Chronic inflammatory diseases are common and seriously affect people’s life, like COPD, Asthma, inflammatory bowel diseases, especially atherosclerosis related diseases (heart attack, stroke and peripheral blood vessel diseases). Many chronic inflammatory diseases are resistant to current anti-inflammatory drugs, like COPD and atherosclerosis related diseases, therefore there is an urgent need to develop new, disease modifying anti-inflammatory drugs. Moxa (Artemisia Argyi) is a plant. Moxa tar (or moxa smoke) is the burning product of its leaves. From clinical experiments, the author finds that Moxa tar has potent and unique anti-inflammatory effect. Its anti-inflammatory property is different from that of any current anti-inflammatory drugs. It not only can suppress chronic inflammation but also can terminate self-perpetuating chronic inflammation which is the underlying mechanism of many incurable inflammatory diseases (like COPD). The author thinks that moxa tar is an important source for developing new anti-inflammatory drug and would like to introduce its anti-inflammatory effect to researchers through his clinical experiments in this article. The methods used in this study are crossover design, i.e., patients serve as their own control, comparing the clinical symptoms and signs before and after moxa tar treatment. Introduction Chronic inflammatory diseases are common and seriously affect people’s life, like COPD, Asthma, atherosclerosis related diseases (heart attack, stroke and peripheral blood vessel diseases), inflammatory bowel diseases, chronic muscle and soft tissue injury and so on. Many chronic inflammatory diseases are resistant to current antiinflammatory drugs, like COPD and atherosclerosis related diseases and therefore there is an urgent need to develop new anti-inflammatory drugs. The current strategy of developing new anti-inflammatory drugs is to target and block certain step or steps in the inflammatory passway via competitive inhibition. Some new anti-inflammatory drugs have been developed, like phosphodiesterase-4 inhibitors, NF-KB inhibitors, adhesion molecule inhibitors, tumour necrosis factor-alpha inhibitors, leukotriene B4 inhibitors, interleukin I receptor inhibitors and so on. Some of these new drugs can suppress chronic inflammation and alleviate clinical symptoms to some extent, but hardly have any curative effect for chronic inflammation. From clinical practising, the author finds that moxa tar (or moxa smoke), a product of burning moxa leaves (Artemisia Argyi leaves), has potent and unique anti-inflammatory effect and it can treat many intractable chronic inflammatory diseases, like COPD, chronic muscle and soft tissue injury, chronic gastritis, angina pectoris, chronic laryngitis, thromboangiitis obliteran (Buerger’s disease) and pulmonary fibrosis. Its anti-inflammatory property is different from that of corticosteroid and other known anti-inflammatory drugs. It not only can treat some corticosteroid resista
{"title":"Moxa Tar, an important source for developing new anti-inflammatory drug","authors":"Q. Zeng","doi":"10.15761/IMM.1000285","DOIUrl":"https://doi.org/10.15761/IMM.1000285","url":null,"abstract":"Chronic inflammatory diseases are common and seriously affect people’s life, like COPD, Asthma, inflammatory bowel diseases, especially atherosclerosis related diseases (heart attack, stroke and peripheral blood vessel diseases). Many chronic inflammatory diseases are resistant to current anti-inflammatory drugs, like COPD and atherosclerosis related diseases, therefore there is an urgent need to develop new, disease modifying anti-inflammatory drugs. Moxa (Artemisia Argyi) is a plant. Moxa tar (or moxa smoke) is the burning product of its leaves. From clinical experiments, the author finds that Moxa tar has potent and unique anti-inflammatory effect. Its anti-inflammatory property is different from that of any current anti-inflammatory drugs. It not only can suppress chronic inflammation but also can terminate self-perpetuating chronic inflammation which is the underlying mechanism of many incurable inflammatory diseases (like COPD). The author thinks that moxa tar is an important source for developing new anti-inflammatory drug and would like to introduce its anti-inflammatory effect to researchers through his clinical experiments in this article. The methods used in this study are crossover design, i.e., patients serve as their own control, comparing the clinical symptoms and signs before and after moxa tar treatment. Introduction Chronic inflammatory diseases are common and seriously affect people’s life, like COPD, Asthma, atherosclerosis related diseases (heart attack, stroke and peripheral blood vessel diseases), inflammatory bowel diseases, chronic muscle and soft tissue injury and so on. Many chronic inflammatory diseases are resistant to current antiinflammatory drugs, like COPD and atherosclerosis related diseases and therefore there is an urgent need to develop new anti-inflammatory drugs. The current strategy of developing new anti-inflammatory drugs is to target and block certain step or steps in the inflammatory passway via competitive inhibition. Some new anti-inflammatory drugs have been developed, like phosphodiesterase-4 inhibitors, NF-KB inhibitors, adhesion molecule inhibitors, tumour necrosis factor-alpha inhibitors, leukotriene B4 inhibitors, interleukin I receptor inhibitors and so on. Some of these new drugs can suppress chronic inflammation and alleviate clinical symptoms to some extent, but hardly have any curative effect for chronic inflammation. From clinical practising, the author finds that moxa tar (or moxa