathway involves two successive steps: 1) conjugation of multiple ubiquitin moieties to the substrate and 2) degradation of the tagged protein by the downstream 26S proteasome complex. Despite intensive research, the unknown still exceeds what we currently know on intracellular protein degradation, and major key questions have remained unsolved. Among these are the modes of specific and timed recognition for the degradation of the many substrates and the mechanisms that underlie aberrations in the system that lead to pathogenesis of diseases.\u003C\u002Fjats:p>","\u003Cjats:p>Giữa thập kỷ 1960 và 1980, hầu hết các nhà khoa học về sự sống tập trung chú ý vào việc nghiên cứu axit nucleic và quá trình dịch mã thông tin mã hóa. Sự phân hủy protein là một lĩnh vực bị bỏ qua, được coi là một quá trình không đặc hiệu và không có lối thoát. Dù có biết rằng protein sẽ quay vòng, nhưng quy mô lớn và đặc hiệu cao của quá trình này, trong đó các protein khác nhau có thời gian bán rã dao động từ vài phút đến vài ngày, đã không được đánh giá đúng mức. Sự phát hiện lysosome bởi Christian de Duve không thay đổi quan điểm này một cách đáng kể, vì rõ ràng rằng bào quan này chủ yếu tham gia vào sự phân hủy các protein ngoại bào, và các protease của chúng không thể đặc hiệu cho cơ chất. Việc phát hiện chuỗi phức tạp của con đường ubiquitin đã cách mạng hóa lĩnh vực này. Hiện tại đã rõ rằng sự phân hủy protein trong tế bào là một quá trình cực kỳ phức tạp, được kiểm soát theo thời gian và được điều chỉnh chặt chẽ, đóng vai trò quan trọng trong nhiều con đường cơ bản trong suốt cuộc đời và cái chết của tế bào cũng như trong sức khỏe và bệnh tật. Với vô số cơ chất bị mục tiêu và vô vàn quá trình liên quan, không có gì bất ngờ khi những sai lệch trong con đường này được liên kết với sự phát sinh bệnh của nhiều bệnh lý, trong đó có một số loại ác tính và thoái hóa thần kinh. Sự phân hủy của một protein qua con đường ubiquitin\u002Fproteasome bao gồm hai bước liên tiếp: 1) sự kết hợp của nhiều moiety ubiquitin với cơ chất và 2) sự phân hủy protein đã được đánh dấu bởi phức hợp proteasome 26S ở hạ lưu. Dù có nghiên cứu sâu rộng, những điều chưa biết vẫn vượt xa những gì chúng ta hiện đang biết về sự phân hủy protein nội bào, và nhiều câu hỏi chính vẫn chưa được giải đáp. Trong số đó có các cơ chế nhận diện đặc hiệu và được xác định theo thời gian cho sự phân hủy của nhiều cơ chất và các cơ chế dẫn đến những sai lệch trong hệ thống gây ra sự phát sinh bệnh của nhiều bệnh lý.\u003C\u002Fjats:p>",{"EN":13683,"VI":13684},"The Ubiquitin-Proteasome Proteolytic Pathway: Destruction for the Sake of Construction","Con đường phân hủy protein ubiquitin-proteasome: Phá hủy vì mục đích xây dựng",{"VOID":13686},"11917093",{"VOID":13688},"10.1152\u002Fphysrev.00027.2001",[102],[101],"https:\u002F\u002Fwww.physiology.org\u002Fdoi\u002F10.1152\u002Fphysrev.00027.2001",[13693,13714],{"id":13694,"sortIndex":36,"researcher":26,"roles":13695,"affiliations":13696,"properties":13707},"efa94c95-b602-4dc2-aa23-d1ff07b85c5d",[],[13697],{"id":13698,"sortIndex":36,"affiliation":13699,"properties":26},"e1d25635-dd8d-44c4-924c-bf3905946797",{"id":13700,"createTime":13701,"updateTime":13701,"relativeEntities":13702,"slug":13703,"properties":13704,"entityType":98,"verifyStatus":28,"verifyTime":26,"verifyNote":26,"syncStatus":28,"languages":26,"translateLanguages":26,"viewCount":36},"3227e599-ec2e-4ca2-8517-06cbb5c09eac","2024-09-25T19:03:13.668+00:00",[],"Faculty-of-Biology-and-the-Institute-for-Catalysis-Science-and-Technology-and-Department-of-Biochemistry-Bruce-Rappaport-Faculty-of-Medicine-Technion-Israel-Institute-of-Technology-Haifa-Israel",{"title":13705},{"EN":13706},"Faculty of Biology and the Institute for Catalysis Science and Technology, and Department of Biochemistry, Bruce Rappaport Faculty of Medicine, Technion-Israel Institute of Technology, Haifa, Israel",{"openalex":13708,"orcid":13710,"title":13712},{"VOID":13709},"A5073166748",{"VOID":13711},"https:\u002F\u002Forcid.org\u002F0000-0002-1222-8104",{"EN":13713},"Michael H. 