Various alloplastic materials have been used on the periodontally diseased ossous defects. Hydroxyapatite, which is used the most common alloplastic material is a non-resorbable form of calcium phosphate and natural coral which is a biodegradable by carbonic anhydrase in osteoclast was introduced recently. The purpose of the present study was to evaluate the clinical effects of porous hydoxyapatite and natural coral on the human periodontal defects. Four males and three females who had adult periodontitis were selected for this study. The teeth that had similar bone loss radiographically and periodontal pocket deeper than 5mm were selected. Gingival recession, pocket depth, plaque index(Silness & Loe), sulcus bleeding index and tooth mobility (measured by Periotest$^{(r)}$) were examined before graft. Before insertion of alloplastic materials, the depth from CEJ to bone crest and from CEJ to base of the osseous defect was recorded. Porous particulate hydroxyapatite(Interpore 200$^{(r)}$, A group) was place on the defect and natural coral(Biocoral$^{(r)}$, B group) was placed on the defect of the opposing tooth. Six months post-surgically the same parameters were recorded by reentry procedures. A and B group showed 0.6mm of mean recession. Mean reduction of pocket depth were 5mm for A group and 4.9mm of B group. Reduced SBI and tooth mobility were recorded. Osseous defect fills of the original defects were 2.9mm for A and 3mm for B group. Percentage defect fills were 71% for A and 59% for B group. The difference of defect fill between pre- and post-insertion was statstically significant(p<0.05). But the difference between the two groups was not significant statistically(p<0.05). The clinical impression at 6 month re-entry and the numerical date indicate that natural coral as well as porous particulate hydoxyapatite has a definite potential as an alloplastic implant in the treatment of periodontal osseous defects.
The purpose of this study was to assess the effect of nutrition education by the difference of BMI(Body Mass Index) group for adults at rural area. Eighty four adults (mean age : 55.9$\pm$11.8) participated in nutrition education program. Data collection includes measured physical status and serum collections for health status. The impact of nutrition KAP (knowledge attitude and practice) and retention was examined among participants who were assessed at program entry, 3 times of education and 1 month of follow-up. The results were as follows: The participants were composed 14 persons of under 20kg/$m^2$ of BMI, 40 persons of 20-25 and 27 persons over 25 of BMI , female 60 persons but male 23 only. Serum albumin and calcium content of female(3.5$\pm$1.2g/㎗, 7.5$\pm$3.9mg/㎗) were significantly lower than males(4.7$\pm$0.9g/㎗, 11.2$\pm$4.6mg/㎗) but there was not significantly different with BMI groups. Serum TG and cholesterol contents of over 25kg/$m^2$ of BMI group(157$\pm$87mg/㎗, 249$\pm$16mg/㎗) were higher than other groups, but significantly different in cholesterol contents only. Via the 10 questions of nutrition attitude, the participants improved significantly between pre and post education(the score of pre, post and after 1 month, 6.5$\pm$1.8, 7.2$\pm$1.5, 7.2$\pm$1.9), and were also attributed to better personal feeling health by modified CMI test, but dietary food habit was not significantly improved. As the differences of BMI groups were compared, 20-25kg/$m^2$ group had better the effect of nutrition education score than other groups, and female had better nutrition attitude and practice score than male.
α1-adrenoceptors link via the G-protein Gq/G11 to both Ca2+ entry and release from stores, but may also activate Rho kinase, which causes calcium sensitization. This study aimed to identify the subtype(s) of α1-adrenoceptor involved in Rho kinase-mediated responses in both rat aorta and mouse spleen, tissues in which contractions involve multiple subtypes of α1-adrenoceptor. Tissues were contracted with cumulative concentrations of noradrenaline (NA) in 0.5 log unit increments, before and in the presence of an antagonist or vehicle. Contractions produced by NA in rat aorta are entirely α1-adrenoceptor mediated as they are competitively blocked by prazosin. The α1A-adrenoceptor antagonist RS100329 had low potency in rat aorta. The α1D-adrenoceptor antagonist BMY7378 antagonized contractions in rat aorta in a biphasic manner: low concentrations blocking α1D-adrenoceptors and high concentrations blocking α1B-adrenoceptors. The Rho kinase inhibitor fasudil (10 µM) significantly reduced aortic contractions in terms of maximum response, suggesting inhibition of α1B-adrenoceptor mediated responses. In the mouse spleen, a tissue in which all 3 subtypes of α1-adrenoceptor are involved in contractions to NA, fasudil (3 µM) significantly reduced both early and late components to the NA contraction, the early component involving α1B- and α1D-adrenoceptors, and the late component involving α1B- and α1A-adrenoceptors. This suggests that fasudil inhibits α1B-adrenoceptor mediated responses. It is concluded that α1D- and α1B-adrenoceptors interact in rat aorta and α1D-, α1A- and α1B-adrenoceptors interact in the mouse spleen to produce contractions and these interactions suggest that one of the receptors preferentially activates Rho kinase, most likely the α1B-adrenoceptor.
