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1. Full Text Specific caspase inhibitor Q‐VD‐OPh prevents neonatal stroke in P7 rat: a role for gender
by Renolleau, Sylvain and Fau, Sébastien and Goyenvalle, Catherine and Joly, Luc‐Marie and Chauvier, David and Jacotot, Etienne and Mariani, Jean and Charriaut‐Marlangue, Christiane
Journal of Neurochemistry, ISSN 0022-3042, 02/2007, Volume 100, Issue 4, pp. 1062 - 1071
Hypoxia–ischaemia in the developing brain results in brain injury with prominent features of apoptosis. In the present study, a third generation dipeptidyl... 
neonatal stroke | brain injury | caspase inhibitor | cell death | gender | Gender | Neonatal stroke | Cell death | Brain injury | Caspase inhibitor | APOPTOSIS-INDUCING FACTOR | NERVOUS-SYSTEM | ACTIVATION | BIOCHEMISTRY & MOLECULAR BIOLOGY | INVOLVEMENT | MECHANISMS | NEUROSCIENCES | CELL-DEATH | HYPOXIA-ISCHEMIA | INFANTS | ISCHEMIC BRAIN-INJURY | MICE | Animals, Newborn | In Situ Nick-End Labeling | Stroke - prevention & control | Humans | Amino Acid Chloromethyl Ketones - therapeutic use | Rats | Male | Caspase Inhibitors | Enzyme Inhibitors - therapeutic use | Gene Expression Regulation - drug effects | Stroke - pathology | Gender Identity | Animals | Statistics, Nonparametric | Quinolines - therapeutic use | Cell Death - drug effects | Neurologic Examination - methods | Neurology | Brain damage | Biochemistry | Gender differences | Rodents | Apoptosis | Quinolines | Enzyme Inhibitors | Neurons and Cognition | Gene Expression Regulation | Neurobiology | Life Sciences | Neurologic Examination | Cerebrovascular Accident | Amino Acid Chloromethyl Ketones | Cell Death | Caspases
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2. Full Text Functional Role of Caspase-1 and Caspase-3 in an ALS Transgenic Mouse Model
by Mingwei Li and Victor O. Ona and Christelle Guégan and Minghua Chen and Vernice Jackson-Lewis and L. John Andrews and Adam J. Olszewski and Philip E. Stieg and Jean-Pyo. Lee and Serge Przedborski and Robert M. Friedlander
Science, ISSN 0036-8075, 4/2000, Volume 288, Issue 5464, pp. 335 - 339
Mutations in the copper/zinc Superoxide dismutase (SOD1) gene produce an animal model of familial amyotrophic lateral sclerosis (ALS), a fatal... 
Bacteriophages | Motor neurons | Spinal cord | Messenger RNA | Disease models | Transgenic animals | Antibodies | Amyotrophic lateral sclerosis | Reports | Mice | Vehicles | NEURONAL APOPTOSIS | MULTIDISCIPLINARY SCIENCES | FAMILY PROTEASES | MICE | AMYOTROPHIC-LATERAL-SCLEROSIS | MEDIATED APOPTOSIS | BRAIN INJURY | TROPHIC FACTOR WITHDRAWAL | INTERLEUKIN-1-BETA CONVERTING-ENZYME | CU,ZN SUPEROXIDE-DISMUTASE | CELL-DEATH | Neuroprotective Agents - therapeutic use | Superoxide Dismutase - genetics | Apoptosis - drug effects | Humans | Amino Acid Chloromethyl Ketones - therapeutic use | Injections, Intraventricular | Caspase 1 - metabolism | Male | Amyotrophic Lateral Sclerosis - drug therapy | Motor Neurons - pathology | Caspases - metabolism | Neuroprotective Agents - pharmacology | Amino Acid Chloromethyl Ketones - pharmacology | Caspase 3 | Amyotrophic Lateral Sclerosis - enzymology | Neuroprotective Agents - administration & dosage | Motor Neurons - drug effects | Superoxide Dismutase - metabolism | Disease Models, Animal | Psychomotor Performance | Cysteine Proteinase Inhibitors - therapeutic use | Interleukin-1 - metabolism | Caspases - genetics | Cysteine Proteinase Inhibitors - administration & dosage | Spinal Cord - enzymology | Mice, Transgenic | Motor Neurons - enzymology | Caspase Inhibitors | Disease Progression | Gene Expression Regulation, Enzymologic | Amyotrophic Lateral Sclerosis - pathology | Amino Acid Chloromethyl Ketones - administration & dosage | Animals | Caspase 1 - genetics | Cysteine Proteinase Inhibitors - pharmacology | Enzyme Activation | Superoxide Dismutase-1 | Nerve Degeneration | Amino Acid Substitution | Neurology | Enzymes | Mutation | Rodents | Genes
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3. Full Text Inhibition of apoptosis induced by ischemia-reperfusion prevents inflammation
by Daemen, M. A and van 't Veer, C and Denecker, G and Heemskerk, V. H and Wolfs, T. G and Clauss, M and Vandenabeele, P and Buurman, W. A
Journal of clinical investigation, ISSN 0021-9738, 1999, Volume 104, Issue 5, pp. 541 - 549
Ischemia followed by reperfusion leads to severe organ injury and dysfunction. Inflammation is considered to be the most important cause of tissue injury in... 
