15 results on '"Yu Shin Kim"'
Search Results
2. In Vivo Calcium Imaging Visualizes Incision-Induced Primary Afferent Sensitization and Its Amelioration by Capsaicin Pretreatment
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Yu Shin Kim, Yan Zhang, Hirotake Ishida, Ratan K. Banik, Ruben Gomez, Hyeonwi Son, and John Shannonhouse
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Pathology ,medicine.medical_specialty ,business.industry ,General Neuroscience ,Sensory system ,Spinal cord ,chemistry.chemical_compound ,medicine.anatomical_structure ,Calcium imaging ,chemistry ,nervous system ,In vivo ,Capsaicin ,medicine ,Nociceptor ,business ,Sensitization ,Research Articles ,Sensory nerve - Abstract
Previous studies have shown that infiltration of capsaicin into the surgical site can prevent incision-induced spontaneous pain like behaviors and heat hyperalgesia. In the present study, we aimed to monitor primary sensory neuron Ca2+activity in the intact dorsal root ganglia (DRG) using Pirt-GCaMP3 male and female mice pretreated with capsaicin or vehicle before the plantar incision. Intraplantar injection of capsaicin (0.05%) significantly attenuated spontaneous pain, mechanical, and heat hypersensitivity after plantar incision. The Ca2+response inin vivoDRG and inin situspinal cord was significantly enhanced in the ipsilateral side compared with contralateral side or naive control. Primary sensory nerve fiber length was significantly decreased in the incision skin area in capsaicin-pretreated animals detected by immunohistochemistry and placental alkaline phosphatase (PLAP) staining. Thus, capsaicin pretreatment attenuates incisional pain by suppressing Ca2+response because of degeneration of primary sensory nerve fibers in the skin.SIGNIFICANCE STATEMENTPostoperative surgery pain is a major health and economic problem worldwide with ∼235 million major surgical procedures annually. Approximately 50% of these patients report uncontrolled or poorly controlled postoperative pain. However, mechanistic studies of postoperative surgery pain in primary sensory neurons have been limited toin vitromodels or small numbers of neurons. Using an innovative, distinctive, and interdisciplinaryin vivopopulational dorsal root ganglia (DRG) imaging (>1800 neurons/DRG) approach, we revealed increased DRG neuronal Ca2+activity from postoperative pain mouse model. This indicates widespread DRG primary sensory neuron plasticity. Increased neuronal Ca2+activity occurs among various sizes of neurons but mostly in small-diameter and medium-diameter nociceptors. Capsaicin pretreatment as a therapeutic option significantly attenuates Ca2+activity and postoperative pain.
- Published
- 2021
3. Meclizine and metabotropic glutamate receptor agonists attenuate severe pain and primary sensory neuron Ca2+ activity in chemotherapy-induced peripheral neuropathy
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Yu Shin Kim, Hirotake Ishida, Matteo Bernabucci, Ruben Gomez, Yan Zhang, Hyeonwi Son, and John Shannonhouse
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Agonist ,business.industry ,medicine.drug_class ,Pharmacology ,medicine.disease ,Receptor antagonist ,Neuroprotection ,Peripheral neuropathy ,nervous system ,Chemotherapy-induced peripheral neuropathy ,Metabotropic glutamate receptor ,Neuropathic pain ,Medicine ,DCPG ,business - Abstract
Chemotherapy-induced peripheral neuropathy (CIPN) affects about 68% of patients undergoing chemotherapy and causes severe neuropathic pain which is debilitating health problem and greatly reduces quality of life. Cisplatin is a commonly used platinum-based chemotherapeutic drug known to cause CIPN, possibly by causing oxidative stress damage to primary sensory neurons. Metabotropic glutamate receptors (mGluRs) are widely hypothesized to be involved in pain processing. Meclizine is an H1 histamine receptor antagonist which is known to have neuroprotective effects including anti-oxidative effect. Here, we used a mouse model of cisplatin-induced CIPN to test agonists of mGluR8 and group II mGluR as well as meclizine as interventions to reduce cisplatin-induced pain. We performed behavioral pain tests and in vivo entire DRG neurons Ca2+ imaging using genetically-encoded Ca2+ indicator, Pirt-GCaMP3 to monitor different drug interventions on a populational ensemble level. CIPN induced increased spontaneous Ca2+ activity in DRG neurons, increased Ca2+ transient amplitudes, and hyperresponses to mechanical, thermal, and chemical stimuli. We found mGluR8 agonist, DCPG, group II mGluR agonist, LY379268, and Histamine1 receptor antagonist, meclizine all significantly attenuated mechanical and thermal pain caused by CIPN. LY379268 and meclizine, but not DCPG, attenuated DRG neuronal Ca2+ activity elevated by CIPN. Furthermore, meclizine attenuated cisplatin-induced weight loss. These results suggest group II mGluR agonist, mGluR8 agonist, and meclizine are excellent candidates to study for mechanisms and new treatment option for CIPN.
