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| 1 | Polyethylene glycol repairs membrane damage and enhances functional recovery: a tissue engineering approach to spinal cord injury显示文摘The integrity of the neuronal membrane is crucial for its function and cellular survival; thus, ineffective repair of damaged membranes may be one of the key elements underlying the neuronal degeneration and overall functional loss that occurs after spinal cord injury (SCi). it has been shown that polyethylene glycol (PEG) can reseal axonal membranes following various injuries in multiple in vitro and in vivo injury models. in addition, PEG may also directly prevent the effects of mitochondria-derived oxidative stress on intracellular components. Thus, PEG repairs mechanically injured cells by at least two distinct pathways: resealing of the disrupted plasma membrane and direct protection of mitochondria. Besides repairing primary membrane damage, PEG treatment also results in significant attenuation of oxidative stress, likely due to its capacity to reseal the membrane, thereby breaking the cycle of cellular damage and free-radical production. Based on this, in addition to the practicality of its application, we expect that PEG may be established as an effective treatment for SCi where membrane disruption and mitochondrial damage are implicated. | Riyi Shi | 2013 | Neuroscience Bulletin2013，29，4： | 8 |
| 2 | Acrolein as a novel therapeutic target for motor and sensory deficits in spinal cord injury显示文摘In the hours to weeks following traumatic spinal cord injuries(SCI), biochemical processes are initiated that further damage the tissue within and surrounding the initial injury site: a process termed secondary injury. Acrolein, a highly reactive unsaturated aldehyde, has been shown to play a major role in the secondary injury by contributing significantly to both motor and sensory deficits. In particular, efforts have been made to elucidate the mechanisms of acrolein-mediated damage at the cellular level and the resulting paralysis and neuropathic pain. In this review, we will highlight the recent developments in the understanding of the mechanisms of acrolein in motor and sensory dysfunction in animal models of SCI. We will also discuss the therapeutic benefits of using acrolein scavengers to attenuate acrolein-mediated neuronal damage following SCI. | Jonghyuck Park Breanne Muratori Riyi Shi | 2014 | Neural Regeneration Research2014，9，7： | 6 |
| 3 | Mechanisms of neuronal membrane sealing following mechanical trauma显示文摘Membrane integrity is crucial for maintaining the intricate signaling and chemically-isolated intracellular environment of neurons; disruption risks deleterious effects, such as unregulated ionic flux, neuronal apoptosis, and oxidative radical damage as observed in spinal cord injury and traumatic brain injury.This paper, in addition to a discussion of the current understanding of cellular tactics to seal membranes, describes two major factors involved in membrane repair.These are line tension, the hydrophobic attractive force between two lipid free-edges, and membrane tension, the rigidity of the lipid bilayer with respect to the tethered cortical cytoskeleton.Ca2+, a major mechanistic trigger for repair processes, increases following fl ux through a membrane injury site, and activates phospholipase enzymes, calpain-mediated cortical cytoskeletal proteolysis, protein kinase cascades, and lipid bilayer microdomain modification.The membrane tension appears to be largely modulated through vesicle dynamics, cytoskeletal organization, membrane curvature, and phospholipase manipulation.Dehydration of the phospholipid gap edge and modification of membrane packaging, as in temperature variation, experimentally impact line tension.Due to the time-sensitive nature of axonal sealing, increasing the effi cacy of axolemmal sealing through therapeutic modifi cation would be of great clinical value, to deter secondary neurodegenerative effects.Better therapeutic enhancement of membrane sealing requires a complete understanding of its intricate underlying neuronal mechanism. | Benjamin K.Hendricks Riyi Shi | 2014 | Neuroscience Bulletin2014，30，4： | 5 |