MEDICINE, RESEARCH & EXPERIMENTAL | ACTIVATING POLYPEPTIDE-II | INJURY | RECEPTOR | ACUTE-RENAL-FAILURE | MECHANISMS | INDUCTION | HYPOXIA | EXPRESSION | INTERLEUKIN-8 | GROWTH-FACTOR-I | Chemotaxis, Leukocyte | Insulin-Like Growth Factor I - pharmacology | Kidney - blood supply | Kidney - pathology | Apoptosis - drug effects | Blood Urea Nitrogen | Humans | Amino Acid Chloromethyl Ketones - therapeutic use | Depression, Chemical | Male | Nephritis - prevention & control | Neoplasm Proteins - metabolism | Caspases - metabolism | Amino Acid Chloromethyl Ketones - pharmacology | Ischemia - complications | Insulin-Like Growth Factor I - administration & dosage | Insulin-Like Growth Factor I - therapeutic use | Ischemia - pathology | In Situ Nick-End Labeling | Cysteine Proteinase Inhibitors - therapeutic use | Cytokines | Drug Administration Schedule | Reperfusion Injury - pathology | Cysteine Proteinase Inhibitors - administration & dosage | Nephritis - etiology | Recombinant Proteins - pharmacology | Amino Acid Chloromethyl Ketones - administration & dosage | Animals | Reperfusion Injury - prevention & control | Cysteine Proteinase Inhibitors - pharmacology | Mice | Protein Processing, Post-Translational | Epidermal Growth Factor - pharmacology | Peroxidase - blood | RNA-Binding Proteins - metabolism
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4. Mechanisms of growth inhibition in human papillomavirus positive and negative cervical cancer cells by the chloromethyl ketone protease inhibitor, succinyl-alanine-alanine-proline-phenylalanine chloromethyl ketone
by Duncan, Kimberly J and Eckert, Kristin A and Clawson, Gary A
Journal of Pharmacology and Experimental Therapeutics, ISSN 0022-3565, 07/2009, Volume 330, Issue 1, pp. 359 - 366
The chymotrypsin-like serine protease inhibitor, succinyl-alanine-alanine-proline-phenylalanine chloromethyl ketone (AAPF(CMK)), has been shown to have... 