A chicken clathrin-associated adaptor protein $3-{\delta}$ subunit 2 (AP3S2) is a subunit of AP3, which is involved in cargo protein trafficking to target membrane with clathrin-coated vesicles. AP3S2 may play a role in virus entry into host cells through clathrin-dependent endocytosis. AP3S2 is also known to participate in metabolic disease developments of progressions, such as liver fibrosis with hepatitis C virus infection and type 2 diabetes mellitus. Chicken AP3S2 (chAP3S2) gene was originally identified as one of the differentially expressed genes (DEGs) in chicken kidney which was fed with different calcium doses. This study aims to characterize the molecular characteristics, gene expression patterns, and transcriptional regulation of chAP3S2 in response to the stimulation of Toll-like receptor 3 (TLR3) to understand the involvement of chAP3S2 in metabolic disease in chicken. As a result, the structure prediction of chAP3S2 gene revealed that the gene is highly conserved among AP3S2 orthologs from other species. Evolutionarily, it was suggested that chAP3S2 is relatively closely related to zebrafish, and fairly far from mammal AP3S2. The transcriptional profile revealed that chAP3S2 gene was highly expressed in chicken lung and spleen tissues, and under the stimulation of poly (I:C), the chAP3S2 expression was down-regulated in DF-1 cells (P<0.05). However, the presence of the transcriptional inhibitors, BAY 11-7085 (Bay) as an inhibitor for nuclear factor ${\kappa}B$ ($NF{\kappa}B$) or Tanshinone IIA (Tan-II) as an inhibitor for activated protein 1 (AP-1), did not affect the expressional level of chAP3S2, suggesting that these transcription factors might be dispensable for TLR3 mediated repression. These results suggest that chAP3S2 gene may play a significant role against viral infection and be involved in TLR3 signaling pathway. Further study about the transcriptional regulation of chAP3S2 in TLR3 pathways and the mechanism of chAP3S2 upon virus entry shall be needed.
Purpose: The entry of bacteria or harmful substances through the epithelial seal of human gingival keratinocytes (HGKs) in the junctional epithelium (JE) is blocked by specialized intercellular junctions such as E-cadherin junctions (ECJs). However, the influence of roughened substrates, which may occur due to apical migration of the JE, root planing, or peri-implantitis, on the development of the ECJs of HGKs remains largely unknown. Methods: HGKs were cultured on substrates with varying levels of roughness, which were prepared by rubbing hydrophobic polystyrene dishes with silicon carbide papers. The activity of c-Jun N-terminal kinase (JNK) was inhibited with SP600125 or by transfection with JNK short hairpin RNA. The development of intercellular junctions was analyzed using scanning electron microscopy or confocal laser scanning microscopy after immunohistochemical staining of the cells for E-cadherin. The expression level of phospho-JNK was assessed by immunoblotting. Results: HGKs developed tight intercellular junctions devoid of wide intercellular gaps on smooth substrates and on rough substrates with low-nanometer dimensions (average roughness $[Ra]=121.3{\pm}13.4nm$), although the ECJs of HGKs on rough substrates with low-nanometer dimensions developed later than those of HGKs on smooth substrates. In contrast, HGKs developed short intercellular junctions with wide intercellular gaps on rough substrates with mid- or high-nanometer dimensions ($Ra=505.3{\pm}115.3nm$, $867.0{\pm}168.6nm$). Notably, the stability of the ECJs was low on the rough substrates, as demonstrated by the rapid destruction of the cell junction following calcium depletion. Inhibition of JNK activity promoted ECJ development in HGKs. JNK was closely associated with cortical actin in the regulation of ECJs in HGKs. Conclusions: These results indicate that on rough substrates with nanometer dimensions, the ECJs of HGKs develop slowly or defectively, and that this effect can be reversed by inhibiting JNK.
