Parental Working Hours and Children's Sedentary Time: A Cross-sectional Analysis of the J-SHINE.

BACKGROUND: Sedentary behaviors are prevalent among children and can have a detrimental effect on their health. Little is known about the influence of parental time on children's sedentary behavior. This study examined the association between parental working hours and children's sedentary time. METHODS: Cross-sectional data were drawn from the Japanese Study on Stratification, Health, Income, and Neighborhood (J-SHINE) in 2010 and 2011. Participants were 886 children aged 7-18 years and their parents. The primary outcome was self-reported sedentary time after school that comprised screen time and non-screen time. The main explanatory variable was parental working hours. We used multiple regression analysis adjusting for sociodemographic factors. RESULTS: Children's mean sedentary time was 222 (standard deviation [SD], 123) min/day; 144 (SD, 108) min/day screen time and 78 (SD, 65) min/day non-screen time. Children whose mothers worked ≥20 hours/week had 28 (95% CI, 9 to 48) min/day longer sedentary time than children of homemakers (240 min/day vs 214 min/day). The longer maternal working hours, the longer sedentary time (P for trend <0.01). In contrast, children whose fathers worked ≥48 hours/week had 82 (95% CI, -156 to -7) min/day shorter sedentary time than children of non-working fathers (179 min/day vs 264 min/day). When limited to children whose fathers worked, there was no statistically significant association between children's sedentary time and paternal working hours. CONCLUSIONS: Children with mothers who work long hours or fathers not working tend to sit more. Supplementing the shortages in resources for childcare may be necessary among those families.

Impaired cutaneous wound healing in mice lacking tetranectin.

Tetranectin was originally purified from human serum on the basis of plasminogen kringle 4-binding properties. Tetranectin enhances plasminogen activation by a tissue-type plasminogen activator so that it has been suggested to play a role in tissue remodeling. We have generated mice with a targeted disruption of the tetranectin gene to elucidate the biological function of tetranectin. In this study, we showed that wound healing was markedly delayed in tetranectin-null mice compared with wild-type mice. A single full-thickness incision was made in the dorsal skin. By 14 days after the incision, the wounds fully healed in all wild-type mice based on the macroscopic closure; in contrast, the progress of wound healing in the tetranectin null mice appeared to be impaired. In histological analysis, wounds of wild-type mice showed complete reepithelialization and healed by 14 days after the incision. However, those of tetranectin-null mice never showed complete reepithelialization at 14 days. At 21 days after the injury, the wound healed and was covered with an epidermis. These results supported the fact that tetranectin may play a role in the wound healing process.

Changes in urinary NTX levels in patients with primary osteoporosis undergoing long-term bisphosphonate treatment.

BACKGROUND: Bisphosphonates, antiresorptive drugs, are widely used to treat osteoporosis patients. However, recent reports indicated that several osteoporosis patients who underwent long-term bisphosphonate therapy subsequently developed severe suppression of bone turnover. We investigated whether urinary crosslinked N-telopeptide of type I collagen (NTX), a bone resorption marker, in osteoporosis patients was highly suppressed during long-term treatment with alendronate or risedronate. METHODS: We investigated 87 primary osteoporosis outpatients who were treated with alendronate or risedronate for more than 2 years. All patients were women, with an average age of 72.6 years. Altogether, 49 patients were treated with alendronate and 38 with risedronate, and the average administration period was 3.5 years. We defined high suppression as NTX being reduced <9.3 nmol bone collagen equivalent/mmol.Cr and a 35% decrease from baseline. RESULTS: In total, 11 of 87 patients (12.6%) had high NTX suppression based on the above criteria. The incidences of high suppression of NTX at 1,2,3,and 4 years after starting the treatment were 0%, 1.1%, 11.9%, and 4.7%, respectively. The average age, bone mineral density, and NTX values at baseline and the administration period were not associated with high suppression of NTX during alendronate or risedronate treatment. Regarding suppression of NTX during long-term treatment, there was no significant difference between alendronate and risedronate. CONCLUSIONS: The results suggested that long-term treatment with bisphosphonates necessitates careful follow-up of the patients.

IGF-I regulates tight-junction protein claudin-1 during differentiation of osteoblast-like MC3T3-E1 cells via a MAP-kinase pathway.