smoke), a product of burning moxa leaves (Artemisia Argyi leaves), has potent and unique anti-inflammatory effect and it can treat many intractable chronic inflammatory diseases, like COPD, chronic muscle and soft tissue injury, chronic gastritis, angina pectoris, chronic laryngitis, thromboangiitis obliteran (Buerger’s disease) and pulmonary fibrosis. Its anti-inflammatory property is different from that of corticosteroid and other known anti-inflammatory drugs. It not only can treat some corticosteroid resista","PeriodicalId":94322,"journal":{"name":"Integrative molecular medicine","volume":"200 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2017-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"74890274","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":"“Brain steatosis” in an obese mouse model during cycles of Famine and Feast the underestimated role of fat (WAT) in brain volume formation","authors":"V. V. Ginneken, E. D. Vries, E. Verheij, J. Greef","doi":"10.15761/IMM.1000283","DOIUrl":"https://doi.org/10.15761/IMM.1000283","url":null,"abstract":"","PeriodicalId":94322,"journal":{"name":"Integrative molecular medicine","volume":"54 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2017-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"85738866","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}
Hiroaki Tanaka, S. Ueno, Ryo Aoyagi, Y. Hatamoto, M. Jaćkowska, Keisuke Shiose, Y. Higaki
Introduction: Understanding the relationship between PGC-1α expression and exercise is important for developing therapeutic exercise programs focusing on the prevention of lifestyle diseases. The current study examined whether easily performed modearte intensity interval exercise can induce PGC-1α gene expression. Methods: Nine subjects performed cycling in one of three protocols: maximal intensity [MIE: 20 ×1 min with 4 min recovery], high intensity [HIE] and a moderate intensity at anaerobic threshold interval exercise [AIE]. Both HIE and AIE were adjusted to obtain the same exercise volume as MIT performed for 5min including recovery time and repeated 20 times. Results: Increase in PGC-1α mRNA expression was observed in all conditions. with a significant increase in plasma epinephrine. ACC phosphorylation also increased in all condition. Conclusion: These findings suggest that easily performed interval exercise at anaerobic threshold induces PGC1α expression which induce aerobic training adaptation.
{"title":"Easily performed interval exercise induces to increase in skeletal muscle PGC-1α gene expression","authors":"Hiroaki Tanaka, S. Ueno, Ryo Aoyagi, Y. Hatamoto, M. Jaćkowska, Keisuke Shiose, Y. Higaki","doi":"10.15761/imm.1000293","DOIUrl":"https://doi.org/10.15761/imm.1000293","url":null,"abstract":"Introduction: Understanding the relationship between PGC-1α expression and exercise is important for developing therapeutic exercise programs focusing on the prevention of lifestyle diseases. The current study examined whether easily performed modearte intensity interval exercise can induce PGC-1α gene expression. Methods: Nine subjects performed cycling in one of three protocols: maximal intensity [MIE: 20 ×1 min with 4 min recovery], high intensity [HIE] and a moderate intensity at anaerobic threshold interval exercise [AIE]. Both HIE and AIE were adjusted to obtain the same exercise volume as MIT performed for 5min including recovery time and repeated 20 times. Results: Increase in PGC-1α mRNA expression was observed in all conditions. with a significant increase in plasma epinephrine. ACC phosphorylation also increased in all condition. Conclusion: These findings suggest that easily performed interval exercise at anaerobic threshold induces PGC1α expression which induce aerobic training adaptation.","PeriodicalId":94322,"journal":{"name":"Integrative molecular medicine","volume":"13 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2017-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"78836595","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":"Conformation, structure, and thermodynamics integrative mechanism related to receptor regulation","authors":"Qinyi Zhao","doi":"10.15761/IMM.1000303","DOIUrl":"https://doi.org/10.15761/IMM.1000303","url":null,"abstract":"","PeriodicalId":94322,"journal":{"name":"Integrative molecular medicine","volume":"102 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2017-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"76104885","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}
STAT3 is an essential cellular transcription factor that activates a cascade of survival and proliferation signaling program in cells upon cytokine and growth factor stimulus. STAT3 forms a converging point for many upstream activated signaling pathways required for maintaining normal and oncogenic condition. As an active transcription factor, it controls transcription of downstream genes involved in various steps of cancer progression like cell proliferation, migration, immune evasion and angiogenesis. It is known to be constitutively active in many cancers with approximately 40% of breast cancer cases positive for activated STAT3. Apart from the wellstudied pY705 activation (canonical pathway), STAT3 is reported to undergo alternative post-translational modifications like pS727 and K685Ac (non-canonical pathway) that are now appearing to be responsible for triggering activated STAT3 in many cancers including breast cancer. Hence, correct designation and targeting ability of these post-translational modifications (PTM) of STAT3 signaling in any particular cancer may hold the key in treating patients with STAT3 overexpression.