| 4 | Mathematical models for foam-diverted acidizing and their applications显示文摘Foam diversion can effectively solve the problem of uneven distribution of acid in layers of different permeabilities during matrix acidizing.Based on gas trapping theory and the mass conservation equation,mathematical models were developed for foam-diverted acidizing,which can be achieved by a foam slug followed by acid injection or by continuous injection of foamed acid.The design method for foam-diverted acidizing was also given.The mathematical models were solved by a computer program.Computed results show that the total formation skin factor,wellhead pressure and bottomhole pressure increase with foam injection,but decrease with acid injection.Volume flow rate in a high-permeability layer decreases,while that in a low-permeability layer increases,thus diverting acid to the low-permeability layer from the high-permeability layer.Under the same formation conditions,for foamed acid treatment the operation was longer,and wellhead and bottomhole pressures are higher.Field application shows that foam slug can effectively block high permeability layers,and improve intake profile noticeably. | Li Songyan Li Zhaomin Lin Riyi | 2008 | Petroleum Science2008，5，2： | 3 |
| 5 | Pathological correlations between traumatic brain injury and chronic neurodegenerative diseases显示文摘Traumatic brain injury is among the most common causes of death and disability in youth and young adults.In addition to the acute risk of morbidity with moderate to severe injuries,traumatic brain injury is associated with a number of chronic neurological and neuropsychiatric sequelae including neurodegenerative diseases such as Alzheimer’s disease and Parkinson’s disease.However,despite the high incidence of traumatic brain injuries and the established clinical correlation with neurodegeneration,the causative factors linking these processes have not yet been fully elucidated.Apart from removal from activity,few,if any prophylactic treatments against post-traumatic brain injury neurodegeneration exist.Therefore,it is imperative to understand the pathophysiological mechanisms of traumatic brain injury and neurodegeneration in order to identify potential factors that initiate neurodegenerative processes.Oxidative stress,neuroinflammation,and glutamatergic excitotoxicity have previously been implicated in both secondary brain injury and neurodegeneration.In particular,reactive oxygen species appear to be key in mediating molecular insult in neuroinflammation and excitotoxicity.As such,it is likely that post injury oxidative stress is a key mechanism which links traumatic brain injury to increased risk of neurodegeneration.Consequently,reactive oxygen species and their subsequent byproducts may serve as novel fluid markers for identification and monitoring of cellular damage.Furthermore,these reactive species may further serve as a suitable therapeutic target to reduce the risk of post-injury neurodegeneration and provide long term quality of life improvements for those suffering from traumatic brain injury. | Marcela Cruz-Haces Jonathan Tang Glen Acosta Joseph Fernandez Riyi Shi | 2017 | Translational Neurodegeneration2017，6，1： | 2 |
| 6 | Acute systemic accumulation of acrolein in mice by inhalation at a concentration similar to that in cigarette smoke显示文摘Cigarette smoke is an important environmental factor associated with a wide array of public health concerns. Acrolein, a component of tobacco smoke and a known toxin to various cell types, may be a key pathological factor mediating the adverse effects linked with tobacco smoke. Although acrolein is known to accumulate in the respiratory system after acute nasal exposure, it is not clear if it accumulates systemically, and less is known in the nervous system. The aim of this study was to assess the degree of acrolein accumulation in the circulation and in the spinal cord following acute acrolein inhalation in mice. Using a laboratory-fabricated inhalation chamber, we found elevated urinary 3-HPMA, an acrolein metabolite, and increased acrolein adducts in the spinal cord after weeks of nasal exposure to acrolein at a concentration similar to that in tobacco smoke. The data indicated that acrolein is absorbed into the circulatory system and some enters the nervous system. It is expected that these findings may facilitate further studies to probe the pathological role of acrolein in the nervous system resulting from smoke and other external sources. | Melissa Tully Lingxing Zheng Glen Acosta Ran Tian Riyi Shi | 2014 | Neuroscience Bulletin2014，30，6： | 2 |
