Aim: This study aimed to investigate factors associated with depression in a sample of elderly Japanese individuals in a rural community and to examine differences among factors associated with individuals living alone or living with others. Methods: Using a population-based sample from rural Japan, we assessed a total of 1552 participants aged 65 years or older by mailing a survey and evaluating responses based on the Geriatric Depression Scale. Factors associated with depression were also examined. Results: We received 964 valid responses. Depressed subjects comprised 20.5% of the sample. Living alone was significantly related to depression. In individuals living alone, depression was associated with loss of appetite, suicidal ideation, financial strain, and worries in life. However, multiple linear regression analyses revealed that the influence of living alone was negated by having a good social support system. Conclusion: These findings confirm that living alone is an important factor in depression among the elderly in a rural part of Japan. Results also confirm what others have found in Western cultures: high levels of social support, awareness of receiving social support, and willingness to receive assistance may reduce the risk of depression.

The aim of this study was to evaluate skeletal pain associated with osteoporosis and to examine the inhibitory effect of bisphosphonate (BP) on pain in an ovariectomized (OVX) mouse model. We evaluated skeletal pain in OVX mice through an examination of pain-like behavior as well as immunohistochemical findings. In addition, we assessed the effects of alendronate (ALN), a potent osteoclast inhibitor, on those parameters. The OVX mice showed a decrease in the pain threshold value, and an increase in the number of c-Fos immunoreactive neurons in laminae I-II of the dorsal horn of the spinal cord. Alendronate caused an increase in the pain threshold value and inhibited c-Fos expression. The serum level of tartrate-resistant acid phosphatase 5b, a marker of osteoclast activity, was significantly negatively correlated with the pain threshold value. Furthermore, we found that an antagonist of the transient receptor potential channel vanilloid subfamily member 1, which is an acid-sensing nociceptor, improved pain-like behavior in OVX mice. These results indicated that the inhibitory effect of BP on osteoclast function might contribute to an improvement in skeletal pain in osteoporosis patients.

ABSTRACT:We have recently demonstrated that pathological changes leading to increased bone resorption by osteoclast activation are related to the induction of pain-like behavior in ovariectomized (OVX) mice. In addition, bisphosphonate and the antagonist of transient receptor potential vanilloid type 1 (TRPV1), an acid-sensing nociceptor, improved the threshold value of pain-like behaviors accompanying an improvement in the acidic environment in the bone tissue based on osteoclast inactivation. The aim of this study was to evaluate the effect of (i) an inhibitor of vacuolar H þ -ATPase, known as an proton pump, (ii) an antagonist of acid-sensing ion channel (ASIC) 3, as another acid-sensing nociceptor, and (iii) the P2X2/3 receptor, as an ATP-ligand nociceptor, on pain-like behavior in OVX mice. This inhibitor and antagonists were found to improve the threshold value of pain-like behavior in OVX mice. These results indicated that the skeletal pain accompanying osteoporosis is possibly associated with the acidic microenvironment and increased ATP level caused by osteoclast activation under a high bone turnover state. Skeletal pain resulting from fragility fractures and skeletal deformity is the most common problem observed in osteoporosis patients. 1 On the other hand, several studies have indicated that osteoporosis patients also experience idiopathic skeletal pain independent of those fractures or deformity. [2][3][4] One factor underlying the induction of idiopathic skeletal pain is the acidic microenvironment created by activated osteoclasts, which results in pain through the same mechanism as that observed for cancer-induced bone pain. 5,6 Moreover, recent studies have demonstrated that bisphosphonate (BP), an anti-bone resorption drug which works via the inhibition of osteoclast activity, improves skeletal pain in osteoporosis patients. 2,3,7 We have also demonstrated that the pathological changes leading to increased bone resorption by osteoclast activation are related to the induction of painlike behavior in an ovariectomized (OVX) mouse model. In addition, BP treatment improved the threshold value of the pain-like behavior accompanied by an improvement in the acidic environment in the bone tissue through osteoclast inactivation. 8 Furthermore, the antagonist to transient receptor potential vanilloid type 1 (TRPV1), a member of a family of polymodal and nonselective cation channels that are predominantly expressed by sensory nerve fibers and sensitized by protons, 9 was also found to improve the threshold value. 8 Therefore, we speculate that the skeletal pain accompanying osteoporosis is associated with the acidic microenvironment resulting from osteoclast activation.On the other hand, with regard to the improvement in the pain threshold, the effect of TRPV1 was likely to be limited in comparison with that of BP. These results encouraged us to clarify the other mechanisms by which pathological changes under a high bone turnover state resulting from osteoclast activation might induce skeletal pain in oste...

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Tetranectin is a plasminogen-binding protein that enhances plasminogen activation, which has been suggested to play a role in tissue remodeling. Recently, we showed that tetranectin has a role in the wound-healing process. In this study, we investigated whether tetranectin plays a role in fracture healing. The fracture-healing process was studied using a femoral osteotomy model in tetranectin-null mice, previously generated by the authors. Radiographic imaging, micro-computed tomography (μCT), and histological analysis were used to evaluate osteotomy healing. In wild-type mice, a callus was apparent from 7 days, and most samples showed marked callus formation and rebridging of the cortices at the osteotomy site at 21 days. In contrast, in the tetranectin-null mice there was no callus formation at 7 days and much less callus formation and no bridging of cortices were observed at 21 days. At 35 days, all osteotomy sites showed clear rebridging, and secondary bone formation was achieved in wild-type mice by 42 days. In contrast, no clear rebridging or secondary bone formation was observed at 42 days in the tetranectin-null mice. Analysis using μCT at 21 days after osteotomy revealed that the callus area in tetranectin-null mice was smaller than that in wild-type mice. Histological analysis also showed that soft tissue and callus formation were smaller in the tetranectin-null mice at the early stage of the healing process after drill-hole injury. These results suggested that tetranectin could have a role in the positive regulation at the early stage of the fracture-healing process, which was reflected in the delayed fracture healing in tetranectin-deficient mice.

The comprehensive ASPs had long-term efficacy for reducing the use of the targeted broad-spectrum antibiotics, maintaining the antibiotic susceptibility of P. aeruginosa, and decreasing the prevalence of MRSA, without adversely affecting clinical outcome.

The expression of Kaposi's sarcoma-associated herpesvirus (KSHV/HHV-8)-encoded proteins is herein demonstrated in Kaposi's sarcoma (KS) and multicentric Castleman's disease (MCD) in a single lymph node derived from a patient with acquired immunodeficiency syndrome. Immunohistochemistry revealed that both lytic and latent KSHV proteins were expressed in cells of the MCD lesion. KSHV-encoded viral interleukin-6 was also detected in follicular dendritic cells of the germinal center. Cytoplasmic localization of open reading frame 59 protein and latency-associated nuclear antigen suggested KSHV activation in the MCD lesion. Moreover, a high copy number of KSHV was detected in the blood. Clinically, pegylated-liposomal doxorubicin induced regression of not only KS, but also lymphadenopathy of the MCD lesion with a decrease in KSHV load and human interleukin-6 in the blood. To the best of the authors' knowledge this is the first case demonstrating differential expression of virus proteins in two KSHV-associated diseases, KS and MCD, in the same section. The case confirms lytic KSHV infection in MCD, and suggests that clinical symptoms of MCD might be closely linked with KSHV activation.

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