Objective: This study was performed to evaluate the efficacy and safety of lurasidone (160 mg/day) compared to quetiapine XR (QXR; 600 mg/day) in the treatment of acutely psychotic patients with schizophrenia. Methods: Patients were randomly assigned to 6 weeks of double-blind treatment with lurasidone 160 mg/day (n=105) or QXR 600 mg/day (n=105). Primary efficacy measure was the change from baseline to week 6 in Positive and Negative Syndrome Scale (PANSS) total score and Clinical Global Impressions severity (CGI-S) score. Adverse events, body measurements, and laboratory parameters were assessed. Results: Lurasidone demonstrated non-inferiority to QXR on the PANSS total score. Adjusted mean±standard error change at week 6 on the PANSS total score was -26.42±2.02 and -27.33±2.01 in the lurasidone and QXR group, respectively. The mean difference score was -0.91 (95% confidence interval -6.35–4.53). The lurasidone group showed a greater reduction in PANSS total and negative subscale on week 1 and a greater reduction in end-point CGI-S score compared to the QXR group. Body weight, body mass index, and waist circumference in the lurasidone group were reduced, with significantly lower mean change compared to QXR. Endpoint changes in glucose, cholesterol, triglycerides, and low-density lipoprotein levels were also significantly lower. The most common adverse drug reactions with lurasidone were akathisia and nausea. Conclusion Lurasidone 160 mg/day was found to be non-inferior to QXR 600 mg/day in the treatment of schizophrenia with comparable efficacy and tolerability. Adverse effects of lurasidone were generally tolerable, and beneficial effects on metabolic parameters can be expected.

Background and Objectives: Smoking is well-established as a risk factor for coronary artery disease. However, recent studies demonstrated favorable results, including reduced mortality, among smokers, which are referred to as the “smoker's paradox”. This study examined the impact of smoking on clinical outcomes in patients with acute myocardial infarction (AMI) undergoing percutaneous coronary intervention (PCI). Methods: Patients with AMI undergoing PCI between 2004 and 2014 were enrolled and classified according to smoking status. The primary endpoint was a composite of major adverse cardiovascular events (MACE) including cardiac death, myocardial infarction, stroke, and revascularization. Results: Among the 10,683 patients, 4,352 (40.7%) were current smokers. Smokers were 10.7 years younger and less likely to have comorbidities such as hypertension, diabetes mellitus, chronic kidney disease, stroke, and prior PCI. Smokers had less MACE (hazard ratio [HR], 0.644; 95% confidence interval [CI], 0.594–0.698; p<0.001) and cardiac death (HR, 0.494; 95% CI, 0.443–0.551; p<0.001) compared to nonsmokers during the 5 years in an unadjusted model. However, after propensity-score matching, smokers showed higher risk of MACE (HR, 1.125; 95% CI, 1.009–1.254; p=0.034) and cardiac death (HR, 1.190; 95% CI, 1.026–1.381; p=0.022). Smoking was a strong independent predictor of lung cancer (propensityscore matched HR, 2.749; 95% CI, 1.416–5.338; p=0.003). Conclusions In contrast to the unadjusted model, smoking is associated with worse cardiovascular outcome and higher incidence of lung cancer after adjustment of various confounding factors. This result can be explained by the characteristics of smokers, which were young and had fewer comorbidities.

Background and Objectives: Smoking is well-established as a risk factor for coronary artery disease. However, recent studies demonstrated favorable results, including reduced mortality, among smokers, which are referred to as the “smoker's paradox”. This study examined the impact of smoking on clinical outcomes in patients with acute myocardial infarction (AMI) undergoing percutaneous coronary intervention (PCI). Methods: Patients with AMI undergoing PCI between 2004 and 2014 were enrolled and classified according to smoking status. The primary endpoint was a composite of major adverse cardiovascular events (MACE) including cardiac death, myocardial infarction, stroke, and revascularization. Results: Among the 10,683 patients, 4,352 (40.7%) were current smokers. Smokers were 10.7 years younger and less likely to have comorbidities such as hypertension, diabetes mellitus, chronic kidney disease, stroke, and prior PCI. Smokers had less MACE (hazard ratio [HR], 0.644; 95% confidence interval [CI], 0.594–0.698; p<0.001) and cardiac death (HR, 0.494; 95% CI, 0.443–0.551; p<0.001) compared to nonsmokers during the 5 years in an unadjusted model. However, after propensity-score matching, smokers showed higher risk of MACE (HR, 1.125; 95% CI, 1.009–1.254; p=0.034) and cardiac death (HR, 1.190; 95% CI, 1.026–1.381; p=0.022). Smoking was a strong independent predictor of lung cancer (propensityscore matched HR, 2.749; 95% CI, 1.416–5.338; p=0.003). Conclusions In contrast to the unadjusted model, smoking is associated with worse cardiovascular outcome and higher incidence of lung cancer after adjustment of various confounding factors. This result can be explained by the characteristics of smokers, which were young and had fewer comorbidities.