- Published
- 2021
4. Mast cell-specific receptor/corticotropin-releasing factor axis regulates alcohol withdrawal-associated headache
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Yu Shin Kim, Yan Zhang, Hirotake Ishida, John Shannonhouse, Ruben Gomez, Hyeonwi Son, and Armen N. Akopian
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medicine.medical_specialty ,business.industry ,Dura mater ,Degranulation ,Vasodilation ,Alcohol ,Mast cell ,chemistry.chemical_compound ,Endocrinology ,medicine.anatomical_structure ,Allodynia ,chemistry ,Internal medicine ,medicine ,medicine.symptom ,Receptor ,business ,Headache pain - Abstract
Rehabilitation from alcohol addiction or abuse is challenging due to alcohol withdrawal symptoms. Headache is a severe alcohol withdrawal symptom that frequently contributes to rehabilitation failure. Despite the need for treating alcohol withdrawal-induced headache, there is no appropriate therapeutic option available. Development of improved therapeutics will depend on obtaining a clearer understanding of alcohol withdrawal-induced headache pain mechanisms. Here, we show that the mast cell-specific receptor MrgprB2 controls development of alcohol withdrawal-induced headache. Withdrawing alcohol from alcohol-acclimated mice induces strong headache behaviors, including facial allodynia, facial pain expressions, and reduced walking movement, symptoms often observed in humans suffering from headache. Observed pain behaviors were abolished in MrgprB2-deficient mice. We observed in vivo spontaneous activation and hypersensitization of trigeminal ganglia neurons in alcohol withdrawal mice, but not in MrgprB2-deficient mice. Corticotropin-releasing factor (CRF) was increased in dura mater after alcohol withdrawal. Injection of CRF into dura mater resulted in activation of trigeminal ganglia neurons and vasodilation, which was accompanied by headache behavior. In cells, CRF evoked Ca2+ transients via MrgprB2 or human MrgprX2. The results indicate that alcohol withdrawal causes headache via mast cell degranulation in dura mater. The process is under control of MrgprB2/MrgprX2, which would appear to represent a potential target for treating alcohol withdrawal-related headache.
