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您的检索式：作者名="Benjamin L.Woolbright"
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| 1 | The impact of sterile inflammation in acute liver injury显示文摘Background:The liver has a number of functions in innate immunity.These functions predispose the liver to innate immune-mediated liver injury when inflammation goes unchecked.Significant progress has been made in the last 25 years on sterile inflammatory liver injury in a number of models;however,a great deal of controversy and many questions about the nature of sterile inflammation still exist.Aim:The goal of this article is to review sterile inflammatory liver injury using both a basic approach to what constitutes the inflammatory injury,and through examination of current models of liver injury and inflammation.This information will be tied to human patient conditions when appropriate.Relevance for patients:Inflammation is one of the most critical factors for managing in-patient liver disease in a number of scenarios.More information is needed for both scientists and clinicians to develop rational treatments. | Benjamin L.Woolbright Hartmut Jaeschke | 2017 | Journal of Clinical & Translational Research2017，3，1： | 2 |
| 2 | Natural products as a means of overcoming cisplatin chemoresistance in bladder cancer显示文摘Cisplatin remains an integral part of the treatment for muscle invasive bladder cancer.A large number of patients do not respond to cisplatin-based chemotherapy and efficacious salvage regimens are limited.Immunotherapy has offered a second line of treatment;however,only approximately 20% of patients respond,and molecular subtyping of tumors indicates there may be significant overlap in those patients that respond to cisplatin and those patients that respond to immunotherapy.As such,restoring sensitivity to cisplatin remains a major hurdle to improving patient care.One potential source of compounds for enhancing cisplatin is naturally derived bioactive products such as phytochemicals,flavonoids and others.These compounds can activate a diverse array of different pathways,many of which can directly promote or inhibit cisplatin sensitivity.The purpose of this review is to understand current drug development in the area of natural products and to assess how these compounds may enhance cisplatin treatment in bladder cancer patients. | Ganeshkumar Rajendran John A.Taylor III Benjamin L.Woolbright | 2021 | Cancer Drug Resistance2021，4，1： | 0 |
| 3 | Lack of direct cytotoxicity of extracellular ATP against hepatocytes:role in the mechanism of acetaminophen hepatotoxicity显示文摘Background:Acetaminophen(APAP)hepatotoxicity is a major cause of acute liver failure in many countries.Mechanistic studies in mice and humans have implicated formation of a reactive metabolite,mitochondrial dysfunction and oxidant stress as critical events in the pathophysiology of APAP-induced liver cell death.It was recently suggested that ATP released from necrotic cells can directly cause cell death in mouse hepatocytes and in a hepatoma cell line(HepG2).Aim:To assess if ATP can directly cause cell toxicity in hepatocytes and evaluate their relevance in the human system.Methods:Primary mouse hepatocytes,human HepG2 cells,the metabolically competent human HepaRG cell line and freshly isolated primary human hepatocytes were exposed to 10-100μM ATP or ATγPin the presence or absence of 5-10 mM APAP for 9-24 h.Results:ATP or ATγP was unable to directly cause cell toxicity in all 4 types of hepatocytes.In addition,ATP did not enhance APAP-induced cell death observed in primary mouse or human hepatocytes,or in HepaRG cells as measured by LDH release and by propidium iodide staining in primary mouse hepatocytes.Furthermore,addition of ATP did not cause mitochondrial dysfunction or enhance APAP-induced mitochondrial dysfunction in primary murine hepatocytes,although ATP did cause cell death in murine RAW macrophages.Conclusions:It is unlikely that ATP released from necrotic cells can significantly affect cell death in human or mouse liver during APAP hepatotoxicity.Relevance for patients:Understanding the mechanisms of APAP-induced cell injury is critical for identifying novel therapeutic targets to prevent liver injury and acute liver failure in APAP overdose patients. | Yuchao Xie Benjamin L.Woolbright Milan Kos Mitchell R.McGill Kenneth Dorko Sean C.Kumer Timothy M.Schmitt Hartmut Jaeschke | 2015 | Journal of Clinical & Translational Research2015，1，2： | 0 |
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