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H, 1997, J Cell Sci, 110, 1793, 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JW, 2001, J Cell Sci, 114, 845, 10.1242\u002Fjcs.114.5.845",{"doi":15366},"10.1242\u002Fjcs.114.5.845",{"id":26,"text":15368,"url":26,"identifiers":15369},"10.1074\u002Fjbc.M100034200",{"doi":15368},{"id":26,"text":15371,"url":26,"identifiers":15372},"10.1074\u002Fjbc.273.10.5461",{"doi":15371},{"id":26,"text":15374,"url":26,"identifiers":15375},"10.1126\u002Fscience.279.5354.1219",{"doi":15374},{"id":26,"text":15377,"url":26,"identifiers":15378},"10.1126\u002Fscience.282.5394.1721",{"doi":15377},{"id":26,"text":15380,"url":26,"identifiers":15381},"10.1016\u002FS0014-5793(99)01072-8",{"doi":15380},{"id":26,"text":15383,"url":26,"identifiers":15384},"10.1016\u002F0092-8674(95)90271-6",{"doi":15383},{"id":26,"text":15386,"url":26,"identifiers":15387},"10.1073\u002Fpnas.98.3.974",{"doi":15386},{"id":26,"text":15389,"url":26,"identifiers":15390},"10.1073\u002Fpnas.240347797",{"doi":15389},{"id":26,"text":15392,"url":26,"identifiers":15393},"10.1074\u002Fjbc.M910378199",{"doi":15392},{"id":26,"text":15395,"url":26,"identifiers":15396},"10.1016\u002FS0092-8674(00)00057-X",{"doi":15395},{"id":26,"text":15398,"url":26,"identifiers":15399},"10.1016\u002FS1097-2765(00)80156-2",{"doi":15398},{"id":26,"text":15401,"url":26,"identifiers":15402},"10.1186\u002F1471-2091-2-7",{"doi":15401},{"id":26,"text":15404,"url":26,"identifiers":15405},"10.1038\u002F23293",{"doi":15404},{"id":26,"text":15407,"url":26,"identifiers":15408},"10.1016\u002FS0959-440X(00)00075-0",{"doi":15407},{"id":26,"text":15410,"url":26,"identifiers":15411},"10.1074\u002Fjbc.274.37.26008",{"doi":15410},{"id":15413,"createTime":15414,"updateTime":15415,"relativeEntities":15416,"slug":15417,"properties":15418,"entityType":799,"verifyStatus":25,"verifyTime":15414,"verifyNote":801,"syncStatus":28,"languages":15434,"translateLanguages":15435,"viewCount":36,"primaryUrl":15436,"fullTextUrl":26,"authors":15437,"publicationType":826,"publisherRelationship":15459,"citationCount":15490,"citationInfo":15491,"publishDate":15502,"publishYear":2978,"citationAnalyzeStatus":28,"lastCitationAnalyze":26,"indexDatabases":26,"openAccess":26,"references":15503,"isForceReanalyzing":2871},"dd8906f5-ec13-4d9f-be76-0d4438b36266","2024-09-23T22:21:48.071+00:00","2025-02-08T00:07:15.801+00:00",[],"Physiology-and-Neurobiology-of-Stress-and-Adaptation-Central-Role-of-the-Brain",{"mag":15419,"keywords":15421,"openalex":15422,"abstract":15424,"title":15427,"pm":15430,"doi":15432},{"VOID":15420},"2144101679",{"VI":786},{"VOID":15423},"W2144101679",{"EN":15425,"VI":15426},"\u003Cjats:p>The brain is the key organ of the response to stress because it determines what is threatening and, therefore, potentially stressful, as well as the physiological and behavioral responses which can be either adaptive or damaging. Stress involves two-way communication between the brain and the cardiovascular, immune, and other systems via neural and endocrine mechanisms. Beyond the “flight-or-fight” response to acute stress, there are events in daily life that produce a type of chronic stress and lead over time to wear and tear on the body (“allostatic load”). Yet, hormones associated with stress protect the body in the short-run and promote adaptation (“allostasis”). The brain is a target of stress, and the hippocampus was the first brain region, besides the hypothalamus, to be recognized as a target of glucocorticoids. Stress and stress hormones produce both adaptive and maladaptive effects on this brain region throughout the life course. Early life events influence life-long patterns of emotionality and stress responsiveness and alter the rate of brain and body aging. The hippocampus, amygdala, and prefrontal cortex undergo stress-induced structural remodeling, which alters behavioral and physiological responses. As an adjunct to pharmaceutical therapy, social and behavioral interventions such as regular physical activity and social support reduce the chronic stress burden and benefit brain and body health and resilience.