• 대한수의사회지
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• 제7권1호
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• pp.74-77
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• 1963

The histological and cytological characteristics of pancreatic islets of chickens were studied along with the distribution and size of islets and weight of chicken pancreas versus body weight. The following is a summarg of the present work. 1. The weight

• Journal of Microbiology and Biotechnology
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• 제9권4호
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• pp.522-524
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• 1999

A discontinuous Percoll gradient was used to separate islets from the collagenase-treated mouse pancreas easily and rapidly. Since the osmolality of Percoll is very low, adjustment of its osmolality to 340 mOs/kg $H_2$O was essential for securing the optimal separation. A discontinuous gradient layering with Percoll solution of 1.09 g, 1.07g, and1.05g/m, respectively, when centrifuged at 800$\times$g for 10 min, resulted in an optimal condition for separation and yielded a banding pattern with an even distribution of islet cells. No significant difference was observed in the morphological features between the Percoll-isolated and the manually-isolated islets. In conclusion, the discontinuous Percoll gradient can be effectively used to isolate the pancreatic islets from mice with four-fold higher efficiency compared to the handpicking method.

• 약학회지
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• 제42권4호
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• pp.408-413
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• 1998

To establish prediabetes in vitro/ model concerning the etiology of Insulin Dependent Diabetes Mellitus (IDDM) in cellular level we have designed experimental prediabefic model in pancreatic beta cells. RINm5F, HIT-T15 and isolated rat islets were chosen as pancreatic beta cells. Since interleukin-$1{\beta}$-induced beta cell cytotoxicity has been implicated in the autoimmune cytotoxicity of IDDM, we used inteleukin-$1{\beta}$ as diabetogenic agent. For establishment of prediabetic in vitro model, the degree of beta cell deterioration was determined by cell proliferation, insulin release and morphological appearance. Cell proliferation, insulin release and morphology were changed dose-dependently in condition that inteleuldn-$1{\beta}$ was exposured to pancreatic beta cells. The concentration and exposure time of interleukin-$1{\beta}$ to set up prediabetic model in beta cell lines and isolated rat islets were 100${\sim}$1000U/ml, 48hr. And 25${\sim}$100U/ml, 48hr, respectively.

• IMMUNE NETWORK
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• 제4권1호
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• pp.53-59
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• 2004

Background: Minor histocompatibility HY antigen, as a transplantation antigen, has been known to cause graft rejection in MHC (major histocompatibility complex) matched donor-recipient. The aim of our study is to investigate the role of male antigen (HY) disparity on MHC matched pancreatic islet transplantation and to examine the mechanism of the immune reaction. Methods: Pancreatic islets were isolated and purified by collagen digestion followed by Ficoll gradient. The isolated islets of male C57BL6/J were transplanted underneath the kidney capsule of syngeneic female mice rendered diabetic with streptozotocine. Blood glucose was monitored for the rejection of engrafted islets. After certain period of time, tail to flank skin transplantation was performed either on mouse transplanted with HY mismatched islets or on sham treated mouse. The rejection was monitored by scoring gross pathology of the engrafted skin. Results: HY mismatched islets survived more than 300 days in 14 out of 15 mice. The acceptance of second party graft (male B6 islets) and the rejection of third party graft (male BALB/c islets) in these mice suggested the tolerance to islets with HY disparity. B6 Skin with HY disparity was rejected on day $25{\pm}7$. However, HY mismatched skin transplanted on the mice tolerated to HY mismatched islets survived more than 240 days. Tetramer staining in these mice indicated the CTL recognizing MHC Db/Uty was not deleted or anergized. Conclusion: The islet transplantation across HY disparity induced tolerance to HY antigen in C57BL6 mouse, which in turn induced tolerance to HY mismatched skin, which otherwise would be rejected within 25 days. The MHC tetramer staining suggested the underlying mechanisms would not be clonal deletion or anergy.

• 한국생물공학회:학술대회논문집
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• 한국생물공학회 2000년도 추계학술발표대회 및 bio-venture fair
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• pp.695-698
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• 2000

We studied the viability and function of islet with monomethoxy polyethylene glycol (mPEG) grafted onto its membrane. Islets were isolated from rat and were repeatedly reacted with activated mPEG (mw 5000) in order to increase grafting density. The density of grafted PEG on the islet membrane was confirmed by Fluorescein-PEG-NHS. An assessment of islet viability using AO / PI staining method showed that multiple PEGylation did not reduce islet viability. The function of PEG grafted islets was evaluated by measuring released insulin from islets. Insulin secreted from the PEGylated islets for 1 h did not show any significant difference compared to control (non-PEGylated) islets. In addition, PEGylated islets responded in the same pattern as control islets in the perifusion test.

• The Korean Journal of Physiology and Pharmacology
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• 제7권4호
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• pp.211-215
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• 2003

To examine the localization pattern of phospholipase D2 (PLD2) in the pancreatic islet (the islet of Langerhans) depending on species, we conducted a morphological experiment in the rat and guinea pig. Since individual islets display a typical topography with a central core of B cell mass and a peripheral boundary of A, D, and PP cells, double immunofluorescent staining with a panel of antibodies was performed to identify PLD2-immunoreactive cells in the islets PLD2 immunoreactivity was mainly present in A and PP cells of the rat pancreatic islets. And yet, in the guinea pig, PLD2 immunoreactivity was exclusively localized in A cells, and not in PP cells. These findings suggest a possibility that PLD2 is mainly located in A cells of rodent pancreatic islets, and that the existence of PLD2 in PP cells is not universal in all species. Based on these results, it is suggested that PLD2 may play a significant role in the function of A and/or PP cells via a PLD-mediated signaling pathway.

