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As well as the established medical disciplines, Frontiers in Medicine is launching new sections that together will facilitate - the use of patient-reported outcomes under real world conditions - the exploitation of big data and the use of novel information and communication tools in the assessment of new medicines - the scientific bases for guidelines and decisions from regulatory authorities - access to medicinal products and medical devices worldwide - addressing the grand health challenges around the world",{"EN":19},"Frontiers in Medicine","PUBLISHER","PENDING",null,0,[25],{"id":26,"createTime":27,"updateTime":28,"relativeEntities":29,"label":30,"description":32,"parentId":22,"standard":22,"scholarHubFieldId":22},"0254e3e5-c28d-4a33-83da-81bc94d29ffd","2023-05-29T10:24:00.931+00:00","2023-11-21T07:56:41.438+00:00",[],{"EN":31},"Medicine (miscellaneous)",{},[34],{"id":35,"createTime":36,"updateTime":37,"relativeEntities":38,"slug":39,"properties":40,"entityType":43,"verifyStatus":21,"verifyTime":22,"verifyNote":22,"syncStatus":21,"languages":22,"translateLanguages":22,"viewCount":44,"url":22,"parentIds":45,"statistic":22},"57a1b006-1eeb-4af3-bad6-598ed57cbdc4","2023-05-29T10:24:21.833+00:00","2024-02-09T17:22:19.223+00:00",[],"Frontiers-Media-S-A-",{"title":41},{"EN":42},"Frontiers Media S.A.","AFFILIATION",5,[],[47,66],{"id":48,"indexDatabase":49,"url":61,"indexYears":62,"academicFieldIds":63,"indexDatabaseRanking":65},"4052debd-eeee-41a8-9550-0fe8cc85a757",{"id":50,"createTime":51,"updateTime":52,"relativeEntities":53,"label":54,"description":56,"key":58,"publicationTags":59,"standard":22},"3c7051d4-eb7d-4c57-a56b-36fc74c5d1e9","2023-05-22T09:57:18.509+00:00","2025-11-21T10:07:52.274+00:00",[],{"EN":55,"VI":55},"Scopus - Elsevier",{"EN":55,"VI":57},"Cơ sở dữ liệu Scopus thuộc Elsevier","scopus",[60],"SCOPUS","https:\u002F\u002Fwww.scopus.com\u002Fsourceid\u002F21100868809","2014-2025",[64],"e89cebf4-fecf-4b74-8ab4-88fca891e4c2","SCOPUS__Q1",{"id":67,"indexDatabase":68,"url":82,"indexYears":22,"academicFieldIds":83,"indexDatabaseRanking":22},"65b97f39-36aa-419d-b11e-788c5be239f0",{"id":69,"createTime":70,"updateTime":71,"relativeEntities":72,"label":73,"description":75,"key":78,"publicationTags":79,"standard":22},"a4921856-b128-4d9f-8f1f-e80813d3bbd4","2023-05-22T09:59:31.026+00:00","2025-11-21T10:07:52.153+00:00",[],{"EN":74,"VI":74},"ISI\u002FSCIE - Science Citation Index Expanded",{"VI":76,"EN":77},"Cơ sở dữ liệu SCIE","SCIE database","scie",[80,81],"SCIE","ISI","https:\u002F\u002Fwww.scopus.com\u002Fsourceid\u002Fnull",[84],"c796e0e3-2c7c-4993-b16f-e2f1a695268e","https:\u002F\u002Fwww.frontiersin.org\u002Fjournals\u002Fmedicine#",{"impactFactor":23,"impactFactorByYear":87,"i10Index":23,"i10IndexLast5Year":23,"totalPublication":88,"totalPublicationByYear":89,"totalCitation":90,"totalCitationByYear":91,"totalCitationPerPublication":92,"totalCitationPerPublicationByYear":93,"hindexLast5Year":88,"hindex":88},{},3,{"2022":88},18,{"2022":90},6,{"2022":92},{"meta":95,"data":97},{"total":96},"35",[98,500,858,1059,1485,2050,2460,3839,4286,4649],{"id":99,"createTime":100,"updateTime":100,"relativeEntities":101,"slug":102,"properties":103,"entityType":119,"verifyStatus":120,"verifyTime":100,"verifyNote":121,"syncStatus":21,"languages":122,"translateLanguages":22,"viewCount":23,"primaryUrl":124,"fullTextUrl":22,"authors":125,"publicationType":278,"publisherRelationship":279,"citationCount":312,"citationInfo":313,"publishDate":22,"publishYear":22,"citationAnalyzeStatus":21,"lastCitationAnalyze":22,"indexDatabases":22,"openAccess":22,"references":315,"isForceReanalyzing":499},"af5fd5b8-e4b5-46b3-b27e-39caa6451ad5","2024-09-05T23:56:41.703+00:00",[],"Exogenous-HMGB1-Promotes-the-Proliferation-and-Metastasis-of-Pancreatic-Cancer-Cells",{"mag":104,"keywords":106,"pmc":107,"openalex":109,"abstract":111,"title":113,"pm":115,"doi":117},{"VOID":105},"3177637549",{},{"VOID":108},"8595098",{"VOID":110},"W3177637549",{"EN":112},"\u003Cjats:p>\u003Cjats:bold>Background:\u003C\u002Fjats:bold> Exogenous HMGB1 plays a vital role in tumor recurrence, and HMGB1 is ubiquitous in the tumor microenvironment. However, the mechanism of action is still unclear. We investigated the role of exogenous HMGB1 in tumor proliferation and metastasis using human SW1990 and PANC-1 cells after radiotherapy and explored the possible molecular mechanism.