TRANSFORMATION | HEAD | APOPTOSIS | SEQUENCES | DRUGS | CARCINOMAS | PHARMACOLOGY & PHARMACY | TYPE-16 | NUCLEAR SCAFFOLD | LINES | CYCLE | Uterine Cervical Neoplasms - enzymology | Humans | Amino Acid Chloromethyl Ketones - therapeutic use | Uterine Cervical Neoplasms - drug therapy | Uterine Cervical Neoplasms - pathology | Oligopeptides - therapeutic use | Serine Proteinase Inhibitors - therapeutic use | Growth Inhibitors - therapeutic use | Amino Acid Chloromethyl Ketones - pharmacology | Tosyllysine Chloromethyl Ketone - metabolism | Cell Line, Tumor | Uterine Cervical Neoplasms - virology | Female | Papillomaviridae | Oligopeptides - pharmacology | Growth Inhibitors - pharmacology | Serine Proteinase Inhibitors - pharmacology | Tosyllysine Chloromethyl Ketone - antagonists & inhibitors
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5. Full Text Combination of necroptosis and apoptosis inhibition enhances cardioprotection against myocardial ischemia–reperfusion injury
by Koshinuma, Shizuka and Koshinuma, Shizuka and Miyamae, Masami and Miyamae, Masami and Kaneda, Kazuhiro and Kaneda, Kazuhiro and Kotani, Junichiro and Kotani, Junichiro and Figueredo, Vincent M and Figueredo, Vincent M
Journal of Anesthesia, ISSN 0913-8668, 4/2014, Volume 28, Issue 2, pp. 235 - 241
Necroptosis has been proposed as a mode of cell death that is a caspase-independent programmed necrosis. We investigated whether necroptosis is involved in... 
Heart | Necrostatin-1 | Pain Medicine | Emergency Medicine | Medicine & Public Health | Necroptosis | Intensive / Critical Care Medicine | Anesthesiology | Ischemia–reperfusion | Ischemia-reperfusion | INFARCT SIZE | RIP1 KINASE | NECROSTATIN | ANESTHESIOLOGY | CELL-DEATH | Heart - physiopathology | Necrosis - drug therapy | Guinea Pigs | Apoptosis - drug effects | Amino Acid Chloromethyl Ketones - therapeutic use | Imidazoles - administration & dosage | Male | Myocardium - pathology | Necrosis - pathology | Indoles - administration & dosage | Myocardial Reperfusion Injury - physiopathology | Cardiotonic Agents - therapeutic use | Myocardial Reperfusion Injury - pathology | Amino Acid Chloromethyl Ketones - administration & dosage | Animals | Cardiotonic Agents - administration & dosage | Necrosis - physiopathology | Caspase 3 - analysis | Heart - drug effects | Indoles - therapeutic use | Hemodynamics - drug effects | Imidazoles - therapeutic use | Myocardial Reperfusion Injury - drug therapy | Drug Therapy, Combination | Care and treatment | Physiological aspects | Myocardial ischemia | Development and progression | Genetic aspects | Research | Reperfusion injury | Apoptosis
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6. Full Text Delayed, Long-Term Administration of the Caspase Inhibitor Q-VD-OPh Reduced Brain Injury Induced by Neonatal Hypoxia-Ischemia
by Han, Wei and Sun, Yanyan and Wang, Xiaoyang and Zhu, Changlian and Blomgren, Klas and Institutionen för neurovetenskap och fysiologi, sektionen för klinisk neurovetenskap och rehabilitering and Institute of Clinical Sciences, Section for the Health of Women and Children, Department of Pediatrics and Göteborgs universitet and Gothenburg University and Sahlgrenska Academy and Institute of Neuroscience and Physiology, Department of Clinical Neuroscience and Rehabilitation and Sahlgrenska akademin and Institutionen för kliniska vetenskaper, sektionen för kvinnors och barns hälsa, Avdelningen för pediatrik
Developmental Neuroscience, ISSN 0378-5866, 03/2014, Volume 36, Issue 1, pp. 64 - 72
Apoptosis contributes greatly to the morphological and biochemical features of cell death after neonatal cerebral hypoxia-ischemia (HI), making this mode of... 