\u003C\u002Fjats:p>","\u003Cjats:p>Não bộ là cơ quan chủ chốt trong phản ứng với căng thẳng bởi vì nó xác định điều gì là đe dọa và do đó, có khả năng gây căng thẳng, cũng như các phản ứng sinh lý và hành vi có thể là thích ứng hoặc tổn hại. Căng thẳng bao gồm sự giao tiếp hai chiều giữa não và các hệ thống tim mạch, miễn dịch, và các hệ thống khác thông qua các cơ chế thần kinh và nội tiết. Ngoài phản ứng \"chiến đấu hoặc bỏ chạy\" đối với căng thẳng cấp tính, có những sự kiện trong cuộc sống hàng ngày gây ra một loại căng thẳng mãn tính và theo thời gian dẫn đến tổn hại cho cơ thể (\"tải trọng allostatic\"). Tuy nhiên, các hormone liên quan đến căng thẳng bảo vệ cơ thể trong ngắn hạn và thúc đẩy sự thích ứng (\"allostasis\"). Não bộ là mục tiêu của căng thẳng, và hồi hải mã là vùng não đầu tiên, bên cạnh vùng dưới đồi, được công nhận là mục tiêu của glucocorticoid. Căng thẳng và các hormone căng thẳng tạo ra cả các hiệu ứng thích ứng và không thích ứng lên vùng não này trong suốt cuộc đời. Những sự kiện trong thời kỳ đầu đời ảnh hưởng đến các mô hình cảm xúc và phản ứng với căng thẳng suốt đời và làm thay đổi tỷ lệ lão hóa của não và cơ thể. Hồi hải mã, hạch hạnh nhân và vỏ não trước trán trải qua sự tái cấu trúc cấu trúc do căng thẳng gây ra, điều này làm thay đổi các phản ứng hành vi và sinh lý. Như một biện pháp bổ trợ cho liệu pháp dược phẩm, các can thiệp xã hội và hành vi như hoạt động thể chất đều đặn và hỗ trợ xã hội làm giảm gánh nặng căng thẳng mãn tính và có lợi cho sức khỏe và sức sống của não và cơ thể.\u003C\u002Fjats:p>",{"EN":15428,"VI":15429},"Physiology and Neurobiology of Stress and Adaptation: Central Role of the Brain","Sinh lý học và thần kinh sinh học của căng thẳng và thích ứng: Vai trò trung tâm của não",{"VOID":15431},"17615391",{"VOID":15433},"10.1152\u002Fphysrev.00041.2006",[102],[101],"https:\u002F\u002Fwww.physiology.org\u002Fdoi\u002F10.1152\u002Fphysrev.00041.2006",[15438],{"id":15439,"sortIndex":36,"researcher":26,"roles":15440,"affiliations":15441,"properties":15452},"d80b24da-dd5a-4e21-9161-d3fba8e54f51",[],[15442],{"id":15443,"sortIndex":36,"affiliation":15444,"properties":26},"4c49431a-d6fe-4330-a4eb-6f56bc023bc4",{"id":15445,"createTime":15446,"updateTime":15446,"relativeEntities":15447,"slug":15448,"properties":15449,"entityType":98,"verifyStatus":28,"verifyTime":26,"verifyNote":26,"syncStatus":28,"languages":26,"translateLanguages":26,"viewCount":36},"c61cfdc9-3077-490e-b6ef-7c673312caff","2024-09-23T22:21:48.087+00:00",[],"Harold-and-Margaret-Milliken-Hatch-Laboratory-of-Neuroendocrinology-The-Rockefeller-University-New-York-New-York-10021-USA-mcewen-rockefeller-edu",{"title":15450},{"EN":15451},"Harold and Margaret Milliken Hatch, Laboratory of Neuroendocrinology, The Rockefeller University, New York, New York 10021, USA. mcewen@rockefeller.edu",{"openalex":15453,"orcid":15455,"title":15457},{"VOID":15454},"A5035103174",{"VOID":15456},"https:\u002F\u002Forcid.org\u002F0000-0002-5288-7892",{"EN":15458},"Bruce S. 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In:Coping With the Environment: Neural and Endocrine Mechanisms.New York: Oxford Univ. Press, 2000, p. 211–234.",{},{"id":26,"text":16654,"url":26,"identifiers":16655},"10.1016\u002FS0166-4328(98)00147-8",{"doi":16654},{"id":26,"text":16657,"url":26,"identifiers":16658},"10.1037\u002F0735-7044.119.5.1389",{"doi":16657},{"id":26,"text":16660,"url":26,"identifiers":16661},"10.1002\u002Fhipo.20167",{"doi":16660},{"id":26,"text":16663,"url":26,"identifiers":16664},"10.1073\u002Fpnas.95.7.4066",{"doi":16663},{"id":26,"text":16666,"url":26,"identifiers":16667},"10.1073\u002Fpnas.0400208101",{"doi":16666},{"id":26,"text":16669,"url":26,"identifiers":16670},"10.1016\u002FS0018-506X(02)00026-0",{"doi":16669},{"id":26,"text":16672,"url":26,"identifiers":16673},"Wood PB.Fibromyalgia syndrome: a central role for the hippocampus—a theoretical construct.J Musculoskeletal Pain12: 19–26, 