\u003C\u002Fjats:p>\u003Cjats:p>\u003Cjats:bold>Materials and Methods:\u003C\u002Fjats:bold> Residual PANC-1 cells and SW1990 cells were isolated after radiotherapy. The supernatant after radiotherapy was collected. The relative expression of HMGB1 was evaluated by Enzyme Linked Immunosorbent Assay (ELISA). Electron microscope (EMS) was used to collect the images of pancreatic cancer cells pre and post radiotherapy treatment. The proliferation of pancreatic cancer cells which were treated with different radiation doses was measured by Carboxy Fluorescein Succinimidyl Ester (CFSE). The migration rates of pancreatic cancer cells were measured by wound healing assays. Subsequently, the expression of related proteins was detected by Western Blot. \u003Cjats:italic>In vivo\u003C\u002Fjats:italic>, the subcutaneous pancreatic tumor models of nude mice were established, and therapeutic capabilities were tested.\u003C\u002Fjats:p>\u003Cjats:p>\u003Cjats:bold>Results:\u003C\u002Fjats:bold> HMGB1 was detected in the supernatant of pancreatic cancer cells after radiotherapy. The results of CFSE showed that exogenous HMGB1 promotes the proliferation and metastasis of pancreatic cancer cells. The western blot results showed activation of p-GSK 3β and up-regulation of N-CA, Bcl-2, and Ki67 in response to HMGB1 stimulation, while E-CA expression was down-regulated in pancreatic cancer cells in response to HMGB1 stimulation. \u003Cjats:italic>In vivo\u003C\u002Fjats:italic>, ethyl pyruvate (EP, HMGB1 inhibitor) inhibits the growth of tumors and HMGB1 promotes the proliferation of tumors after radiation.\u003C\u002Fjats:p>\u003Cjats:p>\u003Cjats:bold>Conclusion:\u003C\u002Fjats:bold> Radiotherapy induces HMGB1 release into the extracellular space. Exogenous HMGB1 promotes the proliferation and metastasis of PANC-1 cells and SW1990 cells by activation of p-GSK 3β which is mediated by Wnt pathway.\u003C\u002Fjats:p>",{"EN":114},"Exogenous HMGB1 Promotes the Proliferation and Metastasis of Pancreatic Cancer Cells",{"VOID":116},"34805222",{"VOID":118},"10.3389\u002Ffmed.2021.756988","PUBLICATION","VERIFIED","Auto Verify",[123],"EN","https:\u002F\u002Fwww.frontiersin.org\u002Farticles\u002F10.3389\u002Ffmed.2021.756988\u002Ffull",[126,148,166,183,205,226,242,261],{"id":127,"sortIndex":128,"researcher":22,"roles":129,"affiliations":130,"properties":141},"ec0e1bf1-df51-4418-b653-1064c600d251",7,[],[131],{"id":132,"sortIndex":23,"affiliation":133,"properties":22},"8ef36139-6538-4833-a514-a54abe52dce2",{"id":134,"createTime":135,"updateTime":135,"relativeEntities":136,"slug":137,"properties":138,"entityType":43,"verifyStatus":21,"verifyTime":22,"verifyNote":22,"syncStatus":21,"languages":22,"translateLanguages":22,"viewCount":23},"2971e72a-2a97-4806-8f57-f220f75f4eaf","2024-09-05T23:56:41.716+00:00",[],"Department-of-Radiology-Jiangsu-Province-Hospital-of-Chinese-Medicine-Affiliated-Hospital-of-Nanjing-University-of-Chinese-Medicine-China",{"title":139},{"EN":140},"Department of Radiology, Jiangsu Province Hospital of Chinese Medicine, Affiliated Hospital of Nanjing University of Chinese Medicine, China",{"openalex":142,"orcid":144,"title":146},{"VOID":143},"A5030677018",{"VOID":145},"https:\u002F\u002Forcid.org\u002F0000-0001-6681-7345",{"EN":147},"Zhongqiu Wang",{"id":149,"sortIndex":150,"researcher":22,"roles":151,"affiliations":152,"properties":159},"ab345796-e86c-42ea-8ae5-f4102effd8e3",1,[],[153],{"id":154,"sortIndex":23,"affiliation":155,"properties":22},"85f9d645-916f-4582-8ef1-79f2fddd35b3",{"id":134,"createTime":135,"updateTime":135,"relativeEntities":156,"slug":137,"properties":157,"entityType":43,"verifyStatus":21,"verifyTime":22,"verifyNote":22,"syncStatus":21,"languages":22,"translateLanguages":22,"viewCount":23},[],{"title":158},{"EN":140},{"openalex":160,"orcid":162,"title":164},{"VOID":161},"A5007569895",{"VOID":163},"https:\u002F\u002Forcid.org\u002F0000-0003-4902-6298",{"EN":165},"Shuai