1.Socio-demographic profile and psychiatric comorbidity of subjects with pathological gambling.
Munidasa WINSLOW ; Mythily SUBRAMANIAM ; Shijia QIU ; Arthur LEE
Annals of the Academy of Medicine, Singapore 2010;39(2):122-128
INTRODUCTIONPathological gambling is defined as the failure to resist the impulse to gamble despite disruption to personal, family and vocational life. It appears to be highly comorbid with psychiatric disorders. This study aims to describe the socio-demographic profile and comorbidity of 40 pathological gamblers compared to controls.
MATERIALS AND METHODSQuestionnaires were administered to 40 cases (90% male, mean age = 38.3, SD = 10.0) scoring 5 or more in the South Oaks Gambling Screen (SOGS) and verified to be pathological gamblers based on DSM-IV criteria and 40 age-and-gender-matched controls.
RESULTSStudy results showed that the prevalence of lifetime DSM-IV diagnoses were significantly different between cases and controls (chi(2) = 16.4, P <0.001), with 67.5% of the cases and 22.5% of the controls meeting the criteria, respectively. Eighty percent of the cases had at least one personality disorder compared to 45% in the control (chi(2) = 10.5, P <0.005). The common lifetime disorders observed in the cases were substance abuse disorder and anxiety while common personality disorders were obsessive-compulsive, avoidant and paranoid.
CONCLUSIONThis study highlights the high rates of comorbidity in a largely Chinese sample in an Asian setting and the importance of assessing pathological gamblers for comorbidities.
Adult ; Asia ; ethnology ; Comorbidity ; Demography ; Female ; Gambling ; psychology ; Humans ; Male ; Mental Disorders ; epidemiology ; ethnology ; Middle Aged
2.Human Papillomavirus Infection–Associated Adenoid Cystic Carcinoma of the Hard Palate.
Arthur Minwoo CHUNG ; Dong Il SUN ; Eun Sun JUNG ; Youn Soo LEE
Journal of Pathology and Translational Medicine 2017;51(3):329-331
No abstract available.
Adenoids*
;
Carcinoma, Adenoid Cystic*
;
Humans*
;
Palate, Hard*
3.Primary Neurilemmoma of the Thyroid Gland Clinically Mimicking Malignant Thyroid Nodule.
Young Sub LEE ; Jee Soon KIM ; Arthur Minwoo CHUNG ; Woo Chan PARK ; Tae Jung KIM
Journal of Pathology and Translational Medicine 2016;50(2):168-171
No abstract available.
Neurilemmoma*
;
Thyroid Gland*
;
Thyroid Nodule*
4.FDG Uptake in the Pathologically Proven Papillary Thyroid Cancer.
Tae Sung KIM ; Mijin YUN ; Arthur CHO ; Jong Doo LEE
Nuclear Medicine and Molecular Imaging 2007;41(1):22-29
PURPOSE: Metastatic thyroid cancers with I-131 uptake have been known to show no increase of FDG uptake whereas those without I-131 uptake tend to demonstrate increased uptake on PET. In this study, we evaluated the degree of FDG uptake in primary thyroid cancers of papillary histology before surgery. MATERIAL AND METHODS: Forty FDG PET studies were performed on the patients who had papillary cancer proven by fine needle aspiration. The degree of FDG uptake was visually categorized as positive or negative (positive if the tumor showed discernible FDG; negative if the tumor didn't) and the peak standard uptake value (peak SUV) of the papillary thyroid cancer (PTC) were compared with the size of PTC. RESULTS: The mean size of 26 PTC with positive FDG uptake was 1.9+/-1.4 cm(0.5~5 cm). In 13 PTC with negative FDG uptake, the mean size of those was 0.5+/-0.2 cm (0.2~0.9 cm). All PTC larger than 1cm (2.5+/-1.4 cm, 1~5 cm) have positive FDG uptake (peak SUV=6.4+/-5.7, 1.7~22.7). Among the micropapillary thyroid cancer (microPTC; PTC smaller than 1cm), 8 microPTC show positive FDG uptake(peak SUV=2.9+/-1.3, 1.7~5.5), while 13 microPTC show negative finding(peak SUV=1.3+/-0.2, 1.1~1.7). The size of microPTC with positive FDG uptake is significantly larger than that of microPTC with negative FDG uptake (0.7+/-0.1 cm vs 0.4+/-0.2 cm, p=0.01). CONCLUSION: All PTCs larger than 1cm show positive FDG uptake in our study. In other words, thyroid lesions larger than 1cm with negative FDG uptake are unlikely to be PTC. So far, only poorly differentiated thyroid cancers are known to show increased FDG uptake. Our results seem to be contradictory to what is known in the literature. Further study is needed to understand better the significance of increased FDG uptake in PTC in relation to expression of NIS and GLUT.