• Journal of Microbiology and Biotechnology
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• 제32권12호
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• pp.1615-1621
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• 2022

Tissue regeneration is the ultimate treatment for many degenerative diseases, however, repair and regeneration of damaged organs or tissues remains a challenge. Previously, we showed that B1 Ab and H3 Ab induce stem cells to differentiate into microglia and brown adipocyte-like cells, while trafficking to the brain and heart, respectively. Here, we present data showing that another selected agonist antibody, P1 antibody, induces the migration of cells to the pancreatic islets and differentiates human stem cells into beta-like cells. Interestingly, our results suggest the purified P1 Ab induces beta-like cells from fresh, human CD34⁺ hematopoietic stem cells and mouse bone marrow. In addition, stem cells with P1 Ab bound to expressed periostin (POSTN), an extracellular matrix protein that regulates tissue remodeling, selectively migrate to mouse pancreatic islets. Thus, these results confirm that our in vivo selection system can be used to identify antibodies from our library which are capable of inducing stem cell differentiation and cell migration to select tissues for the purpose of regenerating and remodeling damaged organ systems.

• The Korean Journal of Physiology and Pharmacology
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• 제7권5호
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• pp.261-266
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• 2003

Type 1 diabetes is an organ-specific autoimmune disease caused by the cytotoxic T cells-mediated destruction of the insulin-producing beta cells in the Langerhans pancreatic islets. Hepatocyte growth factor (HGF) is a potent mitogen and a promoter of proliferation of insulin producing beta cells of pancreatic islets. To study the role of HGF via viral vector in the development of streptozotocin (STZ)-induced diabetes in mice, we have developed an adenoviral vector genetically engineered to carry the gene for human HGF (hHGF) and evaluate the change of blood glucose, insulin level, and insulin-secreting beta cells of pancreatic islets. We demonstrate that the treatment with hHGF gene prevented the development of STZ-induced diabetes and increased serum insulin level to above normal range. Furthermore, it preserved pancreatic beta cells from destruction. These in vivo results may support previous findings that HGF is insulinotropic agent for beta cells and HGF treatment renders the cells to be resistant to the development of diabetes from STZ administration. We suggest that an adenoviral mediated hHGF gene therapy is a good candidate for the prevention and treatment of type 1 diabetes.

• 대한수의학회지
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• 제42권1호
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• pp.21-28
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• 2002

ICR 마우스 췌장에 존재하는 내분비세포의 부위별 분포 및 상대적 빈도를 4 종류의 항혈청 즉, insulin, glucagon, somatostatin 및 human pancreatic polypeptide (PP)을 사용하여 면역조직화학적 방법으로 관찰하였다. 마우스의 췌장은 췌장섬, 외분비부 및 췌관의 3 부분으로 구별되었으며, 췌장섬은 이들 면역반응세포들의 출현 부위에 따라 다시 중심부분, mantle부분 및 가장자리부분으로 다시 세분되었다. 췌장섬의 경우, insulin 면역반응세포들은 주로 췌장섬의 중심부분과 mantle 부분에서 주로 관찰되었으나, somatostatin, glucagon 및 PP 면역반응세포들은 다양한 출현빈도를 나타내며 주로 mantle부분과 가장자리부분에 걸쳐 관찰되었다. 또한 극소수의 PP 면역반응세포들은 췌장섬의 중심부분에서도 관찰되었다. 외분비부에서도 insulin, glucagon, somatostatin 및 PP 면역반응세포들 모두 관찰되었으며, 주로 외분비 샘포 세포 사이공간에서 관찰되었다. 췌관에서는 insulin 및 glucagon 면역반응세포들이 소수 또는 극소수의 빈도로 췌관 상피세포 사이공간에서 관찰되었으며, 극소수의 PP 면역반응세포들 역시 췌관상피 아래부위에서 관찰되었으나, somatostatin 면역반응세포들은 이 부위에서 관찰되지 않았다.

• 대한수의학회지
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• 제40권3호
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• pp.421-430
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• 2000

태아기, 신생아기, 생후 1개월령, 6개월령 및 성체의 한국재래산양 췌장에서 pancreatic poluypeptide(PP) 면역반응세포의 분포 및 출현빈도를 PAP 법에 의해 검색하였다. 외분비부에서는 모든 연령에서 관찰되었으며 췌장세포 사이에 분포하였다. PP 면역반응세포는 신생아가기에서 생후 1개월에 증가한 후 점차 감소하였다. 췌도관에서는 PP 면역반응세포가 생후 1개월부터 관찰되면 그후 점차 감소하였다. 췌도관에서는 PP 면역반응세포가 생후 1개월부터 관찰되면 그후 점차 감소하였다. 이들 면역반응세포는 생후 1개월령 및 6개월령의 췌도관 상피하 결합조직에서 소수 관찰되었다. 그러나 성체에서는 췌도관 상피세포 사이에서 극소수 관찰되었다. 그러나 성체에서는 췌도관 상피세포 사이에서 극소수 관찰되었다. 내분비부(췌장섬)에서 PP 면역반응세포는 신생아기부터 관찰되며, 생후 1개월령부터의 PP면역세포의 분포는 췌장성 주변부에 중등도 또는 소수가 산재하는 것과 다수의 PP 면역반응세포가 췌도 전체 (생후 1개월령)또는 췌도 중앙부(생후 6개월령)에 산재하는 것 등 두가지 유형을 나타내었다. 결론적으로 한국 재래산양의 췌장에 있어서 PP 면역반응세포의 분포와 출현빈도는 발생단계에 따라 상이하였다. 이는 발생단계 동안의 식이성 및 생리학적 조건변화가 이와같은 상이함을 유발하는 요인이 된 것으로 사료된다.