Original Paper | Open Field | MCP-1 | CCL3 | IL-4 | CCL2 | Brain tissue loss | Cylinder Rearing Test | IL-10 | MIP-1 alpha | ACTIVATION | RAT | FOCAL CEREBRAL-ISCHEMIA | MECHANISMS | DEVELOPMENTAL BIOLOGY | MATURATION | NEUROSCIENCES | NEUROPROTECTION | CELL-DEATH | PATHOLOGICAL APOPTOSIS | STROKE | MICE | Caspase Inhibitors - administration & dosage | Microglia - metabolism | Microglia - drug effects | Cell Count | Amino Acid Chloromethyl Ketones - therapeutic use | Caspase 3 - metabolism | Hypoxia-Ischemia, Brain - drug therapy | Motor Activity - drug effects | Male | Treatment Outcome | Quinolines - administration & dosage | Brain - drug effects | Brain - metabolism | Amino Acid Chloromethyl Ketones - administration & dosage | Animals | Caspase Inhibitors - therapeutic use | Behavior, Animal - drug effects | Chemokine CCL3 - metabolism | Chemokine CCL2 - metabolism | Mice | Quinolines - therapeutic use | Hypoxia-Ischemia, Brain - metabolism | Neurologi | Pediatrics | Pediatrik | Neurology
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7. Combined and individual use of pancaspase inhibitor Q-VD-OPh and NMDA receptor antagonist riluzole in experimental spinal cord injury
by Can, H and Aydoseli, A and Gomleksiz, C and Goker, B and Altunrende, ME and Dolgun, M and Sencer, A
ULUSAL TRAVMA VE ACIL CERRAHI DERGISI-TURKISH JOURNAL OF TRAUMA & EMERGENCY SURGERY, ISSN 1306-696X, 11/2017, Volume 23, Issue 6, pp. 452 - 458
BACKGROUND: We investigated the effects of an N-methyl-D-aspartate receptor antagonist, riluzole, and a pancaspase inhibitor and basic apoptosis mediator,... 
spinal cord injury | RAT | NMDA receptor antagonist | riluzole | FOCAL CEREBRAL-ISCHEMIA | Q-VD-OPh | MECHANISMS | STRIATONIGRAL DEGENERATION | PHARMACOTHERAPY | MEMANTINE | CASPASE-3 INHIBITOR | pancaspase inhibitor | RECOVERY | EMERGENCY MEDICINE | necrosis | neuroprotection | IMPROVES | caspases | Apoptosis | Necrosis - drug therapy | Neuroprotective Agents - therapeutic use | Spinal Cord Injuries - drug therapy | Apoptosis - drug effects | Amino Acid Chloromethyl Ketones - therapeutic use | Rats | Male | Quinolines - administration & dosage | Rats, Sprague-Dawley | Necrosis - prevention & control | Quinolines - pharmacology | Riluzole - administration & dosage | Amino Acid Chloromethyl Ketones - administration & dosage | Animals | Neuroprotective Agents - pharmacology | Amino Acid Chloromethyl Ketones - pharmacology | Riluzole - therapeutic use | Quinolines - therapeutic use | Riluzole - pharmacology | Spinal Cord Injuries - physiopathology | Neuroprotective Agents - administration & dosage | Disease Models, Animal
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8. Full Text Caspase-1 inhibitor prevents neurogenic pulmonary edema after subarachnoid hemorrhage in mice
by Suzuki, Hidenori and Sozen, Takumi and Hasegawa, Yu and Chen, Wanqiu and Zhang, John H
Stroke, ISSN 0039-2499, 12/2009, Volume 40, Issue 12, pp. 3872 - 3875
Background and Purpose-We examined the effects of a caspase-1 inhibitor, N-Ac-Tyr-Val-Ala-Asp-chloromethyl ketone (Ac-YVAD-CMK), on neurogenic pulmonary edema... 
Subarachnoid hemorrhage | Pulmonary edema | Caspase-1 inhibitor | Apoptosis | pulmonary edema | subarachnoid hemorrhage | RATS | apoptosis | ACUTE LUNG INJURY | PERIPHERAL VASCULAR DISEASE | caspase-1 inhibitor | EARLY BRAIN-INJURY | CLINICAL NEUROLOGY | Interleukin-1beta - drug effects | Lung - innervation | Apoptosis - drug effects | Amino Acid Chloromethyl Ketones - therapeutic use | Caspase 1 - metabolism | Pulmonary Edema - etiology | Dose-Response Relationship, Drug | Pulmonary Edema - physiopathology | Amino Acid Chloromethyl Ketones - pharmacology | Interleukin-1beta - metabolism | Disease Models, Animal | In Situ Nick-End Labeling | Cysteine Proteinase Inhibitors - therapeutic use | Injections, Intraperitoneal | Treatment Outcome | Lung - physiopathology | Subarachnoid Hemorrhage - complications | Enzyme Activation - drug effects | Caspase Inhibitors | Pulmonary Edema - drug therapy | Animals | Cysteine Proteinase Inhibitors - pharmacology | Lung - drug effects | Biomarkers | Mice | Apoptosis - physiology | Enzyme Activation - physiology
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9. Full Text Cysteine protease inhibitors cure an experimental Trypanosoma cruzi infection
by Engel, Juan C and Doyle, Patricia S and Hsieh, Ivy and McKerrow, James H
Journal of Experimental Medicine, ISSN 0022-1007, 08/1998, Volume 188, Issue 4, pp. 725 - 734
Trypanosoma cruzi is the causative agent of Chagas' disease. The major protease, cruzain, is a target for the development of new chemotherapy. We report the... 