- Published
- 2021
5. Acute and Chronic Pain from Facial Skin and Oral Mucosa: Unique Neurobiology and Challenging Treatment
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Man-Kyo Chung, Sheng Wang, Yu Shin Kim, and Se Lim Oh
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mucosa pain ,Review ,medicine.disease_cause ,Mice ,0302 clinical medicine ,Trigeminal neuralgia ,Skin Physiological Phenomena ,Oral mucosa ,Biology (General) ,Spectroscopy ,Skin ,Chronic pain ,orofacial pain ,General Medicine ,Burning mouth syndrome ,Computer Science Applications ,Chemistry ,medicine.anatomical_structure ,medicine.symptom ,Irritation ,chronic pain ,Orofacial pain ,QH301-705.5 ,Catalysis ,Inorganic Chemistry ,03 medical and health sciences ,Facial Pain ,medicine ,Animals ,Humans ,Physical and Theoretical Chemistry ,Periodontitis ,Molecular Biology ,QD1-999 ,Mouth ,business.industry ,Organic Chemistry ,Mouth Mucosa ,030206 dentistry ,Trigeminal Neuralgia ,medicine.disease ,Chronic periodontitis ,stomatognathic diseases ,Face ,Neuralgia ,Intractable pain ,Trigeminal Nerve Injuries ,business ,Neuroscience ,030217 neurology & neurosurgery - Abstract
The oral cavity is a portal into the digestive system, which exhibits unique sensory properties. Like facial skin, the oral mucosa needs to be exquisitely sensitive and selective, in order to detect harmful toxins versus edible food. Chemosensation and somatosensation by multiple receptors, including transient receptor potential channels, are well-developed to meet these needs. In contrast to facial skin, however, the oral mucosa rarely exhibits itch responses. Like the gut, the oral cavity performs mechanical and chemical digestion. Therefore, the oral mucosa needs to be insensitive, to some degree, in order to endure noxious irritation. Persistent pain from the oral mucosa is often due to ulcers, involving both tissue injury and infection. Trigeminal nerve injury and trigeminal neuralgia produce intractable pain in the orofacial skin and the oral mucosa, through mechanisms distinct from those seen in the spinal area, which is particularly difficult to predict or treat. The diagnosis and treatment of idiopathic chronic pain, such as atypical odontalgia (idiopathic painful trigeminal neuropathy or post-traumatic trigeminal neuropathy) and burning mouth syndrome, remain especially challenging. The central integration of gustatory inputs might modulate chronic oral and facial pain. A lack of pain in chronic inflammation inside the oral cavity, such as chronic periodontitis, involves the specialized functioning of oral bacteria. A more detailed understanding of the unique neurobiology of pain from the orofacial skin and the oral mucosa should help us develop novel methods for better treating persistent orofacial pain.
- Published
- 2021
6. Mast Cell-Specific Receptor/Corticotropin-Releasing Factor Axis Regulates Alcohol Withdrawal-Associated Headache
- Author
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Hirotake Ishida, Yan Zhang, John Shannonhouse, Ruben Gomez, Yu Shin Kim, Hyeonwi Son, and Armen N. Akopian
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medicine.medical_specialty ,business.industry ,Dura mater ,Degranulation ,Alcohol ,Vasodilation ,Alcohol use disorder ,Mast cell ,medicine.disease ,chemistry.chemical_compound ,medicine.anatomical_structure ,Endocrinology ,Allodynia ,chemistry ,Internal medicine ,medicine ,medicine.symptom ,Receptor ,business - Abstract
Rehabilitation from alcohol addiction or abuse is challenging due to alcohol withdrawal symptoms. Headache is a severe alcohol withdrawal symptom that frequently contributes to rehabilitation failure. Despite the need for treating alcohol withdrawal-induced headache, there is no appropriate therapeutic option available. Development of improved therapeutics will depend on obtaining a clearer understanding of alcohol withdrawal-induced headache pain mechanisms. Here, we show that the mast cell-specific receptor MrgprB2 controls development of alcohol withdrawal-induced headache. Withdrawing alcohol from alcohol-acclimated mice induces strong headache behaviors, including facial allodynia, facial pain expressions, and reduced walking movement, symptoms often observed in humans suffering from headache. Observed pain behaviors were abolished in MrgprB2-deficient mice. We observed in vivo spontaneous activation and hypersensitization of trigeminal ganglia neurons in alcohol withdrawal mice, but not in MrgprB2-deficient mice. Corticotropin-releasing factor (CRF) was increased in dura mater after alcohol withdrawal. Injection of CRF into dura mater resulted in activation of trigeminal ganglia neurons and vasodilation, which was accompanied by headache behavior. In cells, CRF evoked Ca2+ transients via MrgprB2 or human MrgprX2. The results indicate that alcohol withdrawal causes headache via mast cell degranulation in dura mater. The process is under control of MrgprB2/MrgprX2, which would appear to represent a potential target for treating alcohol withdrawal-related headache.