2004.",{},{"id":26,"text":16675,"url":26,"identifiers":16676},"10.1016\u002Fj.mehy.2003.10.013",{"doi":16675},{"id":26,"text":16678,"url":26,"identifiers":16679},"10.1016\u002Fj.pain.2005.12.014",{"doi":16678},{"id":26,"text":16681,"url":26,"identifiers":16682},"10.1016\u002F0006-8993(90)90778-A",{"doi":16681},{"id":26,"text":16684,"url":26,"identifiers":16685},"10.1016\u002Fj.psyneuen.2005.01.007",{"doi":16684},{"id":26,"text":16687,"url":26,"identifiers":16688},"10.1080\u002F10253890500156663",{"doi":16687},{"id":26,"text":16690,"url":26,"identifiers":16691},"10.1111\u002Fj.1460-9568.2006.04948.x",{"doi":16690},{"id":26,"text":16693,"url":26,"identifiers":16694},"10.1073\u002Fpnas.071562698",{"doi":16693},{"id":26,"text":16696,"url":26,"identifiers":16697},"10.1001\u002Farchpsyc.1994.03950090033005",{"doi":16696},{"id":26,"text":16699,"url":26,"identifiers":16700},"10.1016\u002FS0031-9384(96)00363-0",{"doi":16699},{"id":26,"text":16702,"url":26,"identifiers":16703},"10.1210\u002Fen.2006-0020",{"doi":16702},{"id":26,"text":16705,"url":26,"identifiers":16706},"10.1002\u002Fcne.20823",{"doi":16705},{"id":16708,"createTime":16709,"updateTime":16710,"relativeEntities":16711,"slug":16712,"properties":16713,"entityType":799,"verifyStatus":25,"verifyTime":16709,"verifyNote":801,"syncStatus":28,"languages":16729,"translateLanguages":16730,"viewCount":36,"primaryUrl":16731,"fullTextUrl":26,"authors":16732,"publicationType":826,"publisherRelationship":16753,"citationCount":16785,"citationInfo":16786,"publishDate":16796,"publishYear":16797,"citationAnalyzeStatus":28,"lastCitationAnalyze":26,"indexDatabases":26,"openAccess":26,"references":16798,"isForceReanalyzing":2871},"e2b71981-7c44-4800-b325-b972ec9603e2","2024-08-30T22:42:08.972+00:00","2025-02-08T00:08:14.147+00:00",[],"The-stress-response-in-fish",{"mag":16714,"keywords":16716,"openalex":16717,"abstract":16719,"title":16722,"pm":16725,"doi":16727},{"VOID":16715},"2136061619",{"VI":786},{"VOID":16718},"W2136061619",{"EN":16720,"VI":16721},"\u003Cjats:p> The stress response in teleost fish shows many similarities to that of the terrestrial vertebrates. These concern the principal messengers of the brain-sympathetic-chromaffin cell axis (equivalent of the brain-sympathetic-adrenal medulla axis) and the brain-pituitary-interrenal axis (equivalent of the brain-pituitary-adrenal axis), as well as their functions, involving stimulation of oxygen uptake and transfer, mobilization of energy substrates, reallocation of energy away from growth and reproduction, and mainly suppressive effects on immune functions. There is also growing evidence for intensive interaction between the neuroendocrine system and the immune system in fish. Conspicuous differences, however, are present, and these are primarily related to the aquatic environment of fishes. For example, stressors increase the permeability of the surface epithelia, including the gills, to water and ions, and thus induce systemic hydromineral disturbances. High circulating catecholamine levels as well as structural damage to the gills and perhaps the skin are prime causal factors. This is associated with increased cellular turnover in these organs. In fish, cortisol combines glucocorticoid and mineralocorticoid actions, with the latter being essential for the restoration of hydromineral homeostasis, in concert with hormones such as prolactin (in freshwater) and growth hormone (in seawater). Toxic stressors are part of the stress literature in fish more so than in mammals. This is mainly related to the fact that fish are exposed to aquatic pollutants via the extensive and delicate respiratory surface of the gills and, in seawater, also via drinking. The high bioavailability of many chemicals in water is an additional factor. Together with the variety of highly sensitive perceptive mechanisms in the integument, this may explain why so many pollutants evoke an integrated stress response in fish in addition to their toxic effects at the cell and tissue levels. Exposure to chemicals may also directly compromise the stress response by interfering with specific neuroendocrine control mechanisms. Because hydromineral disturbance is inherent to stress in fish, external factors such as water pH, mineral composition, and ionic calcium levels have a significant impact on stressor intensity. Although the species studied comprise a small and nonrepresentative sample of the almost 20,000 known teleost species, there are many indications that the stress response is variable and flexible in fish, in line with the great diversity of adaptations that enable these animals to live in a large variety of aquatic habitats. \u003C\u002Fjats:p>","\u003Cjats:p> Phản