Ren",{"id":167,"sortIndex":23,"researcher":22,"roles":168,"affiliations":169,"properties":176},"6778269a-7cf8-4c5a-9cc0-bc6700e46be7",[],[170],{"id":171,"sortIndex":23,"affiliation":172,"properties":22},"cc0252aa-4a82-46f0-b688-835dd84a5f5f",{"id":134,"createTime":135,"updateTime":135,"relativeEntities":173,"slug":137,"properties":174,"entityType":43,"verifyStatus":21,"verifyTime":22,"verifyNote":22,"syncStatus":21,"languages":22,"translateLanguages":22,"viewCount":23},[],{"title":175},{"EN":140},{"openalex":177,"orcid":179,"title":181},{"VOID":178},"A5100629852",{"VOID":180},"https:\u002F\u002Forcid.org\u002F0000-0003-1394-6404",{"EN":182},"Li Zhu",{"id":184,"sortIndex":185,"researcher":22,"roles":186,"affiliations":187,"properties":198},"cbde36c1-9742-4aa1-a171-b2539c423bb6",2,[],[188],{"id":189,"sortIndex":23,"affiliation":190,"properties":22},"e525dbdb-f9a0-45e3-80d3-797a8c76c275",{"id":191,"createTime":192,"updateTime":192,"relativeEntities":193,"slug":194,"properties":195,"entityType":43,"verifyStatus":21,"verifyTime":22,"verifyNote":22,"syncStatus":21,"languages":22,"translateLanguages":22,"viewCount":23},"eb6fc029-b075-493c-9d53-f52a25247e9c","2024-09-05T23:56:41.741+00:00",[],"Department-of-Radiology-Johns-Hopkins-University-School-of-Medicine-United-States",{"title":196},{"EN":197},"Department of Radiology, Johns Hopkins University School of Medicine, United States",{"openalex":199,"orcid":201,"title":203},{"VOID":200},"A5005189001",{"VOID":202},"https:\u002F\u002Forcid.org\u002F0000-0003-1209-1918",{"EN":204},"Marcus J. 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thận mãn tính (CKD) đã được công nhận là một vấn đề sức khỏe cộng đồng hàng đầu trên toàn thế giới. Thông qua tác động của nó lên nguy cơ tim mạch và bệnh thận giai đoạn cuối, CKD ảnh hưởng trực tiếp đến gánh nặng bệnh tật và tỷ lệ tử vong toàn cầu. Quản lý CKD một cách tối ưu trong khuôn khổ cổ điển bao gồm kiểm soát huyết áp, điều trị albumin niệu bằng cách sử dụng ức chế men chuyển angiotensin hoặc thuốc chẹn thụ thể angiotensin II, tránh các chất độc hại cho thận tiềm tàng và béo phì, điều chỉnh liều thuốc, và giảm nguy cơ tim mạch. Bệnh tiểu đường có thể chiếm hơn một nửa gánh nặng của CKD, và béo phì là yếu tố đã được thúc đẩy chính cho căn bệnh này. Các loại thuốc hạ đường huyết mới, chẳng hạn như ức chế đồng vận chuyển natri-glucose 2, đã cho thấy khả năng làm chậm sự suy giảm của GFR, mang lại lợi ích bổ sung trong việc giảm cân, cũng như các kết quả liên quan đến tim mạch và thận. Mặt khác, một thế hệ mới của các chất đối kháng thụ thể mineralocorticoid không steroid gần đây đã được phát triển nhằm đạt được sự ức chế thụ thể chọn lọc, giảm thiểu tác dụng phụ như tăng kali máu và do đó làm cho các thuốc này phù hợp để sử dụng cho bệnh nhân CKD. Hơn nữa, hai liệu pháp hạ kali máu mới đã chứng minh khả năng cải thiện dung nạp, cho phép liều cao hơn của các chất ức chế hệ renin-angiotensin và do đó nâng cao tác dụng bảo vệ thận của chúng. Bất kể nguyên nhân của nó, CKD được đặc trưng bởi khả năng tái tạo thận bị giảm, tổn thương mạch máu nhỏ, stress oxy hóa và viêm, dẫn tới xơ hóa và sự mất nephron tiến triển và không thể hồi phục. Do đó, cần có một phương pháp tiếp cận toàn diện nhằm nhắm vào các quá trình đa dạng và các bối cảnh sinh học liên quan đến sự tiến triển của CKD. Đến nay, các can thiệp trị liệu khi đã thiết lập tình trạng xơ hóa ống kẽ đã được chứng minh là không đủ, vì vậy nỗ lực nghiên cứu nên tập trung vào việc khám phá các cơ chế bệnh lý sớm. Một loạt các phương pháp điều trị mới nhắm đến các yếu tố điều chỉnh epigenetic hiện đang trải qua các thử nghiệm giai đoạn II hoặc giai đoạn III và có thể cung cấp hoạt động điều chỉnh đồng thời để điều chỉnh các khía cạnh khác nhau của sự tiến triển CKD.