Han, Seong Rok;Hyun, Dong Keun;Park, Chong Oon;Ha, Young Soo;Kim, Joon Mee
Journal of Korean Neurosurgical Society
/
v.29
no.10
/
pp.1296-1302
/
2000
Objective : Traumatic brain injury including diffuse axonal injury has been shown to result in a decrease in brainfree magnesium concentration, an endogenous inhibitor of calcium entry into neuron, that is associated with the development of neurological motor deficits. The goal of this study is to establish the therapeutic window during which the therapy with $MgSO_4$ and/or hypothermia improve damaged neurons by TUNEL stain. Method : Moderate brain injury was induced in 64 adult Sprague-Dawley rats, weighing 350 to 450gm each, by using a simple weight-drop device(Marmarou model). The animals were randomly assigned to four groups(sixteen rats each, a control group, a group treated with $MgSO_4$, a group treated with hypothermia, and a group treated with $MgSO_4$ and hypothermia) and the rats in each group were sacrificed and studied after 12 hrs, 24 hrs, 1 wk, and 2 wks after insult. In hypothermic group, these rats were subjected to hypothermia after injury, with their rectal temperatures maintained at $32^{\circ}C$ for 1 hour. After 1-hour period of hypothermia, rewarming to normothermic level was accomplished over 30-minute period. In the groups treated $MgSO_4$, hypothermia and $MgSO_4$ were subsequently treated with $MgSO_4$($750{\mu}moles/kg$) infused intra-muscularly at 30 minutes after trauma. Result : In all treated groups, a significant reduction in TUNEL positive cells was found in comparison with the control group each time(p<0.001). Between treatment groups, No differnce was seen 12hrs, 24hrs, and 1wk. However, hypothermic group treated with or without $MgSO_4$ showed more significant reduction in apoptotic cells than group treated with $MgSO_4$ 2 weeks after trauma(p<0.05). However, hypothermic group treated with $MgSO_4$ showed no significant reduction in apoptotic cells compared with hypothermic group(p>0.05). Conclusion : These findings suggest that both hypothermia and $MgSO_4$ significantly improve pathological changes. Otherwise simultaneously $MgSO_4$ and hypothermia treatment groups is failed to provide additional neuroprotection. These results may be relevant to the design of future clinical trials of therapeutic hypothermia and $MgSO_4$ for traumatic brain injury.
In the present work, we show that tamoxifen(Tam)-induced cytotoxicity is due to the mitochondrial-dependent pathway triggered by the intracellular $Ca^{2+}$ increase in MCF-7 human breast cancer cells. Tam induced the intracellular $Ca^{2+}$ increase. According to the experimental results with $Ca^{2+}$ channel blockers, Tam-induced $Ca^{2+}$ uptake seemed to depend on the voltage-sensitive $Ca^{2+}$ channel at the early stage, but at later stages the intracellular $Ca^{2+}$ increases are more likely due partly to the release of stored $Ca^{2+}$ and partly to the capacitative $Ca^{2+}$ or other entry pathways. Tam-induced $Ca^{2+}$ increase led to the release of cytochrome c from mitochondria into the cytosol and the change of mitochondrial membrane potential. In MCF-7 cells, caspase-7 plays a key role in the downstream of apoptosis because caspase-3 is absent. In the cells treated with Tam, caspase-7 cleavage was increased almost two-fold. There was no marked alteration in the level of anti-apoptotic Bcl-2 protein; however, the cells showed increased expression of pro-apoptotic Bax protein more than two-fold in response to Tam. These results imply that the apoptotic signaling pathway activated by Tam is likely to be mediated via the mitochondrial-dependent pathway.