ứng căng thẳng ở cá xương có nhiều điểm tương đồng với phản ứng của các động vật có xương sống trên cạn. Điều này liên quan đến các thông điệp chính từ trục não - giao cảm - tế bào chromaffin (tương đương với trục não - giao cảm - tủy thượng thận) và trục não - tuyến yên - thận (tương đương với trục não - tuyến yên - thượng thận), cùng với các chức năng của chúng, bao gồm kích thích sự hấp thụ và chuyển giao oxy, huy động các chất nền năng lượng, phân bổ lại năng lượng ra khỏi tăng trưởng và sinh sản, và chủ yếu có ảnh hưởng ức chế đến chức năng miễn dịch. Cũng có bằng chứng ngày càng tăng về sự tương tác mạnh mẽ giữa hệ thần kinh nội tiết và hệ miễn dịch ở cá. Tuy nhiên, có những khác biệt rõ ràng, và những khác biệt này chủ yếu liên quan đến môi trường nước của cá. Ví dụ, các yếu tố gây căng thẳng làm tăng tính thẩm thấu của bề mặt biểu mô, bao gồm cả mang, đối với nước và ion, do đó gây ra sự rối loạn hydromineral hệ thống. Mức catecholamine tuần hoàn cao cũng như thiệt hại cấu trúc đối với mang và có thể là da là những yếu tố chính gây ra. Điều này liên quan đến sự quay vòng tế bào tăng cao ở các cơ quan này. Ở cá, cortisol kết hợp tác dụng của glucocorticoid và mineralocorticoid, với mineralocorticoid là cần thiết cho việc phục hồi cân bằng hydromineral, cùng với các hormone như prolactin (trong nước ngọt) và hormone tăng trưởng (trong nước biển). Các yếu tố gây căng thẳng độc hại là một phần của tài liệu nghiên cứu về căng thẳng ở cá nhiều hơn so với ở động vật có vú. Điều này chủ yếu liên quan đến thực tế rằng cá tiếp xúc với các chất ô nhiễm trong nước thông qua bề mặt hô hấp rộng lớn và nhạy cảm của mang, và trong nước biển, cũng qua uống nước. Tính sinh khả dụng cao của nhiều hóa chất trong nước là một yếu tố bổ sung. Cùng với sự đa dạng của các cơ chế cảm nhận cực kỳ nhạy cảm trong lớp biểu bì, điều này có thể giải thích tại sao rất nhiều chất ô nhiễm gây ra phản ứng căng thẳng tích hợp ở cá ngoài các tác động độc hại của chúng ở mức tế bào và mô. Việc tiếp xúc với các hóa chất cũng có thể trực tiếp ảnh hưởng đến phản ứng căng thẳng bằng cách can thiệp vào các cơ chế kiểm soát thần kinh nội tiết cụ thể. Vì rối loạn hydromineral là vốn có trong căng thẳng ở cá, nên các yếu tố bên ngoài như pH của nước, thành phần khoáng và nồng độ ion canxi có tác động đáng kể đến cường độ của yếu tố gây căng thẳng. Mặc dù các loài được nghiên cứu là một mẫu nhỏ và không đại diện cho gần 20.000 loài cá xương được biết đến, có nhiều dấu hiệu cho thấy phản ứng căng thẳng có tính biến đổi và linh hoạt ở cá, phù hợp với sự đa dạng lớn của các thích ứng cho phép những động vật này sống trong một loạt các môi trường sống dưới nước.",{"EN":16723,"VI":16724},"The stress response in fish","Phản ứng căng thẳng ở cá",{"VOID":16726},"9234959",{"VOID":16728},"10.1152\u002Fphysrev.1997.77.3.591",[102],[101],"https:\u002F\u002Fwww.physiology.org\u002Fdoi\u002F10.1152\u002Fphysrev.1997.77.3.591",[16733],{"id":16734,"sortIndex":36,"researcher":26,"roles":16735,"affiliations":16736,"properties":16748},"6d161b76-0625-4417-be26-95db9cfae07f",[],[16737],{"id":16738,"sortIndex":36,"affiliation":16739,"properties":26},"fe7d116f-773e-47dc-add5-91b3da8fa466",{"id":16740,"createTime":16741,"updateTime":16742,"relativeEntities":16743,"slug":16744,"properties":16745,"entityType":98,"verifyStatus":28,"verifyTime":26,"verifyNote":26,"syncStatus":28,"languages":26,"translateLanguages":26,"viewCount":36},"40a46ce8-eca2-4212-bec6-4adf3e717049","2024-01-12T06:53:38.837+00:00","2024-08-30T22:42:08.988+00:00",[],"Department-of-Animal-Physiology-University-of-Nijmegen-The-Netherlands-",{"title":16746},{"VI":16747},"Department of Animal Physiology, University of Nijmegen, The Netherlands.",{"openalex":16749,"title":16751},{"VOID":16750},"A5087887867",{"EN":16752},"S.E. Wendelaar