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151.
Jing Luo Petr Baranov Sherrina Patel Hong Ouyang John Quach Frances Wu Austin Qiu Hongrong Luo Caroline Hicks Jing Zeng Jing Zhu Jessica Lu Nicole Sfeir Cindy Wen Meixia Zhang Victoria Reade Sara Patel John Sinden Xiaodong Sun Peter Shaw Michael Young Kang Zhang 《The Journal of biological chemistry》2014,289(10):6362-6371
Cell transplantation is a potential therapeutic strategy for retinal degenerative diseases involving the loss of photoreceptors. However, it faces challenges to clinical translation due to safety concerns and a limited supply of cells. Human retinal progenitor cells (hRPCs) from fetal neural retina are expandable in vitro and maintain an undifferentiated state. This study aimed to investigate the therapeutic potential of hRPCs transplanted into a Royal College of Surgeons (RCS) rat model of retinal degeneration. At 12 weeks, optokinetic response showed that hRPC-grafted eyes had significantly superior visual acuity compared with vehicle-treated eyes. Histological evaluation of outer nuclear layer (ONL) characteristics such as ONL thickness, spread distance, and cell count demonstrated a significantly greater preservation of the ONL in hRPC-treated eyes compared with both vehicle-treated and control eyes. The transplanted hRPCs arrested visual decline over time in the RCS rat and rescued retinal morphology, demonstrating their potential as a therapy for retinal diseases. We suggest that the preservation of visual acuity was likely achieved through host photoreceptor rescue. We found that hRPC transplantation into the subretinal space of RCS rats was well tolerated, with no adverse effects such as tumor formation noted at 12 weeks after treatment. 相似文献
152.
A system identification approach for developing model predictive controllers of antibody quality attributes in cell culture processes
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Brandon Downey John Schmitt Justin Beller Brian Russell Anthony Quach Elizabeth Hermann David Lyon Jeffrey Breit 《Biotechnology progress》2017,33(6):1647-1661
As the biopharmaceutical industry evolves to include more diverse protein formats and processes, more robust control of Critical Quality Attributes (CQAs) is needed to maintain processing flexibility without compromising quality. Active control of CQAs has been demonstrated using model predictive control techniques, which allow development of processes which are robust against disturbances associated with raw material variability and other potentially flexible operating conditions. Wide adoption of model predictive control in biopharmaceutical cell culture processes has been hampered, however, in part due to the large amount of data and expertise required to make a predictive model of controlled CQAs, a requirement for model predictive control. Here we developed a highly automated, perfusion apparatus to systematically and efficiently generate predictive models using application of system identification approaches. We successfully created a predictive model of %galactosylation using data obtained by manipulating galactose concentration in the perfusion apparatus in serialized step change experiments. We then demonstrated the use of the model in a model predictive controller in a simulated control scenario to successfully achieve a %galactosylation set point in a simulated fed‐batch culture. The automated model identification approach demonstrated here can potentially be generalized to many CQAs, and could be a more efficient, faster, and highly automated alternative to batch experiments for developing predictive models in cell culture processes, and allow the wider adoption of model predictive control in biopharmaceutical processes. © 2017 The Authors Biotechnology Progress published by Wiley Periodicals, Inc. on behalf of American Institute of Chemical Engineers Biotechnol. Prog., 33:1647–1661, 2017 相似文献
153.
ABSTRACTMacroautophagy/autophagy deregulation has been observed in perpetuated inflammation and the proliferation of tumor cells. However, the mechanisms underlying these changes have yet to be well-identified. UVRAG is one of the key players of autophagy, but its role in vivo remained puzzling. Our recent study utilized a mouse model with inducible expression of a cancer-derived frameshift (FS) mutation in UVRAG that dominant-negatively inhibits wild-type UVRAG, resulting in impaired stimulus-induced autophagy. The systemically compromised autophagy, particularly mitophagy, notably increases inflammation and associated pathologies. Furthermore, our discovery indicates that time-dependent autophagy suppression and ensuing CTNNB1/β-catenin activation may serve as one tumor-promoting mechanism underpinning age-related cancer susceptibility. 相似文献
154.
