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Clinical calcium最新文献

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[Molecular mechanism for feeding and food preference regulation]. [摄食与食物偏好调控的分子机制]。
Clinical calcium Pub Date : 2016-03-01
Yasuhiko Minokoshi
{"title":"[Molecular mechanism for feeding and food preference regulation].","authors":"Yasuhiko Minokoshi","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Feeding behavior is regulated by homeostatic and hedonic mechanisms. NPY/AgRP neurons in the arcuate hypothalamus are involved in the homeostatic regulation, and dopaminergic neurons in the ventral tegmental area regulating the nucleus of accumbens are involved in the hedonic regulation, respectively. Food preference also appears to be regulated by both homeostatic and hedonic mechanisms. However, molecular mechanism for food preference regulation remains elusive and further studies are necessary.</p>","PeriodicalId":502100,"journal":{"name":"Clinical calcium","volume":"26 3","pages":"405-11"},"PeriodicalIF":0.0,"publicationDate":"2016-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145351301","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
[Renal hypophosphatemia:pathophysiology and treatment]. 肾性低磷血症：病理生理及治疗。
Clinical calcium Pub Date : 2016-02-01
Takashi Sekine
{"title":"[Renal hypophosphatemia:pathophysiology and treatment].","authors":"Takashi Sekine","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Serum level of phosphate is regulated by the kidney, especially proximal tubule. The transcellular transport of phosphate in the proximal tubule is mediated via Na dependent transporters, i.e., NPT2a and NPT2b at the luminal membrane, and unknown channel at the basolateral side. The transport of phosphate via NPT2a and NPT2b is further regulated by factors, such as PTH, FGF23, and 1,25(OH)(2)D. Several hereditary diseases that cause hypophoshatemia specically are known. In addition, dysfunction of proximal tubule may develop Fanconi syndrome, which also causes hypherphosphaturia. In this section, I describe the renal mechanisms of phosphate handling and the causes of hypophosphatemia along with its treatment.</p>","PeriodicalId":502100,"journal":{"name":"Clinical calcium","volume":"26 2","pages":"284-94"},"PeriodicalIF":0.0,"publicationDate":"2016-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145351027","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
[Vitamin D dependency and its treatment]. [维生素D依赖性及其治疗]。
Clinical calcium Pub Date : 2016-02-01
Sachiko Kitanaka
{"title":"[Vitamin D dependency and its treatment].","authors":"Sachiko Kitanaka","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Vitamin D dependency is classified to vitamin D-dependent rickets type 1 which shows defective 1,25(OH)(2)D production, and vitamin D-dependent rickets type 2 which shows end-organ unresponsiveness to 1,25(OH)(2)D. Recent advance in the molecular analysis of these diseases revealed variety in the presentation and in the inheritance patterns. Molecular diagnosis would be preferable for adequate therapy especially in type 2.</p>","PeriodicalId":502100,"journal":{"name":"Clinical calcium","volume":"26 2","pages":"277-83"},"PeriodicalIF":0.0,"publicationDate":"2016-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145351039","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
[Vitamin D insufficiency/deficiency:its clinical significance and treatment]. [维生素D不足/缺乏症：临床意义及治疗]。
Clinical calcium Pub Date : 2016-02-01
Ryo Okazaki
{"title":"[Vitamin D insufficiency/deficiency:its clinical significance and treatment].","authors":"Ryo Okazaki","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Vitamin D insufficiency/deficiency, a medical condition in which vitamin D store is decreased, is the most frequent cause of decreased action of vitamin D. Severer form vitamin D deficiency can cause hypocalcemia and rickets/osteomalacia. Milder form vitamin D insufficiency also harms bone health via secondary hyperparathyroidism, the increase in fracture risk, and poor responses to anti-osteoporotic medications. Diagnosis can only be made by measuring serum 25(OH)D, which is not currently covered by the Japanese health insurance policy. In Japan, the guideline for the diagnosis vitamin D insufficiency/deficiency is in the process of drafting. According to the current provisional guideline draft that was made in public, vitamin D deficiency would be defined by serum 25(OH)D level less than 20 ng/mL whereas vitamin D insufficiency would refer to the state in which serum 25(OH)D level is between 20 and 30 ng/mL.</p>","PeriodicalId":502100,"journal":{"name":"Clinical calcium","volume":"26 2","pages":"251-8"},"PeriodicalIF":0.0,"publicationDate":"2016-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145351089","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
