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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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The main objectives of the journal include: providing an intellectual platform for Vietnamese and international scholars; promoting interdisciplinary studies in social sciences and humanities; becoming the leading journal in social sciences and humanities in Vietnam; being indexed by worldwide databases and having academic recognition internationally in the near future.\\nThe journal is currently indexed by Google Scholar, WorldCat, Open Archives, Cosmos Impact Factor, Advanced Sciences Index, Scientific Indexing Services, CrossRef, EBSCO Information Services and Vietnam National University’s digital archive.\\n\"},{\"attributes\":{\"bold\":true},\"insert\":\"Journal of Social Sciences and Humanities-Vietnam\"},{\"insert\":\"\\n\"},{\"attributes\":{\"bold\":true},\"insert\":\"ISSN 2354-1172, email: tapchikhxhnv@gmail.com, tckhxhnv@vnu.edu.vn\"},{\"insert\":\"\\n\"}]}","{\"ops\":[{\"insert\":\"Được thành lập ngày 31\u002F8\u002F2015 (giấy phép hoạt động số 155\u002FGP-BVHTT ngày 11 tháng 5 năm 2015 của Bộ Thông tin và Truyền thông, mã số tiêu chuẩn quốc tế ISSN 2354-1172), Tạp chí Khoa học Xã hội và Nhân văn (Journal of Social Sciences and Humanities) là ấn phẩm khoa học chính thức, duy nhất của Trường Đại học Khoa học Xã hội và Nhân văn, ĐHQG Hà Nội, phát triển và kế thừa Chuyên san Khoa học Xã hội và Nhân văn, Tạp chí Khoa học, ĐHQG Hà Nội.\\nTạp chí xuất bản định kỳ (04 số tiếng Việt\u002Fnăm và 02 số tiếng Anh\u002Fnăm), có nhiệm vụ \"},{\"attributes\":{\"italic\":true},\"insert\":\"công bố, giới thiệu các công trình nghiên cứu khoa học khoa học xã hội và nhân văn của các tác giả là các nhà khoa học trong và ngoài nước, phục vụ giảng dạy, học tập và nghiên cứu khoa học\"},{\"insert\":\". 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And the first issue was published in January 1998 with ISSN 1859-0128. Since then, STDJ has become the most important scientific forum of scientists from VNU-HCM as well as other universities. The magazine has undergone 20 years of development and has become a bridge for scientific exchanges, as well as enriching reference materials for the faculty, doctoral students, students of VNU-HCM in particular and other universities, institutes...\"},{\"attributes\":{\"align\":\"justify\"},\"insert\":\"\\n\"},{\"insert\":\"Science and Technology Development Journal - Health Sciences (STDJ-HS) is a subjournal of Science and Technology Development Journal since 2020.\"},{\"attributes\":{\"align\":\"justify\"},\"insert\":\"\\n\"},{\"insert\":\" \"},{\"attributes\":{\"align\":\"justify\"},\"insert\":\"\\n\"},{\"attributes\":{\"bold\":true},\"insert\":\"2. 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We compare these effects based on the experience in Iranian veterans exposed to the agent during the Iran‐Iraq conflict (1983–88). The first clinical manifestations of sulfur mustard poisoning occurred in the eyes with a sensation of grittiness, lacrimation, photophobia, blepharospasm, and corneal ulceration. Respiratory effects appeared as rhinorhea, laryngitis, tracheobronchitis, and dyspnoea. Skin lesions varied from erythema to bullous necrotization. Initial leukocytosis and lymphopenia returned to normal within four weeks in recovered patients, but marked cytopenia with bone marrow failure occurred in fatal cases. Late toxic effects of sulfur mustard were most commonly found in lungs, skin and eyes. Main respiratory complications were chronic obstructive pulmonary disease, bronchiectasis, asthma, large airway narrowing, and pulmonary fibrosis. Late skin lesions were hyperpigmentation, dry skin, atrophy, and hypopigmentation. Fifteen of the severely intoxicated patients were diagnosed with delayed keratitis, having corneal vascularization, thinning, and epithelial defect. Respiratory complications exacerbated over time, while cutaneous and ocular lesions decreased or remained constant. Both the severity and frequency of bronchiectatic lesions increased during long‐term follow‐up. The only deteriorating cutaneous complication was dry skin. The maximum incidence of delayed kaeratitis was observed 15 to 20 years after initial exposure. 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Hunger signals may be generated in peripheral organs (e.g. ghrelin) but most of them are expressed in the hypothalamus (neuropeptide Y, orexins, agouti‐related peptide, melanin concentrating hormone, endogenous opiates and dopamine) and are expressed during situations of energy deficiency. Some satiety signals, such as cholecystokinin, glucagon‐like peptide 1, peptide YY and enterostatin are released from the digestive tract in response to food intake. Others, such as leptin and insulin, are mobilized in response to perturbations in the nutritional state. Still others are generated in neurones of the hypothalamus (α‐melanocyte‐stimulating hormone and serotonin). Satiety signals act by inhibiting the expression of hunger signals and\u002For by blunting their effect. Palatable food, i.e. food rich in fat and sugar, up‐regulates the expression of hunger signals and satiety signals, at the same time blunting the response to satiety signals and activating the reward system. 