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엄민식,박원우,서승철,이진호,조주연,최혜영,이찬희,임소덕 白中央醫療院 2005 仁濟醫學 Vol.26 No.1
Relapsing polychondritis is an uncommon multisystemic disease which is characterized by recurrent episodes of inflammation and progressive destruction of cartilaginous tissue. The cause of relapsing polychondritis is unclear and suspected to be autoimmune pathophysiology. It involves cartilage of nose, vertebra, trachea, peripheral joint as well as structures of eye, heart, blood vessels or inner ear. Auricular chondritis is present in almost all patients, and multiple arthritis, nasal chondritis, saddle nose, eye involvement, laryngotracheal involvement and skin manifestations are also present. We report a case of relapsing polychondritis presented a arthritis with review of literatures.
Lim, So Dug,Kim, Wanseop,Ahn, Geunghwan,Kwon, Ghee Young Blackwell Publishing Asia 2007 Pathology international Vol.57 No.9
<P>Renal angiomyolipoma (AML) is a benign but progressive tumor that occasionally requires non-surgical therapy and there appears to be a possibility that epidermal growth factor (EGF) is associated with pathogenesis of renal AML. The response to gefitinib, anti-epidermal growth factor receptor (EGFR) agent and a prime example of target therapy, reportedly has been correlated with the presence of mutations within the tyrosine kinase (TK) domain of <I>EGFR</I> or the expression of its truncated form, <I>EGFR</I> variant III. Therefore the purpose of the present paper was to investigate EGFR protein expression and gene mutations in exons 18, 19 and 21 in 40 renal AML. No <I>EGFR</I> gene mutations of TK domain were detected in any of the 40 cases studied and strong immunostaining was found in 5% of the renal AML cases. The present findings indicate that in renal AML, anti-EGFR treatment may not be promising but that there is a possibility that EGFR is associated with renal AML pathogenesis.</P>
Gliadin intake induces oxidative-stress responses in <i>Caenorhabditis elegans</i>
Lim, So Dug,Min, Hyemin,Youn, Esther,Kawasaki, Ichiro,Shim, Yhong-Hee Elsevier 2018 Biochemical and biophysical research communication Vol.503 No.3
<P><B>Abstract</B></P> <P>Clinical attention to gluten-related disorders, such as celiac disease and nonceliac gluten sensitivity, is on the rise. However, identifying the pathophysiological mechanisms of gluten-related disorders remains elusive. Gliadin, a component of gluten, is known to play a major role in gluten toxicity. <I>Caenorhabditis elegans</I> has been widely used as the predominant experimental animal model to study toxicity and stress response in biomedical research. We investigated the stress response induced by gliadin intake in <I>C. elegans</I> to evaluate its toxicity and found brood size, body bending, and pumping rates to be significantly altered in response to gliadin. Notably, reactive oxygen species (ROS) production and <I>Pgst-4::GFP</I> transgene expression, an indicator of the oxidative-stress response, were significantly increased after gliadin intake. Reduced pumping rates were most likely caused by gliadin-induced oxidative stress, since pumping rates in oxidative stress-sensitive <I>mev-1</I> mutants were more severely reduced than in oxidative stress-resistant <I>daf-2</I> mutants following gliadin intake. Our results indicated that gluten/gliadin intake in <I>C. elegans</I> triggered ROS production and induced an oxidative stress response that reduced pumping rates and decreased brood size. We suggest <I>C. elegans</I> to be a useful model system for studying gluten/gliadin toxicity.</P> <P><B>Highlights</B></P> <P> <UL> <LI> Locomotion behavior and brood size were reduced in <I>C. elegans</I> fed with gliadin. </LI> <LI> ROS production and oxidative-stress responses were increased with gliadin intake. </LI> <LI> Reduction in pumping rate was caused by the gliadin-induced oxidative stress. </LI> </UL> </P>
Kwi-Dug Yun,Min-Kyung Ji,Hyun-Pil Lim,Hyun-Seung Kim,Sang-Won Park,Hong-So Yang,Han-Sung Joo 대한치과보철학회 2015 The Journal of Advanced Prosthodontics Vol.7 No.3
PURPOSE This study evaluated the fracture load of customized zirconia abutments with titanium insert according to preparation depths, with or without 5-year artificial aging. MATERIALS AND METHODS Thirty-six identical lithium disilicate crowns (IPS e.max press) were fabricated to replace a maxillary right central incisor and cemented to the customized zirconia abutment with titanium insert on a 4.5×10 mm titanium fixture. Abutments were fabricated with 3 preparation depths (0.5 mm, 0.7 mm, and 0.9 mm). Half of the samples were then processed using thermocycling (temperature: 5-55℃, dwelling time: 120s) and chewing simulation (1,200,000 cycles, 49 N load). All specimens were classified into 6 groups depending on the preparation depth and artificial aging (non-artificial aging groups: N5, N7, N9; artificial aging groups: A5, A7, A9). Static load was applied at 135 degrees to the implant axis in a universal testing machine. Statistical analyses of the results were performed using 1-way ANOVA, 2-way ANOVA, independent t-test and multiple linear regression. RESULTS The fracture loads were 539.28 ± 63.11 N (N5), 406.56 ± 28.94 N (N7), 366.66 ± 30.19 N (N9), 392.61 ± 50.57 N (A5), 317.94 ± 30.05 N (A7), and 292.74 ± 37.15 N (A9). The fracture load of group N5 was significantly higher than those of group N7 and N9 (P<.017). Consequently, the fracture load of group A5 was also significantly higher than those of group A7 and A9 (P<.05). After artificial aging, the fracture load was significantly decreased in all groups with various preparation depths (P<.05). CONCLUSION The fracture load of a single anterior implant restored with lithium disilicate crown on zirconia abutment with titanium insert differed depending on the preparation depths. After 5-year artificial aging, the fracture loads of all preparation groups decreased significantly.
An Autopsy-proven Case-based Review of Autoimmune Encephalitis
심유미,김성익,So Dug Lim,이광훈,Eric Eunshik Kim,Jae Kyung Won,Sung-Hye Park 한국뇌신경과학회 2024 Experimental Neurobiology Vol.33 No.1
Autoimmune encephalitis (AIE) is a type of immunoreactive encephalitic disorder and is recognized as the most prevalent noninfectious encephalitis. Nevertheless, the rarity of definitive AIE diagnosis through biopsy or autopsy represents a significant hurdle to understanding and managing the disease. In this article, we present the pathological findings of AIE and review the literature based on a distinct case of AIE presenting as CD8+ T-lymphocyte predominant encephalitis. We describe the clinical progression, diagnostic imaging, laboratory data, and autopsy findings of an 80-year-old deceased male patient. The patient was diagnosed with pulmonary tuberculosis 6 months before death and received appropriate medications. A week before admission to the hospital, the patient manifested symptoms such as a tendency to sleep, decreased appetite, and confusion. Although the patient temporally improved with medication including correction of hyponatremia, the patient progressed rapidly and died in 6 weeks. The brain tissue revealed lymphocytic infiltration in the gray and white matter, leptomeninges, and perivascular infiltration with a predominance of CD8+ T lymphocytes, suggesting a case of AIE. There was no detectable evidence of viral infection or underlying neoplasm. The autopsy revealed that this patient also had Alzheimer’s disease, atherosclerosis, arteriolosclerosis, and aging-related tau astrogliopathy. This report emphasizes the pivotal role of pathological examination in the diagnosis of AIE, especially when serological autoantibody testing is not available or when a patient is suspected of having multiple diseases.