Clinical calcium最新文献

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[Epidemiology of FGF23-related hypophosophatemic diseases]. [fgf23相关低血糖疾病的流行病学]。
Clinical calcium Pub Date : 2016-02-01
Itsuro Endo
{"title":"[Epidemiology of FGF23-related hypophosophatemic diseases].","authors":"Itsuro Endo","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Through the studies of patients with hypophosphatemic rickets/osteomalacia, fibroblast growth factor 23(FGF23)has emerged as a humoral factor that reduces serum phosphate. Discovery of FGF23 as an essential regulator of phosphate homeostasis has markedly improved our understanding of phosphate homeostasis and hypophosphatemic or hyperphosphatemic disorders. A nationwide epidemiologic survey of FGF23-related hypophosphatemic diseases indicated that the patients showed FGF23 levels of above 30 pg/mL by intact assay in the presence of hypophosphatemia. The survey also showed that prevalence and biochemical data before and after treatment of the diseases. Novel therapeutic methods for these disorders may be developed by elucidation of the mechanism of action of FGF23.</p>","PeriodicalId":502100,"journal":{"name":"Clinical calcium","volume":"26 2","pages":"223-31"},"PeriodicalIF":0.0,"publicationDate":"2016-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145351111","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}
引用次数: 0
[Pathogenesis and clinical condition of hyperphosphatemic diseases]. [高磷酸盐血症的发病机制和临床症状]
Clinical calcium Pub Date : 2016-02-01
Naoto Hamano, Masafumi Fukagawa
{"title":"[Pathogenesis and clinical condition of hyperphosphatemic diseases].","authors":"Naoto Hamano, Masafumi Fukagawa","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Phosphorus is essential mineral to life, which has the multiple roles like postural maintenance or production of energy in the cells. Phosphate overload is harmful and compensatory mechanisms exist. Phosphate is abolished through kidneys and target organ of the compensatory mechanism is also kidneys. It is necessary to evaluate renal function and source of phosphate for estimating the cause of hyperphosphatemia. Acute hyperphosphatemia may cause severe acute kidney injury and avoidance of massive phosphate overload is needed. Chronic hyperphosphatemia have an impact on prognosis because the risk of cardiovascular event increases. Adequate restriction of phosphate intake and use of phosphate absorbent is needed for improvement of prognosis of patients with chronic kidney disease.</p>","PeriodicalId":502100,"journal":{"name":"Clinical calcium","volume":"26 2","pages":"207-13"},"PeriodicalIF":0.0,"publicationDate":"2016-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138816149","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}
引用次数: 0
[Diagnostic criteria for vitamin D-deficient rickets and hypocalcemia-]. [维生素d缺乏性佝偻病和低钙血症的诊断标准]。
Clinical calcium Pub Date : 2016-02-01
Keiichi Ozono
{"title":"[Diagnostic criteria for vitamin D-deficient rickets and hypocalcemia-].","authors":"Keiichi Ozono","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Vitamin D deficiency causes rickets or osteomalacia, which is associated with hypomineralization of bone and chondrocytes, and/or hypocalcemia. Accumulating evidence indicates increase in frequency of vitamin D deficiency due to insufficient intake of vitamin D and calcium and decrease in sunshine. It is necessary for clinician to diagnose vitamin D deficiency accurately and treat patients with vitamin D deficiency adequately. For the purpose, clinical guideline or expert opinion on vitamin D deficiency has been reported.</p>","PeriodicalId":502100,"journal":{"name":"Clinical calcium","volume":"26 2","pages":"215-22"},"PeriodicalIF":0.0,"publicationDate":"2016-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145351026","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}
引用次数: 0
[Pathogenesis of hypophosphatemia]. [低磷血症的发病机制]。
Clinical calcium Pub Date : 2016-02-01
Yasuhiro Takeuchi
{"title":"[Pathogenesis of hypophosphatemia].","authors":"Yasuhiro Takeuchi","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Chronic hypophosphatemia is seriously involved in several disorders of musculoskeletal system. Symptoms of patients are usually non-specific, such as pain with or without muscle weakness on lower extremities and are often hard to be correctly diagnosed. It is clinically important for physicians to understand pathogenesis and clinical features of hypophosphatemia and its related diseases.</p>","PeriodicalId":502100,"journal":{"name":"Clinical calcium","volume":"26 2","pages":"199-205"},"PeriodicalIF":0.0,"publicationDate":"2016-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145351047","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}
引用次数: 0
[Regulatory mechanism of circulating inorganic phosphate]. [循环无机磷酸盐的调控机制]。
Clinical calcium Pub Date : 2016-02-01
Toshimi Michigami
{"title":"[Regulatory mechanism of circulating inorganic phosphate].","authors":"Toshimi Michigami","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Circulating level of phosphate is altered by age and diet, and is also controlled by several hormones such as parathyroid hormone(PTH), 1,25-dihydroxyvitamin D[1,25(OH)2D]and fibroblast growth factor 23(FGF23). The main function of PTH and 1,25(OH)2D is maintaining calcium homeostasis, while FGF23 plays a central role in phosphate metabolism. PTH suppresses phosphate reabsorption in the proximal tubules to increase the renal phosphate wasting, while 1,25(OH)2D facilitates the intestinal phosphate absorption. FGF23 increases the renal phosphate wasting and reduces the production of 1,25(OH)2D. Of note, these hormones mutually regulate one another. The production of FGF23 is also regulated by various local factors. The mechanism for sensing the phosphate availability still remains unknown, and further investigation is required.</p>","PeriodicalId":502100,"journal":{"name":"Clinical calcium","volume":"26 2","pages":"193-8"},"PeriodicalIF":0.0,"publicationDate":"2016-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145351095","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}
引用次数: 0