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The single cell gel electrophoresis (comet) assay is a technically simple and fast method that detects genotoxicity in virtually any mammalian cell type without requirement for cell culture. This review discusses the strength of the comet assay in biomonitoring at its present state of validation. The simple version of the alkaline comet assay detects DNA migration caused by strand breaks, alkaline labile sites, and transient repair sites. By incubation with bacterial glycosylase\u002Fendonuclease enzymes, broad classes of oxidative DNA damage, alkylations, and ultraviolet light‐induced photoproducts are detected as additional DNA migration. The most widely measured enzyme sensitive sites have been those detected by formamidopyrimidine DNA glycosylase (FPG) and endonuclease III (ENDOIII). Reports from biomonitoring studies show that the basal level of DNA damage in leukocytes is influenced be a variety of lifestyle and environmental exposures, including exercise, air pollution, sunlight, and diet. Although not all types of carcinogenic exposures should be expected to damage DNA in leukocytes, the comet assay is a valuable method for detection of genotoxic exposure in humans. However, the predictive value of the comet assay is unknown because it has not been investigated in prospective cohort studies. Also, it is important that the performance of the assay is investigated in multi‐laboratory validation trials. As a tool in risk assessment the comet assay can be used in characterization of hazards.\u003C\u002Fjats:p>",{"EN":1664},"The Alkaline Comet Assay: Towards Validation in Biomonitoring of DNA Damaging Exposures",{"VOID":1666},"16623855",{"VOID":1668},"10.1111\u002Fj.1742-7843.2006.pto_167.x","2024-09-13T06:14:45.809+00:00",[102],"https:\u002F\u002Fonlinelibrary.wiley.com\u002Fdoi\u002F10.1111\u002Fj.1742-7843.2006.pto_167.x",[1673],{"id":1674,"sortIndex":36,"researcher":26,"roles":1675,"affiliations":1676,"properties":1688},"d6826239-2593-4703-9b47-b002ae3b0bef",[],[1677],{"id":1678,"sortIndex":36,"affiliation":1679,"properties":26},"470834c6-e712-4c68-a150-981bbe2f3125",{"id":1680,"createTime":1681,"updateTime":1682,"relativeEntities":1683,"slug":1684,"properties":1685,"entityType":98,"verifyStatus":28,"verifyTime":26,"verifyNote":26,"syncStatus":28,"languages":26,"translateLanguages":26,"viewCount":36},"027173a8-66c6-4abb-b15e-121653b08328","2024-09-13T06:14:43.449+00:00","2025-06-11T15:51:08.110+00:00",[],"Institute-of-Public-Health-University-of-Copenhagen-%C3%98ster-Farimagsgade-5-Building-B-2nd-Floor-P-O-Box-2099-DK-1014-Copenhagen-K-Denmark-p-moller-pubhealth-ku-dk",{"title":1686},{"EN":1687},"Institute of Public Health, University of Copenhagen, Øster Farimagsgade 5, Building B, 2nd Floor, P.O. 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Pharmacology Toxicology, 96, 1",{},{"id":26,"text":1799,"url":26,"identifiers":1800},"10.1093\u002Fajcn\u002F76.2.303",{"doi":1799},{"id":26,"text":1802,"url":26,"identifiers":1803},"10.1016\u002Fj.mrfmmm.2004.02.018",{"doi":1802},{"id":26,"text":1805,"url":26,"identifiers":1806},"Møller P., 2000, The comet assay as a rapid test in biomonitoring occupational exposure to DNA‐damaging agents and effect of confounding factors, Cancer Epidemiol. Biomarkers Prev., 9, 1005",{},{"id":26,"text":1808,"url":26,"identifiers":1809},"10.1096\u002Ffj.01-0386com",{"doi":1808},{"id":26,"text":1811,"url":26,"identifiers":1812},"Møller P., 2003, No effect of 600 g fruit and vegetables per day on oxidative DNA damage and repair in healthy human non‐smokers, Cancer Epidemiol. Biomarkers Prev., 12, 1016",{},{"id":26,"text":1814,"url":26,"identifiers":1815},"10.1080\u002F10715760400016824",{"doi":1814},{"id":26,"text":1817,"url":26,"identifiers":1818},"10.1016\u002Fj.mrfmmm.2004.02.020",{"doi":1817},{"id":26,"text":1820,"url":26,"identifiers":1821},"10.1007\u002Fs00394-004-0470-6",{"doi":1820},{"id":26,"text":1823,"url":26,"identifiers":1824},"10.1093\u002Fajcn\u002F67.6.1210",{"doi":1823},{"id":26,"text":1826,"url":26,"identifiers":1827},"10.2307\u002F3577279",{"doi":1826},{"id":26,"text":1829,"url":26,"identifiers":1830},"Olive P. L., 2002, The comet assay. An overview of techniques, Meth. Mol. Biol., 203, 179",{},{"id":26,"text":1832,"url":26,"identifiers":1833},"10.1158\u002F1055-9965.EPI-04-0509",{"doi":1832},{"id":26,"text":1835,"url":26,"identifiers":1836},"10.1080\u002F095530099140807",{"doi":1835},{"id":26,"text":1838,"url":26,"identifiers":1839},"10.1080\u002F1071576031000150788",{"doi":1838},{"id":26,"text":1841,"url":26,"identifiers":1842},"Rothman N., 1995, Biomarkers and occupational health: Progress and perspectives, 109",{},{"id":26,"text":1844,"url":26,"identifiers":1845},"10.1080\u002F10408440008951123",{"doi":1844},{"id":26,"text":1847,"url":26,"identifiers":1848},"10.1093\u002Fjn\u002F134.12.3362",{"doi":1847},{"id":26,"text":1850,"url":26,"identifiers":1851},"10.1016\u002Fj.mrgentox.2005.07.001",{"doi":1850},{"id":26,"text":1853,"url":26,"identifiers":1854},"10.1016\u002F0014-4827(88)90265-0",{"doi":1853},{"id":26,"text":1856,"url":26,"identifiers":1857},"10.1093\u002Fcarcin\u002Fbgg037",{"doi":1856},{"id":26,"text":1859,"url":26,"identifiers":1860},"10.1016\u002Fj.mrgentox.2003.08.002",{"doi":1859},{"id":26,"text":1862,"url":26,"identifiers":1863},"Sørensen M., 2003, Personal exposure to PM2.5 and biomarkers of DNA damage, Cancer Epidemiol. Biomarkers Prev., 12, 191",{},{"id":26,"text":1865,"url":26,"identifiers":1866},"Tice R. R., 1995, Environmental mutagenesis, 315",{},{"id":26,"text":1868,"url":26,"identifiers":1869},"10.1093\u002Fmutage\u002F18.2.139",{"doi":1868},{"id":26,"text":1871,"url":26,"identifiers":1872},"10.1289\u002Fehp.7562",{"doi":1871},{"id":1874,"createTime":1875,"updateTime":1875,"relativeEntities":1876,"slug":1877,"properties":1878,"entityType":785,"verifyStatus":25,"verifyTime":1875,"verifyNote":786,"syncStatus":28,"languages":1892,"translateLanguages":26,"viewCount":36,"primaryUrl":1893,"fullTextUrl":26,"authors":1894,"publicationType":828,"publisherRelationship":1936,"citationCount":366,"citationInfo":1967,"publishDate":1182,"publishYear":1183,"citationAnalyzeStatus":28,"lastCitationAnalyze":26,"indexDatabases":26,"openAccess":26,"references":1969,"isForceReanalyzing":1102},"a60c804a-992c-403a-8cbe-38fd0787be34","2024-10-07T13:16:31.723+00:00",[],"Protective-Effects-of-L-Arginine-against-Cisplatin-Induced-Renal-Oxidative-Stress-and-Toxicity-Role-of-Nitric-Oxide",{"mag":1879,"keywords":1881,"openalex":1882,"abstract":1884,"title":1886,"pm":1888,"doi":1890},{"VOID":1880},"2068933269",{},{"VOID":1883},"W2068933269",{"EN":1885},"\u003Cjats:p>\u003Cjats:bold>Abstract:\u003C\u002Fjats:bold> Nephrotoxicity is a dose‐limiting factor