Drug design | Chagas' disease | Cysteine protease | Protease inhibitors | Trypanosoma cruzi | STRAINS | MEDICINE, RESEARCH & EXPERIMENTAL | DESIGN | drug design | CHAGAS-DISEASE | IMMUNOLOGY | IDENTIFICATION | GRANULES | CHEMOTHERAPY | cysteine protease | protease inhibitors | PROTEINASE | BENZNIDAZOLE | Cysteine Proteinase Inhibitors - therapeutic use | Amino Acid Chloromethyl Ketones - therapeutic use | Mice, Inbred C3H | Macrophages - parasitology | Animals | Trypanocidal Agents - pharmacology | Amino Acid Chloromethyl Ketones - pharmacology | Cysteine Proteinase Inhibitors - pharmacology | Chagas Disease - drug therapy | Trypanosoma cruzi - drug effects | Female | Trypanocidal Agents - therapeutic use | Mice | Disease Models, Animal
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10. Full Text Effects of a caspase and a calpain inhibitor on resting energy expenditures in normal and hypermetabolic rats: A pilot Study
by Vana, P.G and Laporte, H.M and Kennedy, R.H and Gamelli, R.L and Majetschak, M
Physiological Research, ISSN 0862-8408, 2016, Volume 65, Issue 3, pp. 537 - 541
Several diseases induce hypermetabolism, which is characterized by increases in resting energy expenditures (REE) and whole body protein loss. Exaggerated... 
Burn | Caspase | Calpain | Hypermetabolism | Resting energy expenditure | SKELETAL-MUSCLE | APOPTOSIS | ACTIVATION | PHYSIOLOGY | INJURY | PROTEOLYSIS | MODEL | Cysteine Proteinase Inhibitors - therapeutic use | Caspase Inhibitors - pharmacology | Dipeptides - therapeutic use | Dipeptides - pharmacology | Amino Acid Chloromethyl Ketones - therapeutic use | Male | Metabolic Diseases - drug therapy | Rats, Sprague-Dawley | Pilot Projects | Animals | Caspase Inhibitors - therapeutic use | Amino Acid Chloromethyl Ketones - pharmacology | Metabolic Diseases - etiology | Cysteine Proteinase Inhibitors - pharmacology | Drug Evaluation, Preclinical | Burns - complications | Energy Metabolism - drug effects | Drugs | Proteins | Medical research | Disease | Protein synthesis | Mortality | Life sciences | Burns | Injuries
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11. Full Text Modulation of radiochemoimmunotherapy-induced B16 melanoma cell death by the pan-caspase inhibitor zVAD-fmk induces anti-tumor immunity in a HMGB1-, nucleotide- and T-cell-dependent manner
by Werthmöller, N and Frey, B and Wunderlich, R and Fietkau, R and Gaipl, U.S
Cell Death and Disease, ISSN 2041-4889, 05/2015, Volume 6, Issue 5, pp. e1761 - e1761
One prerequisite that radiotherapy (RT) and chemotherapy (CT) result in anti-tumor immune responses is triggering of immunogenic cell death forms such as... 
