{"title":"[microRNA].","authors":"S. Kojima, N. Seki","doi":"10.32388/1jlwz7","DOIUrl":"https://doi.org/10.32388/1jlwz7","url":null,"abstract":"","PeriodicalId":19307,"journal":{"name":"Nihon rinsho. Japanese journal of clinical medicine","volume":"318 1","pages":"201-4"},"PeriodicalIF":0.0,"publicationDate":"2020-02-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"86769278","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}
This chapter outlines the current clinical application of interferon for treatment of brain tumor, especially glioma. Since approved as a therapeutic drug for brain tumor originally produced in Japan, interferon-beta has been reported to be effective when it was used alone, in combination with chemo-radiotherapy (ACNU/MCNU as a nitrosourea derivative chemodrug, and radiation for 60 Gy totally). Recently, the regimen of combination with interferon-beta have been improved to obtain a higher efficacy rate. For example, as a fundamental study, temozolomide is an enthusiastic chemodrug to enhance the anti-tumor effect of interferon-beta when it is combined, pre-clinical and clinical trial will be scheduled. As for interferon-beta gene therapy by means of liposome as ad drug delivery system, already clinical trial has been performed and clinical safety and effectiveness have been proved, and it is expected that newly development in the field of gene therapy will be established and improvement of therapeutic results for malignant brain tumor will be achieved.
{"title":"[Glioma].","authors":"H. Handa, J. Takeuchi","doi":"10.32388/myufx5","DOIUrl":"https://doi.org/10.32388/myufx5","url":null,"abstract":"This chapter outlines the current clinical application of interferon for treatment of brain tumor, especially glioma. Since approved as a therapeutic drug for brain tumor originally produced in Japan, interferon-beta has been reported to be effective when it was used alone, in combination with chemo-radiotherapy (ACNU/MCNU as a nitrosourea derivative chemodrug, and radiation for 60 Gy totally). Recently, the regimen of combination with interferon-beta have been improved to obtain a higher efficacy rate. For example, as a fundamental study, temozolomide is an enthusiastic chemodrug to enhance the anti-tumor effect of interferon-beta when it is combined, pre-clinical and clinical trial will be scheduled. As for interferon-beta gene therapy by means of liposome as ad drug delivery system, already clinical trial has been performed and clinical safety and effectiveness have been proved, and it is expected that newly development in the field of gene therapy will be established and improvement of therapeutic results for malignant brain tumor will be achieved.","PeriodicalId":19307,"journal":{"name":"Nihon rinsho. Japanese journal of clinical medicine","volume":"12 1","pages":"1011-45"},"PeriodicalIF":0.0,"publicationDate":"2020-02-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"87771144","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}
Polyarteritis nodosa (PAN) is the systemic necrotizing vasculitis on small and median muscular vessels. Recent studies reveal that PAN consists of classical PAN and microscopic polyangitis (MPA). MPO-ANCA, which is one of anti-neutrophil cytoplasmic antibody (ANCA), is involved in the pathogenesis of MPA. In future, by the progress of research of ANCA, the definition or criteria of systemic vasculitis including PAN or MPA will be changed.