Jang, Mi Soon;Son, Yong;Lee, Cheol;Lee, Ju Hwan;Park, Jeong Hyun;Lee, Myeong Jong
The Korean Journal of Pain
/
v.22
no.1
/
pp.58-64
/
2009
Background: Magnesium is a noncompetitive antagonist of the N-methyl-D aspartate (NMDA) receptor. Magnesium is thought to be involved in opioid tolerance by way of inhibiting calcium entry into cells. Methods: The patients were randomly assigned to three groups according to the anesthetic regimens: Group M received magnesium sulfate and Group C received saline intravenously under remifentanil-based anesthesia. Group S received saline intravenously under sevoflurane based anesthesia in place of remifentanil. The patients in the group M received 25% magnesium sulfate 50 mg/kg in 100 ml of saline, and those patients in groups C and S received an equal volume of saline before induction of anesthesia; this was followed by 10 mg/kg/h infusion of either magnesium sulfate (group M) or an equal volume of saline (groups C and S) until the end of surgery. Pain was assessed on a visual analog scale at 1, 6, 12, 24, and 36 hours after the operation. The time to the first postoperative analgesic requirement and the cumulative analgesic consumption were evaluated in the three groups. Results: The visual analog scales for pain and the cumulative analgesic consumption were significantly greater in group C than in other groups. The time to first postoperative analgesic requirement was significantly shorter in group C than that in the other groups. There were no differences between group M and S for side effects. Conclusions: A relatively high dose and continuous remifentanil infusion is associated with clinically relevant evidence of acute opioid tolerance. NMDA-receptor antagonist, magnesium sulfate as an adjuvant analgesic prevents opioid tolerance in patients who are undergoing major abdominal surgery under high dose and continuous remifentanil infusion-based anesthesia.
Purpose : The progressive deterioration of renal function in children can impose a serious and lifelong impact on their lives. The ultimate goal in the management of children with chronic kidney disease(CKD) is to prolong survival, to prevent complications, and to promote growth and neurodevelopment. The aim of this study is to investigate the risk factors for the decline of renal function in pediatric CKD patients. Methods : Data from patients who met the criteria for the Kidney Disease Outcomes Quality Initiative(K/DOQI) CKD stage 2 to 4 between August 1999 and March 2007 were retrospectively analyzed. The estimated glomerular filtration rate(eGFR) was calculated by the Schwartz formula, using serum creatinine levels and height. We calculated the annual eGFR change from the difference between the baseline eGFR and the last eGFR divided by the duration(years) of the follow-up period. We analyzed the association between the annual eGFR change and factors such as age, gender, K/DOQI stage, underlying renal disease, serum calcium, and inorganic phosphorous during the follow-up period. Results : Sixty one children(44 boys & 17 girls) were enrolled. The age at entry was $7.1{\pm}4.7$ years. The annual eGFR change was $-1.2{\pm}11.9 mL/min/1.73m^2/year$. Our study showed that older age(P=0.005). hypocalcemia(P=0.012), and hypenhosphatemia(P=0.002) were significantly related to more rapid decline in renal function. Conclusion : In pediatric CKD, older age, hypocalcemia and hyperphosphatemia are related to more rapid deterioration of renal function.
본 웹사이트에 게시된 이메일 주소가 전자우편 수집 프로그램이나
그 밖의 기술적 장치를 이용하여 무단으로 수집되는 것을 거부하며,
이를 위반시 정보통신망법에 의해 형사 처벌됨을 유념하시기 바랍니다.
[게시일 2004년 10월 1일]
이용약관
제 1 장 총칙
제 1 조 (목적)
이 이용약관은 KoreaScience 홈페이지(이하 “당 사이트”)에서 제공하는 인터넷 서비스(이하 '서비스')의 가입조건 및 이용에 관한 제반 사항과 기타 필요한 사항을 구체적으로 규정함을 목적으로 합니다.
제 2 조 (용어의 정의)
① "이용자"라 함은 당 사이트에 접속하여 이 약관에 따라 당 사이트가 제공하는 서비스를 받는 회원 및 비회원을
말합니다.
② "회원"이라 함은 서비스를 이용하기 위하여 당 사이트에 개인정보를 제공하여 아이디(ID)와 비밀번호를 부여
받은 자를 말합니다.
③ "회원 아이디(ID)"라 함은 회원의 식별 및 서비스 이용을 위하여 자신이 선정한 문자 및 숫자의 조합을
말합니다.