BACKGROUND: During neurosurgical procedures, patients are often exposed to hypoxic and ischemic brain damage. Cerebral ischemia leads to neuronal cell death and eventually causes neurological impairments. Remifentanil is a new ultra-short acting phenylpiperidine opioid analgesic. In this study, we evaluated remifentanil to determine if it exerts an anti-apoptotic effect in the hippocampal dentate gyrus following transient global ischemia in gerbils. METHODS: Step-down avoidance task, terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assay, and immunohistochemical staining for caspase-3 were performed. RESULTS: The numbers of TUNEL-positive cells and caspase-3-positive cells in the dentate gyrus were increased by ransient global ischemia. Latency in the step-down avoidance task was increased by transient global ischemia. Results revealed that apoptotic cell death in the dentate gyrus was increased significantly following transient global ischemia, resulting in memory impairment. However, treatment with remifentanil suppressed ischemia-induced apoptosis in the dentate gyrus, thereby alleviating the memory impairment that was induced by ischemic cerebral injury. CONCLUSIONS: These results indicate that remifentanil may exert a neuroprotective effect on ischemic brain damage during surgery.
Apoptosis ; Brain ; Brain Ischemia ; Caspase 3 ; Cell Death ; Dentate Gyrus ; Gerbillinae ; Humans ; Ischemia ; Ischemic Attack, Transient ; Memory ; Memory Disorders ; Neurons ; Neuroprotective Agents ; Neurosurgical Procedures ; Piperidines

PURPOSE: To determine the patterns of evaluation and treatment in patients with breast cancer after mastectomy and treated with radiotherapy. A nationwide study was performed with the goal of improving radiotherapy treatment. MATERIALS AND METHODS: A web-based database system for the Korean Patterns of Care Study (PCS) for 6 common cancers was developed. Randomly selected records of 286 eligible patients treated between 1998 and 1999 from 17 hospitals were reviewed. RESULTS: The ages of the study patients ranged from 20 to 80 years (median age 44 years). The pathologic T stage by the AJCC was T1 in 9.7% of the cases, T2 in 59.2% of the cases, T3 in 25.6% of the cases, and T4 in 5.3% of the cases. For analysis of nodal involvement, N0 was 7.3%, N1 was 14%, N2 was 38.8%, and N3 was 38.5% of the cases. The AJCC stage was stage I in 0.7% of the cases, stage IIa in 3.8% of the cases, stage IIb in 9.8% of the cases, stage IIIa in 43% of the cases, stage IIIb in 2.8% of the cases, and IIIc in 38.5% of the cases. There were various sequences of chemotherapy and radiotherapy after mastectomy. Mastectomy and chemotherapy followed by radiotherapy was the most commonly performed sequence in 47% of the cases. Mastectomy, chemotherapy, and radiotherapy followed by additional chemotherapy was performed in 35% of the cases, and neoadjuvant chemoradiotherapy was performed in 12.5% of the cases. The radiotherapy volume was chest wall only in 5.6% of the cases. The volume was chest wall and supraclavicular fossa (SCL) in 20.3% of the cases; chest wall, SCL and internal mammary lymph node (IMN) in 27.6% of the cases; chest wall, SCL and posterior axillary lymph node in 25.9% of the cases; chest wall, SCL, IMN, and posterior axillary lymph node in 19.9% of the cases. Two patients received IMN only. The method of chest wall irradiation was tangential field in 57.3% of the cases and electron beam in 42% of the cases. A bolus for the chest wall was used in 54.8% of the tangential field cases and 52.5% of the electron beam cases. The radiation dose to the chest wall was 45~59.4 Gy (median 50.4 Gy), to the SCL was 45~59.4 Gy (median 50.4 Gy), and to the PAB was 4.8~38.8 Gy, (median 9 Gy) CONCLUSION: Different and various treatment methods were used for radiotherapy of the breast cancer patients after mastectomy in each hospital. Most of treatment methods varied in the irradiation of the chest wall. A separate analysis for the details of radiotherapy planning also needs to be followed and the outcome of treatment is needed in order to evaluate the different processes.
Breast Neoplasms ; Breast* ; Chemoradiotherapy ; Drug Therapy ; Humans ; Korea* ; Lymph Nodes ; Mastectomy* ; Mastectomy, Radical ; Radiotherapy ; Thoracic Wall