{"title":"[Polyarteritis nodosa].","authors":"M. Murakami, S. Ozaki, K. Nakao","doi":"10.32388/6b7u4h","DOIUrl":"https://doi.org/10.32388/6b7u4h","url":null,"abstract":"Polyarteritis nodosa (PAN) is the systemic necrotizing vasculitis on small and median muscular vessels. Recent studies reveal that PAN consists of classical PAN and microscopic polyangitis (MPA). MPO-ANCA, which is one of anti-neutrophil cytoplasmic antibody (ANCA), is involved in the pathogenesis of MPA. In future, by the progress of research of ANCA, the definition or criteria of systemic vasculitis including PAN or MPA will be changed.","PeriodicalId":19307,"journal":{"name":"Nihon rinsho. Japanese journal of clinical medicine","volume":"24 1","pages":"349-54"},"PeriodicalIF":0.0,"publicationDate":"2020-02-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"88505636","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":"[Inulin].","authors":"Y. Iino","doi":"10.32388/uozobu","DOIUrl":"https://doi.org/10.32388/uozobu","url":null,"abstract":"","PeriodicalId":19307,"journal":{"name":"Nihon rinsho. Japanese journal of clinical medicine","volume":"22 1","pages":"1071-3"},"PeriodicalIF":0.0,"publicationDate":"2020-02-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"73891798","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}
Interpretive Information • Congenital adrenal hyperplasia • Adrenal virilizing tumor • Cushing’s disease • Normal children and adults after ACTH administration Clinical Background Normal steroid-producing cells of the adrenal glands and gonads synthesize various steroids from circulating cholesterol ester. This results in small amounts of precursors such as pregnenolone, a 5 C-21 steroid, leaking into the circulation. Most of the circulating pregnenolone is from the adrenal cortex, and levels are modestly increased after ACTH administration in normal children and adults. This assay is useful in diagnosing 3β-hydroxysteroid dehydrogenase (3β-HSD) deficiency, an unusual form of congenital adrenal hyperplasia associated with blocked cortisol synthesis and increased levels of 5 steroids. After diagnosis of 3β-HSD deficiency, the test can evaluate glucocorticoid replacement therapy. The assay is also helpful in suggesting the presence of an adrenal virilizing tumor, since almost all of these tumors secrete large amounts of DHEA-sulfate and pregnenolone. Pregnenolone levels are moderately increased in Cushing’s disease due to ACTH-secreting pituitary adenoma or ectopic causes.
{"title":"[Pregnenolone].","authors":"S. Nakamura, S. Mikami, T. Futoeda","doi":"10.32388/plyc34","DOIUrl":"https://doi.org/10.32388/plyc34","url":null,"abstract":"Interpretive Information • Congenital adrenal hyperplasia • Adrenal virilizing tumor • Cushing’s disease • Normal children and adults after ACTH administration Clinical Background Normal steroid-producing cells of the adrenal glands and gonads synthesize various steroids from circulating cholesterol ester. This results in small amounts of precursors such as pregnenolone, a 5 C-21 steroid, leaking into the circulation. Most of the circulating pregnenolone is from the adrenal cortex, and levels are modestly increased after ACTH administration in normal children and adults. This assay is useful in diagnosing 3β-hydroxysteroid dehydrogenase (3β-HSD) deficiency, an unusual form of congenital adrenal hyperplasia associated with blocked cortisol synthesis and increased levels of 5 steroids. After diagnosis of 3β-HSD deficiency, the test can evaluate glucocorticoid replacement therapy. The assay is also helpful in suggesting the presence of an adrenal virilizing tumor, since almost all of these tumors secrete large amounts of DHEA-sulfate and pregnenolone. Pregnenolone levels are moderately increased in Cushing’s disease due to ACTH-secreting pituitary adenoma or ectopic causes.","PeriodicalId":19307,"journal":{"name":"Nihon rinsho. Japanese journal of clinical medicine","volume":"112 1","pages":"464-6"},"PeriodicalIF":0.0,"publicationDate":"2020-02-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"81659693","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}
Cystatin C ist ein Cystein-Protease-Inhibitor mit einem Molekulargewicht von 13 kD, das an kein anderes Protein bindet und auf Grund der geringen Größe ausschließlich durch glomeruläre Filtration ausgeschieden wird. Es zeichnet sich durch eine konstante Bildungsrate und damit konstante Plasmakonzentration aus. Die Expression des Cystatin C wird durch ein Gen des sog. „house-keeping“-Typs reguliert, welches eine stabile Produktionsrate garantiert. Es wird in allen kernhaltigen Zellen synthetisiert. Cystatin C wird nicht durch eine Akute-Phase-Reaktion beeinflusst. Cystatin C wird frei von der gesunden Niere filtriert, tubulär rückresorbiert und in den Tubuluszellen vollständig abgebaut. Die Halbwertszeit beträgt ca. 2 Stunden. Die Serumkonzentration hängt deshalb ausschließlich von der glomerulären Filtrationsleistung der Niere ab. Ein Wiedereintritt in die Blutzirkulation erfolgt nicht. Bei Tubulusdysfunktion ist die Absorbtion beeinträchtigt und Cystatin C wird mit dem Urin ausgeschieden. In diesem Fall ist die Cystatin C-Konzentration im Urin ein Maß für die Tubulus-Dysfunktion.