[Intracellular and extracellular functions of phosphorus compound in the body]. [体内磷化合物的细胞内和细胞外功能]。
Clinical calcium Pub Date : 2016-02-01
Hiroko Segawa, Ai Hanazaki, Ken-ichi Miyamoto
{"title":"[Intracellular and extracellular functions of phosphorus compound in the body].","authors":"Hiroko Segawa, Ai Hanazaki, Ken-ichi Miyamoto","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Phosphorus, as a phosphate is a component of bone, cellular membrane, and also high-energy phosphate compounds, and nucleic acids. Also phosphate acts as a buffer to maintain the pH and is concerned with functional regulation of several proteins and intracellular signaling through the phosphorylation/dephosphorylation. Thus phosphorus plays a variety of important roles intracellular and extracellular component. A disorder of phosphate homeostasis results bone disorder and general metabolic dysfunction of all body tissues and organs.</p>","PeriodicalId":502100,"journal":{"name":"Clinical calcium","volume":"26 2","pages":"187-91"},"PeriodicalIF":0.0,"publicationDate":"2016-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145351074","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
[Phosphate metabolism and iron deficiency]. [磷酸盐代谢和缺铁]。
Clinical calcium Pub Date : 2016-02-01
Keitaro Yokoyama
{"title":"[Phosphate metabolism and iron deficiency].","authors":"Keitaro Yokoyama","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Autosomal dominant hypophosphatemic rickets(ADHR)is caused by gain-of-function mutations in FGF23 that prevent its proteolytic cleavage. Fibroblast growth factor 23(FGF23)is a hormone that inhibits renal phosphate reabsorption and 1,25-dihydroxyvitamin D biosynthesis. Low iron status plays a role in the pathophysiology of ADHR. Iron deficiency is an environmental trigger that stimulates FGF23 expression and hypophosphatemia in ADHR. It was reported that FGF23 elevation in patients with CKD, who are often iron deficient. In patients with nondialysis-dependent CKD, treatment with ferric citrate hydrate resulted in significant reductions in serum phosphate and FGF23.</p>","PeriodicalId":502100,"journal":{"name":"Clinical calcium","volume":"26 2","pages":"241-9"},"PeriodicalIF":0.0,"publicationDate":"2016-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145351088","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
[Inhitibion of FGF23 activities as a possible new treatment for patients with FGF23-related hypophosphatemic diseases]. [抑制FGF23活性可能成为治疗FGF23相关低磷血症患者的新方法]。
Clinical calcium Pub Date : 2016-02-01
Yuka Kinoshita
{"title":"[Inhitibion of FGF23 activities as a possible new treatment for patients with FGF23-related hypophosphatemic diseases].","authors":"Yuka Kinoshita","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Excessive actions of fibroblast growth factor 23(FGF23)result in several kinds of hypophosphatemic rickets and osteomalacia. A combination of oral active vitamin D3 and phosphate is the current standard therapy for FGF23-related hypophosphatemia. However, these medications can lead to long-term complications, such as secondary hyperparathyroidism and renal impairment. Therefore, safer and more efficient therapy to correct excessive actions of FGF23 is needed. X-linked hypophosphatemic rickets(XLHR)is the most prevalent form of FGF23-related hypophosphatemia. The efficacy of anti-FGF23 antibody was confirmed in a Hyp mouse, a murine model of XLHR. A recent phase 1 double-blind, placebo-controlled study and the subsequent open-label phase 1/2 study in adults with XLHR showed the safety and the efficacy of human anti-FGF23 antibody, KRN23. KRN23 has a potential for effectively treating patients with XLHR and other types of FGF23-related hypophosphatemia as well.</p>","PeriodicalId":502100,"journal":{"name":"Clinical calcium","volume":"26 2","pages":"233-9"},"PeriodicalIF":0.0,"publicationDate":"2016-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145351098","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
[FGF23 related hypophosphatemic rickets:current therapy and unresolved issues]. [FGF23相关的低磷血症佝偻病：目前的治疗和尚未解决的问题]。
Clinical calcium Pub Date : 2016-02-01
Daisuke Harada, Noriyuki Namba