- Published
- 2021
7. Na+-dependent inactivation of vascular Na+/Ca2+ exchanger responsible for reduced peripheral blood flow in neuropathic pain model
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Shin-ya Saito, Momoka Yamaguchi, Takuma Furukawa, John Shannonhouse, Hirotake Ishida, Tomohisa Ishikawa, and Yu Shin Kim
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Boron Compounds ,Male ,Serotonin ,medicine.medical_specialty ,Contraction (grammar) ,Nifedipine ,Vasodilator Agents ,Vasodilation ,Article ,Sodium-Calcium Exchanger ,Amiloride ,Norepinephrine ,Internal medicine ,medicine ,Animals ,Vasoconstrictor Agents ,Rats, Wistar ,Ouabain ,Calcimycin ,Pharmacology ,Dose-Response Relationship, Drug ,Sodium-calcium exchanger ,business.industry ,Sodium ,Thiourea ,Arteries ,Nerve injury ,Calcium Ionophores ,Disease Models, Animal ,Endocrinology ,15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic Acid ,Blood Circulation ,Neuropathic pain ,Peripheral nerve injury ,Neuralgia ,Calcium ,Sciatic nerve ,medicine.symptom ,business ,Vasoconstriction ,Muscle Contraction - Abstract
Reduced skin blood flow has been reported in neuropathic pain patients as well as various peripheral neuropathic pain model animals. We have previously shown that vasodilators, which improves reduced skin blood flow, correlatively alleviate neuropathic pain in chronic constriction injury (CCI) mice, a model of neuropathic pain from peripheral nerve injury. Here, we sought to elucidate the mechanism underlying the reduced skin blood flow in CCI rats. The skin blood flow of the ipsilateral plantar arteries was significantly reduced compared to that of the contralateral ones 4 weeks after loose ligation of the sciatic nerve. The contraction induced by noradrenaline, serotonin, and U46619, a thromboxane receptor agonist, in the isolated ipsilateral plantar arteries was significantly enhanced compared to that in the contralateral ones. KB-R7943, a Na(+)/Ca(2+) exchanger (NCX) inhibitor, shifted the concentration-response curves of noradrenaline to the left in the contralateral arteries but had no effect on the ipsilateral side. There was no significant difference in concentration-response curves of noradrenaline between the ipsilateral and contralateral arteries in the presence of KB-R7943. Amiloride, a non-specific inhibitor of Na(+) channels and transporters, comparably shifted concentration-response curves of noradrenaline to the left in both the contralateral and ipsilateral arteries. One hundred nM of noradrenaline induced intracellular Ca(2+) elevation in the ipsilateral arteries, which was significantly larger than that induced by 300-nM noradrenaline in the contralateral arteries. These results suggest that reduced peripheral blood flow after nerve injury is due to Na(+)-dependent inactivation of NCX in the ipsilateral plantar arteries.