{"title":"Approaching non-canonical STAT3 signaling to redefine cancer therapeutic strategy","authors":"S. Dimri, Sukanya, A. De","doi":"10.15761/IMM.1000268","DOIUrl":"https://doi.org/10.15761/IMM.1000268","url":null,"abstract":"STAT3 is an essential cellular transcription factor that activates a cascade of survival and proliferation signaling program in cells upon cytokine and growth factor stimulus. STAT3 forms a converging point for many upstream activated signaling pathways required for maintaining normal and oncogenic condition. As an active transcription factor, it controls transcription of downstream genes involved in various steps of cancer progression like cell proliferation, migration, immune evasion and angiogenesis. It is known to be constitutively active in many cancers with approximately 40% of breast cancer cases positive for activated STAT3. Apart from the wellstudied pY705 activation (canonical pathway), STAT3 is reported to undergo alternative post-translational modifications like pS727 and K685Ac (non-canonical pathway) that are now appearing to be responsible for triggering activated STAT3 in many cancers including breast cancer. Hence, correct designation and targeting ability of these post-translational modifications (PTM) of STAT3 signaling in any particular cancer may hold the key in treating patients with STAT3 overexpression.","PeriodicalId":94322,"journal":{"name":"Integrative molecular medicine","volume":"49 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2017-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"87278200","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}
Background: Luteolin is a flavonoid found in various edible plants that exhibits diverse health benefits, including anti-inflammatory and anti-gout effects. However, there has been little clinical investigation of luteolin from the viewpoint of gout prevention. We conducted a clinical trial of supplementation with chrysanthemum flower extract rich in luteolin (LCE) to assess the effect on serum uric acid levels in Japanese men. Methods: We examined the effect of LCE containing 10% luteolin in two double-blind placebo-controlled studies. In the single-dose study, fasting subjects took a capsule containing 100 mg of LCE (10 mg of luteolin) or placebo before ingestion of a high purine base test meal and the serum uric acid level was determined over time. For the repeated-administration study, the subjects ingested placebo or LCE capsule for 4 weeks. Fasting serum uric acid was evaluated before and after ingestion. Results: Oral intake of LCE had no significant influence on serum uric acid. After 4 weeks of LCE ingestion, serum uric acid tended to decrease in the LCE group. A significant decrease of serum uric acid was observed after LCE ingestion in the subjects with a baseline uric acid level of 5.5 to 7.0 mg/dL. There were no abnormalities suggesting adverse effects during or after ingestion of LCE. Conclusion: Ingestion of LCE for 4 weeks reduced the serum uric acid level. Luteolin may be able to prevent gout by controlling uric acid. Abbreviations: XOD: xanthine oxidase; LCE: luteolin-rich chrysanthemum flower extract; CRP: C-reactive protein; AUC: area under the concentration vs. time curve; CFO: chrysanthemum flower oil
{"title":"Luteolin-rich chrysanthemum flower extract suppresses baseline serum uric acid in Japanese subjects with mild hyperuricemia","authors":"M. Hirano, Shogo Takeda, S. Hitoe, H. Shimoda","doi":"10.15761/IMM.1000275","DOIUrl":"https://doi.org/10.15761/IMM.1000275","url":null,"abstract":"Background: Luteolin is a flavonoid found in various edible plants that exhibits diverse health benefits, including anti-inflammatory and anti-gout effects. However, there has been little clinical investigation of luteolin from the viewpoint of gout prevention. We conducted a clinical trial of supplementation with chrysanthemum flower extract rich in luteolin (LCE) to assess the effect on serum uric acid levels in Japanese men. Methods: We examined the effect of LCE containing 10% luteolin in two double-blind placebo-controlled studies. In the single-dose study, fasting subjects took a capsule containing 100 mg of LCE (10 mg of luteolin) or placebo before ingestion of a high purine base test meal and the serum uric acid level was determined over time. For the repeated-administration study, the subjects ingested placebo or LCE capsule for 4 weeks. Fasting serum uric acid was evaluated before and after ingestion. Results: Oral intake of LCE had no significant influence on serum uric acid. After 4 weeks of LCE ingestion, serum uric acid tended to decrease in the LCE group. A significant decrease of serum uric acid was observed after LCE ingestion