in clinical use of cisplatin. The changes in renal haemodynamics were suggested to play a role in cisplatin‐induced nephrotoxicity. The aim of the present study was to investigate the effect of modulation of nitric oxide on the severity of cisplatin‐induced nephrotoxicity using an experimental rat model. A nitric oxide precursor, L‐arginine and an inhibitor of nitric oxide synthase, L‐NAME were used. After six days of cisplatin injection, acute nephrotoxicity was demonstrated by a marked increase in serum creatinine and blood urea nitrogen. Histological examination of the kidneys confirmed the occurrence of renal damage. Moreover, cisplatin induced an increase in the level of lipid peroxides and oxidized glutathione and a depletion of reduced glutathione. The activities of the antioxidant enzymes glutathione peroxidase and superoxide dismutase were also lowered. Besides, there was a reduction in the kidney total nitrate\u002Fnitrite levels. L‐arginine significantly attenuated the oxidative stress and nephrotoxic effect of cisplatin. On the other hand, L‐NAME was found to aggravate cisplatin nephrotoxicity. In conclusion, the decrease in the kidney nitric oxide level contributes, at least in part, in the mechanism underlying the nephrotoxicity of cisplatin. Furthermore, L‐arginine shows nephroprotective effects and might be useful in improving the therapeutic index of cisplatin.\u003C\u002Fjats:p>",{"EN":1887},"Protective Effects of L‐Arginine against Cisplatin‐Induced Renal Oxidative Stress and Toxicity: Role of Nitric Oxide",{"VOID":1889},"15998355",{"VOID":1891},"10.1111\u002Fj.1742-7843.2005.pto_114.x",[102],"https:\u002F\u002Fonlinelibrary.wiley.com\u002Fdoi\u002F10.1111\u002Fj.1742-7843.2005.pto_114.x",[1895,1917],{"id":1896,"sortIndex":115,"researcher":26,"roles":1897,"affiliations":1898,"properties":1910},"26f2aafb-b03d-4aff-a41a-b743810391df",[],[1899],{"id":1900,"sortIndex":36,"affiliation":1901,"properties":26},"7c123f2a-8caf-45dc-bc82-7356bf26bbcd",{"id":1902,"createTime":1903,"updateTime":1904,"relativeEntities":1905,"slug":1906,"properties":1907,"entityType":98,"verifyStatus":28,"verifyTime":26,"verifyNote":26,"syncStatus":28,"languages":26,"translateLanguages":26,"viewCount":36},"9510dc6b-677c-4f93-a856-fc4fd0ff6c4f","2023-12-23T10:12:36.893+00:00","2024-10-07T13:16:31.755+00:00",[],"Department-of-Pharmacology-and-Toxicology-Faculty-of-Pharmacy-Ain-Shams-University-Egypt",{"title":1908},{"VI":1909},"Department of Pharmacology and Toxicology, Faculty of Pharmacy, Ain Shams University, Egypt",{"openalex":1911,"orcid":1913,"title":1915},{"VOID":1912},"A5102986096",{"VOID":1914},"https:\u002F\u002Forcid.org\u002F0000-0002-0537-4445",{"EN":1916},"Ebtehal El‐Demerdash",{"id":1918,"sortIndex":36,"researcher":26,"roles":1919,"affiliations":1920,"properties":1931},"d8c032f6-4664-42d3-9643-febd4e64b550",[],[1921],{"id":1922,"sortIndex":36,"affiliation":1923,"properties":26},"c811f418-f473-4a5d-a476-78f51c6e8a8b",{"id":1924,"createTime":1925,"updateTime":1925,"relativeEntities":1926,"slug":1927,"properties":1928,"entityType":98,"verifyStatus":28,"verifyTime":26,"verifyNote":26,"syncStatus":28,"languages":26,"translateLanguages":26,"viewCount":36},"ac0d8d01-226d-4541-9c21-3530ac5c6f5a","2024-10-07T13:16:31.741+00:00",[],"Department-of-Pharmacology-and-Toxicology-Faculty-of-Pharmacy-Cairo-University-and",{"title":1929},{"EN":1930},"Department of Pharmacology and Toxicology, Faculty of Pharmacy, Cairo University, and",{"openalex":1932,"title":1934},{"VOID":1933},"A5101115341",{"EN":1935},"Samira Saleh",{"url":26,"publisher":1937,"properties":1962},{"id":659,"createTime":660,"updateTime":661,"relativeEntities":1938,"slug":663,"properties":1939,"entityType":24,"verifyStatus":28,"verifyTime":26,"verifyNote":26,"syncStatus":28,"languages":26,"translateLanguages":26,"viewCount":36,"subjectFields":1945,"manageAffiliations":1946,"indexDatabases":1947,"url":761,"thumbnailPath":26,"statistic":26,"gsStatistic":26,"type":26,"analyzePriority":26},[],{"country":1940,"issn":1941,"introduce":1942,"eissn":1943,"title":1944},{"VOID":666},{"VOID":668},{"EN":670},{"VOID":672},{"EN":674},[],[],[1948,1955],{"id":721,"indexDatabase":1949,"url":734,"indexYears":735,"academicFieldIds":1954,"indexDatabaseRanking":740},{"id":723,"createTime":724,"updateTime":725,"relativeEntities":1950,"label":1951,"description":1952,"key":731,"publicationTags":1953,"standard":26},[],{"EN":728,"VI":728},{"EN":728,"VI":730},[733],[737,738,739],{"id":742,"indexDatabase":1956,"url":757,"indexYears":26,"academicFieldIds":1961,"indexDatabaseRanking":26},{"id":744,"createTime":745,"updateTime":746,"relativeEntities":1957,"label":1958,"description":1959,"key":753,"publicationTags":1960,"standard":26},[],{"EN":749,"VI":749},{"VI":751,"EN":752},[755,756],[759,760],{"volume":1963,"pages":1964,"issue":1966},{"VOID":1174},{"VOID":1965},"91-97",{"VOID":1178},{"total":366,"publishYear":26,"statisticByYear":1968},{"2012":158,"2013":356,"2014":158,"2015":135,"2016":52,"2017":53,"2018":135,"2019":50,"2020":52,"2021":59,"2022":135,"2023":114,"2024":111},[1970,1973,1976,1979,1982,1985,1988,1991,1994,1998,2001,2004,2007,2010,2013,2016,2019,2022,2025,2028,2031,2034,2037,2040,2044,2047,2050,2053,2056,2059,2062,2065,2068,2071,2074,2077,2080,2083,2086,2089],{"id":26,"text":1971,"url":26,"identifiers":1972},"10.1038\u002Fki.1995.213",{"doi":1971},{"id":26,"text":1974,"url":26,"identifiers":1975},"10.1097\u002F00007890-199711150-00002",{"doi":1974},{"id":26,"text":1977,"url":26,"identifiers":1978},"10.1006\u002Fphrs.2000.0724",{"doi":1977},{"id":26,"text":1980,"url":26,"identifiers":1981},"10.1016\u002FS0270-9295(03)00089-5",{"doi":1980},{"id":26,"text":1983,"url":26,"identifiers":1984},"10.1046\u002Fj.1523-1755.1998.00767.x",{"doi":1983},{"id":26,"text":1986,"url":26,"identifiers":1987},"10.1016\u002FS0014-2999(00)00025-X",{"doi":1986},{"id":26,"text":1989,"url":26,"identifiers":1990},"Cernadas M. R., 1992, Renal and systemic effects of amino acids administered separately: comparison between L‐arginine and