{"title":"[FGF23 related hypophosphatemic rickets:current therapy and unresolved issues].","authors":"Daisuke Harada, Noriyuki Namba","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>FGF23-related hypophosphatemic rickets is basically treated with active vitamin D and phosphorus. The treatment goals are to minimize bone deformity and improve adult height in children, and to relieve pain and decrease osteomalacia in adult. However, since they do not target the underlying molecular defect, bone deformity can worsen during growth and adult height is suboptimal restricted. Many adult patients suffer from enthesopathy leading to symptoms such as spinal cord compression and debilitating pain. At present, no treatment is effective in preventing or revenging this complication. The recently developed anti-FGF23 antibody may potentially be a more fundamental treatment.</p>","PeriodicalId":502100,"journal":{"name":"Clinical calcium","volume":"26 2","pages":"269-76"},"PeriodicalIF":0.0,"publicationDate":"2016-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145351071","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
[NF-κB signaling pathways and the future perspectives of bone disease therapy using selective inhibitors of NF-κB]. [NF-κB信号通路和NF-κB选择性抑制剂治疗骨病的未来前景]。
Clinical calcium Pub Date : 2016-02-01
Eijiro Jimi, Hidefumi Fukushima
{"title":"[NF-κB signaling pathways and the future perspectives of bone disease therapy using selective inhibitors of NF-κB].","authors":"Eijiro Jimi, Hidefumi Fukushima","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>The transcriptional factor nuclear factor κB(NF-κB)regulates the expression of a wide variety of genes that are involved in immune and inflammatory responses, proliferation, and tumorigenesis. NF-κB consists of five members, such as p65(RelA), RelB, c-Rel, p50/p105(NF-κB1), and p52/p100(NF-κB2). There are two distinct NF-κB activation pathways, termed the classical and alternative NF-κB signaling pathways. Since mice lacking both p50 and p52 subunits developed typical osteopetrosis, due to total lack of osteoclasts, NF-κB is also important osteoclast differentiation. A selective NF-κB inhibitor blocked receptor activator of NF-κB ligand(RANKL)-induced osteoclastogenesis both in vitro and in vivo. Recent findings have shown that inactivation of NF-κB enhances osteoblast differentiation in vitro and bone formation in vivo. NF-κB is constitutively activated in many cancers including oral squamous cell carcinoma(OSCC), and is involved in the invasive characteristics of OSCC. A selective NF-κB inhibitor also prevented jaw bone destruction by OSCC by reduced osteoclast numbers in animal model. Thus the inhibition of NF-κB might useful for the treatment of bone diseases, such as arthritis, osteoporosis, periodontitis, and bone invasion by OSCC by inhibiting bone resorption and by stimulating bone formation.</p>","PeriodicalId":502100,"journal":{"name":"Clinical calcium","volume":"26 2","pages":"298-304"},"PeriodicalIF":0.0,"publicationDate":"2016-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145351091","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
[Treatment for CKD-MBD(Chronic Kidney Disease-Mineral and Bone Disorder)]. [CKD-MBD（慢性肾脏-矿物质和骨骼疾病）的治疗]。
Clinical calcium Pub Date : 2016-02-01
Yuko Iwashita, Yu Iwashita, Takafumi Ito, Takashi Shigematsu
{"title":"[Treatment for CKD-MBD(Chronic Kidney Disease-Mineral and Bone Disorder)].","authors":"Yuko Iwashita, Yu Iwashita, Takafumi Ito, Takashi Shigematsu","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>CKD is a common disease that is estimated to develop one in eight persons in Japan. The CKD itself is highly risk factor on the cardiac/vascular mortality. In addition,a new concept has been proposed \"CKD-MBD\". CKD-MBD is composed of a combination of abnormal mineral metabolism, abnormal bone, and extra skeletal calcification with cardiovascular high mortality. Treatment for CKD-MBD is a wide-ranging. We aim to decline cardiovascular event, fracture, and mortality rate of patients with CKD. The main therapeutic target for CKD-MBD becomes the phosphate control. Today, we can use of the VRDA, Calcimimetics and muti-phosphate binders as a lot of pharmacological intervention.</p>","PeriodicalId":502100,"journal":{"name":"Clinical calcium","volume":"26 2","pages":"259-67"},"PeriodicalIF":0.0,"publicationDate":"2016-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145351075","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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