{"title":"[Fragility Fractures in Hemodialysis Patients. Bone-derived turnover markers in chronic kidney disease G5D.]","authors":"Yasuo Imanishi","doi":"CliCa180810751079","DOIUrl":"https://doi.org/CliCa180810751079","url":null,"abstract":"<p><p>It is well established that patients with maintenance hemodialysis increased fracture rates compared with the general population, incident hip fractures are associated with substantial morbidity and mortality. To prevent fractures in hemodialysis patients, bone turnover markers are useful as well as measurement of bone mineral density.</p>","PeriodicalId":10389,"journal":{"name":"Clinical calcium","volume":"28 8","pages":"1075-1079"},"PeriodicalIF":0.0,"publicationDate":"2018-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36345556","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":"[Rickets/Osteomalacia. The function and mechanism of vitamin D action.]","authors":"Makoto Makishima","doi":"CliCa181013191326","DOIUrl":"https://doi.org/CliCa181013191326","url":null,"abstract":"<p><p>The antirickets factor vitamin D exhibits its action through activation of vitamin D receptor(VDR). The active form of vitamin D, 1α,25-dihydroxyvitamin D3[1,25(OH)2D3], is a potent VDR ligand, and contributes to the maintenance of calcium homeostasis by enhancing intestinal calcium absorption, renal calcium reabsorption and bone resorption. 1,25(OH)2D3 also regulates bone formation, phosphorus metabolism and vitamin D metabolism. Experimental and epidemiological evidence has shown vitamin D actions on cellular proliferation and differentiation, immunity and inflammation, and cardiovascular function. Vitamin D derivatives and VDR ligands may be useful for the treatment of osteoporosis, malignancy, autoimmune and inflammatory disease and cardiovascular disease as well as rickets and osteomalacia.</p>","PeriodicalId":10389,"journal":{"name":"Clinical calcium","volume":"28 10","pages":"1319-1326"},"PeriodicalIF":0.0,"publicationDate":"2018-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36537411","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":"[Bone and calcium metabolism associated with malignancy. Bone metastasis of prostate cancer:overview of clinical features and treatments.]","authors":"Kazuhiro Suzuki, Yoshiyuki Miyazawa","doi":"CliCa181114411449","DOIUrl":"https://doi.org/CliCa181114411449","url":null,"abstract":"<p><p>Bones are the most frequent sites in patients with progressive prostate cancer. Spinal column and pelvic bone are vulnerable for metastasis, and osteoblastic lesions are frequently observed. Imaging evaluation is performed using bone scintigrapy with 99mTc, CT or MRI. Extent of disease is categorized as EOD score, and it is still used for evaluation of bone metastasis in clinical trials. Clinical guidelines recommend the uses of bone modifying agents including zoledronic acid and denosumab for bone metastasis in patients with castration-resistant prostate cancer. New androgen targeted agents, enzalutamide and abiraterone, or taxans, docetaxel and cabazitaxel, show clinical efficacy for bone metastasis of prostate cancer. Recently, metastasis free survival(MFS)has been approved as a primary endpoint for nonmetastatic castration-resistant prostate cancer. For this category, enzalutamide and apalutamide have been approved for patients with nonmetastatic castration-resistant prostate cancer. Treatment and follow-up strategy is now dramatically changed in the area of bone metastasis of prostate cancer.</p>","PeriodicalId":10389,"journal":{"name":"Clinical calcium","volume":"28 11","pages":"1441-1449"},"PeriodicalIF":0.0,"publicationDate":"2018-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36673414","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":"[Homeostasis and Disorder of Musculoskeletal System.Molecular signaling and its pathogenic alterations in neuromuscular junction formation.]","authors":"Ryo Ueta, Yuji Yamanashi","doi":"CliCa1803360366","DOIUrl":"https://doi.org/CliCa1803360366","url":null,"abstract":"<p><p>The neuromuscular junction(NMJ)is the synapse between a motor neuron and the skeletal muscle that is essential for muscle contraction. Impairments at the NMJ lead to neuromuscular-transmission pathologies characterized by fatigable muscle weakness. Muscle-specific receptor tyrosine kinase MuSK plays key roles in NMJ formation. Over the past decade, studies examining the NMJ formation signals have identified molecules involved in the signaling pathways and have promoted a better understanding of characteristic molecular mechanisms for MuSK activation. Unlike many other receptor tyrosine kinases, MuSK is regulated by the cytoplasmic activator Dok-7 in addition to the extracellular activator agrin. It is well established that all of these molecules are indispensable in the formation and maintenance of the NMJ. In this chapter, we review molecular signaling, particularly MuSK signaling, in the formation of the NMJ and the altered molecular signaling associated with neuromuscular disorders.</p>","PeriodicalId":10389,"journal":{"name":"Clinical calcium","volume":"28 3","pages":"360-366"},"PeriodicalIF":0.0,"publicationDate":"2018-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"35889743","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":"[Homeostasis and Disorder of Musculoskeletal System.Humoral factors produced by osteocytes as druggable targets for skeletal diseases.]","authors":"Seiji Fukumoto","doi":"CliCa1803307312","DOIUrl":"https://doi.org/CliCa1803307312","url":null,"abstract":"<p><p>Osteocytes have several functions such as sensing mechanical load to bone and regulating osteoclastic bone resorption. In addition, osteocytes secrete several humoral factors that affect bone and other organs. FGF23 produced by osteocytes works as a hormone that reduces serum phosphate level. Sclerostin suppresses bone formation by inhibiting Wnt signals. Drugs that inhibit the activities of these factors are now under investigation as new therapeutic measures.