Biopsy, Fine-Needle
;
Humans
;
Thyroid Gland*
;
Thyroid Neoplasms*
;
Thyroid Nodule
5.Clinical Significance of Myocardial Uptake on F-18 FDG PET/CT Performed in Oncologic Patients.
Ho Jin CHO ; Arthur CHO ; Jong Doo LEE ; Won Jun KANG
Nuclear Medicine and Molecular Imaging 2009;43(6):519-525
PURPOSE: F-18 fluorodeoxyglucose (FDG) uptake of myocardium is influenced by various factors. Increased glycolysis, and subsequent increased F-18 FDG uptake has been reported in ischemic cardiomyopathy. However, clinical significance of incidentally found myocardial F-18 FDG uptake has not been clarified. We retrospectively reviewed the degree and pattern of myocardial uptake in patients without history of ischemic heart disease who underwent torso F-18 FDG PET/CT for evaluation of neoplastic disease. MATERIALS AND METHODS: From January 2005 to June 2009, 77 patients who underwent F-18 FDG PET/CT and Tc-99m sestamibi stress/rest SPECT within 3 months were enrolled. RESULTS: Of 77 patients, 55 (71.4%) showed increased F-18 FDG uptake in the myocardium. In this population, 40 showed uniform uptake pattern, while 15 showed focal uptake. In patients with uniform uptake, 17 showed decreased uptake in the septum without perfusion defect on myocardial SPECT. Remaining 23 patients showed uniform uptake, with 1 reversible perfusion defect and 1 fixed perfusion defect. In 15 patients with focal uptake, 9 showed increased F-18 FDG uptake in the base, and only 1 of them showed reversible perfusion defect on myocardial SPECT. In the remaining 6 focal uptake group, 4 had reversible perfusion defect in the corresponding wall, and 1 had apical hypertrophy. CONCLUSION: We demonstrated that septal defect pattern and basal uptake pattern in the myocardium may represent normal variants. Focal myocardial uptake other than normal variants on oncologic torso F-18 FDG PET/CT with routine fasting protocol may suggest ischemic heart disease, thus further evaluation is warranted.
Cardiomyopathies
;
Fasting
;
Glycolysis
;
Humans
;
Hypertrophy
;
Ischemia
;
Myocardial Ischemia
;
Myocardium
;
Perfusion
;
Retrospective Studies
;
Tomography, Emission-Computed, Single-Photon
;
Torso
6.Prognostic Value of 18F-Fluorodeoxyglucose Positron Emission Tomography in Patients with Resectable Pancreatic Cancer.
Hye Jin CHOI ; Chang Moo KANG ; Woo Jung LEE ; Si Young SONG ; Arthur CHO ; Mijin YUN ; Jong Doo LEE ; Joo Hang KIM ; Jae Hoon LEE
Yonsei Medical Journal 2013;54(6):1377-1383
PURPOSE: We evaluated the prognostic value of 18F-2-fluoro-2-deoxyglucose positron emission tomography (FDG PET) in patients with resectable pancreatic cancer. MATERIALS AND METHODS: We retrospectively reviewed the medical records of pancreatic cancer patients who underwent curative resection, which included 64 consecutive patients who had preoperative FDG PET scans. For statistical analysis, the maximal standardized uptake value (SUVmax) of primary pancreatic cancer was measured. Survival time was estimated by the Kaplan-Meier method, and Cox's proportional hazard model was used to determine whether SUVmax added new predictive information concerning survival together with known prognostic factors. p<0.05 indicated statistical significance. RESULTS: Overall survival (OS) and disease-free survival (DFS) were respectively 42.9 months (27.6-58.2; 95% CI) and 14.9 months (10.1-19.7; 95% CI). When subjects were divided into two groups according to SUVmax with a cutoff value of 3.5, the high SUVmax group (n=32; SUVmax >3.5) showed significantly shorter OS and DFS than the low SUVmax group. Multivariate analysis of OS and DFS showed that both high SUVmax and poor tumor differentiation were independent poor prognostic factors. CONCLUSION: Our study showed that degree of FDG uptake was an independent prognostic factor in pancreatic cancer patients who underwent curative resection.