- Published
- 2021
8. Visualization of Peripheral Neuron Sensitization in a Surgical Mouse Model of Osteoarthritis by In Vivo Calcium Imaging
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Richard J. Miller, P.B. Tran, Yu Shin Kim, Xinzhong Dong, Rachel E. Miller, S. Ishihara, and Anne-Marie Malfait
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0301 basic medicine ,Pathology ,medicine.medical_specialty ,business.industry ,Immunology ,Sham surgery ,Hindlimb ,Sensory neuron ,03 medical and health sciences ,030104 developmental biology ,0302 clinical medicine ,medicine.anatomical_structure ,Calcium imaging ,nervous system ,Rheumatology ,Dorsal root ganglion ,In vivo ,Anesthesia ,Hyperalgesia ,medicine ,Nociceptor ,Immunology and Allergy ,medicine.symptom ,business ,030217 neurology & neurosurgery - Abstract
Objective The purpose of this study was to develop a method for analyzing sensory neuron responses to mechanical stimuli in vivo, and to evaluate whether these neuronal responses change after destabilization of the medial meniscus (DMM). Methods DMM or sham surgery was performed in 10-week old male C57BL/6 wild-type or Pirt-GCaMP3+/- mice. All experiments were performed eight weeks after surgery. Knee and hind paw hyperalgesia were assessed in wild-type mice. The retrograde label DiI was injected into the ipsilateral knee to quantify the number of knee-innervating neurons in the L4 dorsal root ganglion (DRG) in wild-type mice. In vivo calcium imaging was performed on the ipsilateral L4 DRG of Pirt-GCaMP3+/- mice as mechanical stimuli (paw pinch, knee pinch, knee twist) were applied to the ipsilateral hind limb. Results Eight weeks after surgery, DMM mice had more hyperalgesia in the knee and hind paw compared to sham mice. Intra-articular injection of DiI labeled similar numbers of neurons in the L4 DRG of sham and DMM mice. Increased numbers of sensory neurons responded to all three mechanical stimuli in DMM mice, as assessed by in vivo calcium imaging. The majority of responses in sham and DMM mice were in small-to-medium-sized neurons, consistent with the size of nociceptors. The magnitude of responses was similar between sham and DMM mice. Conclusions We demonstrated that increased numbers of small-to-medium sized DRG neurons respond to mechanical stimuli 8 weeks after DMM surgery, suggesting that nociceptors have become sensitized by lowering the response threshold. This article is protected by copyright. All rights reserved.
- Published
- 2017
9. Coupled Activation of Primary Sensory Neurons Contributes to Chronic Pain
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Michael Anderson, Dwight E. Bergles, Catherine Gong, David C. Spray, Pamela Colleen LaVinka, Feng Quan Zhou, Qin Zheng, Yun Guan, Le Anne Young, Menachem Hanani, Xinzhong Dong, Kyoungsook Park, Amit Agarwal, Yu Shin Kim, Shao Qiu He, and Saijilafu
- Subjects
0301 basic medicine ,Sensory Receptor Cells ,Mice, Transgenic ,Sensory system ,Article ,Mice ,03 medical and health sciences ,0302 clinical medicine ,Downregulation and upregulation ,Ganglia, Spinal ,Neuroplasticity ,Animals ,Medicine ,Neuronal Plasticity ,business.industry ,General Neuroscience ,Chronic pain ,Gap junction ,Gap Junctions ,medicine.disease ,Up-Regulation ,030104 developmental biology ,medicine.anatomical_structure ,nervous system ,Hyperalgesia ,Neuroglia ,Chronic Pain ,medicine.symptom ,business ,Neuroscience ,030217 neurology & neurosurgery - Abstract
Primary sensory neurons in the DRG play an essential role in initiating pain by detecting painful stimuli in the periphery. Tissue injury can sensitize DRG neurons, causing heightened pain sensitivity, often leading to chronic pain. Despite the functional importance, how DRG neurons function at a population level is unclear due to the lack of suitable tools. Here we developed an imaging technique that allowed us to simultaneously monitor the activities of >1,600 neurons/DRG in live mice and discovered a striking neuronal coupling phenomenon that adjacent neurons tend to activate together following tissue injury. This coupled activation occurs among various neurons and is mediated by an injury-induced upregulation of gap junctions in glial cells surrounding DRG neurons. Blocking gap junctions attenuated neuronal coupling and mechanical hyperalgesia. Therefore, neuronal coupling represents a new form of neuronal plasticity in the DRG and contributes to pain hypersensitivity by “hijacking” neighboring neurons through gap junctions.
