{"title":"Complexity and Diversity of Polycomb Group Proteins: How Do They Work?","authors":"Yi‐Chung Chien","doi":"10.4247/AM.2018.ABI204","DOIUrl":"https://doi.org/10.4247/AM.2018.ABI204","url":null,"abstract":"","PeriodicalId":93243,"journal":{"name":"Adaptive medicine","volume":"115 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2018-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"80303764","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Tumor Biomarkers in Nipple Discharge of Breast Cancer: Current Status and Future Perspectives","authors":"Yawen Wang","doi":"10.4247/AM.2018.ABI206","DOIUrl":"https://doi.org/10.4247/AM.2018.ABI206","url":null,"abstract":"","PeriodicalId":93243,"journal":{"name":"Adaptive medicine","volume":"23 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2018-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"85693920","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Changes of Serum NO, IL-6 and TNF-α in the Qinghai-Tibet Plateau with High Altitude Alcoholic Liver Disease and Their Clinical Significances","authors":"Zhao Wu","doi":"10.4247/AM.2018.ABI200","DOIUrl":"https://doi.org/10.4247/AM.2018.ABI200","url":null,"abstract":"","PeriodicalId":93243,"journal":{"name":"Adaptive medicine","volume":"5 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2018-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"79162590","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2017-01-01Epub Date: 2017-03-31DOI: 10.4247/am.2017.abg170
Juliann G Kiang
Mild hypoxia induced by 20% hemorrhage results in increases in few cytokine concentrations and sclerostin levels in blood, but shows no changes in bone formation, bone marrow cellularity, and gastrointestinal (GI) integrity and no systemic bacterial infection as well as no subsequent mortality. On the other hand, severe hypoxia induced by 40% hemorrhage causes significant increases in most cytokine concentrations, GI injury, lung injury, systemic bacterial infection, cellular ATP reduction and subsequent mortality. The severe hypoxia drastically damages GI and lung morphology, elevates cytokine concentrations in blood and increases inducible nitric oxide synthase (iNOS) expression in cells that is mediated by transcription factors NF-κB/NF-IL6, subsequently producing free radicals that disrupt mitochondria. ATP depletion, p53 phosphorylation, and caspase-3 activation are found, suggesting cell apoptosis. As a result, mortality occurs. However, when mild hypoxia follows ionizing radiation, the mild hypoxia significantly enhances radiation-induced mortality and acute radiation syndrome, including injury of bone marrow, GI, kidney, and lung. The synergism also occurs at the molecular level, resulting in alteration of microRNAs, amplification of iNOS expression, cytokine increases, sepsis, and ATP depletion. This is the first demonstration of synergistic effects between mild hypoxia and ionizing radiation.
{"title":"Exacerbation of Mild Hypoxia on Acute Radiation Syndrome and Subsequent Mortality.","authors":"Juliann G Kiang","doi":"10.4247/am.2017.abg170","DOIUrl":"10.4247/am.2017.abg170","url":null,"abstract":"<p><p>Mild hypoxia induced by 20% hemorrhage results in increases in few cytokine concentrations and sclerostin levels in blood, but shows no changes in bone formation, bone marrow cellularity, and gastrointestinal (GI) integrity and no systemic bacterial infection as well as no subsequent mortality. On the other hand, severe hypoxia induced by 40% hemorrhage causes significant increases in most cytokine concentrations, GI injury, lung injury, systemic bacterial infection, cellular ATP reduction and subsequent mortality. The severe hypoxia drastically damages GI and lung morphology, elevates cytokine concentrations in blood and increases inducible nitric oxide synthase (iNOS) expression in cells that is mediated by transcription factors NF-κB/NF-IL6, subsequently producing free radicals that disrupt mitochondria. ATP depletion, p53 phosphorylation, and caspase-3 activation are found, suggesting cell apoptosis. As a result, mortality occurs. However, when mild hypoxia follows ionizing radiation, the mild hypoxia significantly enhances radiation-induced mortality and acute radiation syndrome, including injury of bone marrow, GI, kidney, and lung. The synergism also occurs at the molecular level, resulting in alteration of microRNAs, amplification of iNOS expression, cytokine increases, sepsis, and ATP depletion. This is the first demonstration of synergistic effects between mild hypoxia and ionizing radiation.</p>","PeriodicalId":93243,"journal":{"name":"Adaptive medicine","volume":"9 1","pages":"28-33"},"PeriodicalIF":0.0,"publicationDate":"2017-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8491646/pdf/nihms-1737221.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39492016","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Juliann G Kiang, Bradley R Garrison, Nikolai V Gorbunov
