경희대학교 의과대학·의학전문대학원

성 동진

, M.D.-St. Luke’s Hospital at St. Louis

내과 매칭

김성수 교수님

,

가장 높게 랭크한

St. Louis 지역 내과 프로그램으로 매칭 되었습니다 .  

병원의

이름은 St. Luke's Hospital 입니다 .  Washington Univ.

와 St. Louis Univ.

의대와 강한 Affiliation

을 가지고 있습니다 . 하나님께 감사드리고 교수님께도 감

사를 드립니다

.  H1 비자도 받을 수 있게 되어 더욱 기쁩니다 .  

갈 수록 극심해져가는 미국 레지던트 지원 경쟁에서 올해 많은 한국 선생님들이 고배

를 마셨습니다

.  99/99 같은 뛰어난 점수를 가지고 있어도 또는 10 군데 이상의 인

터뷰를 본 선생님들도 매칭에 실패하였습니다

.   하지만 교수님의 도움으로 2 년 전

리서치를 시작하기 위해 곤잘레스 교수님과 연락을 하게 되고 1 년 8 개월이라는 시

간동안 리서치 경력과 페이퍼는 물론이고 영어와 미국사람들과의 대인관계 기술도 늘

게 되어 인터뷰에서 좋은 인상을 남기고 올 수 있었습니다

.  

교수님께 감사드리고 5 월에 찾아뵙고 다시 인사 드리겠습니다

.  

성동진 드림

 ongjin (Luke) Sung, M.D.

Postdoctoral Research Fellow, Physician Department of Ophthalmology

State University of New York at Buffalo Mailling address:

Medical Research (VAMC), 3495 Bailey Ave. Buffalo, NY 14215

(Cell Phone) 716-868-9146

(Fax) 716-862-6526

Fig 29-1Amphibolic intermediates formed from

the carbon skeletons of amino acids.

Figure 1 The insulin resistance syndrome. Insulin

resistance initially manifests itself as the constellation of symptoms that comprise the insulin resistance

syndrome (shown in the orange circle). Ultimately,

insulin resistance can evolve into a number of diseases (shown in the red circle).

Fig. 1. Interplay between CNS and other tissues in the

pathophysiology of type 2 diabetes and the metabolic

syndrome. ANS, autonomic nervous system; FFA, free fatty

acids; HPA, hypothalamo–pituitary–adrenal system; VLDL,

very low density lipoprotein.

Figure 1. Metabolic Staging of Type 2 DiabetesType 2 diabetes is characterized by a progressive decrease in insulin action, followed by an inability of the β cell to

compensate for insulin resistance. Insulin resistance is the first lesion, due to interactions among genes, aging, and metabolic changes produced by obesity. Insulin resistance in visceral fat leads to increased fatty acid production, which

exacerbates insulin resistance in liver and muscle. The β cell compensates for insulin resistance by secreting more insulin. Ultimately, the β cell can no longer

The brain receives various forms of metabolic information from peripheral organs/tissues through humoral and neuronal pathways. These inputs are probably integrated and processed in the brain, leading to appropriate

systemic responses. Several signals, as therapeutic targets, are discussed in this article.

Scheme of the neuronal pathways involved in energy homeostasis.

Neuronal signals from WAT modulate hypothalamic leptin sensitivity,

thereby regulating feeding behavior. In addition, the liver transmits

information regarding excess energy to the brain via the afferent vagus,

thereby activating the sympathetic nervous system which in turn

enhances energy expenditure and lipolysis. The autonomic nervous

system, as exemplified by these neuronal circuits, plays important roles

in regulating energy metabolism.

Role of adipose tissue in peripheral insulin resistance. The fat cell is

essential to the regulation of glucose metabolism and energy homeostasis. Adipocytes of obese type 2 diabetics release FFA that alter muscle glucose uptake and increase hepatic glucose production. Normal adipocytes also release adipocytokines such as leptin and adiponectin which promote lipid combustion and stimulate insulin action in muscle and fat. Leptin also has central effects on food intake and peripheral insulin sensitivity. In obesity and type 2 diabetes, adiponectin secretion is decreased and there is

resistance to the action of leptin. In lipoatrophy, both leptin and adiponectin are low, and extreme insulin resistance develops. Finally, hypertrophied

adipocytes of obese people also release TNF-α and resistin which further exacerbate insulin resistance in peripheral tissues.

Structure of bilirubin diglucuronide (conjugated, "direct-reacting" bilirubin). Glucuronic acid is attached via ester linkage to the two propionic acid groups of bilirubin to form an acylglucuronide.

Conjugation of bilirubin with glucuronic acid. The glucuronate donor, UDP-glucuronic acid, is formed from UDP-glucose as

depicted. The UDP-glucuronosyltransferase is also called bilirubin-UGT.

No Significant Correlation Exists Between Core Promoter Mutations,Viral Replication, and Liver Damage in Chronic Hepatitis B Infection. Hepatology. 2000

Nov;32(5):1154-YOON KEUN CHUN,1 JEE YOUN KIM,1 HONG JUNG WOO,2 SOO MYUNG OH,2 INSUG KANG,1,2 JOOHUN

HA,1,2 AND SUNG SOO KIM1,21:

Phosphatidylinositol 3-Kinase Stimulates Muscle Differentiation by Activating p38 Mitogen-Activated Protein Kinase. BBRC, 24 September 2000, Pages 502-507

Yoon Keun Chuna_{, Jayoung Kim}a_{, Sijoong Kwon}a_{, Soon Hee Choi}a_{, Feng Hong}a_{, Kuen-ai Moon}a_{, Joung Mok Kim}a_,

Sang Lim Choia_{, Bum Shik Kim}b_{, Joohun Ha}a _{and Sung Soo Kim}a, 1

Effects of polyamine depletion by α-difluoromethylornithine on in vitro and in vivo biological properties of 4T1 murine mammary cancer cells .Breast Cancer Res Treat. 2008 Jan;107(1):33-40.

John Yoonkeun Jun1_{, James W. Griffith}2_{, Richard Bruggeman}3_{, Sharlene Washington}1_{, Laurence M. Demers}1, 3_,

Michael F. Verderame1, 4 _{and Andrea Manni}1

Department of Medicine, Pennsylvania State University College of Medicine, 500 University Drive, Hershey, PA, 17033, USA,

Nonobese, insulin-deficient Ins2Akita _{mice develop type 2 diabetes phenotypes including insulin resistance and cardiac}

remodeling. Am J Physiol Endocrinol Metab. 2007 Dec;293(6):E1687-96.

Eun-Gyoung Hong,1,2 _{Dae Young Jung,}1 _{Hwi Jin Ko,}1 _{Zhiyou Zhang,}1 _{Zhexi Ma,}1_{John Y. Jun,}1,3_{Jae Hyeong Kim,}1

Andrew D. Sumner,4 _{Thomas C. Vary,}1 _{Thomas W. Gardner,}1,5 _{Sarah K. Bronson,}1 _{and Jason K. Kim}11_Department

of Cellular and Molecular Physiology, Pennsylvania State University College of Medicine, Hershey, Pennsylvania;

2_{Department of Internal Medicine, Section of Endocrinology, Hallym University College of Medicine, Seoul, South Korea;} 3_{Division of Endocrinology, Diabetes and Metabolism,} 4_{Cardiology, and} 5_{Ophthalmology, Department of Internal Medicine,}