| 7 | Heating of heavy oil by circulating hot water in closed double casing in ultra-deep wells显示文摘In heavy oil production,the loss of energy to ambient surroundings decreases the temperature of the heavy oil flowing upwards in a vertical wellbore,which increases the oil viscosity and the oil may not flow normally in the wellbore.Therefore,it is necessary to lower the heavy oil viscosity by heating methods to allow it to be lifted easily.Heating of heavy oil in an oil well is achieved by circulating hot water in annuli in the well(tubing-casing annulus,casing-casing annulus).In this paper,based on heat transfer principles and fluid flow theory,a model is developed for produced fluids and hot water flowing in a vertical wellbore.The temperature and pressure of produced fluids and hot water in the wellbore are calculated and the effect of hot water on heavy oil temperature is analyzed.Calculated results show that the hot water circulating in the annuli may effectively heat the heavy oil in the tubing,so as to significantly reduce both oil viscosity and resistance to oil flow. | Lin Riyi Wang Fangzheng Wang Xinwei | 2012 | Petroleum Science2012，9，4： | 1 |
| 8 | Decreased functions of astrocytes on carbon nanofiber materials显示文摘 | Janice L. McKenzie Michael C. Waid Riyi Shi Thomas J. Webster | 2003 | Biomaterials2003，，7： | 1 |
| 9 | Current advances in neurotrauma research:diagnosis, neuroprotection,and neurorepair显示文摘Traumatic brain injury(TBI)and spinal cord injury(SCI)causes significant cell death(Raghupathi et al.,1995;DeKosky et al.,1998;Hall et al.,2005;Farkas and Povlishock,2007)and tissue lesion in the neocortex(Lighthall et al.,1989;Lyeth et al.,1990),leaving many patients with substantial motor disability and cognitive impairment(Hamm et al.,1992;Scheff et al.,1997).Unfortunately,at present,there are no | Jinhui Chen Riyi Shi | 2014 | Neural Regeneration Research2014，9，11： | 1 |
| 10 | Modeling of lifting heavy oil assisted by enclosed thermal fluid circulation in hollow rod显示文摘 | Songyan Li Zhaomin Li Binfei Li Riyi Lin | 2010 | Journal of Petroleum Science and Engineering2010，，1： | 1 |
| 11 | Accumulation of Acrolein–Protein Adducts after Traumatic Spinal Cord Injury显示文摘 | Jian Luo Koji Uchida Riyi Shi | | 0，，： | 1 |
| 12 | Acrolein scavenger dimercaprol offers neuroprotection in an animal model of Parkinson’s disease:implication of acrolein and TRPA1显示文摘Background:The mechanisms underlying lesions of dopaminergic(DA)neurons,an essential pathology of Parkinson’s disease(PD),are largely unknown,although oxidative stress is recognized as a key factor.We have previously shown that the pro-oxidative aldehyde acrolein is a critical factor in PD pathology,and that acrolein scavenger hydralazine can reduce the elevated acrolein,mitigate DA neuron death,and alleviate motor deficits in a 6-hydroxydopamine(6-OHDA)rat model.As such,we hypothesize that a structurally distinct acrolein scavenger,dimercaprol(DP),can also offer neuroprotection and behavioral benefits.Methods:DP was used to lower the elevated levels of acrolein in the basal ganglia of 6-OHDA rats.The acrolein levels and related pathologies were measured by immunohistochemistry.Locomotor and behavioral effects of 6-OHDA injections and DP treatment were examined using the open field test and rotarod test.Pain was assessed using mechanical allodynia,cold hypersensitivity,and plantar tests.Finally,the effects of DP were assessed in vitro on SK-N-SH dopaminergic cells exposed to acrolein.Results:DP reduced acrolein and reversed the upregulation of pain-sensing transient receptor potential ankyrin 1(TRPA1)channels in the substantia nigra,striatum,and cortex.DP also mitigated both motor and sensory deficits typical of PD.In addition,DP lowered acrolein and protected DA-like cells in vitro.Acrolein’s ability to upregulate TRPA1 was also verified in vitro using cell lines.Conclusions:These results further elucidated the acrolein-mediated pathogenesis and reinforced the critical role of acrolein in PD while providing strong arguments for anti-acrolein treatments as a novel and feasible strategy to combat neurodegeneration in PD.Considering the extensive involvement of acrolein in various nervous system illnesses and beyond,anti-acrolein strategies may have wide applications and broad impacts on human health. | Liangqin Shi Yazhou Lin Yucheng Jiao Seth AHerr Jonathan Tang Edmond Rogers Zhengli Chen Riyi Shi | 2021 | Translational Neurodegeneration2021，10，2： | 0 |