in the subjects with a baseline uric acid level of 5.5 to 7.0 mg/dL. There were no abnormalities suggesting adverse effects during or after ingestion of LCE. Conclusion: Ingestion of LCE for 4 weeks reduced the serum uric acid level. Luteolin may be able to prevent gout by controlling uric acid. Abbreviations: XOD: xanthine oxidase; LCE: luteolin-rich chrysanthemum flower extract; CRP: C-reactive protein; AUC: area under the concentration vs. time curve; CFO: chrysanthemum flower oil","PeriodicalId":94322,"journal":{"name":"Integrative molecular medicine","volume":"28 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2017-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"86680125","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}
Pancreatic ductal adenocarcinoma (PDAC) arises from epithelia of pancreas. Despite its low incidence, it is the most lethal cancer type. Although the poor outcome is largely secondary to the high proportion of patients who are diagnosed with advanced disease, the prognosis of PDAC is also influenced by the inherent biological aggressiveness and the high metastatic potential of this malignancy. Treatment options remain limited with little progress over the last decades. Some improvements in surgical outcome occur in patients who also receive chemotherapy and/or radiotherapy, however, the impact on long-term survival has been minimal owing to the intense resistance of PDAC to all extent treatments regimen. Hence, there is an urgent need to 1) gain better understanding of the biology of PDAC; 2) to develop early detection and prevention programs; 3) to identify new therapeutic strategies to improve quality of life and survivorship. In this review, first, we will summarise the state of knowledge of PDAC pathogenesis with a particular the focus on the molecular characteristics causing therapeutic resistance. Then, we will briefly review current and emerging approaches in the PDAC care. Lastly, we will highlight the integrative approaches in the light of new experimental and clinical research conducted with the aim of moving towards personalised therapy in patients with PDAC.
{"title":"Scientific rationale for integrative and personalised strategies for pancreatic ductal adenocarcinoma management","authors":"Peyda Korhan, R. Verkerk, W. Critchley","doi":"10.15761/IMM.1000310","DOIUrl":"https://doi.org/10.15761/IMM.1000310","url":null,"abstract":"Pancreatic ductal adenocarcinoma (PDAC) arises from epithelia of pancreas. Despite its low incidence, it is the most lethal cancer type. Although the poor outcome is largely secondary to the high proportion of patients who are diagnosed with advanced disease, the prognosis of PDAC is also influenced by the inherent biological aggressiveness and the high metastatic potential of this malignancy. Treatment options remain limited with little progress over the last decades. Some improvements in surgical outcome occur in patients who also receive chemotherapy and/or radiotherapy, however, the impact on long-term survival has been minimal owing to the intense resistance of PDAC to all extent treatments regimen. Hence, there is an urgent need to 1) gain better understanding of the biology of PDAC; 2) to develop early detection and prevention programs; 3) to identify new therapeutic strategies to improve quality of life and survivorship. In this review, first, we will summarise the state of knowledge of PDAC pathogenesis with a particular the focus on the molecular characteristics causing therapeutic resistance. Then, we will briefly review current and emerging approaches in the PDAC care. Lastly, we will highlight the integrative approaches in the light of new experimental and clinical research conducted with the aim of moving towards personalised therapy in patients with PDAC.","PeriodicalId":94322,"journal":{"name":"Integrative molecular medicine","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2017-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"90744805","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}
Kazutoshi Nakano, T. Nakayama, Y. Shirato, N. Nakayama, E. Tachikawa, Kaori Sasaki, Mikako Tarashima, Kayoko Saito, M. Ōsawa
