• Journal of Embryo Transfer
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• v.25 no.3
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• pp.201-206
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• 2010

Two male reticulated giraffes (Giraffa camelopardalis reticulata), 21-year-old, died of nutritional deficiency that primarily caused by serious tooth wear at Seoul Zoo in winter. A 970 kg-weighed giraffe showed tooth wear of premolars, molars and incisors at necropsy. A foreign body in the rumen, congestion and ulcer of abomasum and duodenum were also observed. Mild appearance of serous fat atrophy in pericardial sac suggests that lack of nutritional intake caused by tooth wear can become harmful enough to threat life. At the necropsy of a 1,290 kg-weighed giraffe, a large quantity of sandy soil were found in the rumen which would stuck the pathway of well-fermented ruminal contents at esophageal groove. Nutritional deficiency could be suspected to urge this giraffe to graze grass on the ground along with sandy soil. Secondarily, the soil damaged teeth and become a culprit making irregular tooth wear and mild serous fat atrophy. Nutritionally good care of geriatric animals is needed especially for browsing animals like giraffes and critically in winter season.

• Proceedings of the Korean Society for Bioinformatics Conference
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• 2001.10a
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• pp.1-9
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• 2001

scale genomic and postgenomic data means that many of the challenges in biomedical research are now challenges in computational sciences and information technology. The informatics revolutions both in clinical informatics and bioinformatics will change the current paradigm of biomedical sciences and practice of clinical medicine, including diagnostics, therapeutics, and prognostics. Postgenome informatics, powered by high throughput technologies and genomic-scale databases, is likely to transform our biomedical understanding forever much the same way that biochemistry did a generation ago. In this talk, 1 will describe how these technologies will in pact biomedical research and clinical care, emphasizing recent advances in biochip-based functional genomics. Basic data preprocessing with normalization and filtering, primary pattern analysis, and machine teaming algorithms will be presented. Issues of integrated biochip informatics technologies including multivariate data projection, gene-metabolic pathway mapping, automated biomolecular annotation, text mining of factual and literature databases, and integrated management of biomolecular databases will be discussed. Each step will be given with real examples from ongoing research activities in the context of clinical relevance. Issues of linking molecular genotype and clinical phenotype information will be discussed.

• Journal of mucopolysaccharidosis and rare diseases
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• v.2 no.2
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• pp.46-49
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• 2016

Achondroplasia is autosomal dominant genetic disease and fibroblast growth factor receptor 3 (FGFR3) is currently known to be the only gene that causes achondroplasia. Gain-of function mutation in fibroblast-growth-factor-receptor 3 (FGFR3) causes the disease and C-type natriuretic peptide (CNP) antagonizes FGFR3 downstream signaling by inhibiting the pathway of mitogen-activated protein kinase (MAPK). As FGFR3-related skeletal dysplasias are caused by growth attenuation of the cartilage, chondrocytes appear to be unique in their response to FGFR3 activation. However, the full spectrum of molecular events by which FGFR3 mediates its signaling is just beginning to emerge. This article summaries the mechanisms of FGFR3 function in skeletal dysplasias, the extraordinary cellular manifestations of FGFR3 signaling in chondrocytes, and finally, the progress toward therapy for ACH.

• Archives of Plastic Surgery
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• v.48 no.4
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• pp.384-388
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• 2021

Adequate positioning of the hand is a critical step in hand fracture operative repair that can impact both the clinical outcome and the efficiency of the operation. In this paper, we introduce the use of a thermoplastic splint with an added thumb stabilizing component as a means to increase the surgeon's autonomy and to streamline the patient care pathway. The thermoplastic splint is custom fabricated preoperatively by the specialist hand therapist. The splint is used prior, during, and post operation with minimal modification. The thumb component assists maintaining the forearm in a stable pronated position whilst drilling and affixing metal work. This is demonstrated in the video of removal of metal work and open reduction and internal fixation of a metacarpal fracture.