Bonga",{"url":26,"publisher":16754,"properties":16779},{"id":659,"createTime":660,"updateTime":661,"relativeEntities":16755,"slug":663,"properties":16756,"entityType":24,"verifyStatus":28,"verifyTime":26,"verifyNote":26,"syncStatus":28,"languages":26,"translateLanguages":26,"viewCount":36,"subjectFields":16762,"manageAffiliations":16763,"indexDatabases":16764,"url":771,"thumbnailPath":26,"statistic":26,"gsStatistic":26,"type":26,"analyzePriority":26},[],{"country":16757,"issn":16758,"introduce":16759,"eissn":16760,"title":16761},{"VOID":666},{"VOID":668},{"EN":670},{"VOID":672},{"EN":674},[],[],[16765,16772],{"id":731,"indexDatabase":16766,"url":744,"indexYears":745,"academicFieldIds":16771,"indexDatabaseRanking":751},{"id":733,"createTime":734,"updateTime":735,"relativeEntities":16767,"label":16768,"description":16769,"key":741,"publicationTags":16770,"standard":26},[],{"EN":738,"VI":738},{"EN":738,"VI":740},[743],[747,748,749,750],{"id":753,"indexDatabase":16773,"url":768,"indexYears":26,"academicFieldIds":16778,"indexDatabaseRanking":26},{"id":755,"createTime":756,"updateTime":757,"relativeEntities":16774,"label":16775,"description":16776,"key":764,"publicationTags":16777,"standard":26},[],{"EN":760,"VI":760},{"VI":762,"EN":763},[766,767],[770],{"volume":16780,"pages":16782,"issue":16784},{"VOID":16781},"77",{"VOID":16783},"591-625",{"VOID":9007},3901,{"total":16785,"publishYear":26,"statisticByYear":16787},{"2012":351,"2013":16788,"2014":16789,"2015":615,"2016":16790,"2017":13770,"2018":364,"2019":16791,"2020":16792,"2021":16793,"2022":16794,"2023":617,"2024":16795},196,217,147,225,211,202,180,99,"1997-07-01",1997,[],{"id":16800,"createTime":16801,"updateTime":16802,"relativeEntities":16803,"slug":16804,"properties":16805,"entityType":799,"verifyStatus":25,"verifyTime":16801,"verifyNote":801,"syncStatus":28,"languages":16820,"translateLanguages":16821,"viewCount":36,"primaryUrl":16822,"fullTextUrl":26,"authors":16823,"publicationType":826,"publisherRelationship":16867,"citationCount":16899,"citationInfo":16900,"publishDate":16909,"publishYear":16910,"citationAnalyzeStatus":28,"lastCitationAnalyze":26,"indexDatabases":26,"openAccess":26,"references":16911,"isForceReanalyzing":2871},"f5f8b3bc-6335-4208-aa6b-bbb99604235d","2024-09-23T10:08:38.288+00:00","2025-02-08T00:09:12.457+00:00",[],"The-Free-Radical-Theory-of-Aging-Matures",{"mag":16806,"keywords":16808,"openalex":16809,"abstract":16811,"title":16814,"pm":16817,"doi":16819},{"VOID":16807},"2113007696",{"VI":786},{"VOID":16810},"W2113007696",{"EN":16812,"VI":16813},"\u003Cjats:p>Beckman, Kenneth B., and Bruce N. Ames. The Free Radical Theory of Aging Matures. Physiol. Rev. 78: 547–581, 1998. — The free radical theory of aging, conceived in 1956, has turned 40 and is rapidly attracting the interest of the mainstream of biological research. From its origins in radiation biology, through a decade or so of dormancy and two decades of steady phenomenological research, it has attracted an increasing number of scientists from an expanding circle of fields. During the past decade, several lines of evidence have convinced a number of scientists that oxidants play an important role in aging. (For the sake of simplicity, we use the term oxidant to refer to all “reactive oxygen species,” including O\u003Cjats:sup>−\u003C\u002Fjats:sup>\u003Cjats:sub>2\u003C\u002Fjats:sub>⋅, H\u003Cjats:sub>2\u003C\u002Fjats:sub>O\u003Cjats:sub>2\u003C\u002Fjats:sub>, and ⋅OH, even though the former often acts as a reductant and produces oxidants indirectly.) The pace and scope of research in the last few years have been particularly impressive and diverse. The only disadvantage of the current intellectual ferment is the difficulty in digesting the literature. Therefore, we have systematically reviewed the status of the free radical theory, by categorizing the literature in terms of the various types of experiments that have been performed. These include phenomenological measurements of age-associated oxidative stress, interspecies comparisons, dietary restriction, the manipulation of metabolic activity and oxygen tension, treatment with dietary and pharmacological antioxidants, in vitro senescence, classical and population genetics, molecular genetics, transgenic organisms, the study of human diseases of aging, epidemiological studies, and the ongoing elucidation of the role of active oxygen in biology.