Comparative Evaluation of Nanofibrous Scaffolding for Bone Regeneration in Critical-Size Calvarial Defects

Woo, Kyung Mi,Chen, Victor J.,Jung, Hong-Moon,Kim, Tae-Il,Shin, Hong-In,Baek, Jeong-Hwa,Ryoo, Hyun-Mo,Ma, Peter X. Mary Ann Liebert 2009 Tissue engineering. Part A Vol.15 No.8

<P>In a previous study we found that nanofibrous poly(l-lactic acid) (PLLA) scaffolds mimicking collagen fibers in size were superior to solid-walled scaffolds in promoting osteoblast differentiation and bone formation in vitro. In this study we used an in vivo model to confirm the biological properties of nanofibrous PLLA scaffolds and to evaluate how effectively they support bone regeneration against solid-walled scaffolds. The scaffolds were implanted in critical-size defects made on rat calvarial bones. Compared with solid-walled scaffolds, nanofibrous scaffolds supported substantially more new bone tissue formation, which was confirmed by micro-computed tomography measurement and von Kossa staining. Goldner's trichrome staining showed abundant collagen deposition in nanofibrous scaffolds but not in the control solid-walled scaffolds. The cells in these scaffolds were immuno-stained strongly for Runx2 and bone sialoprotein (BSP). In contrast, solid-walled scaffolds implanted in the defects were stained weakly with trichrome, Runx2, and BSP. These in vivo results demonstrate that nanofibrous architecture enhances osteoblast differentiation and bone formation.</P>

Isolation and expression analysis of stimulator of interferon gene from olive flounder, Paralichthys olivaceus

Ma, Jeong-In,Kang, Sunhye,Jeong, Hyung-Bok,Lee, Jehee The Korean Society of Fisheries and Aquatic Scienc 2018 Fisheries and Aquatic Sciences Vol.21 No.3

Stimulator of interferon gene (STING) is induced by various inflammatory agents, such as lipopolysaccharide and microbial pathogens, including virus and bacteria. In this study, we obtained a full-length cDNA of a STING homolog from olive flounder using rapid amplification of cDNA ends PCR technique. The full-length cDNA of Paralichthys olivaceus STING (PoSTING) was 1442 bp in length and contained a 1209-bp open reading frame that translated into 402 amino acids. The theoretical molecular mass of the predicted protein sequence was 45.09 kDa. In the PoSTING protein, three transmembrane domains and the STING superfamily domain were identified as characteristic features. Quantitative real-time PCR revealed that PoSTING expressed in all the tissues analyzed, but showed the highest level in the spleen. Temporal expression analysis examined the significantly upregulated expression of PoSTING mRNA after viral hemorrhagic septicemia virus (VHSV) stimulation. In contrast, no significant changes in the PoSTING expression were detected in Edwardsiella tarda-challenged group compared to the un-injected control. The expression of P. olivaceus type I interferon (PoIFN-I) was also highly upregulated upon VHSV challenge. These results suggest that STING might be involved in the essential immune defense against viral infection together with the activation of IFN-I in olive flounder.

Paricalcitol attenuates cyclosporine-induced kidney injury in rats

Park, Jeong Woo,Bae, Eun Hui,Kim, In Jin,Ma, Seong Kwon,Choi, Chan,Lee, JongUn,Kim, Soo Wan International Society of Nephrology 2010 Kidney international Vol.77 No.12

Despite its benefits, the clinical use of cyclosporine A (CsA) is limited by its nephrotoxic properties. Because paricalcitol (19-nor-1,25-hydroxyvitamin D<SUB>2</SUB>) has renoprotective effects, we tested whether it can blunt renal dysfunction and fibrosis in a rat model of CsA-induced nephropathy. Treatment with CsA decreased creatinine clearance, increased monocyte/macrophage infiltration, and increased the expression of inflammatory cytokines within the kidney. Paricalcitol reduced the decline in kidney function and pro-fibrotic changes and also blunted the increased transforming growth factor (TGF)-β1 expression and Smad signaling. Using an in vitro model, we treated HK-2 cells with CsA and found that paricalcitol attenuated the CsA-induced increases in phosphorylated extracellular signal-regulated and c-Jun N-terminal kinases, and also prevented the activation of nuclear factor-κB. Paricalcitol effectively prevented TGF-β1-induced epithelial-to-mesenchymal transitions and extracellular matrix accumulation as evidenced by attenuated collagen deposition and fibrosis in CsA-treated rats. In addition, paricalcitol decreased the number of TUNEL-positive nuclei and reduced the expression of pro-apoptotic markers in CsA-treated HK-2 cells. Thus, paricalcitol appears to attenuate CsA-induced nephropathy by suppression of inflammatory, pro-fibrotic, and apoptotic factors through inhibition of the nuclear factor-κB, Smad, and mitogen-activated protein kinase signaling pathways.