Radiation combined injury is defined as an ionizing radiation exposure received in combination with other trauma or physiological insults. The range of radiation threats we face today includes everything from individual radiation exposures to mass casualties resulting from a terrorist nuclear incident, and many of these exposure scenarios include the likelihood of additional traumatic injury. Radiation combined injury sensitizes target organs and cells and exacerbates acute radiation syndrome. Organs and cells with high sensitivity to combined injury are the skin, the hematopoietic system, the gastrointestinal tract, spermatogenic cells, and the vascular system. Among its many effects, radiation combined injury results in decreases in lymphocytes, macrophages, neutrophils, platelets, stem cells, and tissue integrity; activation of the iNOS/NF-κB/NF-IL6 and p53/Bax pathways; and increases in DNA single and double strand breaks, TLR signaling, cytokine concentrations, bacterial infection, and cytochrome c release from mitochondria to cytoplasm. These alterations lead to apoptosis and autophagy and, as a result, increased mortality. There is a pressing need to understand more about the body's response to combined injury in order to be able to develop effective countermeasures, since few currently exist. In this review, we summarize what is known about how combined injury modifies the radiation response, with a special emphasis on DNA damage/repair, signal transduction pathways, apoptosis, and autophagy. We also describe current and prospective countermeasures relevant to the treatment and prevention of combined injury.
{"title":"Radiation Combined Injury: DNA Damage, Apoptosis, and Autophagy.","authors":"Juliann G Kiang, Bradley R Garrison, Nikolai V Gorbunov","doi":"10.4247/AM.2010.ABA004","DOIUrl":"https://doi.org/10.4247/AM.2010.ABA004","url":null,"abstract":"<p><p>Radiation combined injury is defined as an ionizing radiation exposure received in combination with other trauma or physiological insults. The range of radiation threats we face today includes everything from individual radiation exposures to mass casualties resulting from a terrorist nuclear incident, and many of these exposure scenarios include the likelihood of additional traumatic injury. Radiation combined injury sensitizes target organs and cells and exacerbates acute radiation syndrome. Organs and cells with high sensitivity to combined injury are the skin, the hematopoietic system, the gastrointestinal tract, spermatogenic cells, and the vascular system. Among its many effects, radiation combined injury results in decreases in lymphocytes, macrophages, neutrophils, platelets, stem cells, and tissue integrity; activation of the iNOS/NF-κB/NF-IL6 and p53/Bax pathways; and increases in DNA single and double strand breaks, TLR signaling, cytokine concentrations, bacterial infection, and cytochrome c release from mitochondria to cytoplasm. These alterations lead to apoptosis and autophagy and, as a result, increased mortality. There is a pressing need to understand more about the body's response to combined injury in order to be able to develop effective countermeasures, since few currently exist. In this review, we summarize what is known about how combined injury modifies the radiation response, with a special emphasis on DNA damage/repair, signal transduction pathways, apoptosis, and autophagy. We also describe current and prospective countermeasures relevant to the treatment and prevention of combined injury.</p>","PeriodicalId":93243,"journal":{"name":"Adaptive medicine","volume":"2 1","pages":"1-10"},"PeriodicalIF":0.0,"publicationDate":"2010-04-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8491956/pdf/nihms-1739722.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39492015","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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