우리나라 주요 항만의 입출항 통항패턴을 연구하기 위한 사전 연구로서, 부산항에 입·출항하는 위험화물운반선의 통항량을 항만운영정보시스템(Port Management Information Systim, Port-MIS) 자료를 이용하여 사전 조사하고, 통항량이 가장 높은 각 계절별 연속 3일을 선별하였다. 해양안전종합정보시스템(General Information Center on Maritime Safety & Security, GICOMS) 자료를 이용하여 선별된 12일간 위험화물운반선의 부산항 주요 통항로의 통항 패턴을 분석하였다. 또한 주요 입출항 지점인 북항 오륙도 방파제와 감천항 동방파제의 위험화물운반선의 통항 이격거리를 분석하였다. 항로 단면에서 선박의 궤적이 정규분포를 이룬다는 가정을 근거로 해상교통안전진단 등에서 정규분포의 누적 확률분포 함수를 이용하여 충돌확률을 추정하여 사용하고 있지만, 오륙도 방파제 입출항 및 감천항 동방파제 입항에서의 선박의 항해 궤적은 KS-test 및 SW-test를 이용한 정규성 검정결과 정규분포를 따르지 않는 것으로 평가되었다. 특히 북항에서는 선박의 우측통항 경향이 두드러지게 나타났다. 일반적인 통항이론의 적용보다는 항만의 특성에 맞는 통항모델을 개발하여, 해상교통안전진단 등에서 적용하는 것이 바람직하여 이에 대한 후속연구가 필요할 것으로 판단된다.

본 연구에서는 해양·수산분야의 대학생 자원봉사활동에 대한 자료를 수집하여 활동유형을 유류방제작업, 어촌봉사활동, 해안 정화작업 등으로 분석하였다. 또한 자원봉사 참여자 대부분은 환경보호, 보람, 사회교류, 특별체험, 자연과의 동화측면에서 만족하고 있었다. 주제측면에서 체계성, 효율성, 활동의 다양성, 자원홍보활용, 봉사이후 보상, 자기봉사역량 측면에서 불만족스러워 한다. 이러한 연구 결과를 바탕으로 대학생 자원봉사의 정책적 측면에서 해양·수산분야의 자원봉사를 증진시킬 수 있는 방안을 제안하였다.

This study was conducted to investigate the preventing effects of OPB (Rehmannia glutinosa Libosch and Eleutherococcus senticosus Max extracts) and combined OPB/Calcium therapy on bone loss in ovariectomized rats. Sixty Sprague Dawley rats of 12-week-old were divided into eight groups: OVX (ovariectomized), OPBL (OPB 50 mg/kg), OPBM (OPB100 mg/kg), OPBH (OPB 200 mg/kg), OPBL/CAL(OPBL+CAL), OPBM/CAL (OPBM+CAL), OPBH/CAL (OPBH+CAL) and CAL (Calcium citrate 88.33 mg/kg+1, 25-dihydroxy-vitamin D₃33.33 IU/kg). Bone mineral density (BMD), bone mineral content (BMC), bone strength indices and cortical thickness were analyzed by peripheral quantitative computerized tomography (pQCT). pQCT scanning showed that OVX induced a significant decrease in trabecular bone mineral density and bone mineral content in the proximal tibia (-36.4 ±24%, -21.8±12.7%).These decreases were significantly prevented by the administration of OPBM and OPBM/CAL. Cortical BMD and BMC of tibia were slightly enhanced by OPB and OPB/CAL. However there was no significant difference between OVX and OPB, OPB/CAL treated group. Bone strength indices and cortical thickness were not significantly different. Our results suggest that OPB and combined OPB/Calcium therapy are effective in preventing the development of bone loss induced by ovariectomy in rats.

We performed the present study to investigate whether Rehmannia glutinosa Libosch (RG) extracts (RGX) and Eleutherococcus senticosus Max (ES) extracts (ESX) play any roles in bone metabolism. We examined cellular activities of bone cells by measurement of osteoblastic cell viability, osteoprotegerin (OPG) secretion from osteoblasts, osteoclastogenesis, and osteoclastic activity. There is no cytotoxicity from osteoblasts after treatment with RGX and ESX. The secretion of OPG from the osteoblasts showed marked increases after treatment with RGX and ESX. In addition, RGX and ESX treatment decreased the number of tartrate-resistant acid phosphatase-positive multinucleated cells and the resorption areas. RGX and ESX, when mixed at optimal ratios, induced synergic effects, in vitro. OPB, which showed synergic effects, is the extract of natural ingredients RG and ES mixed at a raw material weight ratio of 4 : 1. It can be suspected that extracts of RG and ES mixtures contains active ingredients involved in bone tissue metabolism and may be effective in improving osteoporosis.

The importance of phytoestrogens to human health is currently being actively investigated. Hesperidin, abundantly found in citrus fruits, is known to possess antioxidant, anticancer, and anti-inflammatory effects. Recently, it has been reported that hesperidin inhibits bone loss and decreases serum and hepatic lipids in ovariectomized mice. In our study, to determine the possible role of hesperidin in the regulation of bone metabolism, we observed the effects of hesperidin on the proliferation and activity of osteoblasts, as well as the effects of hesperidin on osteoclast generation and activity. We observed that, when treated with hesperidin, the number and viability of osteoblastic cells increased, alkaline phosphatase (ALP) activity of osteoblastic cells increased, and osteoprotegerin (OPG) secretion from MG63 cells decreased. Hesperidin treatment had no effect on the osteoclast generation and activity in the bone marrow cell culture, but decreased the number and resorptive activity of osteoclasts generated from RAW/264.7 cells. Taken together, these results indicate that hesperidin increases the proliferation and activity of osteoblasts, while inhibiting generation and activity of osteoclasts. Although the precise role of hesperidin remains to be elucidated, our study suggests that it is one of the important modulators of bone metabolism.