④ "비밀번호(패스워드)"라 함은 회원이 자신의 비밀보호를 위하여 선정한 문자 및 숫자의 조합을 말합니다.
제 3 조 (이용약관의 효력 및 변경)
① 이 약관은 당 사이트에 게시하거나 기타의 방법으로 회원에게 공지함으로써 효력이 발생합니다.
② 당 사이트는 이 약관을 개정할 경우에 적용일자 및 개정사유를 명시하여 현행 약관과 함께 당 사이트의
초기화면에 그 적용일자 7일 이전부터 적용일자 전일까지 공지합니다. 다만, 회원에게 불리하게 약관내용을
변경하는 경우에는 최소한 30일 이상의 사전 유예기간을 두고 공지합니다. 이 경우 당 사이트는 개정 전
내용과 개정 후 내용을 명확하게 비교하여 이용자가 알기 쉽도록 표시합니다.
제 4 조(약관 외 준칙)
① 이 약관은 당 사이트가 제공하는 서비스에 관한 이용안내와 함께 적용됩니다.
② 이 약관에 명시되지 아니한 사항은 관계법령의 규정이 적용됩니다.
제 2 장 이용계약의 체결
제 5 조 (이용계약의 성립 등)
① 이용계약은 이용고객이 당 사이트가 정한 약관에 「동의합니다」를 선택하고, 당 사이트가 정한
온라인신청양식을 작성하여 서비스 이용을 신청한 후, 당 사이트가 이를 승낙함으로써 성립합니다.
② 제1항의 승낙은 당 사이트가 제공하는 과학기술정보검색, 맞춤정보, 서지정보 등 다른 서비스의 이용승낙을
포함합니다.
제 6 조 (회원가입)
서비스를 이용하고자 하는 고객은 당 사이트에서 정한 회원가입양식에 개인정보를 기재하여 가입을 하여야 합니다.
제 7 조 (개인정보의 보호 및 사용)
당 사이트는 관계법령이 정하는 바에 따라 회원 등록정보를 포함한 회원의 개인정보를 보호하기 위해 노력합니다. 회원 개인정보의 보호 및 사용에 대해서는 관련법령 및 당 사이트의 개인정보 보호정책이 적용됩니다.
제 8 조 (이용 신청의 승낙과 제한)
① 당 사이트는 제6조의 규정에 의한 이용신청고객에 대하여 서비스 이용을 승낙합니다.
② 당 사이트는 아래사항에 해당하는 경우에 대해서 승낙하지 아니 합니다.
- 이용계약 신청서의 내용을 허위로 기재한 경우
- 기타 규정한 제반사항을 위반하며 신청하는 경우
제 9 조 (회원 ID 부여 및 변경 등)
① 당 사이트는 이용고객에 대하여 약관에 정하는 바에 따라 자신이 선정한 회원 ID를 부여합니다.
② 회원 ID는 원칙적으로 변경이 불가하며 부득이한 사유로 인하여 변경 하고자 하는 경우에는 해당 ID를
해지하고 재가입해야 합니다.
③ 기타 회원 개인정보 관리 및 변경 등에 관한 사항은 서비스별 안내에 정하는 바에 의합니다.
제 3 장 계약 당사자의 의무
제 10 조 (KISTI의 의무)
① 당 사이트는 이용고객이 희망한 서비스 제공 개시일에 특별한 사정이 없는 한 서비스를 이용할 수 있도록
하여야 합니다.
② 당 사이트는 개인정보 보호를 위해 보안시스템을 구축하며 개인정보 보호정책을 공시하고 준수합니다.
③ 당 사이트는 회원으로부터 제기되는 의견이나 불만이 정당하다고 객관적으로 인정될 경우에는 적절한 절차를
거쳐 즉시 처리하여야 합니다. 다만, 즉시 처리가 곤란한 경우는 회원에게 그 사유와 처리일정을 통보하여야
합니다.
제 11 조 (회원의 의무)
① 이용자는 회원가입 신청 또는 회원정보 변경 시 실명으로 모든 사항을 사실에 근거하여 작성하여야 하며,
허위 또는 타인의 정보를 등록할 경우 일체의 권리를 주장할 수 없습니다.