\u003C\u002Fjats:p>","\u003Cjats:p>Chronic kidney disease (CKD) has been recognized as a leading public health problem worldwide. Through its effect on cardiovascular risk and end-stage kidney disease, CKD directly affects the global burden of morbidity and mortality. Classical optimal management of CKD includes blood pressure control, treatment of albuminuria with angiotensin-converting enzyme inhibitors or angiotensin II receptor blockers, avoidance of potential nephrotoxins and obesity, drug dosing adjustments, and cardiovascular risk reduction. Diabetes might account for more than half of CKD burden, and obesity is the most important prompted factor for this disease. New antihyperglycemic drugs, such as sodium-glucose-cotransporter 2 inhibitors have shown to slow the decline of GFR, bringing additional benefit in weight reduction, cardiovascular, and other kidney outcomes. On the other hand, a new generation of non-steroidal mineralocorticoid receptor antagonist has recently been developed to obtain a selective receptor inhibition reducing side effects like hyperkalemia and thereby making the drugs suitable for administration to CKD patients. Moreover, two new potassium-lowering therapies have shown to improve tolerance, allowing for higher dosage of renin-angiotensin system inhibitors and therefore enhancing their nephroprotective effect. Regardless of its cause, CKD is characterized by reduced renal regeneration capacity, microvascular damage, oxidative stress and inflammation, resulting in fibrosis and progressive, and irreversible nephron loss. Therefore, a holistic approach should be taken targeting the diverse processes and biological contexts that are associated with CKD progression. To date, therapeutic interventions when tubulointerstitial fibrosis is already established have proved to be insufficient, thus research effort should focus on unraveling early disease mechanisms. An array of novel therapeutic approaches targeting epigenetic regulators are now undergoing phase II or phase III trials and might provide a simultaneous regulatory activity that coordinately regulate different aspects of CKD progression.\u003C\u002Fjats:p>",{"VI":1078,"EN":1079},"Những Hiểu Biết Về Điều Trị Trong Sự Tiến Triển Của Bệnh Thận Mãn Tính","Therapeutic Insights in Chronic Kidney Disease 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In both the 7- and 19-day studies, ALLN-346 oral therapy resulted in the normalization of urine uric acid excretion and a significant reduction of hyperuricemia by 44 and 28% when therapy was given with food over 24 h or was limited for up to 6 h, respectively. Fractional excretion of uric acid (FEUA) was normalized with ALLN-346 therapy. 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is a multisystem granulomatous disease of unknown origin that has variable clinical course and can affect nearly any organ. It has a chronic course in about 25% of patients. Corticosteroids (CS) are the cornerstone of therapy but their long-term use is associated with cumulative toxicity. Commonly used CS-sparing agents include methotrexate, cyclophosphamide, azathioprine, and mycophenolate mofetil. Twenty to forty percentage of sarcoidosis patients are refractory to these therapies or develop severe adverse events. Therefore, additional and targeted CS-sparing agents are needed for chronic sarcoidosis. Macrophage activation, interferon response, and formation of the granuloma are mainly mediated by T helper-1 responses. Different pro-inflammatory cytokines such as interleukin (IL)-8, IL-12, IL-6, and tumor necrosis factor-alpha (TNF-α) have been shown to be highly expressed in sarcoidosis-affected tissues. As a result of increased production of these cytokines, Janus kinase-signal transducer and activator of transcription (JAK-STAT) signaling is constitutively active in sarcoidosis. Several studies of biological agents that target TNF-α have reported their efficacy and appear today as a second line option in refractory sarcoidosis. Some case series report a positive effect of tocilizumab an anti-IL-6 monoclonal antibody in this setting. More recently, JAK inhibition appears as a new promising strategy. This review highlights key advances on the management of chronic refractory sarcoidosis. 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