• Journal of Digestive Cancer Research
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• v.2 no.1
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• pp.11-14
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• 2014

Competency for practicing gastroenterology in the United States requires accredited training in Internal Medicine, followed by accredited training in gastroenterology and hepatology. The structured training encompasses a 3-year period after graduation with a medical degree for internal medicine, followed by a 3-year period for gastroenterology and hepatology. Within the gastroenterology training period, competency in oncology knowledge and procedural approaches to luminal and solid gastrointestinal organ cancers is required, whereas knowledge competency but not procedural competency is required in areas of advanced endoscopic procedures for cancer care. Only general knowledge, but not competency, is required for areas such as chemotherapy, which can be obtained with further optional training in a structured 2-year oncology fellowship program. Although there is no standardization to date for including full oncology training within a gastroenterology training program in the United States, there is great interest from gastroenterology professional societies to include a pathway for trainees within the gastroenterology training program.

• Journal of The Korean Society of Inherited Metabolic disease
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• v.23 no.2
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• pp.15-20
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• 2023

Galactosemia is an inborn error disorder of carbohydrate metabolism, caused by metabolic disturbances at various stages of the Leloir pathway. In patients with galactosemia, accurate diagnosis and appropriate care are essential to avoid complications and unnecessary treatments. And a careful differential diagnosis of the type of galactosemia is crucial. Even with an appropriate galactose-restricted diet, long-term complications may occur, especially in patients with classic galactosemia. So new treatment options are being developed. In this review, we will review the new symptoms of each subtype that have been reported recently and GALM (Galactose mutarotase) deficiency, a new form of galactosemia, and treatment policies according to recent guidelines.

• Tuberculosis and Respiratory Diseases
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• v.57 no.5
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• pp.449-460
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• 2004

Background : PS-341 is a novel, highly selective and potent proteasome inhibitor, which showed cytotoxicity against some tumor cells. Its anti-tumor activity has been suggested to be associated with modulation of the expression of apoptosis-associated proteins, such as p53, $p21^{WAF/CIP1}$, $p27^{KIP1}$, NF-${\kappa}B$, Bax and Bcl-2. c-Jun N-terminal kinase (JNK) and glycogen synthase kinase-$3{\beta}$ (GSK-$3{\beta}$) are important modulators of apoptosis. However, their role in PS-341-induced apoptosis is unclear. This study was undertaken to elucidate the role of JNK and GSK-$3{\beta}$ in the PS-341-induced apoptosis in lung cancer cells. Method : NCI-H157 and A549 cells were used in the experiments. The cell viability was assayed using the MTT assay and apoptosis was evaluated by proteolysis of PARP. The JNK activity was measured by an in vitro immuno complex kinase assay and by phosphorylation of endogenous c-Jun. The protein expression was evaluated by Western blot analysis. Dominant negative JNK1 (DN-JNK1) and GSK-$3{\beta}$ were overexpressed using plasmid and adenovirus vectors, respectively. Result : PS-341 reduced the cell viability via apoptosis, activated JNK and increased the c-Jun expression. Blocking of the JNK activation by overexpression of DN-JNK1, or pretreatment with SP600125, suppressed the apoptosis induced by PS-341. The activation of caspase 3 was mediated by JNK activation. Blocking of the caspase 3 activation suppressed PS-341-induced apoptosis. PS-341 activated the phosphatidylinositol 3-kinase (PI3K)/Akt pathway, but its blockade enhanced the PS-341-induced cell death via apoptosis. GSK-$3{\beta}$ was inactivated by PS-341 via the PI3K/Akt pathway. Overexpression of constitutively active GSK-$3{\beta}$ enhanced PS-341-induced apoptosis; in contrast, this was suppressed by dominant negative GSK-$3{\beta}$ (DN-GSK-$3{\beta}$). Inactivation of GSK-$3{\beta}$ by pretreatment with lithium chloride or the overexpression of DN-GSK-$3{\beta}$ suppressed both the JNK activation and c-Jun up-regulation induced by PS-341. Conclusion : The JNK/caspase pathway is involved in PS-341-induced apoptosis, which is negatively regulated by the PI3K/Akt-mediated inactivation of GSK-$3{\beta}$ in lung cancer cells.