L929 CELLS | DENDRITIC CELLS | APOPTOTIC CELLS | TOLL-LIKE RECEPTORS | TISSUE-DAMAGE | TUMOR-CELLS | MALIGNANT-MELANOMA | IONIZING-RADIATION | GROUP BOX-1 PROTEIN | RADIATION-THERAPY | CELL BIOLOGY | Apyrase - therapeutic use | Apoptosis - drug effects | Apoptosis - radiation effects | Dacarbazine - therapeutic use | Dendritic Cells - immunology | Melanoma, Experimental - drug therapy | Melanoma, Experimental - radiotherapy | Amino Acid Chloromethyl Ketones - therapeutic use | Chemoradiotherapy | Lymphocyte Activation - immunology | HMGB1 Protein - metabolism | Hyperthermia, Induced | B7-2 Antigen - immunology | Radiation, Ionizing | Mice, Inbred C57BL | Tumor Necrosis Factor-alpha - secretion | Myeloid Differentiation Factor 88 - genetics | Histocompatibility Antigens Class II - biosynthesis | Macrophages, Peritoneal - immunology | Melanoma, Experimental - pathology | Combined Modality Therapy | Homeodomain Proteins - genetics | Mice, Knockout | Animals | Apoptosis - immunology | B7-2 Antigen - biosynthesis | Histocompatibility Antigens Class II - immunology | Caspase Inhibitors - therapeutic use | Interferon-gamma - immunology | Cell Line, Tumor | Mice | CD8-Positive T-Lymphocytes - immunology | Interferon-gamma - biosynthesis | Original
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12. Full Text Caspase inhibitor affords neuroprotection with delayed administration in a rat model of neonatal hypoxic-ischemic brain injury
by Cheng, Yu and Deshmukh, Mohanish and D'Costa, Anselm and Demaro, Joseph A and Gidday, Jeffrey M and Shah, Aarti and Sun, Yuling and Jacquin, Mark F and Johnson Jr, Eugene M and Holtzman, David M
Journal of Clinical Investigation, ISSN 0021-9738, 05/1998, Volume 101, Issue 9, pp. 1992 - 1999
Programmed cell death (apoptosis) is a normal process in the developing nervous system. Recent data suggest that certain features seen in the process of... 
Caspase | Cerebral palsy | Hypoxia | Ischemia | Cell death | MEDICINE, RESEARCH & EXPERIMENTAL | hypoxia | APOPTOSIS | ICE FAMILY PROTEASES | cell death | NUCLEAR-DNA FRAGMENTATION | GERBIL | DAMAGE | caspase | ischemia | NERVE GROWTH-FACTOR | PROGRAMMED CELL-DEATH | HIPPOCAMPUS | NEURONAL DEATH | cerebral palsy | EXPRESSION | Animals, Newborn | DNA Damage - drug effects | Staining and Labeling - methods | Coumarins - metabolism | Cysteine Proteinase Inhibitors - therapeutic use | Hypoxia - drug therapy | Apoptosis - drug effects | Cysteine Proteinase Inhibitors - administration & dosage | Amino Acid Chloromethyl Ketones - therapeutic use | Injections, Intraperitoneal | Injections, Intraventricular | Rats | Oligopeptides - metabolism | Rats, Sprague-Dawley | Amino Acid Chloromethyl Ketones - administration & dosage | Animals | Ligation | Time Factors | Brain Ischemia - drug therapy | Carotid Arteries - surgery
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13. Full Text Radiosensitization of solid tumors by Z-VAD, a pan-caspase inhibitor
by Luigi Moretti and Kwang Woon Kim and Dae Kwang Jung and Christopher D. Willey and Bo Lu
Molecular Cancer Therapeutics, ISSN 1535-7163, 05/2009, Volume 8, Issue 5, pp. 1270 - 1279
Despite recent advances in the management of breast and lung cancer, novel treatment strategies are still needed to further improve patient outcome. The... 