Antiapoptotic Effect of Paricalcitol in Gentamicin-induced Kidney Injury

Sang Heon Suh,Ko Eun Lee,Jeong Woo Park,In Jin Kim,Ok Kim,Chang Seong Kim,Joon Seok Choi,Eun Hui Bae,Seong Kwon Ma,Jong Un Lee,Soo Wan Kim 대한생리학회-대한약리학회 2013 The Korean Journal of Physiology & Pharmacology Vol.17 No.5

While the anti-apoptotic effect of paricalcitol has been demonstrated in various animal models, it is not yet clear whether paricalcitol attenuates the apoptosis in gentamicin (GM)-induced kidney injury. We investigated the effect of paricalcitol on apoptotic pathways in rat kidneys damaged by GM. Rats were randomly divided into three groups: 1) Control group (n=8), where only vehicle was delivered, 2) GM group (n=10), where rats were treated with GM (150 mg/kg/day) for 7 days, 3) PARI group (n=10), where rats were co-treated with paricalcitol (0.2 Ռg/kg/day) and GM for 7 days. Paricalcitol attenuated renal dysfunction by GM administration in biochemical profiles. In terminal deoxynu-cleotidyl transferase dUTP nick end labeling staining, increased apoptosis was observed in GM group, which was reversed by paricalcitol co-treatment. Immunoblotting using protein samples from rat cortex/outer stripe of outer medulla showed increased Bax/Bcl-2 ratio and cleaved form of caspase-3 in GM group, both of which were reversed by paricalcitol. The phosphorylated Jun-N-terminal kinase (JNK) expression was increase in GM, which was counteracted by paricalcitol. The protein expression of p-Akt and nitro-tyrosine was also enhanced in GM-treated rats compared with control rats, which was reversed by paricalcitol co-treatment. Paricalcitol protects GM-induced renal injury by antiapoptotic mechanisms, including inhibition of intrinsic apoptosis pathway and JNK.

Increased Expression of Endothelin-1 and CYP11B2 in Gentamicin-Induced Nephropathy in Rat Kidney

( Eun Hui Bae ),( In Jin Kim ),( Yoon Wha Oh ),( Woo Kyun Bae ),( Jeong Woo Park ),( Seong Kwon Ma ),( Nam Ho Kim ),( Chul Choi ),( Jong Un Lee ),( Suhn Hee Kim ),( Soo Wan Kim ) 대한신장학회 2007 Kidney Research and Clinical Practice Vol.26 No.6

Purpose : An altered activity of vasoactive hormones as well as aldosterone synthase (CYP11B2) in the kidney may involve the pathogenesis of gentamicin-induced nephropathy. The present study was designed to investigate whether there are changes of local renin-angiotensin-aldosterone system (RAAS) and endothelin (ET) in the kidney of gentamicin-induced nephropathy in rats. Methods : Male Sprague-Dawley rats (180-200 g) were intramuscularly injected with gentamicin (100 mg/kg per day) for 5 days. Vehicle was given for the control rats. The mRNA expression of local renin-angiotensin system, aldosterone synthase (CYP11B2), ET system and transforming grow factor-β1 (TGF-β1) was determined in the kidney by real-time polymerase chain reaction. The protein expression of TGF-β in the kidney was determined by immunoblotting and immunohistochemistry. Results : Following the gentamicin treatment, a renal failure was noted as evidenced by increased serum concentrations of creatinine along with a decrease of its clearance. TGF-β1 expression was significantly increased in the kidney in gentamicin treated rats compared with that in controls. The abundance of ET-1 mRNA was significantly increased. The endothelin type A receptor expression was decreased while endothelin type B receptor was not changed. The expression of angiotensin converting enzyme 1 (ACE1) and ACE2 was decreased, whereas renin expression was not changed. The CYP11B2 expression was significantly increased in gentamicin treated rats, while mineralocorticoid receptor expression was not changed. Conclusion : The expression of ET-1 and CYP11B2 was up-regulated which may play a role in the pathogenesis of gentamicin-induced nephropathy.