• Journal of Gastric Cancer
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• v.5 no.2
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• pp.95-100
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• 2005

Purpose: Critical pathways (CP), also known as clinical pathways, are management plans that display goals for patients and have led to improved outcomes for many disease entities. This study was aimed at developing a critical pathway for the surgical treatment of gastric cancer patients and evaluating its usefulness. Materials and Methods: A CP was developed and implemented by a team of surgeons, nurses, nutritionists, and administrative officials. Among the 117 patients who received curative gastrectomies for gastric cancer at Kangnam St. Mary's Hospital, The Catholic University of Korea, between October 2003 and August 2004, 26 patients were treated according to the CP. We evaluated its usefulness by comparing the clinical characterisctics, postoperative progress, hospital stays, and costs between the CP and the non-CP groups. Patient satisfaction was also surveyed with questionnaires. Results: Of the initial 26 patients in the CP group, two were excluded from the final evaluation; one patient had a duodenal stump leakage, and the other had a gastric stasis postoperatively. In 8 patients, protocol violation occurred; six patients refused to be discharged on the $7^{th}$ postoperative day, one patient who had an gastric staisis postoperatively stayed for 2 additional days, and one patient who needed ICU care stayed for 4 additional days. The drop-out rate was $7.7\%$ (2/26), and the variance rate was $30.8\%$ (8/26). The mean hospital stay was 11.3 days ($10\~15$ days) for the CP group compared with 17.5 days ($9\∼68$ days) for the non-CP group, resulting in a difference of about 6 days (P<0.05). The mean hospital stays after surgery were 10.3 days ($7\∼68$ days) and 8.3 days ($7\∼12$ days) for the non-CP and the CP groups, respectively, but the difference was statistically not significant (P>0.05). The mean charge during the hospital stay was higher in the non-CP group ( $\\$ 6,292,200) than in the CP group ( $\\$ 4,863,685). The charge per hospital day was higher in the CP group ( $\\$ 430,414) than in the non-CP group ( $\\$ 359,554). Patient satisfaction was higher in the CP group than in the non-CP group. Conclusion: By developing and applying a critical pathway in the surgical treatment of stomach cancer patients, we could reduce the length of hospital stay as well as the cost. A multi-centered prospective study to establish a standard treatment pathway and to demonstrate its effectiveness is needed in the future.

• Journal of Life Science
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• v.24 no.7
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• pp.762-768
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• 2014

Diet exerts a major stress on the body and may affect gene expression and physiological functions. Understanding of cellular responses during starvation is necessary in developing strategies to reduce damage caused by diet. In this study, we isolated 10 genes (Comt, RGN, Scd1, Temt, Idi1, Fabp5, Car3, Cyp2c70, Pinx1, and Poldip3) that are down-regulated in starvation and are closely related to liver metabolism. Water supply during starvation had no effect on the induction of apoptosis, autophagy, and ERQC. The genes down-regulated by starvation were associated with many related pathways rather than limited to the liver homeostasis pathway. Water supply during starvation is important. However, maintaining NaCl homeostasis is more important. The results are thought to be closely related to gender-specific metabolism in starvation and NaCl.

• Molecules and Cells
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• v.42 no.4
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• pp.292-300
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• 2019

Immunometabolism, defined as the interaction of metabolic pathways with the immune system, influences the pathogenesis of metabolic diseases. Metformin and carbon monoxide (CO) are two pharmacological agents known to ameliorate metabolic disorders. There are notable similarities and differences in the reported effects of metformin and CO on immunometabolism. Metformin, an anti-diabetes drug, has positive effects on metabolism and can exert anti-inflammatory and anti-cancer effects via adenosine monophosphate-activated protein kinase (AMPK)-dependent and AMPK-independent mechanisms. CO, an endogenous product of heme oxygenase-1 (HO-1), can exert anti-inflammatory and antioxidant effects at low concentration. CO can confer cytoprotection in metabolic disorders and cancer via selective activation of the protein kinase R-like endoplasmic reticulum (ER) kinase (PERK) pathway. Both metformin and CO can induce mitochondrial stress to produce a mild elevation of mitochondrial ROS (mtROS) by distinct mechanisms. Metformin inhibits complex I of the mitochondrial electron transport chain (ETC), while CO inhibits ETC complex IV. Both metformin and CO can differentially induce several protein factors, including fibroblast growth factor 21 (FGF21) and sestrin2 (SESN2), which maintain metabolic homeostasis; nuclear factor erythroid 2-related factor 2 (Nrf2), a master regulator of the antioxidant response; and REDD1, which exhibits an anticancer effect. However, metformin and CO regulate these effects via different pathways. Metformin stimulates p53- and AMPK-dependent pathways whereas CO can selectively trigger the PERK-dependent signaling pathway. Although further studies are needed to identify the mechanistic differences between metformin and CO, pharmacological application of these agents may represent useful strategies to ameliorate metabolic diseases associated with altered immunometabolism.