lung cancer | Angiogenesis | breast cancer | autophagy | caspase | MAMMALIAN TARGET | BREAST-CANCER | LUNG-CANCER | APOPTOSIS | IN-VITRO | ANGIOGENESIS | ONCOLOGY | AUTOPHAGIC CELL-DEATH | MICROVESSEL DENSITY | IONIZING-RADIATION | CANCER-THERAPY | Autophagy - radiation effects | Humans | Amino Acid Chloromethyl Ketones - therapeutic use | Necrosis - pathology | Autophagy - drug effects | Neovascularization, Pathologic - pathology | Radiation-Sensitizing Agents - therapeutic use | Amino Acid Chloromethyl Ketones - pharmacology | Amino Acid Chloromethyl Ketones - metabolism | Female | Neoplasms - radiotherapy | Radiation-Sensitizing Agents - pharmacology | Necrosis - metabolism | Combined Modality Therapy | Caspase Inhibitors | Neoplasms - drug therapy | Radiation Tolerance - drug effects | Xenograft Model Antitumor Assays | Animals | Mice, Nude | Radiation-Sensitizing Agents - metabolism | Cell Line, Tumor | Cell Proliferation - drug effects | Mice | Neovascularization, Pathologic - metabolism | Neoplasms - pathology | Cell Proliferation - radiation effects
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14. Full Text A new mouse mutant of the Cdh23 gene with early-onset hearing loss facilitates evaluation of otoprotection drugs
by Han, F and Yu, H and Tian, C and Chen, H.E and Benedict-Alderfer, C and Zheng, Y and Wang, Q and Han, X and Zheng, Q.Y
Pharmacogenomics Journal, ISSN 1470-269X, 02/2012, Volume 12, Issue 1, pp. 30 - 44
We report a novel mutation (erlong, erl) of the cadherin 23 (Cdh23) gene in a mouse model for DFNB12 characterized by progressive hearing loss beginning from... 
mutation | apoptosis | hearing loss | mouse model | Cdh23 | Z-VAD-FMK | SYNDROME TYPE 1D | CADHERIN GENE | INBRED STRAINS | TIP-LINK | NONSYNDROMIC DEAFNESS | HAIR-CELLS | USHER-SYNDROME | GENETICS & HEREDITY | PHARMACOLOGY & PHARMACY | MICE | MUTATIONS | Neuroprotective Agents - therapeutic use | Amino Acid Sequence | Age Factors | Mice, Inbred C57BL | Amino Acid Chloromethyl Ketones - therapeutic use | Hair Cells, Auditory, Outer - drug effects | Molecular Sequence Data | Hearing Loss - pathology | Genetic Complementation Test | Mice, Inbred C3H | Hearing Loss - genetics | Hair Cells, Auditory, Outer - pathology | Point Mutation | Animals | Neuroprotective Agents - pharmacology | Amino Acid Chloromethyl Ketones - pharmacology | Mice | Cadherins - genetics | Drug Evaluation, Preclinical | Disease Models, Animal | Gene mutations | Physiological aspects | Cadherins | Genetic aspects | Research | Health aspects | Risk factors | Hearing loss
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15. Full Text Protective effect of caspase inhibition on compression‐induced muscle damage
by Teng, Bee T and Tam, Eric W and Benzie, Iris F and Siu, Parco M
The Journal of Physiology, ISSN 0022-3751, 07/2011, Volume 589, Issue 13, pp. 3349 - 3369
Non‐technical summary  A pressure ulcer, also known as a pressure sore, bedsore or decubitus ulcer, results from localized ulcerated tissue breakdown caused by... 
RAT SKELETAL-MUSCLE | OXIDATIVE STRESS | IN-VITRO | PHYSIOLOGY | DOXORUBICIN-INDUCED APOPTOSIS | DEEP TISSUE-INJURY | CARDIAC DYSFUNCTION | MEDIATED CLEAVAGE | GASTROCNEMIUS-MUSCLE | AGED RATS | NEUROSCIENCES | CELL-DEATH | Compressive Strength - physiology | Neuroprotective Agents - therapeutic use | Caspases - physiology | Apoptosis - drug effects | Caspases - genetics | Muscular Diseases - enzymology | Amino Acid Chloromethyl Ketones - therapeutic use | Rats | Male | Muscular Diseases - pathology | Random Allocation | Caspase Inhibitors | Rats, Sprague-Dawley | Animals | Neuroprotective Agents - pharmacology | Amino Acid Chloromethyl Ketones - pharmacology | Compressive Strength - drug effects | Muscular Diseases - prevention & control | Apoptosis - physiology | Bedsores | Messenger RNA | Implants, Artificial | Prosthesis | Proteases | Heat shock proteins | Orthopedic equipment and supplies | Tumor proteins | Animal control | Prostheses | Pressure ulcers | Autophagy | Rodents | Apoptosis | Skeletal Muscle and Exercise
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