Antiapoptotic Effect of Paricalcitol in Gentamicin-induced Kidney Injury

Suh, Sang Heon,Lee, Ko Eun,Park, Jeong Woo,Kim, In Jin,Kim, Ok,Kim, Chang Seong,Choi, Joon Seok,Bae, Eun Hui,Ma, Seong Kwon,Lee, Jong Un,Kim, Soo Wan The Korean Society of Pharmacology 2013 The Korean Journal of Physiology & Pharmacology Vol.17 No.5

While the anti-apoptotic effect of paricalcitol has been demonstrated in various animal models, it is not yet clear whether paricalcitol attenuates the apoptosis in gentamicin (GM)-induced kidney injury. We investigated the effect of paricalcitol on apoptotic pathways in rat kidneys damaged by GM. Rats were randomly divided into three groups: 1) Control group (n=8), where only vehicle was delivered, 2) GM group (n=10), where rats were treated with GM (150 mg/kg/day) for 7 days, 3) PARI group (n=10), where rats were co-treated with paricalcitol (0.2 ${\mu}g/kg/day$) and GM for 7 days. Paricalcitol attenuated renal dysfunction by GM administration in biochemical profiles. In terminal deoxynucleotidyl transferase dUTP nick end labeling staining, increased apoptosis was observed in GM group, which was reversed by paricalcitol co-treatment. Immunoblotting using protein samples from rat cortex/outer stripe of outer medulla showed increased Bax/Bcl-2 ratio and cleaved form of caspase-3 in GM group, both of which were reversed by paricalcitol. The phosphorylated Jun-N-terminal kinase (JNK) expression was increase in GM, which was counteracted by paricalcitol. The protein expression of p-Akt and nitro-tyrosine was also enhanced in GM-treated rats compared with control rats, which was reversed by paricalcitol co-treatment. Paricalcitol protects GM-induced renal injury by antiapoptotic mechanisms, including inhibition of intrinsic apoptosis pathway and JNK.

Effects of Rosiglitazone on Heat Shock Protein and the Endothelin System in Deoxycorticosterone Acetate-Salt Hypertensive Rats

( Eun Hui Bae ),( In Jin Kim ),( Jeong Woo Park ),( Seong Kwon Ma ),( Ki Chul Choi ),( Jong Un Lee ),( Soo Wan Kim ) 대한전해질학회 2008 Electrolytes & Blood Pressure Vol.6 No.1

The deoxycorticosterone acetate (DOCA)-salt rat is known as a model of volume dependent hypertension and characterized by increased cardiac endothelin-1 (ET-1) content. Recently, it has been reported that rosiglitazone (RGT), a peroxisome proliferator-activated subtype gamma receptor agonist, shows blood pressure lowering effect. We investigated whether DOCA-salt hypertension is associated with altered expression of heat shock proteins (HSP) and ET-1 in the heart, aorta, and kidney, and whether RGT changes HSP expression and ET-1 in association with its blood pressure lowering effect. Two weeks after the silastic DOCA (200 mg/kg) strips implantation, DOCA-salt rats were randomly divided to receive control diet with or without RGT (10 mg/kg/day) for another 2 weeks. The mRNA expression of ET-1 was determined by real time polymerase chain reaction. The expression of HSP was determined by semiquantitative immunoblotting. In DOCA-salt rats, systolic blood pressure was markedly increased, while creatinine clearance decreased. RGT treatment attenuated high blood pressure and decreased creatinine clearance in DOCA-salt rats. The mRNA expression of ET-1 was increased in DOCA-salt rats compared to controls, which was counteracted by RGT treatment. The protein expression of HSP70, HSP32, and HSP25 was increased in the kidney and heart in DOCA-salt rats, which was attenuated by RGT treatment in the kidney, but not in the heart. In conclusion, increased expression of ET-1 may play a role in the pathogenesis of hypertension in DOCA-salt rats, which was counteracted by the treatment of RGT. Up-regulation of HSP70, HSP32, and HSP25 in the kidney and heart may play a role in organ protection against a variety of stresses.

전남지역에서 생산되고 있는 차들의 항산화, α-Glucosidase 저해 및 항염증 활성

김진영(Jin Young Kim),조정용(Jeong-Yong Cho),박경진(Kyung Jin Park),박숙(Sook Park),문희(Hee Moon),안양준(Yang Joon An),하훈(Hoon Ha),양수인(Soo In Yang),마승진(Seung Jin Ma),나환식(Hwan Sik Na) 한국차학회 2016 한국차학회지 Vol.22 No.2

The aim of this study was to investigate and compare antioxidative, α-glucosidase inhibitory, and anti-inflammation activities of five teas [Boseong green tea (BG), Damyang Jukro tea (DJ), Gurye yellow tea (GY), Boseong black tea (BB), and Jangheung Chungtaejeon tea (JC)] produced in Jeollanamdo. BG and JC showed higher radical-scavenging activities than the other tea samples in the in vitro assays of 1,1-diphenyl-2-picrylhydrazyl nitrite radicals. In addition, BG and JC were more effective in inhibiting α-glucosidase than GY and BB. DJ, having low radical scavenging activity showed high α-glucosidase inhibitory activity, which was similar to those of BG and JC. All of the tea samples had weak cytotoxicities on macrophage RAW 264.7 cells at a concentration of 100 μg/mL. They also showed anti-inflammatory activities via the suppression of inducible nitric oxide synthase and nitrite oxide production in LPS-induced RAW 264.7 cells, although their activities were slightly different. These results indicate that the tea manufacturing method and environmental factors of tea cultivation play an important role in enhancing the biological activities of the tea samples.