Aged
;
Aged, 80 and over
;
Disease-Free Survival
;
Female
;
Fluorodeoxyglucose F18/*diagnostic use
;
Humans
;
Male
;
Middle Aged
;
Pancreatic Neoplasms/*diagnosis/mortality
;
Positron-Emission Tomography/*methods
;
Retrospective Studies
7.KRAS Mutation Test in Korean Patients with Colorectal Carcinomas: A Methodological Comparison between Sanger Sequencing and a Real-Time PCR-Based Assay.
Sung Hak LEE ; Arthur Minwoo CHUNG ; Ahwon LEE ; Woo Jin OH ; Yeong Jin CHOI ; Youn Soo LEE ; Eun Sun JUNG
Journal of Pathology and Translational Medicine 2017;51(1):24-31
BACKGROUND: Mutations in the KRAS gene have been identified in approximately 50% of colorectal cancers (CRCs). KRAS mutations are well established biomarkers in anti–epidermal growth factor receptor therapy. Therefore, assessment of KRAS mutations is needed in CRC patients to ensure appropriate treatment. METHODS: We compared the analytical performance of the cobas test to Sanger sequencing in 264 CRC cases. In addition, discordant specimens were evaluated by 454 pyrosequencing. RESULTS: KRAS mutations for codons 12/13 were detected in 43.2% of cases (114/264) by Sanger sequencing. Of 257 evaluable specimens for comparison, KRAS mutations were detected in 112 cases (43.6%) by Sanger sequencing and 118 cases (45.9%) by the cobas test. Concordance between the cobas test and Sanger sequencing for each lot was 93.8% positive percent agreement (PPA) and 91.0% negative percent agreement (NPA) for codons 12/13. Results from the cobas test and Sanger sequencing were discordant for 20 cases (7.8%). Twenty discrepant cases were subsequently subjected to 454 pyrosequencing. After comprehensive analysis of the results from combined Sanger sequencing–454 pyrosequencing and the cobas test, PPA was 97.5% and NPA was 100%. CONCLUSIONS: The cobas test is an accurate and sensitive test for detecting KRAS-activating mutations and has analytical power equivalent to Sanger sequencing. Prescreening using the cobas test with subsequent application of Sanger sequencing is the best strategy for routine detection of KRAS mutations in CRC.
Biomarkers
;
Codon
;
Colorectal Neoplasms*
;
Humans
8.Early-life exposure to endocrine disrupting chemicals associates with childhood obesity.
Chunxue YANG ; Hin Kiu LEE ; Alice Pik Shan KONG ; Lee Ling LIM ; Zongwei CAI ; Arthur C.K CHUNG
Annals of Pediatric Endocrinology & Metabolism 2018;23(4):182-195
Increasing prevalence of childhood obesity poses threats to the global health burden. Because this rising prevalence cannot be fully explained by traditional risk factors such as unhealthy diet and physical inactivity, early-life exposure to endocrine disrupting chemicals (EDCs) is recognized as emerging novel risk factors for childhood obesity. EDCs can disrupt the hormone-mediated metabolic pathways, affect children’s growth and mediate the development of childhood obesity. Many organic pollutants are recently classified to be EDCs. In this review, we summarized the epidemiological and laboratory evidence related to EDCs and childhood obesity, and discussed the possible mechanisms underpinning childhood obesity and early-life exposure to non-persistent organic pollutants (phthalates, bisphenol A, triclosan) and persistent organic pollutants (dichlorodiphenyltrichloroethane, polychlorinated biphenyls, polybrominated diphenyl ethers, per- and polyfluoroalkyl substances). Understanding the relationship between EDCs and childhood obesity helps to raise public awareness and formulate public health policy to protect the youth from exposure to the harmful effects of EDCs.