non‐nitric oxide donor amino acids, J. Pharm. Exp. Therap., 263, 1023",{},{"id":26,"text":1992,"url":26,"identifiers":1993},"Ellman G. L., 1959, Tissue sulfhydryl groups, Arch. Biochem. Biophys., 74, 214",{},{"id":26,"text":1995,"url":26,"identifiers":1996},"Fabinay D. L., 1971, Automated reaction rate method for determination of serum creatinine with the CentrifiChem, Clin. Chem., 17, 696, 10.1093\u002Fclinchem\u002F17.8.696",{"doi":1997},"10.1093\u002Fclinchem\u002F17.8.696",{"id":26,"text":1999,"url":26,"identifiers":2000},"Garnick M. B., 1988, Acute renal failure, 621",{},{"id":26,"text":2002,"url":26,"identifiers":2003},"Garza‐Quintero R., 1993, Conversion of structure in ATP‐depleted proximal tubules: role of calcium, polyphosphoinositides and glycine, Amer. J. Physiol., 265, F605",{},{"id":26,"text":2005,"url":26,"identifiers":2006},"10.1046\u002Fj.1523-1755.2002.00233.x",{"doi":2005},{"id":26,"text":2008,"url":26,"identifiers":2009},"10.1590\u002FS0100-879X2003000700017",{"doi":2008},{"id":26,"text":2011,"url":26,"identifiers":2012},"10.1038\u002Fki.1991.210",{"doi":2011},{"id":26,"text":2014,"url":26,"identifiers":2015},"10.1097\u002F01.ju.0000105073.67242.eb",{"doi":2014},{"id":26,"text":2017,"url":26,"identifiers":2018},"10.1007\u002FBF00686332",{"doi":2017},{"id":26,"text":2020,"url":26,"identifiers":2021},"10.1093\u002Fndt\u002F12.12.2478",{"doi":2020},{"id":26,"text":2023,"url":26,"identifiers":2024},"10.1016\u002F0006-2952(94)90269-0",{"doi":2023},{"id":26,"text":2026,"url":26,"identifiers":2027},"10.1093\u002Fjnci\u002F81.10.724",{"doi":2026},{"id":26,"text":2029,"url":26,"identifiers":2030},"10.1016\u002FS0021-9258(19)52451-6",{"doi":2029},{"id":26,"text":2032,"url":26,"identifiers":2033},"10.1006\u002Fphrs.2002.0968",{"doi":2032},{"id":26,"text":2035,"url":26,"identifiers":2036},"Marklund S. L., 1985, Handbook of methods for oxygen radical research, 243",{},{"id":26,"text":2038,"url":26,"identifiers":2039},"10.1006\u002Fniox.2000.0319",{"doi":2038},{"id":26,"text":2041,"url":26,"identifiers":2042},"Mistry P., 1991, The effects of cisplatin on the concentration of protein thiols and glutathione in the rat kidney, Cancer Chemother. Pharmacol., 28, 277, 10.1007\u002FBF00685535",{"doi":2043},"10.1007\u002FBF00685535",{"id":26,"text":2045,"url":26,"identifiers":2046},"Moncada S., 1991, Nitric oxide: physiology, pathophysiology and pharmacology, Pharmacol. Rev., 43, 109",{},{"id":26,"text":2048,"url":26,"identifiers":2049},"10.1016\u002FS1043-6618(03)00040-9",{"doi":2048},{"id":26,"text":2051,"url":26,"identifiers":2052},"10.1007\u002FBF00255906",{"doi":2051},{"id":26,"text":2054,"url":26,"identifiers":2055},"10.1016\u002F0003-2697(79)90738-3",{"doi":2054},{"id":26,"text":2057,"url":26,"identifiers":2058},"10.1006\u002Fphrs.1999.0569",{"doi":2057},{"id":26,"text":2060,"url":26,"identifiers":2061},"10.1042\u002Fbj0940705",{"doi":2060},{"id":26,"text":2063,"url":26,"identifiers":2064},"Paglia D. E., 1967, Studies on the quantitative and qualitative characterization of erythrocyte glutathione peroxidase, J. Lab. Clin. Med., 70, 158",{},{"id":26,"text":2066,"url":26,"identifiers":2067},"10.1038\u002F333664a0",{"doi":2066},{"id":26,"text":2069,"url":26,"identifiers":2070},"10.1021\u002Fac50011a034",{"doi":2069},{"id":26,"text":2072,"url":26,"identifiers":2073},"10.1159\u002F000069714",{"doi":2072},{"id":26,"text":2075,"url":26,"identifiers":2076},"10.1016\u002F0006-2952(92)90725-X",{"doi":2075},{"id":26,"text":2078,"url":26,"identifiers":2079},"10.1016\u002F0003-2697(69)90064-5",{"doi":2078},{"id":26,"text":2081,"url":26,"identifiers":2082},"10.1016\u002FS0305-7372(97)90012-8",{"doi":2081},{"id":26,"text":2084,"url":26,"identifiers":2085},"10.1038\u002Fki.1991.58",{"doi":2084},{"id":26,"text":2087,"url":26,"identifiers":2088},"Winston J. A., 1985, Reduced renal blood flow in early cisplatin‐induced acute renal failure in the rat, Amer. J. Physiol., 249, F490",{},{"id":26,"text":2090,"url":26,"identifiers":2091},"10.1016\u002F0006-2952(94)90383-2",{"doi":2090},{"id":2093,"createTime":2094,"updateTime":2094,"relativeEntities":2095,"slug":2096,"properties":2097,"entityType":785,"verifyStatus":25,"verifyTime":2094,"verifyNote":786,"syncStatus":28,"languages":2111,"translateLanguages":26,"viewCount":36,"primaryUrl":2112,"fullTextUrl":26,"authors":2113,"publicationType":828,"publisherRelationship":2238,"citationCount":366,"citationInfo":2270,"publishDate":2272,"publishYear":2273,"citationAnalyzeStatus":28,"lastCitationAnalyze":26,"indexDatabases":26,"openAccess":26,"references":2274,"isForceReanalyzing":1102},"d7c8d486-a1c8-4439-ae9a-395fd68d92e5","2024-09-30T15:47:11.401+00:00",[],"Hypotensive-and-Vasorelaxant-Effects-of-Citronellol-a-Monoterpene-Alcohol-in-Rats",{"mag":2098,"keywords":2100,"openalex":2101,"abstract":2103,"title":2105,"pm":2107,"doi":2109},{"VOID":2099},"2096364717",{},{"VOID":2102},"W2096364717",{"EN":2104},"\u003Cjats:p>\u003Cjats:bold>Abstract: \u003C\u002Fjats:bold> Citronellol is an essential oil constituent from the medicinal plants \u003Cjats:italic>Cymbopogon citratus\u003C\u002Fjats:italic>, \u003Cjats:italic>Cymbopogon winterianus\u003C\u002Fjats:italic> and \u003Cjats:italic>Lippia alba\u003C\u002Fjats:italic> which are thought to possess antihypertensive properties. Citronellol‐induced cardiovascular effects were evaluated in this study. In rats, citronellol (1–20 mg\u002Fkg, i.v.) induced hypotension, which was not affected by pre‐treatment with atropine, hexamethonium, \u003Cjats:italic>N\u003C\u002Fjats:italic>\u003Cjats:sup>ω\u003C\u002Fjats:sup>‐nitro‐\u003Cjats:sc>l\u003C\u002Fjats:sc>‐arginine methyl ester hydrochloride or indomethacin, and tachycardia, which was only attenuated by pre‐treatment with atropine and hexamethonium. These responses were less than those obtained for nifedipine, a reference drug. In intact rings of rat mesenteric artery pre‐contracted with 10 μM phenylephrine, citronellol induced relaxations (\u003Cjats:italic>p\u003C\u002Fjats:italic>D\u003Cjats:sub>2\u003C\u002Fjats:sub> = 0.71 ± 0.11; \u003Cjats:italic>E\u003C\u002Fjats:italic>\u003Cjats:sub>max\u003C\u002Fjats:sub> = 102 ± 5%; n = 6) that were not affected by endothelium removal, after tetraethylamonium in rings without endothelium pre‐contracted with KCl 80 mM. Citronellol strongly antagonized (maximal inhibition = 97 ± 4%; n = 6) the contractions induced by CaCl\u003Cjats:sub>2\u003C\u002Fjats:sub> (10\u003Cjats:sup>−6\u003C\u002Fjats:sup> to 3 × 10\u003Cjats:sup>−3 \u003C\u002Fjats:sup>M) and did not induce additional effects on the maximal response of nifedipine (10 μM). Finally, citronellol inhibited the contractions induced by 10 μM phenylephrine or 20 mM caffeine. The present results suggest that citronellol lowers blood pressure by a direct effect on the vascular smooth muscle leading to vasodilation.