It is widely believed that evolutionarily advanced cells require nuclei rich in DNA to proliferate, while mitochondria isolated from nuclei cannot proliferate. We have developed a novel stable cell line, designated “mitochondrial cells (MitoCells)”, maintaining active mitochondria, the majority of which lacked nuclei. MitoCells can be continuously generated in culture. Herein, we report proliferation studies of MitoCells. We found that the nuclear DNA-less (nDNA-less) MitoCells, which were sorted with flow cytometry and were filtrated with 1.2 μmeter and 3 μmeter isopore membrane filters, could exist and proliferate. We also confirmed that the sorted nDNA-less MitoCells had mitochondrial DNA(mtDNA) with T9176C mutation analysis and that the unsorted MitoCells had SURF-1 gene of nDNA. These results suggest that MitoCells could have prokaryotic nature with both mtDNA and nDNA. Introduction The eukaryotes, by definition and in contrast to prokaryotes, have a nucleus, which contains most of the cell’s DNA, enclosed by double layered membranes [1]. The prokaryotes have no nucleus and have few or no organelles. Eukaryotes must have a nucleus and mitochondria in order to exist and proliferate with some exceptions [2-4]. Mitochondria which are isolated from nuclei are believed to be unable to exist or proliferate [5,6]. It is hypothesized that most of the ancestral mitochondrial genome was transferred to the nucleus as the symbiotic relationship between eukaryotes and ancestral mitochondria developed [7-9]. The respiratory chain /oxidative phosphorylation system (OPHOS) has five complexes, the polypeptides of which are encoded by mitochondrial DNA (mtDNA) and/or nuclear DNA (nDNA): only 13 polypeptides are encoded by mtDNA: complex I has 7 polypeptides encoded by mtDNA, complex II none, complex III one, complex IV three and complex V two. All other polypeptides of mitochondria are encoded by nDNA. We reported a series of novel stable cell lines, designated “mitochondrial cells (MitoCells)”, derived from cybrids obtained by fusing mitochondria-less HeLa cells with platelets [10,11]. All MitoCells have active mitochondria. The majority of these MitoCells lack nuclei but have a small amount of DNA, while the minority (less than 3 percent) have the same amount of DNA as cells with nuclei (nDNA-rich). We have recently reported that the MitoCells can survive under anaerobic condition and they could produce energy employing an anaerobic metabolic pathway, maintaining the electron transport enzyme activities, but losing the activity of tricarboxylic acid (TCA) cycle by means of mitochondrial enzyme assay and Western blot analyses [12]. This report suggests that energy production of MitoCells is far from the original cybrid cells which are eukaryote, although the MitoCells have enough polypeptides encoded by mtDNA and nDNA for maintaining their lives. Although most MitoCells have no nuclei, they can be continuously generated in culture. Therefore, it is important
{"title":"Proliferation without nuclei suggests mitochondrial cells (MitoCells) to be prokaryotic nature","authors":"Kazutoshi Nakano, T. Nakayama, Y. Shirato, N. Nakayama, E. Tachikawa, Kaori Sasaki, Mikako Tarashima, Kayoko Saito, M. Ōsawa","doi":"10.15761/IMM.1000267","DOIUrl":"https://doi.org/10.15761/IMM.1000267","url":null,"abstract":"It is widely believed that evolutionarily advanced cells require nuclei rich in DNA to proliferate, while mitochondria isolated from nuclei cannot proliferate. We have developed a novel stable cell line, designated “mitochondrial cells (MitoCells)”, maintaining active mitochondria, the majority of which lacked nuclei. MitoCells can be continuously generated in culture. Herein, we report proliferation studies of MitoCells. We found that the nuclear DNA-less (nDNA-less) MitoCells, which were sorted with flow cytometry and were filtrated with 1.2 μmeter and 3 μmeter isopore membrane filters, could exist and proliferate. We also confirmed that the sorted nDNA-less MitoCells had mitochondrial DNA(mtDNA) with T9176C mutation analysis and that the unsorted MitoCells had SURF-1 gene of nDNA. These results suggest that MitoCells could have prokaryotic nature with both mtDNA and nDNA. Introduction The eukaryotes, by definition and in contrast to prokaryotes, have a nucleus, which contains most of the cell’s DNA, enclosed by double layered membranes [1]. The prokaryotes have no nucleus and have few or no organelles. Eukaryotes must have a nucleus and mitochondria in order to exist and proliferate with some exceptions [2-4]. Mitochondria which are isolated from nuclei are believed to be unable to exist or proliferate [5,6]. It is hypothesized that most of the ancestral mitochondrial genome was transferred to the nucleus as the symbiotic relationship between eukaryotes and ancestral mitochondria developed [7-9]. The respiratory chain /oxidative phosphorylation system (OPHOS) has five complexes, the polypeptides of which are encoded by mitochondrial DNA (mtDNA) and/or nuclear DNA (nDNA): only 13 polypeptides are encoded by mtDNA: complex I has 7 polypeptides encoded by mtDNA, complex II none, complex III one, complex IV three and complex V two. All other polypeptides of mitochondria are encoded by nDNA. We reported a series