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Journal of Biological Chemistry, ISSN 0021-9258, 09/2007, Volume 282, Issue 36, pp. 26089 - 26100
Although principally produced by the pancreas to degrade dietary proteins in the intestine, trypsins are also expressed in the nervous system and in epithelial... 
Life Sciences & Biomedicine | Biochemistry & Molecular Biology | Science & Technology | Hyperalgesia - chemically induced | Inflammation - chemically induced | Inflammation - pathology | Receptors, Proteinase-Activated - metabolism | Capsaicin - pharmacology | Edema - genetics | Receptor, PAR-1 - metabolism | Humans | Male | Receptor, PAR-1 - deficiency | Receptor, PAR-2 - deficiency | Hyperalgesia - pathology | Inflammation - metabolism | Trypsin Inhibitors - chemistry | Trypsin - pharmacology | Trypsin - genetics | Granulocytes - pathology | Granulocytes - metabolism | Nociceptors - pathology | Recombinant Proteins - metabolism | Hyperalgesia - metabolism | Rats | Recombinant Proteins - chemistry | Recombinant Proteins - genetics | Recombinant Proteins - pharmacology | Trypsin - metabolism | Rats, Sprague-Dawley | Mice, Knockout | Edema - metabolism | Animals | Hyperalgesia - genetics | Calcium Signaling - drug effects | Enteropeptidase - chemistry | Ganglia, Spinal - pathology | Inflammation - genetics | Receptor, PAR-2 - physiology | Receptors, Thrombin - metabolism | Mice | Nociceptors - metabolism | Aprotinin - chemistry | Edema - chemically induced | Pain Measurement | Edema - pathology | Trypsin - chemistry | Ganglia, Spinal - metabolism | Index Medicus | Nociceptors/metabolism | Aprotinin/chemistry | Edema/chemically induced | Recombinant Proteins/chemistry | Receptor, PAR-1/deficiency | Enteropeptidase/chemistry | Capsaicin/pharmacology | Inflammation/chemically induced | Receptors, Proteinase-Activated/metabolism | Granulocytes/metabolism | Trypsin Inhibitors/chemistry | Ganglia, Spinal/metabolism | Receptor, PAR-2/deficiency | Calcium Signaling/drug effects | Trypsin/chemistry | Hyperalgesia/chemically induced | Receptors, Thrombin/metabolism
Journal Article
Journal Article
Gastroenterology (New York, N.Y. 1943), ISSN 0016-5085, 12/2009, Volume 137, Issue 6, pp. 2084 - 2095.e3
Background & Aims The transient receptor potential (TRP) channel family includes transducers of mechanical and chemical stimuli for visceral sensory neurons.... 
Gastroenterology and Hepatology | Gastroenterology & Hepatology | Life Sciences & Biomedicine | Science & Technology | Hyperalgesia - chemically induced | Immunohistochemistry | Intestinal Mucosa - metabolism | Intestinal Mucosa - physiopathology | Mechanotransduction, Cellular - drug effects | Capsaicin - pharmacology | Neuroanatomical Tract-Tracing Techniques | Receptor, PAR-2 - metabolism | Colon - drug effects | Afferent Pathways - physiopathology | Colon - innervation | Male | Ganglia, Spinal - physiopathology | Nodose Ganglion - metabolism | Trinitrobenzenesulfonic Acid | Pelvis - innervation | RNA, Messenger - metabolism | Transient Receptor Potential Channels - deficiency | Action Potentials | Nodose Ganglion - physiopathology | Splanchnic Nerves - physiopathology | In Situ Hybridization | Colitis - chemically induced | Nodose Ganglion - drug effects | Colon - physiopathology | Female | Transient Receptor Potential Channels - metabolism | Bradykinin - pharmacology | Disease Models, Animal | Afferent Pathways - metabolism | Hyperalgesia - metabolism | Mice, Inbred C57BL | Reverse Transcriptase Polymerase Chain Reaction | Pressure | Stimulation, Chemical | Colon - metabolism | Hyperalgesia - physiopathology | Mice, Knockout | Animals | Colitis - physiopathology | Transient Receptor Potential Channels - genetics | TRPA1 Cation Channel | Colitis - metabolism | Splanchnic Nerves - metabolism | Mice | Ganglia, Spinal - drug effects | Pain Measurement | Ganglia, Spinal - metabolism | Index Medicus | Abridged Index Medicus
Journal Article
Neuropharmacology, ISSN 0028-3908, 04/2017, Volume 116, pp. 315 - 327
Joint pain is a major clinical problem mainly associated to osteoarthritis, and characterized by articular cartilage degradation resulting in a complex chronic... 
Dynorphin | Opioids | Anhedonia | Anxiety | Cognition | Osteoarthritis | KOR | Pharmacology & Pharmacy | Neurosciences | Neurosciences & Neurology | Life Sciences & Biomedicine | Science & Technology | Arthralgia - pathology | Microglia - metabolism | Spinal Cord - metabolism | Enkephalins - metabolism | Epigenesis, Genetic | Hyperalgesia - psychology | Hyperalgesia - pathology | Enkephalins - genetics | Spinal Cord - pathology | Cognition - physiology | Microglia - pathology | Acetylation | Osteoarthritis - pathology | Receptors, Opioid, kappa - genetics | Arthralgia - psychology | Disease Models, Animal | Emotions - physiology | Protein Precursors - genetics | Hyperalgesia - metabolism | Mice, Inbred C57BL | Amygdala - metabolism | Receptors, Opioid, kappa - metabolism | Osteoarthritis - metabolism | Hippocampus - pathology | Chronic Pain - psychology | Chronic Pain - pathology | Amygdala - pathology | Corticotropin-Releasing Hormone - metabolism | Mice, Knockout | Protein Precursors - metabolism | Chronic Pain - metabolism | Hippocampus - metabolism | Osteoarthritis - psychology | Animals | Arthralgia - metabolism | Histones - metabolism | Corticotropin releasing hormone | Epigenetic inheritance | Analysis | Arthralgia | ACTH | Missing in action | Chronic pain | Index Medicus | Artrosi | Cognició | Angoixa | Dolor | Neuropèptids
Journal Article
Molecular pain, ISSN 1744-8069, 01/2011, Volume 7, Issue 1, pp. 1744-8069-7-40 - 40
Journal Article
The Journal of neuroscience, ISSN 1529-2401, 05/2004, Volume 24, Issue 18, pp. 4300 - 4312
Journal Article
Journal Article