\u003C\u002Fjats:p>",{"EN":2106},"Hypotensive and Vasorelaxant Effects of Citronellol, a Monoterpene Alcohol, in Rats",{"VOID":2108},"20002067",{"VOID":2110},"10.1111\u002Fj.1742-7843.2009.00492.x",[102],"https:\u002F\u002Fonlinelibrary.wiley.com\u002Fdoi\u002F10.1111\u002Fj.1742-7843.2009.00492.x",[2114,2135,2155,2170,2187,2204,2221],{"id":2115,"sortIndex":59,"researcher":26,"roles":2116,"affiliations":2117,"properties":2128},"04f20ac3-cd50-4efd-86bb-97e0ed5535f0",[],[2118],{"id":2119,"sortIndex":36,"affiliation":2120,"properties":26},"78c2bc04-3e56-437b-bc3a-6b98174e580c",{"id":2121,"createTime":2122,"updateTime":2122,"relativeEntities":2123,"slug":2124,"properties":2125,"entityType":98,"verifyStatus":28,"verifyTime":26,"verifyNote":26,"syncStatus":28,"languages":26,"translateLanguages":26,"viewCount":36},"1659c3e0-33aa-4d1a-a2a5-0ef640c4506f","2024-09-30T15:47:11.452+00:00",[],"Laboratory-of-Pharmaceutical-Technology-LTF-Federal-University-of-Para%C3%ADba-Jo%C3%A3o-Pessoa-PB-Brazil",{"title":2126},{"EN":2127},"Laboratory of Pharmaceutical Technology (LTF), Federal University of Paraíba, João Pessoa-PB, Brazil",{"openalex":2129,"orcid":2131,"title":2133},{"VOID":2130},"A5039582274",{"VOID":2132},"https:\u002F\u002Forcid.org\u002F0000-0001-8783-4806",{"EN":2134},"Isac Almeida de Medeiros",{"id":2136,"sortIndex":36,"researcher":26,"roles":2137,"affiliations":2138,"properties":2150},"7b36be83-f69b-4135-ae27-96d9d7e3e997",[],[2139],{"id":2140,"sortIndex":36,"affiliation":2141,"properties":26},"1d061908-5e9e-4215-8794-1be2f68f657c",{"id":2142,"createTime":2143,"updateTime":2144,"relativeEntities":2145,"slug":2146,"properties":2147,"entityType":98,"verifyStatus":28,"verifyTime":26,"verifyNote":26,"syncStatus":28,"languages":26,"translateLanguages":26,"viewCount":36},"34acec1b-8b77-4e40-90b8-f32c96401df6","2024-02-07T11:21:42.612+00:00","2024-09-30T15:47:11.425+00:00",[],"Department-of-Physiology-Federal-University-of-Sergipe-S%C3%A3o-Cristov%C3%A3o-SE-Brazil",{"title":2148},{"VI":2149},"Department of Physiology, Federal University of Sergipe, São Cristovão, SE, Brazil",{"openalex":2151,"title":2153},{"VOID":2152},"A5037473141",{"EN":2154},"Joana F. A. Bastos",{"id":2156,"sortIndex":115,"researcher":26,"roles":2157,"affiliations":2158,"properties":2165},"134991ed-8197-4c7a-8e74-eeb04d34cb18",[],[2159],{"id":2160,"sortIndex":36,"affiliation":2161,"properties":26},"2e1dd732-c367-4e13-966f-7b46b57de7d2",{"id":2142,"createTime":2143,"updateTime":2144,"relativeEntities":2162,"slug":2146,"properties":2163,"entityType":98,"verifyStatus":28,"verifyTime":26,"verifyNote":26,"syncStatus":28,"languages":26,"translateLanguages":26,"viewCount":36},[],{"title":2164},{"VI":2149},{"openalex":2166,"title":2168},{"VOID":2167},"A5065759302",{"EN":2169},"Ítalo José Alves 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Transgenic mice overexpressing alpha2A-adrenoceptors in pancreatic beta-cells show altered regulation of glucose homeostasis, Diabetologia, 43, 899, 10.1007\u002Fs001250051467",{"doi":2600},"10.1007\u002Fs001250051467",{"id":26,"text":2602,"url":26,"identifiers":2603},"Hamamdzic, 1995, Regulation of alpha 2-adrenergic receptor expression and signaling in pancreatic beta-cells, Am J Physiol, 269, E162",{},{"id":26,"text":2605,"url":26,"identifiers":2606},"Davani, 2004, Aged transgenic mice with increased glucocorticoid sensitivity in pancreatic beta-cells develop diabetes, Diabetes, 53, S51, 10.2337\u002Fdiabetes.53.2007.S51",{"doi":2607},"10.2337\u002Fdiabetes.53.2007.S51",{"id":26,"text":2609,"url":26,"identifiers":2610},"Rosmond, 2002, A C-1291G polymorphism in the alpha2A-adrenergic receptor gene (ADRA2A) promoter is associated with cortisol escape from dexamethasone and elevated glucose levels, J Intern Med, 251, 252, 10.1046\u002Fj.1365-2796.2002.00961.x",{"doi":2611},"10.1046\u002Fj.1365-2796.2002.00961.x",{"id":26,"text":2613,"url":26,"identifiers":2614},"Boesgaard, 2010, Variants at DGKB\u002FTMEM195, ADRA2A, GLIS3 and C2CD4B loci are associated with reduced glucose-stimulated beta cell function in middle-aged Danish people, Diabetologia, 53, 1647, 10.1007\u002Fs00125-010-1753-5",{"doi":2615},"10.1007\u002Fs00125-010-1753-5",{"id":26,"text":2617,"url":26,"identifiers":2618},"Dupuis, 2010, New genetic loci implicated in fasting glucose homeostasis and their impact on type 2 diabetes risk, Nat Genet, 42, 105, 10.1038\u002Fng.520",{"doi":2619},"10.1038\u002Fng.520",{"id":26,"text":2621,"url":26,"identifiers":2622},"Rosengren, 2010, Overexpression of alpha2A-adrenergic receptors contributes to type 2 diabetes, Science, 327, 217, 10.1126\u002Fscience.1176827",{"doi":2623},"10.1126\u002Fscience.1176827",{"id":26,"text":2625,"url":26,"identifiers":2626},"Small, 2006, Complex haplotypes derived from noncoding polymorphisms of the intronless alpha2A-adrenergic gene diversify receptor expression, Proc Natl Acad Sci USA, 103, 5472, 10.1073\u002Fpnas.0601345103",{"doi":2627},"10.1073\u002Fpnas.0601345103",{"id":26,"text":2629,"url":26,"identifiers":2630},"Berlin, 1994, Reduction of hyperglycemia after oral glucose load by the new alpha 2-adrenergic receptor antagonist SL 84.0418 in healthy subjects, Clin Pharmacol Ther, 55, 338, 