| 13 | Elevated axonal membrane permeability and its correlation with motor deficits in an animal model of multiple sclerosis显示文摘Background:It is increasingly clear that in addition to myelin disruption,axonal degeneration may also represent a key pathology in multiple sclerosis(MS).Hence,elucidating the mechanisms of axonal degeneration may not only enhance our understanding of the overall MS pathology,but also elucidate additional therapeutic targets.The objective of this study is assess the degree of axonal membrane disruption and its significance in motor deficits in EAE mice.Methods:Experimental Autoimmune Encephalomyelitis was induced in mice by subcutaneous injection of myelin oligodendrocyte glycoprotein/complete Freud’s adjuvant emulsion,followed by two intraperitoneal injections of pertussis toxin.Behavioral assessment was performed using a 5-point scale.Horseradish Peroxidase Exclusion test was used to quantify the disruption of axonal membrane.Polyethylene glycol was prepared as a 30%(w/v)solution in phosphate buffered saline and injected intraperitoneally.Results:We have found evidence of axonal membrane disruption in EAE mice when symptoms peak and to a lesser degree,in the pre-symptomatic stage of EAE mice.Furthermore,polyethylene glycol(PEG),a known membrane fusogen,significantly reduces axonal membrane disruption in EAE mice.Such PEG-mediated membrane repair was accompanied by significant amelioration of behavioral deficits,including a delay in the emergence of motor deficits,a delay of the emergence of peak symptom,and a reduction in the severity of peak symptom.Conclusions:The current study is the first indication that axonal membrane disruption may be an important part of the pathology in EAE mice and may underlies behavioral deficits.Our study also presents the initial observation that PEG may be a therapeutic agent that can repair axolemma,arrest axonal degeneration and reduce motor deficits in EAE mice. | Gary Leung Melissa Tully Jonathan Tang Shengxi Wu Riyi Shi | 2017 | Translational Neurodegeneration2017，6，1： | 0 |
| 14 | Critical role of mitochondrial aldehyde dehydrogenase 2 in acrolein sequestering in rat spinal cord injury显示文摘Lipid peroxidation-derived aldehydes,such as acrolein,the most reactive aldehyde,have emerged as key culprits in sustaining post-spinal cord injury(SCI)secondary pathologies leading to functional loss.Strong evidence suggests that mitochondrial aldehyde dehydrogenase-2(ALDH2),a key oxidoreductase and powerful endogenous anti-aldehyde machinery,is likely important for protecting neurons from aldehydesmediated degeneration.Using a rat model of spinal cord contusion injury and recently discovered ALDH2 activator(Alda-1),we planned to validate the aldehyde-clearing and neuroprotective role of ALDH2.Over an acute 2 day period post injury,we found that ALDH2 expression was significantly lowered post-SCI,but not so in rats given Alda-1.This lower enzymatic expression may be linked to heightened acrolein-ALDH2 adduction,which was revealed in co-immunoprecipitation experiments.We have also found that administration of Alda-1 to SCI rats significantly lowered acrolein in the spinal cord,and reduced cyst pathology.In addition,Alda-1 treatment also resulted in significant improvement of motor function and attenuated post-SCI mechanical hypersensitivity up to 28 days post-SCI.Finally,ALDH2 was found to play a critical role in in vitro protection of PC12 cells from acrolein exposure.It is expected that the outcome of this study will broaden and enhance anti-aldehyde strategies in combating post-SCI neurodegeneration and potentially bring treatment to millions of SCI victims.All animal work was approved by Purdue Animal Care and Use Committee(approval No.1111000095)on January 1,2021. | Seth A.Herr Liangqin Shi Thomas Gianaris Yucheng Jiao Siyuan Sun Nick Race Scott Shapiro Riyi Shi | 2022 | Neural Regeneration Research2022，17，7： | 0 |
| 15 | Potassium channel blockers restore axonal conduction in CNS trauma and diseases显示文摘Myelin damage in the central nervous system(CNS)plays an important role in motor and sensory dysfunction(Shi and Sun,2011).This neuropathology is observed widely in neurotrauma such as spinal cord injuries(SCI)and is also a distinguishing feature of many neurological diseases such as multiple sclerosis(MS)and amyotrophic lateral sclerosis(ALS)(Shi and Sun,2011).Damage to myelin structure leads to severe | Jessica C.Page Riyi Shi | 2016 | Neural Regeneration Research2016，11，8： | 0 |
| 16 | A perspective on recent findings and future strategies for reactive aldehyde removal in spinal cord injury显示文摘Acrolein in spinal cord injury:The propensity of reactive aldehydes such as acrolein to both initiate and perpetuate tissue damage after spinal cord injury (SCI) is well established.Formed primarily from lipid peroxidation,acrolein is known to be one of the most reactive aldehydes.Acrolein will quickly overwhelm endogenous clearance mechanisms and antioxidants,and form adductswith lipids,proteins,and DNA. | Seth A.Herr Anna J.Prall Riyi Shi | 2023 | Neural Regeneration Research2023，18，10： | 0 |
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