Adolescent
;
Diet
;
Endocrine Disruptors*
;
Global Health
;
Halogenated Diphenyl Ethers
;
Humans
;
Metabolic Networks and Pathways
;
Pediatric Obesity*
;
Polychlorinated Biphenyls
;
Prevalence
;
Public Health
;
Risk Factors
9.A Case of von Hippel-Lindau Disease with Colorectal Adenocarcinoma, Renal Cell Carcinoma and Hemangioblastomas.
Su Jin HEO ; Choong Kun LEE ; Kyu Yeon HAHN ; Gyuri KIM ; Hyuk HUR ; Sung Hoon CHOI ; Kyung Seok HAN ; Arthur CHO ; Minkyu JUNG
Cancer Research and Treatment 2016;48(1):409-414
von Hippel-Lindau (VHL) disease is an autosomal dominant inherited tumor syndrome associated with mutations of the VHL tumor suppressor gene located on chromosome 3p25. The loss of functional VHL protein contributes to tumorigenesis. This condition is characterized by development of benign and malignant tumors in the central nervous system (CNS) and the internal organs, including kidney, adrenal gland, and pancreas. We herein describe the case of a 74-year-old man carrying the VHL gene mutation who was affected by simultaneous colorectal adenocarcinoma, renal clear cell carcinoma, and hemangioblastomas of CNS.
Adenocarcinoma*
;
Adrenal Glands
;
Aged
;
Carcinogenesis
;
Carcinoma, Renal Cell*
;
Central Nervous System
;
Colorectal Neoplasms
;
Genes, Tumor Suppressor
;
Hemangioblastoma*
;
Humans
;
Kidney
;
Pancreas
;
von Hippel-Lindau Disease*
10.Differential Immunohistochemical Profiles for Distinguishing Prostate Carcinoma and Urothelial Carcinoma.
Woo Jin OH ; Arthur Minwoo CHUNG ; Jee Soon KIM ; Ji Heun HAN ; Sung Hoo HONG ; Ji Yeol LEE ; Yeong Jin CHOI
Journal of Pathology and Translational Medicine 2016;50(5):345-354
BACKGROUND: The pathologic distinction between high-grade prostate adenocarcinoma (PAC) involving the urinary bladder and high-grade urothelial carcinoma (UC) infiltrating the prostate can be difficult. However, making this distinction is clinically important because of the different treatment modalities for these two entities. METHODS: A total of 249 patient cases (PAC, 111 cases; UC, 138 cases) collected between June 1995 and July 2009 at Seoul St. Mary's Hospital were studied. An immunohistochemical evaluation of prostatic markers (prostate-specific antigen [PSA], prostate-specific membrane antigen [PSMA], prostate acid phosphatase [PAP], P501s, NKX3.1, and α-methylacyl coenzyme A racemase [AMACR]) and urothelial markers (CK34βE12, p63, thrombomodulin, S100P, and GATA binding protein 3 [GATA3]) was performed using tissue microarrays from each tumor. RESULTS: The sensitivities of prostatic markers in PAC were 100% for PSA, 83.8% for PSMA, 91.9% for PAP, 93.7% for P501s, 88.3% for NKX 3.1, and 66.7% for AMACR. However, the urothelial markers CK34βE12, p63, thrombomodulin, S100P, and GATA3 were also positive in 1.8%, 0%, 0%, 3.6%, and 0% of PAC, respectively. The sensitivities of urothelial markers in UC were 75.4% for CK34βE12, 73.9% for p63, 45.7% for thrombomodulin, 22.5% for S100P, and 84.8% for GATA3. Conversely, the prostatic markers PSA, PSMA, PAP, P501s, NKX3.1, and AMACR were also positive in 9.4%, 0.7%, 18.8%, 0.7%, 0%, and 8.7% of UCs, respectively. CONCLUSIONS: Prostatic and urothelial markers, including PSA, NKX3.1, p63, thrombomodulin, and GATA3 are very useful for differentiating PAC from UC. The optimal combination of prostatic and urothelial markers could improve the ability to differentiate PAC from UC pathologically.
Acid Phosphatase
;
Adenocarcinoma
;
Carrier Proteins
;
Coenzyme A
;
Humans
;
Immunohistochemistry
;
Membranes
;
Prostate*
;
Seoul
;
Thrombomodulin
;
Urinary Bladder