In mice receiving i.v. low doses of 3H-LSD the accumulation of radioactivity in brain appears to reflect a selective binding to high affinity sites as indicated by the heterogenous regional distribution (paralleling that observed in in vitro binding studies) and by the saturable character of the process (ED50 around 30μg.kg?1 in cerebral cortex).The identity of the binding sites was assessed in various regions by administration of agonists or antagonists of different neurotransmitters. In cortex specific accumulation of 3H-LSD was easily prevented by administration of serotonin antagonists (cyproheptadine, methysergide, methiothepin) or by tryptamine derivatives (psilocin, psilocybin, dimethyltryptamine) and 5-hydroxytryptophan + pargyline. Among neuroleptics some prevented 3H-LSD binding (spiperone, haloperidol) whereas 1mg.kg?1 pimozide was ineffective. In addition a large variety of agents (adrenergic, cholinergic, morphine) were ineffective. These data suggest a selective binding to cortical serotonin receptors. 相似文献
155.
M Morgan Conn Joe Kappock Dale Drueckhammer Richard Cammack Dennis Hall Tony Cass Jon D Stewart Graham RL Cousins Jeremy KM Sanders Sabine Flitsch Philip AS Lowden Richard Newman 《Current opinion in chemical biology》1999,3(6):631
A selection of interesting papers that were published in the two months before our press date in major journals most likely to report significant results in chemical biology. 相似文献
156.
KM Abha Mishra Runesh Podili Teja S. Pathlavath Kalyan K. Sethi 《Journal of biochemical and molecular toxicology》2023,37(8):e23409
Since the outbreak of highly virulent coronaviruses, significant interest was assessed to the brain and heart axis (BHA) in severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)-affected patients. The majority of clinical reports accounted for unusual symptoms associated with SARS-CoV-2 infections which are of the neurological type, such as headache, nausea, dysgeusia, anosmia, and cerebral infarction. The SARS-CoV-2 enters the cells through the angiotensin-converting enzyme (ACE-2) receptor. Patients with prior cardiovascular disease (CVD) have a higher risk of COVID-19 infection and it has related to various cardiovascular (CV) complications. Infected patients with pre-existing CVDs are also particularly exposed to critical health outcomes. Overall, COVID-19 affected patients admitted to intensive care units (ICU) and exposed to stressful environmental constraints, featured with a cluster of neurological and CV complications. In this review, we summarized the main contributions in the literature on how SARS-CoV-2 could interfere with the BHA and its role in affecting multiorgan disorders. Specifically, the central nervous system involvement, mainly in relation to CV alterations in COVID-19-affected patients, is considered. This review also emphasizes the biomarkers and therapy options for COVID-19 patients presenting with CV problems. 相似文献
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Rohan H. C. Palmer Emma C. Johnson Hyejung Won Renato Polimanti Manav Kapoor Apurva Chitre Molly A. Bogue Chelsie E. Benca-Bachman Clarissa C. Parker Anurag Verma Timothy Reynolds Jason Ernst Michael Bray Soo Bin Kwon Dongbing Lai Bryan C. Quach Nathan C. Gaddis Laura Saba Hao Chen Michael Hawrylycz Shan Zhang Yuan Zhou Spencer Mahaffey Christian Fischer Sandra Sanchez-Roige Anita Bandrowski Qing Lu Li Shen Vivek Philip Joel Gelernter Laura J. Bierut Dana B. Hancock Howard J. Edenberg Eric O. Johnson Eric J. Nestler Peter B. Barr Pjotr Prins Desmond J. Smith Schahram Akbarian Thorgeir Thorgeirsson Dave Walton Erich Baker Daniel Jacobson Abraham A. Palmer Michael Miles Elissa J. Chesler Jake Emerson Arpana Agrawal Maryann Martone Robert W. Williams 《Genes, Brain & Behavior》2021,20(6):e12738
The National Institute on Drug Abuse and Joint Institute for Biological Sciences at the Oak Ridge National Laboratory hosted a meeting attended by a diverse group of scientists with expertise in substance use disorders (SUDs), computational biology, and FAIR (Findability, Accessibility, Interoperability, and Reusability) data sharing. The meeting's objective was to discuss and evaluate better strategies to integrate genetic, epigenetic, and 'omics data across human and model organisms to achieve deeper mechanistic insight into SUDs. Specific topics were to (a) evaluate the current state of substance use genetics and genomics research and fundamental gaps, (b) identify opportunities and challenges of integration and sharing across species and data types, (c) identify current tools and resources for integration of genetic, epigenetic, and phenotypic data, (d) discuss steps and impediment related to data integration, and (e) outline future steps to support more effective collaboration—particularly between animal model research communities and human genetics and clinical research teams. This review summarizes key facets of this catalytic discussion with a focus on new opportunities and gaps in resources and knowledge on SUDs. 相似文献
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