{"title":"[Cystatin C].","authors":"Shin-ichiro Okizaki, Tatsumi Moriya","doi":"10.32388/wkmqi6","DOIUrl":"https://doi.org/10.32388/wkmqi6","url":null,"abstract":"Cystatin C ist ein Cystein-Protease-Inhibitor mit einem Molekulargewicht von 13 kD, das an kein anderes Protein bindet und auf Grund der geringen Größe ausschließlich durch glomeruläre Filtration ausgeschieden wird. Es zeichnet sich durch eine konstante Bildungsrate und damit konstante Plasmakonzentration aus. Die Expression des Cystatin C wird durch ein Gen des sog. „house-keeping“-Typs reguliert, welches eine stabile Produktionsrate garantiert. Es wird in allen kernhaltigen Zellen synthetisiert. Cystatin C wird nicht durch eine Akute-Phase-Reaktion beeinflusst. Cystatin C wird frei von der gesunden Niere filtriert, tubulär rückresorbiert und in den Tubuluszellen vollständig abgebaut. Die Halbwertszeit beträgt ca. 2 Stunden. Die Serumkonzentration hängt deshalb ausschließlich von der glomerulären Filtrationsleistung der Niere ab. Ein Wiedereintritt in die Blutzirkulation erfolgt nicht. Bei Tubulusdysfunktion ist die Absorbtion beeinträchtigt und Cystatin C wird mit dem Urin ausgeschieden. In diesem Fall ist die Cystatin C-Konzentration im Urin ein Maß für die Tubulus-Dysfunktion.","PeriodicalId":19307,"journal":{"name":"Nihon rinsho. Japanese journal of clinical medicine","volume":"41 1","pages":"419-25"},"PeriodicalIF":0.0,"publicationDate":"2020-02-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"79057621","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}
Serratia species, in particular, Serratia marcescens frequently causes bloodstream infections. Recently, several outbreaks of nosocomial bloodstream infections due to S. marcescens have been reported in Japan. Although Serratia is an opportunistic pathogen, the organism can develop endotoxin shock and multiple organ failure because of being gram-negative rod when a number of bacteria invade the bloodstream. Serratia in the intestinal tract can invade bloodstream endogenously in compromised hosts. However, the possible causes of an outbreak are contamination of antiseptics, and consequent contamination of transfusion. To prevent outbreaks of S. marcescens bloodstream infection, management of antiseptics and transfusion in addition to contact precaution should be taken.
{"title":"[Serratia].","authors":"Y. Hirakata","doi":"10.32388/n3915x","DOIUrl":"https://doi.org/10.32388/n3915x","url":null,"abstract":"Serratia species, in particular, Serratia marcescens frequently causes bloodstream infections. Recently, several outbreaks of nosocomial bloodstream infections due to S. marcescens have been reported in Japan. Although Serratia is an opportunistic pathogen, the organism can develop endotoxin shock and multiple organ failure because of being gram-negative rod when a number of bacteria invade the bloodstream. Serratia in the intestinal tract can invade bloodstream endogenously in compromised hosts. However, the possible causes of an outbreak are contamination of antiseptics, and consequent contamination of transfusion. To prevent outbreaks of S. marcescens bloodstream infection, management of antiseptics and transfusion in addition to contact precaution should be taken.","PeriodicalId":19307,"journal":{"name":"Nihon rinsho. Japanese journal of clinical medicine","volume":"115 1","pages":"2156-60"},"PeriodicalIF":0.0,"publicationDate":"2020-02-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"79078640","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}
C-reactive protein (CRP) was discovered by Tillett and Francis in 1930. The name CRP arose because it was first identified as a substance in the serum of patients with acute inflammation that reacted with the "c" carbohydrate antibody of the capsule of pneumococcus.CRP is a pentameric protein synthesized by the liver, whose level rises in response to inflammation. CRP is an acute-phase reactant protein that is primarily induced by the IL-6 action on the gene responsible for transcription of CRP during the acute phase of an inflammatory/infectious process. There is some question of whether dysregulation of the role of CRP in the clearance of apoptotic cells and cellular debris plays a role in the pathogenesis of systemic lupus erythematosus (SLE), but this has not been definitively demonstrated. It has been demonstrated to have some protective properties in animal studies on lung tissue in alveolitis by reducing neutrophil-mediated damage to the alveoli and protein leakage into the lung.CRP has both proinflammatory and anti-inflammatory properties. It plays a role in the recognition and clearance of