Effects of high-intensity interval walking training on physical fitness and blood pressure in middle-aged and older people

Reproduced from Mayo Clin Proc., with permission), permission is hereby granted to place a pdf of Nemoto, K et al. Effects of high-intensity interval walking training on physical fitness and blood pressure in middle-aged and older people. Mayo Clin Proc. 82 (7):803-811 into the institutional repository of Shinshu University at https://soar-ir.shinshu-u.ac.jp/ArticleMAYO CLINIC PROCEEDINGS. 82(7): 803-811 (2007)journal articl

Platelet-rich plasma for regeneration of neural feedback pathways around dental implants: a concise review and outlook on future possibilities

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Treatment of OPG-deficient mice with WP9QY, a RANKL-binding peptide, recovers alveolar bone loss by suppressing osteoclastogenesis and enhancing osteoblastogenesis.

Osteoblasts express two key molecules for osteoclast differentiation, receptor activator of NF-κB ligand (RANKL) and osteoprotegerin (OPG), a soluble decoy receptor for RANKL. RANKL induces osteoclastogenesis, while OPG inhibits it by blocking the binding of RANKL to RANK, a cellular receptor of RANKL. OPG-deficient (OPG–/–) mice exhibit severe alveolar bone loss with enhanced bone resorption. WP9QY (W9) peptide binds to RANKL and blocks RANKL-induced osteoclastogenesis. W9 is also reported to stimulate bone formation in vivo. Here, we show that treatment with W9 restores alveolar bone loss in OPG–/–mice by suppressing osteoclastogenesis and enhancing osteoblastogenesis. Administration of W9 or risedronate, a bisphosphonate, to OPG–/–mice significantly decreased the osteoclast number in the alveolar bone. Interestingly, treatment with W9, but not risedronate, enhanced Wnt/β-catenin signaling and induced alveolar bone formation in OPG–/–mice. Expression of sclerostin, an inhibitor of Wnt/β-catenin signaling, was significantly lower in tibiae of OPG–/–mice than in wild-type mice. Treatment with risedronate recovered sclerostin expression in OPG–/–mice, while W9 treatment further suppressed sclerostin expression. Histomorphometric analysis confirmed that bone formation-related parameters in OPG–/–mice, such as osteoblast number, osteoblast surface and osteoid surface, were increased by W9 administration but not by risedronate administration. These results suggest that treatment of OPG–/–mice with W9 suppressed osteoclastogenesis by inhibiting RANKL signaling and enhanced osteoblastogenesis by attenuating sclerostin expression in the alveolar bone. Taken together, W9 may be a useful drug to prevent alveolar bone loss in periodontitis

Immunolocalization of DMP1 and sclerostin in the epiphyseal trabecule and diaphyseal cortical bone of osteoprotegerin deficient mice

In order to define the osteocytic function in accelerated bone remodeling, we examined the distribution of the osteocytic lacunar-canalicular system (OLCS) and osteocyte-secreting molecules-dentin matrix protein (DMP) 1 and sclerostin-in the epiphyses and cortical bones of osteoprotegerin deficient (OPG-/-) mice. Silver impregnation visualized a well-arranged OLCS in the wild-type epiphyses and cortical bone, whereas OPG-/- mice had an irregular OLCS in the epiphyses, but well-arranged canaliculi in the cortical bone. DMP1-positive osteocytes were evenly distributed throughout the wild-type epiphyses and cortical bone, as well as the OPG-/- cortical bone. However, OPG-/- epiphyses revealed weak DMP1-immunoreactivity. Thus, osteocytes appear to synthesize more DMP1 as the OLCS becomes regular. In contrast, sclerostin-immunoreactivity was significantly diminished in the OPG-/- epiphyses and cortical bone. In OPG-/- epiphyses and cortical bone, triple staining demonstrated few sclerostin-positive osteocytes in the periphery of a thick cell layer of alkaline phosphatase-positive osteoblasts and many tartrate resistant acid phosphatasepositive osteoclasts. Summarizing, the regular distribution of OLCS may affect DMP1 synthesis, while the cellular activities of osteoclasts and osteoblasts rather than the regularity of OLCS may ultimately influence sclerostin synthesis

Age specific prevalence of impairment and disability relating to hemiplegic stroke in the Hai District of northern Tanzania

OBJECTIVES—To determine the age specific prevalence of impairment and disability relating to hemiplegic stroke in one rural area of Tanzania.
METHODS—During the yearly house to house census of the study population of 148 135 (85 152 aged 15 and over) in August 1994, specific questions were asked to identify those who might be disabled from stroke. People thus identified were subsequently interviewed and examined by one investigator. In those in whom the clinical diagnosis of stroke was confirmed a more detailed interview and examination relating to risk factors and recovery was carried out.
RESULTS—One hundred and eight patients, 61 men and 47 women, were identified with a median age of 70 (range 18-100). Median age at first stroke was 65 years. The age specific rates in this study were lower than previous studies in developed countries. All were cared for at home although 23 (21%) were bedbound.
CONCLUSIONS—Although prevalence of impairment and disability related to stroke in this population as a whole was low this is mainly explained by the age structure, with less than 6% being aged 65 and over. Age standardised rates for stroke with residual disability were about half those found in previous studies in developed countries. Death from stroke in Africa may be higher but data are limited. With the demographic transition stroke is likely to become a more important cause of disability in sub-Saharan Africa.