② 당 사이트가 관계법령 및 개인정보 보호정책에 의거하여 그 책임을 지는 경우를 제외하고 회원에게 부여된
ID의 비밀번호 관리소홀, 부정사용에 의하여 발생하는 모든 결과에 대한 책임은 회원에게 있습니다.
③ 회원은 당 사이트 및 제 3자의 지적 재산권을 침해해서는 안 됩니다.
제 4 장 서비스의 이용
제 12 조 (서비스 이용 시간)
① 서비스 이용은 당 사이트의 업무상 또는 기술상 특별한 지장이 없는 한 연중무휴, 1일 24시간 운영을
원칙으로 합니다. 단, 당 사이트는 시스템 정기점검, 증설 및 교체를 위해 당 사이트가 정한 날이나 시간에
서비스를 일시 중단할 수 있으며, 예정되어 있는 작업으로 인한 서비스 일시중단은 당 사이트 홈페이지를
통해 사전에 공지합니다.
② 당 사이트는 서비스를 특정범위로 분할하여 각 범위별로 이용가능시간을 별도로 지정할 수 있습니다. 다만
이 경우 그 내용을 공지합니다.
제 13 조 (홈페이지 저작권)
① NDSL에서 제공하는 모든 저작물의 저작권은 원저작자에게 있으며, KISTI는 복제/배포/전송권을 확보하고
있습니다.
② NDSL에서 제공하는 콘텐츠를 상업적 및 기타 영리목적으로 복제/배포/전송할 경우 사전에 KISTI의 허락을
받아야 합니다.
③ NDSL에서 제공하는 콘텐츠를 보도, 비평, 교육, 연구 등을 위하여 정당한 범위 안에서 공정한 관행에
합치되게 인용할 수 있습니다.
④ NDSL에서 제공하는 콘텐츠를 무단 복제, 전송, 배포 기타 저작권법에 위반되는 방법으로 이용할 경우
저작권법 제136조에 따라 5년 이하의 징역 또는 5천만 원 이하의 벌금에 처해질 수 있습니다.
제 14 조 (유료서비스)
① 당 사이트 및 협력기관이 정한 유료서비스(원문복사 등)는 별도로 정해진 바에 따르며, 변경사항은 시행 전에
당 사이트 홈페이지를 통하여 회원에게 공지합니다.
② 유료서비스를 이용하려는 회원은 정해진 요금체계에 따라 요금을 납부해야 합니다.
제 5 장 계약 해지 및 이용 제한
제 15 조 (계약 해지)
회원이 이용계약을 해지하고자 하는 때에는 [가입해지] 메뉴를 이용해 직접 해지해야 합니다.
제 16 조 (서비스 이용제한)
① 당 사이트는 회원이 서비스 이용내용에 있어서 본 약관 제 11조 내용을 위반하거나, 다음 각 호에 해당하는
경우 서비스 이용을 제한할 수 있습니다.
- 2년 이상 서비스를 이용한 적이 없는 경우
- 기타 정상적인 서비스 운영에 방해가 될 경우
② 상기 이용제한 규정에 따라 서비스를 이용하는 회원에게 서비스 이용에 대하여 별도 공지 없이 서비스 이용의
일시정지, 이용계약 해지 할 수 있습니다.
제 17 조 (전자우편주소 수집 금지)
회원은 전자우편주소 추출기 등을 이용하여 전자우편주소를 수집 또는 제3자에게 제공할 수 없습니다.
제 6 장 손해배상 및 기타사항
제 18 조 (손해배상)
당 사이트는 무료로 제공되는 서비스와 관련하여 회원에게 어떠한 손해가 발생하더라도 당 사이트가 고의 또는 과실로 인한 손해발생을 제외하고는 이에 대하여 책임을 부담하지 아니합니다.
제 19 조 (관할 법원)
서비스 이용으로 발생한 분쟁에 대해 소송이 제기되는 경우 민사 소송법상의 관할 법원에 제기합니다.
[부 칙]
1. (시행일) 이 약관은 2016년 9월 5일부터 적용되며, 종전 약관은 본 약관으로 대체되며, 개정된 약관의 적용일 이전 가입자도 개정된 약관의 적용을 받습니다.