복수의 감별에 있어 혈청과 복수내 CEA 및 CA19-9의 가치에 관한 연구

김선민 ( Kim Seon Min ),박경식 ( Park Gyeong Sig ),마상인 ( Ma Sang In ),김휘정 ( Kim Hwi Jeong ),유승박 ( Yu Seung Bag ),조준환 ( Jo Jun Hwan ),이재동 ( Lee Jae Dong ),이중건 ( Lee Jung Geon ) 대한내과학회 1992 대한내과학회지 Vol.42 No.4

Ascites may be caused by various benign and malignant disease, but it is sometimes difficult to determine whether it is caused by benign disease or malignant diseases. In order to determine whether CEA, CA 19-9 in ascitic fluid and serum assist in the diagnosis of malignant disease that causing ascites, we studied 38 cases of malignant ascites and 43 cases of benign ascites patients who were admitted to Seoul Adventist Hospital from April 1989 to December 1990. The results were obtained as follows: 1) The mean value of CEA in serum and ascitic fluid of the malignant ascites group were significantly higher than that of the benign ascites group in serum (p<0.05), in ascites (p<0.01). 2) The mean value of CA 19-9 in serum and ascitic fluid of the malignant ascites group was signficantly higher than that of the benign ascites group was significantly higher than that of the benign ascites group, there was no significance in statistical aspects(p>0.05). 3) The sensitivity of CEA was 81% in ascites, 78% in serum, the sensitivity of CA 19-9 was 63% in ascites, 65% in serum. 4) The sensitivity of CEA was increased to 87% in serum and ascites combinations, the sensitivity of CA 19-9 was also increased to 81% in serum and ascites combinations. The sensitivity was significantly elevated to 92% in case of all tumor marker combinations. 5) There was a significant correlations between serum CEA and ascites CEA, serum CA 19-9 and ascites CA 19-9. (p<0.01, in all cases) It was concluded that the measurement of serum and ascites CEA, CA 19-9 levels is useful lin differention between ascites caused by benign and malignant diseases. Combinantions of each tumor markers in serum and ascites were more accurate than single test.

실명을 주소로 한 신경아세포종 1예

마인열,하정옥,김춘동,이태숙 영남대학교 의과대학 1985 Yeungnam University Journal of Medicine Vol.2 No.1

신생아세포종은 소아기에 발생하는 악성종양중 뇌종양 다음으로 흔히 발생하는 것으로 원발 혹은 전이된 부위에 따라 다양한 임상증상이 나타날 수 있으나 실명을 주소로 한 경우는 드물다. 본 증례는 4세된 남아의 복부에서 기원하여 사골동으로 원위전이하여 갑작스런 실명을 주소로한 신경아세포종으로 cytoxan, vincristine, DTIC, adriamycin 및 VM-26의 병합요법으로 치료하여 실명은 그대로 있으나 복부와 사골동의 종괴는 현저히 감소하였고 환아는 건강이 양호한 상태이다. Neuroblastoma is the most common extracranial solid tumor of childhood which presents various clinical symptoms depending on the primary and metastatic sites. However, it has been rarely reported that sudden onset of blindness was the chief complaint of neuroblastoma. A four years old boy was admitted to the Yeungnam University Hospital with the chief complaint of a sudden onset of blindness due to a distant metastasis of abdominal neuroblastoma to the sphenoid sinus. On admission, both side pupils were dilated without light reflex, fundoscopy showed pale optic disk, electroretinogram was subnormal and visual evoked potential showed no response. The liver was palpable in 3½ finger breadth from the right costal margin and adult fist sized mass was palpable in the right flank. Skull X-ray showed destructed sphenoid bone and clinoid process and brain CT scan showed tumor mass in the sphenoid sinus and left orbit. Ultrasonogram and CT scan of the abdomen showed large tumor masses around the right kidney and para-aortic and retropancreatic lymph node. IVP showed displaced right calyceal system with preserved contour. Left supraclavicular lymph node which appeared after admission was biopsied and it showed poorly differentiated neuroblasts. He was treated according to the multiagent chemotherapy schedule for stage IV neuroblastoma patient of children's cancer study group. Adbominal tumor masses and sphenoid sinus mass were markedly reduced after 2 courses of the combination chemotherapy of cyclophosphamide, vincristine, DTIC, adriamycin and VM-26. Eventhough the blindness was not improved, the patient has been in good clinical condition.