Insulin-like growth factor I (IGF-I) is expressed in many tissues, including bone, and acts on the proliferation and differentiation of osteoblasts as an autocrine/paracrine regulator. Tight-junction proteins have been detected in osteoblasts, and direct cell-to-cell interactions may modulate osteoblast function with respect, for example, to gap junctions. In order to investigate the regulation of expression of tight-junction molecules and of function during bone differentiation, osteoblast-like MC3T3-E1 cells and osteocyte-like MLO-Y4 cells were treated with IGF-I. In both MC3T3-E1 cells and MLO-Y4 cells, the tight-junction molecules occludin, claudin-1, -2, and -6, and the gap-junction molecule connexin 43 (Cx43) were detected by reverse transcription with polymerase chain reaction. In MC3T3-E1 cells but not MLO-Y4 cells, mRNAs of claudin-1, -2, and -6, Cx43, and type I collagen, and proteins of claudin-1 and Cx43 were increased after treatment with IGF-I. Such treatment significantly decreased paracellular permeability in MC3T3-E1 cells. The expression of claudin-1 in MC3T3-E1 cells after IGF-I treatment was mainly upregulated via a mitogen-activated protein (MAP)-kinase pathway and, in part, modulated by a PI3-kinase pathway, whereas Cx43 expression and the mediated gap-junctional intercellular communication protein did not contribute to the upregulation. Furthermore, in MC3T3-E1 cells during wound healing, upregulation of claudin-1 was observed together with an increase of IGF-I and type I collagen. These findings suggest that the induction of tight-junction protein claudin-1 and paracellular permeability during the differentiation of osteoblast-like MC3T3-E1 cells after treatment with IGF-I is regulated via a MAP-kinase pathway, but not with respect to gap junctions.

Underutilization of antiosteoporotic drugs by orthopedic surgeons for prevention of a secondary osteoporotic fracture.

BACKGROUND: Despite the availability of effective treatment and well-publicized treatment guidelines for preventing osteoporotic fractures, there are significant gaps in implementing the recommendations, and it is unknown how many patients are treated for prevention of secondary osteoporotic fractures. In this study, we investigate what percentage of osteoporosis patients were treated with antiosteoporotic drugs after osteoporotic fractures of the hip, wrist, and proximal humerus, and we discuss here the need for improvement in the treatment of osteoporosis following fracture. METHODS: We studied 422 patients with osteoporotic fractures, 91 men and 331 women, with an average age of 77.1 years (range, 52-102 years). The 422 cases consisted of 299 hip fractures, 97 distal radius fractures, and 26 proximal humerus fractures. All patients underwent surgical intervention. The variables were examined to ascertain whether osteoporosis patients were medicated with antiosteoporotic drugs at postfracture. RESULTS: Fifty-five (13%) of the 422 patients received antiosteoporotic medication at postfracture. Pharmaceutical treatment was given in 44 cases (14.7%) of hip fractures, 8 cases (8.2%) of distal radius fractures, and 3 cases (11.5%) of proximal humerus fractures. Thirty-one (7.3% of total) of the 55 patients were taking the same medication pre- and postfracture. Seven (1.7%) of the 55 were administered a different drug compared to before the fracture, and 17 (4%) started to take an antiosteoporotic drug for the first time subsequent to the fracture. CONCLUSIONS: The present rate of treatment is insufficient given the high risk of secondary fractures and the availability of appropriate drugs that would reduce that risk.

p38 MAP-kinase regulates function of gap and tight junctions during regeneration of rat hepatocytes.

BACKGROUND/AIMS: Hepatocyte regeneration is considered to be associated with adaptive changes in expression of gap and tight junctions through multiple signal transduction pathways including p38 MAP-kinase. The role of the stress responsitive MAP-kinase, p38 MAP-kinase, signaling pathway in function of gap and tight junctions was examined during regeneration of rat hepatocytes in vivo and in vitro. METHODS: We examined changes in formation, expression and function of gap and tight junctions in rat livers after 70% partial hepatectomy and in primary cultures of rat hepatocytes, by using a p38 MAP-kinase inhibitor, SB203580. RESULTS: When p38 MAP-kinase was activated during partial hepatectomy, down-regulation of Cx32 and up-regulation of claudin-1 were observed. By SB203580 treatment, the down-regulation of Cx32 was inhibited and the up-regulation of claudin-1 was enhanced, well maintaining the structures of gap and tight junctions. SB203580 treatment did not affect the increase of hepatocyte proliferation. In EGF induced proliferative rat hepatocytes treated with SB203580, the expression and function of Cx32 and claudin-1 were increased. CONCLUSIONS: Dynamic changes of formation of gap and tight junctions during regeneration of rat hepatocytes in vivo and in vitro are in part controlled via a p38 MAP-kinase signaling pathway, and are independent of cell growth.