Nitric oxide(NO) is a labile, uncharged, reactive radical that functions as a sensitive mediator of intercellular communication in diverse tissues. It has been reported that NO is produced by osteoblast and these results may suggest that NO is integrally involved in the regulation of osteoclast formation and osteoclast resorption activity by osteoblastic cells. We examined the effect of cytokines on NO release by mouse bone marrow cell. We also examined the effects of cytokines and sodium nitroprusside(SNP) on the formation of osteoclast-like cell from mouse bone marrow cells in culture. Cytokines stimulated NO production of mouse bone marrow cells, and N-nitro-L-arginine methyl ester, a specific inhibitor of NO synthase, suppressed the cytokine-induced NO production. SNP showed dual action in the generation of osteoclasts. The addition of (30μM)SNP inhibited the formation of tartrate resistant acid phosphatase(TRAP)(+) multinucleated cell, whereas lower concentration(30μM) of SNP enhanced it. Although the precise action of NO remains to be elucidated in detail, the action of NO in osteoclast generation in our studies seems to be associated, at least in part, with bone metabolism and bone pathophysiology.

Leptin, the product of the obese gene, is a circulating hormone secreted primarily from adipocytes. Several results suggest that leptin is important mediators of bone metabolism. The present study was undertaken to determine the effects of leptin on anti-osteoclastogenesis using murine precursors cultured on Ca-P coated plates and on the production of osteoprotegerin (OPG) in osteoblastic cells. Additionally, this study examined the possible involvement of prostaglandin E₂(PGE₂)/вввB/protein kinase C (PKC)-mediated signals on the effect of leptin on anti-osteoclastogenesis to various culture systems of osteoclast precursors. Osteoclast generation was determined by counting tartrate-resistant acid phosphatase positive [TRAP (+)] multinucleated cells (MNCs). Osteoclastic activity was determined by measuring area of resorption pits formed by osteoclasts on Ca-P coated plate. The number of 1,25-dihydroxycholecalciferol 1.25[OH]₂D₃- or PGE₂-induced TRAP (+) MNCs in the mouse bone marrow cell culture decreased significantly after treatment with leptin. The number of receptor activator of NF-kB ligand (RANKL)-induced TRAP (+) MNCs in M-CSF dependent bone marrow macrophage (MDBM) cell or RAW264.7 cell culture decreased significantly with leptin treatment. Indomethacin inhibited osteoclast generation induced by 1.25[OH]₂D₃ and dexamethasone, however, no significant differences were found in the leptin treated group when compared to the corresponding indomethacin group. Phorbol 12-myristate 13-acetate (PMA), a PKC activator, inhibited osteoclast generation induced by 1.25[OH]₂D₃The number of TRAP (+) MNCs decreased significantly with treatment by PMA at concentrations of 0.01 and 0.1μM in culture. Leptin inhibited PMA-mediated osteoclast generation. Isoquinoline-5-sulfonic 2-methyl-1-piperazide dihydrochloride (H7) had no effect on osteoclast generation induced by 1.25[OH]₂D₃ Cell culture treatment with leptin resulted in no significant differences in osteoclast generation compared to the corresponding H7 group. Indomethacin showed no significant effect on TRAP (+) MNCs formation from the RAW264.7 cell line. PMA inhibited TRAP (+) MNCs formation induced by RANKL in the RAW264.7 cell culture. H7 had no effect on osteoclast generation from the RAW264.7 cell line. There was no difference compared with the corresponding control group after treatment with leptin. 1.25[OH]₂D₃- or PGE₂-induced osteoclastic activity decreased significantly with leptin treatment at a concentration of 100 ng/ml in mouse bone marrow cell culture. Indomethacin, PMA, and H7 significantly inhibited osteoclastic activity induced by 1.25[OH]₂D₃ in mouse bone marrow cell culture. No significant differences were found between the leptin treated group and the corresponding control group. The secretion of OPG, a substance known to inhibit osteoclast formation, was detected from the osteoblasts. Treatment by leptin resulted in significant increases in OPG secretion by osteoblastic cells. Taken these results, leptin may be an important regulatory cytokines within the bone marrow microenvironment.

The present study was performed to investigate whether Achyranthes Radix extracts play roles in the bone metabolism. Three kinds of Achyranthes Radix extracts (methylene chloride (MC), ethylacetate (Ea), and water (W)) were used for bioassay. We examined cellular activities of osteoblasts by measurement of cell proliferation rate, alkaline phosphatase (ALP) activity, and calcified nodule formation. Osteoclast generation was assayed by measuring the number of tartrate-resistant acid phosphatase (TRAP) (+) multinucleated cells after culture of osteoclast precursor cells. There was a maximum 20% increase in proliferation rate of osteoblastic cells after treatment with MC. First and second subfraction of MC layer increased proliferation of osteoblast. Ea layer and second subfraction of MC layer increased ALP activity. Also MC layer and second subfraction of MC layer from Achyranthes Radix extracts increased the calcified nodule. MC layer and second subfraction of MC layer from Achyranthes Radix extracts significantly decreased in the number of TRAP (+) multinucleated cells. Taken together, Achyranthes Radix stimulates the proliferation and bioactivities of bone-forming osteoblasts, and inhibits activities of bone-resorbing osteoclasts.