Spontaneous intestinal perforation is characterized by isolated mucosal ulceration with acute inflammation, submucosal edema and serosal inflammation, and considered as a separate clinical entity from necrotizing enterocolitis. The causes of spontaneous intestinal perforation are administration of indomethacin, dexamethasone, umbilical artery catheterization, defect of intestinal musculature, and systemic candidasis. Intestinal perforation caused by defects of intestinal musculature is rare, and its pathogenesis remains uncertain. The authors report one case of a premature infant with defect in intestinal musculature confirmed through postoperation biopsy who was misdiagnosed as intestinal perforation due to necrotizing enterocolitis.
Biopsy ; Catheterization ; Catheters ; Dexamethasone ; Edema ; Enterocolitis, Necrotizing ; Humans ; Indomethacin ; Infant, Newborn ; Infant, Premature ; Inflammation ; Intestinal Perforation* ; Ulcer ; Umbilical Arteries

PURPOSE: Local treatment of rectal tumors have become an alternative to the classic radical operation. However, conventional transanal procedures are limited to tumors located in the lower rectum and the precision of the excision is restricted by the limitation of the surgeon's visualization during the procedure. This report will present our surgical management and functional results after TEM, a new minimally invasive technique for the treatment of rectal tumors. METHODS: From December 1994 to January 2000, 136 patients underwent TEM. All patients were evaluated preoperatively with sigmoidoscopy or colonoscopy with biopsy. The indications for TEM were benign rectal tumors and T1 and T2 malignant rectal tumors with well or moderately differentiation. All patients were followed up 1 month postoperatively and every 3 months thereafter. RESULTS: The mean operation time was 56.5 minutes (25~150 minutes) and the mean postoperative hospital stay was 3.6 days (2~10 days). On the basis of the postoperative evaluations, 56 of the 136 patients proved to have benign tumors while the remaining 80 patients had malignant tumors. One hundred thirty five patients were removed with adequate resection margins. One patient had cancer cell involvement at the resection margin. There were no serious complications. After a mean observation time of 29 months (12~42 months), there were five noted recurrences. Functional results were excellent; 24 of the 136 patients complained of impaired continence or defecation disorders in a review one month postoperatively. These problems improved during the first 6 months after the surgery. CONCLUSIONS: We feel that TEM is an adequate method for removal of benign rectal tumors, and properly selected early rectal cancers.
Biopsy ; Colonoscopy ; Defecation ; Humans ; Length of Stay ; Microsurgery* ; Rectal Neoplasms ; Rectum ; Recurrence ; Sigmoidoscopy

BACKGROUND: One of the major morphologic characteristics of hepatitis B is a hepatocellular regeneration which is induced by massive hepatocyte necrosis and associated with proliferative activity of hepatocytes. The purpose of this study is to document the proliferative activity of hepatocytes in various types of hepatitis B by immunohistochemical staining for proliferative cell nuclear antigen-labelling index (PCNA-LI) and electron microscopy. METHODS: We studied 83 patients with hepatitis B; 11 cases of acute viral hepatitis, 24 cases of mild chronic hepatitis, 34 cases of severe chronic hepatitis with early cirrhosis and 14 cases of severe chronic hepatitis. The PCNA was tested by immunohistochemical staining using anti-PCNA antibody. Furthermore we evaluated the ultrastructure of acinus-forming hepatocytes (AFH) by electron microscopy. RESULTS: The expression rate and labelling index of PCNA were 27.3% and 5.3 +/- 0.9% in acute viral hepatitis, 62.5% and 22.9 +/- 31.7% in mild chronic hepatits, and then 47.1% and 14.1 +/- 24.2% in severe chronic hepatitis with early cirrhosis, respectively (Figure 1). By contrast, no detectable PCNA expression was noted in AFH. Electron microscopic findings showed that hepatocytes forming a rosette underwent marked degenerative changes with sinusoidal capillarization and increased fine strands of collagen fiber in portal area. CONCLUSION: The proliferative acitivity of hepatitis B was significantly decreased in severe chronic hepatitis containing AFH. This result suggested that differences in proliferative activity was associated with hepatic cell necrosis and AFH.
Adolescent ; Adult ; Aged ; Cell Division ; Female ; Hepatitis B, Chronic/*metabolism/*pathology ; Hepatocytes/*metabolism/*ultrastructure ; Human ; Immunohistochemistry ; Male ; Microscopy, Electron ; Middle Age ; Proliferating Cell Nuclear Antigen/*metabolism