10.1038\u002Fclpt.1994.35",{"doi":2631},"10.1038\u002Fclpt.1994.35",{"id":26,"text":2633,"url":26,"identifiers":2634},"Buse, 1970, Effect of alpha-adrenergic blockade on insulin secretion in man, Metabolism, 19, 219, 10.1016\u002F0026-0495(70)90055-7",{"doi":2635},"10.1016\u002F0026-0495(70)90055-7",{"id":26,"text":2637,"url":26,"identifiers":2638},"Kawazu, 1987, Studies of midaglizole (DG-5128). A new type of oral hypoglycemic drug in healthy subjects, Diabetes, 36, 216, 10.2337\u002Fdiabetes.36.2.216",{"doi":2639},"10.2337\u002Fdiabetes.36.2.216",{"id":26,"text":2641,"url":26,"identifiers":2642},"Ortiz-Alonso, 1991, Effect of an oral alpha 2-adrenergic blocker (MK-912) on pancreatic islet function in non-insulin-dependent diabetes mellitus, Metabolism, 40, 1160, 10.1016\u002F0026-0495(91)90210-N",{"doi":2643},"10.1016\u002F0026-0495(91)90210-N",{"id":26,"text":2645,"url":26,"identifiers":2646},"Robertson, 1976, A role for alpha-adrenergic receptors in abnormal insulin secretion in diabetes mellitus, J Clin Invest, 57, 791, 10.1172\u002FJCI108338",{"doi":2647},"10.1172\u002FJCI108338",{"id":26,"text":2649,"url":26,"identifiers":2650},"Schmidt, 1997, Acute alpha 2 blockade by idazoxan increases insulin and lowers plasma glucose during positron emission tomography, Psychopharmacol Bull, 33, 253",{},{"id":26,"text":2652,"url":26,"identifiers":2653},"Ribes, 1984, In vivo stimulation of pancreatic hormone secretion by norepinephrine infusion in the dog, Am J Physiol, 246, E339",{},{"id":26,"text":2655,"url":26,"identifiers":2656},"Östenson, 1988, Alpha 2-adrenoceptor blockade does not enhance glucose-induced insulin release in normal subjects or patients with noninsulin-dependent diabetes, J Clin Endocrinol Metab, 67, 1054, 10.1210\u002Fjcem-67-5-1054",{"doi":2657},"10.1210\u002Fjcem-67-5-1054",{"id":26,"text":2659,"url":26,"identifiers":2660},"Natali, 1998, Effects of acute alpha 2-blockade on insulin action and secretion in humans, Am J Physiol, 274, E57",{},{"id":26,"text":2662,"url":26,"identifiers":2663},"Sciberras, 1994, The effects of a peripherally selective alpha 2-adrenoceptor antagonist, MK-467, on the metabolic and cardiovascular response to exercise in healthy man, Br J Clin Pharmacol, 37, 39, 10.1111\u002Fj.1365-2125.1994.tb04236.x",{"doi":2664},"10.1111\u002Fj.1365-2125.1994.tb04236.x",{"id":26,"text":2666,"url":26,"identifiers":2667},"Morgan, 2001, Imidazoline binding sites in the endocrine pancreas: can they fulfil their potential as targets for the development of new insulin secretagogues?, Curr Pharm Des, 7, 1413, 10.2174\u002F1381612013397366",{"doi":2668},"10.2174\u002F1381612013397366",{"id":26,"text":2670,"url":26,"identifiers":2671},"Efendic, 2002, Two generations of insulinotropic imidazoline compounds, Diabetes, 51, S448, 10.2337\u002Fdiabetes.51.2007.S448",{"doi":2672},"10.2337\u002Fdiabetes.51.2007.S448",{"id":26,"text":2674,"url":26,"identifiers":2675},"Fagerholm, 2008, Alpha2a-adrenoceptor antagonism increases insulin secretion and synergistically augments the insulinotropic effect of glibenclamide in mice, Br J Pharmacol, 154, 1287, 10.1038\u002Fbjp.2008.186",{"doi":2676},"10.1038\u002Fbjp.2008.186",{"id":26,"text":2678,"url":26,"identifiers":2679},"Khosravi, 2006, Control of environmental health and removal of rats by alpha2-adrenergic antagonist and potassium channel blocker, Iran J Environ Health Sci Eng, 3, 255",{},{"id":26,"text":2681,"url":26,"identifiers":2682},"Berridge, 1992, Comparison of the effects of efaroxan and glibenclamide on plasma glucose and insulin levels in rats, Eur J Pharmacol, 213, 213, 10.1016\u002F0014-2999(92)90684-V",{"doi":2683},"10.1016\u002F0014-2999(92)90684-V",{"id":26,"text":2685,"url":26,"identifiers":2686},"Mourtada, 1997, Interactions between imidazoline compounds and sulphonylureas in the regulation of insulin secretion, Br J Pharmacol, 121, 799, 10.1038\u002Fsj.bjp.0701172",{"doi":2687},"10.1038\u002Fsj.bjp.0701172",{"id":26,"text":2689,"url":26,"identifiers":2690},"de Boer, 1996, The pharmacologic profile of mirtazapine, J Clin Psychiatry, 57, 19",{},{"id":26,"text":2692,"url":26,"identifiers":2693},"Garcia-Sevilla, 1981, Alpha 2-adrenoreceptors on human platelets: selective labelling by [3H]clonidine and [3H]yohimbine and competitive inhibition by antidepressant drugs, Eur J Pharmacol, 74, 329, 10.1016\u002F0014-2999(81)90052-2",{"doi":2694},"10.1016\u002F0014-2999(81)90052-2",{"id":26,"text":2696,"url":26,"identifiers":2697},"Kalkman, 2003, Alpha2c-Adrenoceptor blockade by clozapine and other antipsychotic drugs, Eur J Pharmacol, 462, 33, 10.1016\u002FS0014-2999(03)01308-6",{"doi":2698},"10.1016\u002FS0014-2999(03)01308-6",{"id":2700,"createTime":2701,"updateTime":2701,"relativeEntities":2702,"slug":2703,"properties":2704,"entityType":785,"verifyStatus":25,"verifyTime":2718,"verifyNote":786,"syncStatus":28,"languages":2719,"translateLanguages":26,"viewCount":36,"primaryUrl":2720,"fullTextUrl":26,"authors":2721,"publicationType":828,"publisherRelationship":2866,"citationCount":2898,"citationInfo":2899,"publishDate":2901,"publishYear":2902,"citationAnalyzeStatus":28,"lastCitationAnalyze":26,"indexDatabases":26,"openAccess":26,"references":2903,"isForceReanalyzing":1102},"814c6189-591d-4609-bb03-7198f2f4cff6","2024-09-28T20:08:55.424+00:00",[],"Pharmacogenetic-Studies-of-Paclitaxel-in-the-Treatment-of-Ovarian-Cancer",{"mag":2705,"keywords":2707,"openalex":2708,"abstract":2710,"title":2712,"pm":2714,"doi":2716},{"VOID":2706},"2106341748",{},{"VOID":2709},"W2106341748",{"EN":2711},"\u003Cjats:p>\u003Cjats:bold>Abstract: \u003C\u002Fjats:bold> The purpose of this study was to evaluate the role of sequence variants in the CYP2C8, ABCB1 and CYP3A4 genes and the CYP3A4 phenotype for the pharmacokinetics and toxicity of paclitaxel in ovarian cancer patients. Thirty‐eight patients were treated with paclitaxel and carboplatin. The genotypes of CYP2C8*1B, *1C, *2, *3, *4, *5, *6, *7, *8 and P404A, ABCB1 G2677T\u002FA and C3435T, as well as CYP3A4*1B, were determined by pyrosequencing. Phenotyping of CYP3A4 was performed \u003Cjats:italic>in