\u003C\u002Fjats:p>","\u003Cjats:p>Beckman, Kenneth B., và Bruce N. Ames. Lý Thuyết Tự Do Kinh Điển về Lão Hóa Chín Muồi. Physiol. Rev. 78: 547–581, 1998. — Lý thuyết tự do kinh điển về lão hóa, được hình thành vào năm 1956, đã bước sang tuổi 40 và đang nhanh chóng thu hút sự quan tâm của chính dòng chảy nghiên cứu sinh học. Từ những nguồn gốc của nó trong sinh học bức xạ, trải qua một thập kỷ gần như ngủ yên và hai thập kỷ nghiên cứu hiện tượng ổn định, lý thuyết này đã thu hút ngày càng nhiều nhà khoa học từ một loạt lĩnh vực mở rộng. Trong thập kỷ vừa qua, một số bằng chứng đã khiến một số nhà khoa học tin rằng các chất oxy hóa đóng vai trò quan trọng trong quá trình lão hóa. (Để đơn giản, chúng tôi sử dụng thuật ngữ chất oxy hóa để chỉ tất cả các \"quy trình oxy hóa phản ứng\" như O\u003Cjats:sup>−\u003C\u002Fjats:sup>\u003Cjats:sub>2\u003C\u002Fjats:sub>⋅, H\u003Cjats:sub>2\u003C\u002Fjats:sub>O\u003Cjats:sub>2\u003C\u002Fjats:sub> và ⋅OH, mặc dù thành phần trước đó thường hoạt động như một chất khử và sản xuất các chất oxy hóa một cách gián tiếp.) Tốc độ và phạm vi nghiên cứu trong những năm gần đây đặc biệt ấn tượng và đa dạng. Hạn chế duy nhất của sự sôi nổi trí thức hiện tại nằm ở việc khó khăn trong việc tiêu hóa tài liệu. Do đó, chúng tôi đã xem xét một cách hệ thống trạng thái của lý thuyết tự do kinh điển, bằng cách phân loại tài liệu theo các loại thí nghiệm khác nhau đã được thực hiện. Những thí nghiệm này bao gồm những đo lường hiện tượng về stress oxy hóa liên quan đến tuổi tác, so sánh liên loài, hạn chế chế độ ăn uống, thao tác hoạt động chuyển hóa và áp lực oxy, điều trị bằng các chất chống oxy hóa từ chế độ ăn uống và dược phẩm, quá trình lão hóa trong ống nghiệm, di truyền học cổ điển và dân số, di truyền phân tử, sinh vật chuyển gen, nghiên cứu về các bệnh ở người liên quan đến lão hóa, các nghiên cứu dịch tễ học, và những khám phá đang tiếp tục về vai trò của oxy hoạt động trong sinh học.\u003C\u002Fjats:p>",{"EN":16815,"VI":16816},"The Free Radical Theory of Aging Matures","Lý Thuyết Tự Do Kinh Điển về Lão Hóa Chín Muồi",{"VOID":16818},"9562038",{"VOID":1024},[102],[101],"https:\u002F\u002Fwww.physiology.org\u002Fdoi\u002F10.1152\u002Fphysrev.1998.78.2.547",[16824,16846],{"id":16825,"sortIndex":115,"researcher":26,"roles":16826,"affiliations":16827,"properties":16839},"8ef12c77-8f7a-4c54-ac90-78b09f3ab6b6",[],[16828],{"id":16829,"sortIndex":36,"affiliation":16830,"properties":26},"74a7240b-c673-4a71-bcb3-bf4c7be4d7a7",{"id":16831,"createTime":16832,"updateTime":16833,"relativeEntities":16834,"slug":16835,"properties":16836,"entityType":98,"verifyStatus":28,"verifyTime":26,"verifyNote":26,"syncStatus":28,"languages":26,"translateLanguages":26,"viewCount":36},"6d4ef1b9-57d1-4d41-921e-e7705287a382","2023-12-07T21:32:24.782+00:00","2024-12-18T20:12:10.652+00:00",[],"Department-of-Molecular-and-Cell-Biology-University-of-California-Berkeley-California",{"title":16837},{"VI":16838},"Department of Molecular and Cell Biology, University of California, Berkeley, California",{"openalex":16840,"orcid":16842,"title":16844},{"VOID":16841},"A5047067531",{"VOID":16843},"https:\u002F\u002Forcid.org\u002F0009-0005-2891-8993",{"EN":16845},"Bruce N. Ames",{"id":16847,"sortIndex":36,"researcher":26,"roles":16848,"affiliations":16849,"properties":16860},"1acceb3c-07e0-457d-91f9-ec1be1cba4f6",[],[16850],{"id":16851,"sortIndex":36,"affiliation":16852,"properties":26},"9650a73f-cd05-4652-9bbb-6e26a5e451da",{"id":16853,"createTime":16854,"updateTime":16854,"relativeEntities":16855,"slug":16856,"properties":16857,"entityType":98,"verifyStatus":28,"verifyTime":26,"verifyNote":26,"syncStatus":28,"languages":26,"translateLanguages":26,"viewCount":36},"b94af550-7655-4049-a0cc-1970403279d7","2024-09-23T10:08:38.308+00:00",[],"Department-of-Molecular-and-Cell-Biology-University-of-California-Berkeley-94720-3202-USA-",{"title":16858},{"EN":16859},"Department of Molecular and Cell Biology, University of California, Berkeley, 94720-3202, USA.",{"openalex":16861,"orcid":16863,"title":16865},{"VOID":16862},"A5059093059",{"VOID":16864},"https:\u002F\u002Forcid.org\u002F0000-0001-8876-0706",{"EN":16866},"Kenneth B. 