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- 2016
10. In vivo calcium imaging visualizes peripheral neuron sensitization in murine osteoarthritis
- Author
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Richard J. Miller, P.B. Tran, Rachel E. Miller, Anne-Marie Malfait, Xinzhong Dong, and Yu Shin Kim
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0303 health sciences ,Pathology ,medicine.medical_specialty ,business.industry ,Sham surgery ,Hindlimb ,Anatomy ,Sensory neuron ,03 medical and health sciences ,0302 clinical medicine ,medicine.anatomical_structure ,Calcium imaging ,nervous system ,Dorsal root ganglion ,In vivo ,Hyperalgesia ,medicine ,Nociceptor ,medicine.symptom ,business ,030217 neurology & neurosurgery ,030304 developmental biology - Abstract
ObjectiveThe purpose of this study was to develop a method for analyzing sensory neuron responses to mechanical stimuli in vivo, and to evaluate whether these neuronal responses change after destabilization of the medial meniscus (DMM).MethodsDMM or sham surgery was performed in 10-week old male C57BL/6 wild-type or Pirt-GCaMP3+/− mice. All experiments were performed eight weeks after surgery. Knee and hind paw hyperalgesia were assessed in wild-type mice. The retrograde label DiI was injected into the ipsilateral knee to quantify the number of knee-innervating neurons in the L4 dorsal root ganglion (DRG) in wild-type mice. In vivo calcium imaging was performed on the ipsilateral L4 DRG of Pirt-GCaMP3+/− mice as mechanical stimuli (paw pinch, knee pinch, knee twist) were applied to the ipsilateral hind limb.ResultsEight weeks after surgery, DMM mice had more hyperalgesia in the knee and hind paw compared to sham mice. Intra-articular injection of DiI labeled similar numbers of neurons in the L4 DRG of sham and DMM mice. Increased numbers of sensory neurons responded to all three mechanical stimuli in DMM mice, as assessed by in vivo calcium imaging. The majority of responses in sham and DMM mice were in small-to-medium-sized neurons, consistent with the size of nociceptors. The magnitude of responses was similar between sham and DMM mice.ConclusionsWe demonstrated that increased numbers of small-to-medium sized DRG neurons respond to mechanical stimuli 8 weeks after DMM surgery, suggesting that nociceptors have become sensitized by lowering the response threshold.
- Published
- 2017
11. Central Terminal Sensitization of TRPV1 by Descending Serotonergic Facilitation Modulates Chronic Pain
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Ronald Dubner, Yuxia Chu, Pamela Colleen LaVinka, Kyoungsook Park, Zhe Li, Michael J. Caterina, Yu Shin Kim, Xinzhong Dong, Man Li, Shuohao Sun, Ke Ren, Feng Wei, Zongxiang Tang, and Liang Han
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Neuroscience(all) ,TRPV1 ,TRPV Cation Channels ,Serotonergic ,Article ,Mice ,Trigeminal ganglion ,medicine ,Animals ,Sensitization ,Neurons ,business.industry ,General Neuroscience ,Spinal trigeminal nucleus ,Chronic pain ,Nociceptors ,medicine.disease ,Mice, Inbred C57BL ,Disease Models, Animal ,medicine.anatomical_structure ,Spinal Cord ,Trigeminal Ganglion ,nervous system ,Neuropathic pain ,Brainstem ,Capsaicin ,Chronic Pain ,business ,Neuroscience - Abstract
SummaryThe peripheral terminals of primary nociceptive neurons play an essential role in pain detection mediated by membrane receptors like TRPV1, a molecular sensor of heat and capsaicin. However, the contribution of central terminal TRPV1 in the dorsal horn to chronic pain has not been investigated directly. Combining primary sensory neuron-specific GCaMP3 imaging with a trigeminal neuropathic pain model, we detected robust neuronal hyperactivity in injured and uninjured nerves in the skin, soma in trigeminal ganglion, and central terminals in the spinal trigeminal nucleus. Extensive TRPV1 hyperactivity was observed in central terminals innervating all dorsal horn laminae. The central terminal TRPV1 sensitization was maintained by descending serotonergic (5-HT) input from the brainstem. Central blockade of TRPV1 or 5-HT/5-HT3A receptors attenuated central terminal sensitization, excitatory primary afferent inputs, and mechanical hyperalgesia in the territories of injured and uninjured nerves. Our results reveal central mechanisms facilitating central terminal sensitization underlying chronic pain.