vivo\u003C\u002Fjats:italic> with quinine as a probe. The patients were monitored for toxicity and 23 patients underwent a more extensive neurotoxicity evaluation. Patients heterozygous for G\u002FA in position 2677 in ABCB1 had a significantly higher clearance of paclitaxel than most other ABCB1 variants. A lower clearance of paclitaxel was found for patients heterozygous for CYP2C8*3 when stratified according to the ABCB1 G2677T\u002FA genotype. In addition, the CYP3A4 enzyme activity \u003Cjats:italic>in vivo\u003C\u002Fjats:italic> affected which metabolic pathway was dominant in each patient, but not the total clearance of paclitaxel. The exposure to paclitaxel correlated to the degree of neurotoxicity. Our findings suggest that interindividual variability in paclitaxel pharmacokinetics might be predicted by ABCB1 and CYP2C8 genotypes and provide useful information for individualized chemotherapy.\u003C\u002Fjats:p>",{"EN":2713},"Pharmacogenetic Studies of Paclitaxel in the Treatment of Ovarian Cancer",{"VOID":2715},"19143748",{"VOID":2717},"10.1111\u002Fj.1742-7843.2008.00351.x","2024-09-28T20:08:55.423+00:00",[102],"https:\u002F\u002Fonlinelibrary.wiley.com\u002Fdoi\u002F10.1111\u002Fj.1742-7843.2008.00351.x",[2722,2743,2763,2778,2797,2816,2845],{"id":2723,"sortIndex":36,"researcher":26,"roles":2724,"affiliations":2725,"properties":2736},"9d079a64-7c1c-44e4-a502-f34b376b726d",[],[2726],{"id":2727,"sortIndex":36,"affiliation":2728,"properties":26},"0e86613d-9795-4006-a52b-98195b873f15",{"id":2729,"createTime":2730,"updateTime":2730,"relativeEntities":2731,"slug":2732,"properties":2733,"entityType":98,"verifyStatus":28,"verifyTime":26,"verifyNote":26,"syncStatus":28,"languages":26,"translateLanguages":26,"viewCount":36},"b6403669-5ef8-4527-b5cc-59106d1d0f16","2024-09-28T20:08:55.440+00:00",[],"Division-of-Drug-Research-Faculty-of-Health-Sciences-Link%C3%B6ping-University-Link%C3%B6ping-",{"title":2734},{"EN":2735},"Division of Drug Research, Faculty of Health Sciences, Linköping University, Linköping,",{"openalex":2737,"orcid":2739,"title":2741},{"VOID":2738},"A5037660153",{"VOID":2740},"https:\u002F\u002Forcid.org\u002F0000-0002-8015-5728",{"EN":2742},"Henrik Gréen",{"id":2744,"sortIndex":114,"researcher":26,"roles":2745,"affiliations":2746,"properties":2758},"ace120de-d42c-4ad0-b16d-949f019858ee",[],[2747],{"id":2748,"sortIndex":36,"affiliation":2749,"properties":26},"f7230ec8-6919-4ada-a624-902b29c413b7",{"id":2750,"createTime":2751,"updateTime":2752,"relativeEntities":2753,"slug":2754,"properties":2755,"entityType":98,"verifyStatus":28,"verifyTime":26,"verifyNote":26,"syncStatus":28,"languages":26,"translateLanguages":26,"viewCount":36},"1aeab6aa-bc9e-4914-812c-f59b4a94319f","2024-01-19T14:59:13.489+00:00","2024-09-28T20:08:55.465+00:00",[],"Department-of-Oncology-Link%C3%B6ping-University-Hospital-Link%C3%B6ping",{"title":2756},{"VI":2757},"Department of Oncology, Linköping University Hospital, Linköping",{"openalex":2759,"title":2761},{"VOID":2760},"A5034247691",{"EN":2762},"Per Rosenberg",{"id":2764,"sortIndex":135,"researcher":26,"roles":2765,"affiliations":2766,"properties":2773},"863bc790-c97d-4392-b959-e1b80e15b767",[],[2767],{"id":2768,"sortIndex":36,"affiliation":2769,"properties":26},"7fe9c420-e26c-4615-9c4e-cbeb4167c471",{"id":2729,"createTime":2730,"updateTime":2730,"relativeEntities":2770,"slug":2732,"properties":2771,"entityType":98,"verifyStatus":28,"verifyTime":26,"verifyNote":26,"syncStatus":28,"languages":26,"translateLanguages":26,"viewCount":36},[],{"title":2772},{"EN":2735},{"openalex":2774,"title":2776},{"VOID":2775},"A5051955118",{"EN":2777},"Curt 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Stockholm,",{"id":2831,"sortIndex":115,"affiliation":2832,"properties":26},"7b5af760-a14a-49cb-92d9-f1628cee86f3",{"id":2833,"createTime":2834,"updateTime":2834,"relativeEntities":2835,"slug":2836,"properties":2837,"entityType":98,"verifyStatus":28,"verifyTime":26,"verifyNote":26,"syncStatus":28,"languages":26,"translateLanguages":26,"viewCount":36},"1ecea666-a0b9-44ba-892d-9545d1464638","2024-09-28T20:08:55.485+00:00",[],"Present-affiliation-Department-of-Clinical-Toxicology-Central-Laboratories-Blood-Bank-King-Fahad-Medical-City-Riyadh-11525-Kingdom-of-Saudi-Arabia-",{"title":2838},{"EN":2839},"Present affiliation: Department of Clinical Toxicology, Central Laboratories & Blood Bank, King Fahad Medical City, Riyadh 11525, Kingdom of Saudi Arabia.",{"openalex":2841,"title":2843},{"VOID":2842},"A5023965807",{"EN":2844},"Rajaa A. 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Sufficient uteroplacental blood flow is essential for normal pregnancy outcome and is accomplished by the coordinated growth and remodelling of the entire maternal uterine vasculature. The main focus of this MiniReview is to provide information on upstream (pre‐placental) maternal uterine vascular remodelling that facilitates gestational increases in uterine blood flow. Consideration of the three‐dimensional pattern of remodelling (circumferential enlargement \u003Cjats:italic>versus\u003C\u002Fjats:italic> axial elongation), changes in vessel biomechanical properties, and underlying mechanisms [shear stress, nitric oxide, vascular endothelial growth factor (VEGF)\u002Fplacental growth factor (PlGF), the renin–angiotensin system] and pathways (local \u003Cjats:italic>versus\u003C\u002Fjats:italic> systemic; venoarterial exchange) are provided using the rat as the principal animal model, although findings from other species are incorporated wherever possible to provide a comparative perspective. The process of maternal gestational uterine vascular remodelling involves a number of cellular processes and mechanisms, including trophoblast invasion, hyperplasia and hypertrophy, and changes in extracellular matrix composition. In addition, changes in cellular function, e.g. the secretory and contractile properties of smooth muscle and an up‐regulation of endothelial vasodilatory influences may contribute to uteroplacental blood flow increases through changes in tone as well as in structure. Future studies aimed at better understanding the inter‐relationship between changes in vessel structure (remodelling) and function (reactivity) would likely generate new mechanistic insights into the fascinating process of maternal gestational uterine vascular adaptation and provide a more physiological perspective of the underlying cellular processes involved in its regulation.