[Steroids-induced osteoporosis due to the treatment for Pulmonary diseases.] [治疗肺部疾病引起的类固醇性骨质疏松症]
Clinical calcium Pub Date : 2016-01-01
Nobuyuki Horita, Takeshi Kaneko
{"title":"[Steroids-induced osteoporosis due to the treatment for Pulmonary diseases.]","authors":"Nobuyuki Horita, Takeshi Kaneko","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Corticosteroids are key medications to treat pulmonary diseases. A variety of medications, doses, administration route, and duration of corticosteroids were chosen for each of pulmonary diseases. Although corticosteroids are potent medications, they often cause serious adverse effects such as osteoporosis, diabetes, and immunosuppression. Thus, physicians have to properly assess the risk of adverse effects to prevent them. In this review, we discuss the risk of osteoporosis by corticosteroids that are prescribed for pulmonary diseases. Inhaled corticosteroids are not serious risk factors of osteoporosis. If systemic corticosteroids are planned to be administrated in the prednisolone equivalent dosage of 5 mg/day or more for three months or longer, risk of bone fracture have to be assessed regardless of the primary pulmonary disease. If necessary, prophylactic agent such as bisphosphonates should be prescript.</p>","PeriodicalId":502100,"journal":{"name":"Clinical calcium","volume":"26 10","pages":"1459-1465"},"PeriodicalIF":0.0,"publicationDate":"2016-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145351151","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}
引用次数: 0
[Design of mechanobio-materials for cell manipulation and its application for stem cell manipulation.] 细胞操纵机械生物材料的设计及其在干细胞操纵中的应用
Clinical calcium Pub Date : 2016-01-01
Satoru Kidoaki
{"title":"[Design of mechanobio-materials for cell manipulation and its application for stem cell manipulation.]","authors":"Satoru Kidoaki","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Recently, control of mechanobiologic response of cells has been a strong attractive issue for biomaterials sciences in relation to the requirements for optimization of cell-materials interactions. In this mini-review, we survey the typical parameters for designing the biomaterials to manipulate cell mechanobiology, i.e., mechanobio-materials. In addition, from the view of regenerative biomedical engineering, we introduce our recent approaches on the development of mechanobio-materials for stem cell manipulation that ensures the high-qualified stemness.</p>","PeriodicalId":502100,"journal":{"name":"Clinical calcium","volume":"26 12","pages":"1773-1778"},"PeriodicalIF":0.0,"publicationDate":"2016-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145351168","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}
引用次数: 0
[Topics for basic and clinical research in ASBMR 2015]. 【ASBMR 2015基础与临床研究课题】。
Clinical calcium Pub Date : 2016-01-01
Ippei Kanazawa
{"title":"[Topics for basic and clinical research in ASBMR 2015].","authors":"Ippei Kanazawa","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>This is a brief report on selected topics in 37th Annual meeting of ASBMR held in Seattle on October 9-12, 2015. I focused on several interesting presentations of basic and clinical research.</p>","PeriodicalId":502100,"journal":{"name":"Clinical calcium","volume":"26 1","pages":"133-5"},"PeriodicalIF":0.0,"publicationDate":"2016-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145351260","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}
引用次数: 0
[Changes in cytosolic Ca 2+ dynamics associated with muscular dystrophy.] [与肌肉萎缩症相关的胞浆ca2 +动力学变化]
Clinical calcium Pub Date : 2016-01-01
Jun Tanihata, Shin'ichi Takeda
{"title":"[Changes in cytosolic Ca\u0000 <sup>2+</sup>\u0000 dynamics associated with muscular dystrophy.]","authors":"Jun Tanihata, Shin'ichi Takeda","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>\u0000 Duchenne muscular dystrophy(DMD)is X-linked genetic disorder caused by a lack of the membrane-associated protein dystrophin. DMD is characterized by progressive muscle wasting secondary to repeated muscle damage and inadequate repair. The mechanisms underlying the functional impairments in dystrophic muscle have not yet been fully determined. However, several recent studies indicate that elevated intracellular Ca\u0000 <sup>2+</sup>\u0000 homeostasis is a cause or facilitator of the development of muscle weakness in muscular dystrophy. This review focuses on abnormalities of Ca\u0000 <sup>2+</sup>\u0000 homeostasis and the possibilities for treatment by counteracting the Ca\u0000 <sup>2+</sup>\u0000 dysregulation.\u0000 </p>","PeriodicalId":502100,"journal":{"name":"Clinical calcium","volume":"26 12","pages":"1677-1683"},"PeriodicalIF":0.0,"publicationDate":"2016-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145351159","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}
引用次数: 0
[p130Cas-Mediated Regulation of Mechanical Functions of Cells.] [p130cas介导的细胞机械功能调控]
Clinical calcium Pub Date : 2016-01-01
Yasuhiro Sawada, Hiroaki Hirata
{"title":"[p130Cas-Mediated Regulation of Mechanical Functions of Cells.]","authors":"Yasuhiro Sawada, Hiroaki Hirata","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>It is 10 years since we reported Cas as a cell mechano-sensor that converts stretching force to a biochemical signal. While we have been looking into the mechanism of how Cas molecules are extended, it appears that the source of stretching force does not derive from actomyosin contraction, but originates from actin polymerization. Furthermore, we have found that phosphorylated Cas links actomyosin contraction to cell migration by tensin 1-mediated association with inwardly moving actin filaments. Collectively, Cas serves as a force sensor at the cell leading edges as well as a part of force transmission machinery, i.e. clutch, which drives the cell forward.</p>","PeriodicalId":502100,"journal":{"name":"Clinical calcium","volume":"26 12","pages":"1743-1749"},"PeriodicalIF":0.0,"publicationDate":"2016-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145351205","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}
引用次数: 0
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