foreign pathogens and damaged cells by binding to the phosphocholine, phospholipids, histone, chromatin, and fibronectin. It can activate the classic complement pathway and also activates phagocytic cells via Fc receptors to expedite the removal of cellular debris and damaged or apoptotic cells and foreign pathogens. This can become pathologic, however, when it is activated by autoantibodies displaying the phosphocholine arm in auto-immune processes, such as idiopathic thrombocytopenic purpura (ITP). It can also worsen tissue damage in certain cases by activation of the complement system and thus inflammatory cytokines.As compared to the erythrocyte sedimentation rate, which is an indirect test for inflammation, the levels of CRP rise and fall rapidly with the onset and removal of the inflammatory stimulus respectively. Persistently elevated CRP levels can be seen in chronic inflammatory conditions such as chronic infections or inflammatory arthritides such as rheumatoid arthritis.There are numerous causes of an elevated C-reactive protein. These include acute and chronic conditions, and these can be infectious or non-infectious in etiology. However, markedly elevated levels of CRP are most often associated with an infectious cause (an example of pathogen-associated molecular pattern recognition). Trauma can also cause elevations in CRP (alarmin response). More modest elevations tend to be associated with a broader spectrum of etiologies, ranging from sleep disturbances to periodontal disease.
{"title":"[C-reactive protein].","authors":"H. Ohtani, N. Shimetani","doi":"10.32388/imeyzp","DOIUrl":"https://doi.org/10.32388/imeyzp","url":null,"abstract":"C-reactive protein (CRP) was discovered by Tillett and Francis in 1930. The name CRP arose because it was first identified as a substance in the serum of patients with acute inflammation that reacted with the \"c\" carbohydrate antibody of the capsule of pneumococcus.CRP is a pentameric protein synthesized by the liver, whose level rises in response to inflammation. CRP is an acute-phase reactant protein that is primarily induced by the IL-6 action on the gene responsible for transcription of CRP during the acute phase of an inflammatory/infectious process. There is some question of whether dysregulation of the role of CRP in the clearance of apoptotic cells and cellular debris plays a role in the pathogenesis of systemic lupus erythematosus (SLE), but this has not been definitively demonstrated. It has been demonstrated to have some protective properties in animal studies on lung tissue in alveolitis by reducing neutrophil-mediated damage to the alveoli and protein leakage into the lung.CRP has both proinflammatory and anti-inflammatory properties. It plays a role in the recognition and clearance of foreign pathogens and damaged cells by binding to the phosphocholine, phospholipids, histone, chromatin, and fibronectin. It can activate the classic complement pathway and also activates phagocytic cells via Fc receptors to expedite the removal of cellular debris and damaged or apoptotic cells and foreign pathogens. This can become pathologic, however, when it is activated by autoantibodies displaying the phosphocholine arm in auto-immune processes, such as idiopathic thrombocytopenic purpura (ITP). It can also worsen tissue damage in certain cases by activation of the complement system and thus inflammatory cytokines.As compared to the erythrocyte sedimentation rate, which is an indirect test for inflammation, the levels of CRP rise and fall rapidly with the onset and removal of the inflammatory stimulus respectively. Persistently elevated CRP levels can be seen in chronic inflammatory conditions such as chronic infections or inflammatory arthritides such as rheumatoid arthritis.There are numerous causes of an elevated C-reactive protein. These include acute and chronic conditions, and these can be infectious or non-infectious in etiology. However, markedly elevated levels of CRP are most often associated with an infectious cause (an example of pathogen-associated molecular pattern recognition). Trauma can also cause elevations in CRP (alarmin response). More modest elevations tend to be associated with a broader spectrum of etiologies, ranging from sleep disturbances to periodontal disease.","PeriodicalId":19307,"journal":{"name":"Nihon rinsho. Japanese journal of clinical medicine","volume":"42 1 1","pages":"197-200"},"PeriodicalIF":0.0,"publicationDate":"2020-02-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"83518251","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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