BACKGROUND/AIMS: Lamivudine use in patients with decompensated cirrhosis B has been reported to improve the hepatic function and often delay the need for liver transplantation. In the present study, we evaluated the efficacy and safety of long-term lamivudine therapy in patients with decompensated cirrhosis by comparative study using a matched, untreated cohort. METHODS: 41 patients with decompensated cirrhosis B were included for this study (31 male and 10 female; mean age, 50 years; mean observation period, 18 months). They were divided into two groups: a lamivudine treatment group and an untreated control group. 21 patients in the treatment group were treated with lamivudine 75 or 150 mg daily for at least 12 months. Biochemical and serologic markers were evaluated at two to three-month intervals for all patients. Clinical improvement was defined by a decrease in the Child-Pugh score of at least 2 points. RESULTS: During the observation period, 62% (13/21) was responders, 33% (7/21) was breakthrough, and 5% (1/21) was non-responder in the treated group. The mean Child-Pugh score was significantly improved from 8.6 to 6.0 in the treatment group, but aggravated from 8.7 to 10.0 in the control group during the follow-up. The HBeAg seroconversion rate was 31% in the treatment group (5/16) and none in the control group (0/14). Clinical improvement was observed in fifteen of 21 in the treatment group (71%) and only one of 20 in the control group (5%). According to the treatment responses, clinical improvement was observed in ten of 13 responders (77%), four of 7 breakthrough (57%), and one non-responder. CONCLUSIONS: The long-term administration of lamivudine for patients with decompensated cirrhosis B is effective and safe, although breakthrough and non-response occurred in some patients.
Adult ; Antiviral Agents/adverse effects/*therapeutic use ; Comparative Study ; English Abstract ; Female ; Hepatitis B/complications/*drug therapy ; Human ; Lamivudine/adverse effects/*therapeutic use ; Liver Cirrhosis/*virology ; Male ; Middle Aged ; Treatment Outcome

BACKGROUND: One of the limitation during the irradiation of malignant tumor is hazard to normal tissue although it is important and effective tool for treating malignant tumor. We studied the role of interleukin-1 alpha (IL-1alpha) and interleukin-6 (IL-6) in the radiation-induced lung injury especially on fibrosis. METHODS: We irradiated right-side lungs of thirty Sprague-Dawley rats with single fraction of 20 Gy and then sacrificed the animals until 20th week at intervals of two weeks. Both irradiated and unirradiated lung tissues were stained hematoxilin and eosin, Masson trichrome, reticulin and immunohistochemical staining for IL-1alpha and IL-6. The degree of the staining for IL-1alpha and IL-6 were examined semiquantitatively. RESULTS: Two weeks after irradiation interstitial edema and capillary congestion appeared, followed by increase of the monocytes infiltration and proteinaceous material during 4th and 8th week. After eight weeks of irradiation, collagen and reticulin fibers were detected along alveolar wall. 12th to 20th week, fibrosis in interstitium, decreased number of alveoli and thickening of bronchial wall were observed. The degree of immunohistochemical staining for IL-1alpha and IL-6 was increased rapidly during the first three week and then decreased slowly, but remain incresed until 20th week. CONCLUSION: Our Study demonstrate the early and persistent elevation of cytokines IL-1alpha and IL-6 by immunohistochemical stain in rat lung following pulmonary irradiation. We think cytokines are produced immediately after irradiation, make collagen genes turn on and perisist until the expression of late effects become apparent pathologically and clinically.
Animals ; Capillaries ; Collagen ; Cytokines ; Edema ; Eosine Yellowish-(YS) ; Estrogens, Conjugated (USP) ; Fibrosis ; Interleukin-1* ; Interleukin-1alpha ; Interleukin-6* ; Lung Injury ; Lung* ; Monocytes ; Rats* ; Rats, Sprague-Dawley ; Reticulin