</p>","PeriodicalId":10389,"journal":{"name":"Clinical calcium","volume":"28 3","pages":"307-312"},"PeriodicalIF":0.0,"publicationDate":"2018-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"35890263","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":"[Homeostasis and Disorder of Musculoskeletal System.Pathogenesis of musculoskeletal diseases and strategies for their treatment.]","authors":"Takeshi Miyamoto","doi":"CliCa1803301305","DOIUrl":"https://doi.org/CliCa1803301305","url":null,"abstract":"<p><p>Decline of homeostasis in musculoskeletal locomotive organs such as bone and muscle with age leads to age-related diseases such as osteoporosis and muscle atrophy. To date, various findings underlying the pathogenesis of these tissues were accumulated. In this review, we discuss regarding the recent advances in the findings in the treatment for osteoporosis and the strategy for muscle atrophy, and our recent findings on the mechanisms underlying these diseases.</p>","PeriodicalId":10389,"journal":{"name":"Clinical calcium","volume":"28 3","pages":"301-305"},"PeriodicalIF":0.0,"publicationDate":"2018-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"35890264","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":"[Diagnosis and treatment of rheumatoid arthritis:toward the best practice. Pathogenesis of Rheumatoid Arthritis.]","authors":"Keshi Fujio","doi":"CliCa1805601606","DOIUrl":"https://doi.org/CliCa1805601606","url":null,"abstract":"<p><p>Rheumatoid arthritis(RA)has been a disease of unknown cause for many years. However, the etiology is becoming obvious due to the use of biological products in recent years, arthritis model mice in basic immunology and genome wide analysis in genetics etc. In particular, the knowledge of what is effective and what is not effective for biological products directly reveals the pathology of RA. It has also been found that the cytokine dependence of arthritis model mice and RA is not necessarily the same. It is pointed out that the difference may be derived from the presence of anti-citrullinated protein antibody(ACPA). Studies of immune responses against self antigens such as citrullinated protein will provide a clue to elucidate the pathogenesis of RA. Further analysis of genetic polymorphism and epigenome in combination with human immunity is expected to promote understanding of RA.</p>","PeriodicalId":10389,"journal":{"name":"Clinical calcium","volume":"28 5","pages":"601-606"},"PeriodicalIF":0.0,"publicationDate":"2018-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36073270","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":"[Diagnosis and treatment of rheumatoid arthritis:toward the best practice. Towards precision medicine in rheumatoid arthritis.]","authors":"Katsuya Suzuki, Tsutomu Takeuchi","doi":"CliCa1805626629","DOIUrl":"https://doi.org/CliCa1805626629","url":null,"abstract":"<p><p>Biologics made a big paradigm shift in the treatment for rheumatoid arthritis(RA). In the next step, current research for RA shifts from traditional approach for average patients to precision medicine using huge omics data from patients. Multiomics analysis for the specimen from patients will play an important role for the establishment of precision medicine for RA.</p>","PeriodicalId":10389,"journal":{"name":"Clinical calcium","volume":"28 5","pages":"626-629"},"PeriodicalIF":0.0,"publicationDate":"2018-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36073275","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":"[Aging-related frailty and sarcopenia. Epidemiology of Frailty and Sarcopenia.]","authors":"Atsumu Yuki, Fujiko Ando, Hiroshi Shimokata","doi":"CliCa180911831189","DOIUrl":"https://doi.org/CliCa180911831189","url":null,"abstract":"<p><p>Frailty and sarcopenia present significant risks for adverse outcomes such as disability, falls, and mortality in Japanese older adults. Among community-dwelling Japanese older adults, the prevalence of frailty, which was characterized using three or more limitations(shrinking, exhaustion, low activity, slowness, and weakness), was 5.2% and 12.0% in men and women, respectively. The prevalence of sarcopenia based on a diagnosis of low appendicular muscle mass, low grip strength, and low gait speed was 9.6% in men and 7.7% in women. Further, the prevalence of frailty with comorbidity of sarcopenia was 21.6% and 52.2% in men and women, respectively, and the prevalence of sarcopenia with comorbidity of frailty was 28.6% and 34.4% in men and women, respectively. The estimated number of prevalent cases of frailty, pre-frailty, and sarcopenia in Japanese older adults was approximately 3,090,000, 17,950,000, and 2,710,000, respectively.</p>","PeriodicalId":10389,"journal":{"name":"Clinical calcium","volume":"28 9","pages":"1183-1189"},"PeriodicalIF":0.0,"publicationDate":"2018-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36430657","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":"[Thermoregulatory behavior and its central circuit mechanism-What thermosensory pathway drives it?]","authors":"Kazuhiro Nakamura","doi":"CliCa18016572","DOIUrl":"https://doi.org/CliCa18016572","url":null,"abstract":"<p><p>Thermoregulatory behavior in homeothermic animals is an instinctive behavior to reduce the cost of their homeothermy, such as warm-seeking behavior to reduce metabolic energy for heat production in cold environments. A recent study identified the central neural pathway that transmits cutaneous thermosensory information on environmental temperature to drive thermoregulatory behavior. This study proposed that the brain mechanism that drives thermoregulatory behavior does not require conscious\"feeling\"(i.e., perception)of skin temperature mediated by the spinothalamocortical pathway, whereas thermosensory information that ascends through the spinal cord and the lateral parabrachial nucleus of the pons generates thermal comfort and discomfort that drive thermoregulatory behavior.</p>","PeriodicalId":10389,"journal":{"name":"Clinical calcium","volume":"28 1","pages":"65-72"},"PeriodicalIF":0.0,"publicationDate":"2018-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"35689713","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}