of novel stable cell lines, designated “mitochondrial cells (MitoCells)”, derived from cybrids obtained by fusing mitochondria-less HeLa cells with platelets [10,11]. All MitoCells have active mitochondria. The majority of these MitoCells lack nuclei but have a small amount of DNA, while the minority (less than 3 percent) have the same amount of DNA as cells with nuclei (nDNA-rich). We have recently reported that the MitoCells can survive under anaerobic condition and they could produce energy employing an anaerobic metabolic pathway, maintaining the electron transport enzyme activities, but losing the activity of tricarboxylic acid (TCA) cycle by means of mitochondrial enzyme assay and Western blot analyses [12]. This report suggests that energy production of MitoCells is far from the original cybrid cells which are eukaryote, although the MitoCells have enough polypeptides encoded by mtDNA and nDNA for maintaining their lives. Although most MitoCells have no nuclei, they can be continuously generated in culture. Therefore, it is important","PeriodicalId":94322,"journal":{"name":"Integrative molecular medicine","volume":"19 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2017-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"78259886","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}
Y. Nakagawa-Yagi, H. Hara, H. Nakanishi, T. Tasaka, A. Hara
Medical treatment using high-voltage electric potential (HELP) devices to generate an electric field (EF) is an alternative therapy commonly used in Japan. However, the underlying mechanisms of the potential health benefits are not fully understood. To address this issue, we investigated the levels of lyso-form phospholipids using selected reaction monitoring (SRM) analysis in plasma samples obtained from healthy human subjects before and after a single HELP exposure (9 kV/electrode + 9 kV/electrode, 30 min). Lysophosphatidylcholine (lysoPC)-22:4 was significantly upregulated after HELP exposure. However, there was no effect on the levels of lysophosphatidic acid (lysoPA), or other lysoPC species. LysoPC is known to accelerate intestinal movement as a putative endogenous activator of transient receptor potential vanilloid 2 (TRPV2). We further examined the in silico docking simulation of lysoPC-22:4 with TRPV2. Docking results showed that lysoPC-22:4 has good binding energy (-8.2 kcal/mol). Our findings provide new insight into the molecular mechanisms of constipation alleviation by EF therapy.
{"title":"Acute exposure to an electric field induces changes in human plasma lysophosphatidylcholine (lysoPC)-22:4 levels: Molecular insight into the docking of lysoPC-22:4 interaction with TRPV2","authors":"Y. Nakagawa-Yagi, H. Hara, H. Nakanishi, T. Tasaka, A. Hara","doi":"10.15761/IMM.1000274","DOIUrl":"https://doi.org/10.15761/IMM.1000274","url":null,"abstract":"Medical treatment using high-voltage electric potential (HELP) devices to generate an electric field (EF) is an alternative therapy commonly used in Japan. However, the underlying mechanisms of the potential health benefits are not fully understood. To address this issue, we investigated the levels of lyso-form phospholipids using selected reaction monitoring (SRM) analysis in plasma samples obtained from healthy human subjects before and after a single HELP exposure (9 kV/electrode + 9 kV/electrode, 30 min). Lysophosphatidylcholine (lysoPC)-22:4 was significantly upregulated after HELP exposure. However, there was no effect on the levels of lysophosphatidic acid (lysoPA), or other lysoPC species. LysoPC is known to accelerate intestinal movement as a putative endogenous activator of transient receptor potential vanilloid 2 (TRPV2). We further examined the in silico docking simulation of lysoPC-22:4 with TRPV2. Docking results showed that lysoPC-22:4 has good binding energy (-8.2 kcal/mol). Our findings provide new insight into the molecular mechanisms of constipation alleviation by EF therapy.","PeriodicalId":94322,"journal":{"name":"Integrative molecular medicine","volume":"65 1","pages":"1"},"PeriodicalIF":0.0,"publicationDate":"2017-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"84516188","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":"A new dissection procedure for learning of echocardiography","authors":"H. Suenaga","doi":"10.15761/imm.1000297","DOIUrl":"https://doi.org/10.15761/imm.1000297","url":null,"abstract":"","PeriodicalId":94322,"journal":{"name":"Integrative molecular medicine","volume":"6 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2017-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"87518407","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}
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