\u003C\u002Fjats:p>",{"EN":3062},"Physiological Remodelling of the Maternal Uterine Circulation during 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play a central role in inflammation through their direct interaction with other cell types, such as leucocytes and endothelial cells, and by the release of many factors, that is, lipids [such as thromboxane (\u003Cjats:styled-content style=\"fixed-case\">TX\u003C\u002Fjats:styled-content>)\u003Cjats:styled-content style=\"fixed-case\">A\u003C\u002Fjats:styled-content>\u003Cjats:sub>2\u003C\u002Fjats:sub>] and proteins (a wide number of angiogenic and growth factors) stored in α‐granules, and adenosine diphosphate (\u003Cjats:styled-content style=\"fixed-case\">ADP\u003C\u002Fjats:styled-content>), stored in dense granules. These platelet actions trigger autocrine and paracrine activation processes that lead to leucocyte recruitment into different tissues and phenotypic changes in stromal cells which contribute to the development of different disease states, such as atherosclerosis and atherothrombosis, intestinal inflammation and cancer. The signals induced by platelets may cause pro‐inflammatory and malignant phenotypes in other cells through the persistent induction of aberrant expression of cyclooxygenase (\u003Cjats:styled-content style=\"fixed-case\">COX\u003C\u002Fjats:styled-content>)‐2 and increased generation of prostanoids, mainly prostaglandin (\u003Cjats:styled-content style=\"fixed-case\">PG\u003C\u002Fjats:styled-content>)\u003Cjats:styled-content style=\"fixed-case\">E\u003C\u002Fjats:styled-content>\u003Cjats:sub>2\u003C\u002Fjats:sub>. In addition to cardiovascular disease, enhanced platelet activation has been detected in inflammatory disease and intestinal tumourigenesis. Moreover, the results of clinical studies have shown that the antiplatelet drug aspirin reduces the incidence of vascular events and colorectal cancer. All these pieces of evidence support the notion that colorectal cancer and atherothrombosis may share a common mechanism of disease, that is, platelet activation in response to epithelial (in tumourigenesis) and endothelial (in tumourigenesis and atherothrombosis) injury. Extensive translational medicine research is necessary to obtain a definitive mechanistic demonstration of the platelet‐mediated hypothesis of colon tumourigenesis. The results of these studies will be fundamental to support the clinical decision to recommend the use of low‐dose aspirin, and possibly other antiplatelet agents, in primary prevention, that is, even for individuals at low cardiovascular risk.\u003C\u002Fjats:p>",{"EN":3333},"Role of Platelets in Inflammation and Cancer: Novel Therapeutic 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is a chronic inflammatory disease of the airways manifesting in many different phenotypes. Allergic asthma, comprising approximately half of patients with asthma, is characterized by the accumulation of eosinophils into the lungs. Eosinophils release factors that damage the surrounding cells and participate in the maintenance and exacerbation of inflammation. In the absence of any inflammatory survival‐prolonging factors, eosinophils die by apoptosis in few days but in inflamed airways, eosinophil survival is thought to be prolonged due to the surrounding pro‐inflammatory factors such as \u003Cjats:styled-content style=\"fixed-case\">IL\u003C\u002Fjats:styled-content>‐5, \u003Cjats:styled-content style=\"fixed-case\">IL\u003C\u002Fjats:styled-content>‐3 and \u003Cjats:styled-content style=\"fixed-case\">GM\u003C\u002Fjats:styled-content>‐\u003Cjats:styled-content style=\"fixed-case\">CSF\u003C\u002Fjats:styled-content>. Resolution of eosinophilic inflammation is an important goal in the treatment of allergic asthma. Apoptosis is a physiological and non‐inflammatory way to eliminate these harmful cells, and development of drugs targeting eosinophil apoptosis is one possible strategy for the therapy of allergic asthma. Importance of this strategy is supported by the fact that promotion of eosinophil apoptosis is a property of many anti‐asthmatic agents such as glucocorticoids, the current main anti‐inflammatory therapy of asthma, theophylline and leukotriene modifiers. β\u003Cjats:sub>2\u003C\u002Fjats:sub> agonists have been shown to modulate eosinophil longevity by increasing survival. Also, anti‐\u003Cjats:styled-content style=\"fixed-case\">IL\u003C\u002Fjats:styled-content>‐5 antibody mesolizumab has shown efficacy in reducing asthma exacerbations in patients with severe eosinophilic asthma. Many potential future anti‐asthmatic agents, such as \u003Cjats:styled-content style=\"fixed-case\">S\u003C\u002Fjats:styled-content>iglec‐8 activating antibody and novel humanized anti‐\u003Cjats:styled-content style=\"fixed-case\">IL\u003C\u002Fjats:styled-content>‐5 antibody \u003Cjats:styled-content style=\"fixed-case\">MEDI\u003C\u002Fjats:styled-content>‐563, have the property of inducing eosinophil apoptosis. This \u003Cjats:styled-content style=\"fixed-case\">M\u003C\u002Fjats:styled-content>ini\u003Cjats:styled-content style=\"fixed-case\">R\u003C\u002Fjats:styled-content>eview aims to present eosinophil apoptosis as a therapeutic target in the treatment of allergic asthma. We summarize the effects and mechanisms of current and potential future anti‐asthmatic drugs on eosinophil apoptosis and additionally, discuss the potential factors that promote eosinophil longevity in the lungs.\u003C\u002Fjats:p>",{"EN":3735},"Eosinophil Apoptosis as a Therapeutic Target in Allergic 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