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The composition of this microbial community is host specific, evolving throughout an individual's lifetime and susceptible to both exogenous and endogenous modifications. Recent renewed interest in the structure and function of this “organ” has illuminated its central position in health and disease. The microbiota is intimately involved in numerous aspects of normal host physiology, from nutritional status to behavior and stress response. Additionally, they can be a central or a contributing cause of many diseases, affecting both near and far organ systems. The overall balance in the composition of the gut microbial community, as well as the presence or absence of key species capable of effecting specific responses, is important in ensuring homeostasis or lack thereof at the intestinal mucosa and beyond. The mechanisms through which microbiota exerts its beneficial or detrimental influences remain largely undefined, but include elaboration of signaling molecules and recognition of bacterial epitopes by both intestinal epithelial and mucosal immune cells. The advances in modeling and analysis of gut microbiota will further our knowledge of their role in health and disease, allowing customization of existing and future therapeutic and prophylactic modalities.\u003C\u002Fjats:p>","\u003Cjats:p>Vi sinh vật đường ruột là một tập hợp các vi sinh vật sinh sống trong toàn bộ đường tiêu hóa của động vật có vú. Thành phần của cộng đồng vi sinh vật này là đặc trưng cho từng chủ thể, tiến hóa trong suốt cuộc đời của một cá nhân và dễ bị tác động bởi cả những thay đổi bên ngoài và bên trong. Sự quan tâm gần đây đối với cấu trúc và chức năng của \"cơ quan\" này đã làm nổi bật vị trí trung tâm của nó trong sức khỏe và bệnh tật. Vi sinh vật đường ruột có vai trò mật thiết trong nhiều khía cạnh của sinh lý bình thường của chủ thể, từ trạng thái dinh dưỡng đến hành vi và phản ứng với stress. Ngoài ra, chúng có thể là nguyên nhân chính hoặc nguyên nhân góp phần vào nhiều bệnh, ảnh hưởng đến cả các hệ thống cơ quan gần và xa. Sự cân bằng tổng thể trong thành phần của cộng đồng vi sinh vật đường ruột, cũng như sự hiện diện hoặc vắng mặt của các loài vi sinh vật chính có khả năng gây ra các phản ứng cụ thể, là rất quan trọng trong việc đảm bảo trạng thái cân bằng hoặc sự thiếu hụt tại niêm mạc ruột và các khu vực khác. Cơ chế mà vi sinh vật thực hiện lợi ích hoặc ảnh hưởng có hại của chúng vẫn chủ yếu chưa được xác định rõ, nhưng bao gồm cả việc giải phóng các phân tử tín hiệu và việc nhận diện các epitop vi khuẩn bởi cả tế bào biểu mô ruột và tế bào miễn dịch niêm mạc. Những tiến bộ trong việc mô hình hóa và phân tích vi sinh vật đường ruột sẽ nâng cao hiểu biết của chúng ta về vai trò của chúng trong sức khỏe và bệnh tật, cho phép tùy chỉnh các liệu pháp và biện pháp phòng ngừa hiện tại và trong tương lai.\u003C\u002Fjats:p>",{"EN":18036,"VI":18037},"Gut Microbiota in Health and Disease","Vi sinh vật đường ruột trong sức khỏe và bệnh tật",{"VOID":18039},"20664075",{"VOID":18041},"10.1152\u002Fphysrev.00045.2009",[102],[101],"https:\u002F\u002Fwww.physiology.org\u002Fdoi\u002F10.1152\u002Fphysrev.00045.2009",[18046,18067,18084,18101],{"id":18047,"sortIndex":114,"researcher":26,"roles":18048,"affiliations":18049,"properties":18060},"dee3dfdc-6b3e-4247-95b2-aeededb9199b",[],[18050],{"id":18051,"sortIndex":36,"affiliation":18052,"properties":26},"c1978840-89a1-47f9-9d17-737a0fe7e2b6",{"id":18053,"createTime":18054,"updateTime":18054,"relativeEntities":18055,"slug":18056,"properties":18057,"entityType":98,"verifyStatus":28,"verifyTime":26,"verifyNote":26,"syncStatus":28,"languages":26,"translateLanguages":26,"viewCount":36},"2c4c2551-5acf-41c5-bcc7-ebdf9378b324","2024-10-13T00:06:00.593+00:00",[],"Michael-Smith-Laboratories-Department-of-Microbiology-and-Immunology-and-Department-of-Biochemistry-and-Molecular-Biology-The-University-of-British-Columbia-Vancouver-British-Columbia-Canada",{"title":18058},{"EN":18059},"Michael Smith Laboratories, Department of Microbiology and Immunology, and Department of Biochemistry and Molecular Biology, The University of British Columbia, Vancouver, British Columbia, Canada",{"openalex":18061,"orcid":18063,"title":18065},{"VOID":18062},"A5029589860",{"VOID":18064},"https:\u002F\u002Forcid.org\u002F0000-0003-1686-0788",{"EN":18066},"L. 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