- Published
- 2014
12. Implementation of the basic Actions for Virtual Human with Diversity and Reusability
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Geun-Jae Jung, Jong-Hee Park, and Yu-Shin Kim
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Hierarchy ,Engineering ,Root (linguistics) ,Action (philosophy) ,business.industry ,Human–computer interaction ,GRASP ,Ontology ,Artificial intelligence ,business ,Reusability ,Diversity (business) ,Virtual actor - Abstract
In this paper, we attempt to realize the diversity of human actions in a virtual world in terms of the basic actions. We utilize the comprehensive knowledge structure of ontology to organize the human actions into an action hierarchy, each action being the root action of its associated hierarchy of specialized actions. Each basic action is implemented by composing the primitive motions and each basic action in turn by reusing those basic actions. Our approach to the development of these actions is focused more on their diversity and brevity than on their visual realism. Based on this design we develop a method to grasp virtual humans` characteristics and reflect those characteristics on their respective action patterns. We also present a mechanism for the agents to adapt their motions to diverse qualitative changes in environment. We apply these methods to such basic actions as walk, run and throw to demonstrate their viability.
- Published
- 2011
13. In vivo calcium imaging of knee-innervating dorsal root ganglion neurons reveals increased neuronal responsiveness to physical stimuli after dmm surgery
- Author
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K. Park, Xinzhong Dong, Rachel E. Miller, Richard J. Miller, S. Ishihara, A.-M. Malfait, and Yu Shin Kim
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Calcium imaging ,medicine.anatomical_structure ,Dorsal root ganglion ,Rheumatology ,In vivo ,business.industry ,medicine ,Biomedical Engineering ,Orthopedics and Sports Medicine ,Anatomy ,business - Published
- 2015
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14. Nose Shape Optimization of High-speed Train for Minimization of Tunnel Sonic Boom
- Author
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Dong-Ho Lee, Hyeok-Bin Kwon, Yu-shin Kim, Ki-hyeok Jang, and Kwan-jung Yee
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Engineering ,business.industry ,Mechanical Engineering ,Structural engineering ,Industrial and Manufacturing Engineering ,Sonic boom ,Euler equations ,symbols.namesake ,Buckling ,Compressibility ,symbols ,Train ,Shape optimization ,Minification ,business ,Parametric statistics - Abstract
The tunnel booming noise generated during the train-tunnel interaction has been one of the most serious constraints in the development of the high-speed trains. It is well known that the nose shape of the train has the significant influence on the intensity of the booming noise. In this study, the nose shape has been optimized by using the response surface methodology and the axi-symmetric compressible Euler equations. The parametric studies are also performed with respect to the slenderness ratio, the blockage ratio and the train speed to investigate their sensitivities to the optimization results. The results show that it is possible to befine more general design space by introducing the Hicks-Henne shape functions, resulting in the more effective nose shape than that of Maeda. The mechanism and the aspects of the train-tunnel interaction were also investigated discussed from the results of the parametric study.
- Published
- 2001
15. A histamine-independent itch pathway is required for allergic ocular itch
- Author
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Changxiong Guo, William Olson, Qin Liu, Andrew J.W. Huang, Cheng Chiu Huang, Wenqin Luo, Fengxian Li, and Yu Shin Kim
- Subjects
0301 basic medicine ,Immunology ,TRPV Cation Channels ,TRPA1 Channel ,Article ,Mice ,03 medical and health sciences ,Neural Pathway ,chemistry.chemical_compound ,Transient Receptor Potential Channels ,otorhinolaryngologic diseases ,Animals ,Immunology and Allergy ,Medicine ,skin and connective tissue diseases ,TRPA1 Cation Channel ,Conjunctivitis, Allergic ,Mice, Knockout ,Histamine metabolism ,business.industry ,Extramural ,Pruritus ,food and beverages ,medicine.disease ,eye diseases ,Allergic conjunctivitis ,030104 developmental biology ,chemistry ,business ,Biomarkers ,psychological phenomena and processes ,Histamine - Abstract
Non-histaminergic TRPA1 neural pathway is required for the development of allergic ocular itch. Pharmacological inhibition of TRPA1 channel can lead to novel therapeutic strategies to treat ocular itch in severe allergic conjunctivitis.
- Published
- 2016
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