No abstract available.
Lymphoma, T-Cell, Cutaneous*

Depression is a highly prevalent mental health disease that, fortunately, can easily be treated. However, depression is often inadequately managed because only some depressive patients seek professional help, and even when they do, they often discontinue their treatments. Research has shown that there is a high association between suicide and depression. Proper depression management plans help depressive patients adhere to treatment medication and support them in continuing treatment. These efforts for treating depression may reduce suicidal ideation and behavior. Simply giving screening results to clinicians was not enough to have treatment outcomes. Besides informing clinicians of patients' screening results, staff-assisted care, including educating patients, following-up on assessments and treatment schedules, helping patients adhere to prescribed antidepressant medications, and referring to mental health care professionals would be critical to achieving successful treatment outcomes. A higher level of staff-assisted care has been reported to have higher treatment outcomes. Future studies in Korea are needed to establish a depression screening system, including post-screening management programs in primary care or community care settings, and to assess the effectiveness of this system. Attaining a higher depression diagnosis rate through screening and running post-screening management programs with sufficient staffing for treatment adherence will reduce depression relapse and suicidal attempts.
Appointments and Schedules ; Depression ; Humans ; Korea ; Mass Screening ; Mental Health ; Primary Health Care ; Recurrence ; Running ; Suicidal Ideation ; Suicide

To assess the value of endorectal ultrasonography ( ERUS ) in predicting the pathological response to neoadjuvant chemoradiotherapy( NCRT ) for locally advanced rectal cancer( LARC) . Methods Ninety‐nine patients with LARC received NCRT and total mesorectal excision in our hospital were retrospectively analyzed . T he maximum length and thickness of rectal tumor were measured by ERUS both before NCRT ( ERUS1 ) and after NCRT following sugery ( ERUS2 ) ,and the length and thickness reduction rate were calculated . T he patients were classified into good responder group ( n ＝ 47 ) and poor responder group( n ＝ 52 ) ,or pathological complete response ( pCR) group ( n ＝ 25 ) and non‐pCR group ( n＝74) according to pathological tumor regression grade ( T RG ) . T he differences of various parameters were compared between groups . T he correlations between these parameters and T RG grading were analyzed by Spearman correlation analysis . T he ROC curve was used to evaluate the diagnostic efficacy of the parameter . Results T he length and thickness of ERUS2 were significantly shorter than that of ERUS1( all P ＜0 .05) . T he length and thickness of ERUS2 in good responder group were shorter than those in poor responder group ,while the length and thickness reduction rate were higher than those in poor responder group with significant difference ( all P ＜ 0 .05 ) . T he length and thickness of ERUS2 in pCR group were shorter than those in non‐pCR group ,w hile the length and thickness reduction rate were higher than those in non‐pCR group with significant difference ( all P ＜ 0 .05 ) . T he length and thickness of ERUS2 were positively correlated with T RG grading ( r ＝ 0 .577 ,0 .605 ; all P ＜ 0 .01 ) and the length and thickness reduction rate were negatively correlated with T RG grading ( r ＝ －0 .681 ,－0 .598 ; all P ＜0 .01 ) . ROC curve showed the cut‐off value of the length and thickness reduction rate to predict good responder were 41 .34% ,46 .46% , with corresponding AUC areas of 0 .843 ,0 .796 , sensitivity of 74 .5% ,70 .2% , and specificity of 76 .9% ,80 .8% ,respectively . ROC curve showed the cut‐off value of the length and thickness reduction rate to predict pCR were 57 .36% ,58 .52% ,with corresponding AUC areas of 0 .851 and 0 .895 , sensitivity of 68 .0% ,76 .0% ,and specificity of 94 .6% ,93 .2% ,respectively . Conclusions T he changes of length and thickness of tumor after NCRT are well correlated with treatment response . T he length and thickness reduction rate measured on ERUS present high accuracy in prediction of good response and pCR in LARC patients .

PURPOSE: PTEN and DMBT1, candidate tumor suppressor genes on chromosome 10q, were identified based on deletions in glioblastoma and medulloblastoma cell lines. We examined the occurrences and frequencies of allelic deletions on chromosome 10q23 and 10q25 by loss of heterozygosity (LOH) analysis in 24 pediatric brain tumors to investigate the possible involvement of PTEN and DMBT1 gene deletions in the development of pediatric brain tumors. METHOD: LOH was analyzed by polymerase chain reaction (PCR) of PTEN locus on 10q23 using 2 microsatellite markers, D10S608 and D10S579, and of DMBT1 locus on 10q25-q26.1 using a microsatellite marker, D10S587, in 24 pediatric brain tumor (18 medulloblastomas, 3 ependymomas, 2 glioblastomas and 1 supratentorial primitive neuroectodermal tumor) DNAs extracted from archival tissue specimens (case 1-15, 19) or fresh frozen tissue specimens (case 16-18, 20-24). RESULTS: Allelic deletions were detected in 4 of 23 informative cases (17%) on D10S608, 6 of 24 informative cases (25%) on D10S579, and 8 of 24 informative cases (33%) on D10S587. Overall 11 of 24 cases (46%) showed LOH on chromosome 10q at PTEN or DMBT1 loci, and they were 10 medulloblastomas and 1 ependymoma pathologically. Of 18 medulloblastomas, 7 (39%) exhibited LOH at PTEN locus, 8 (44%) exhibited LOH at DMBT1 locus, and 10 (56%) exhibited LOH at one or both of loci. CONCLUSION: Our results support the notion that PTEN and DMBT1 tumor suppressor gene deletions may be involved in the pathogenesis of pediatric brain tumors. Our results also suggested that PTEN and DMBT1 tumor suppressor gene deletions may not be important in molecular mechanism of glioblastoma development in children as in adults.
Adult ; Brain Neoplasms* ; Brain* ; Cell Line ; Child ; DNA ; Ependymoma ; Gene Deletion ; Genes, Tumor Suppressor ; Glioblastoma ; Humans ; Loss of Heterozygosity* ; Medulloblastoma ; Microsatellite Repeats ; Neural Plate ; Polymerase Chain Reaction

Background: s/Aims: Non-invasive models stratifying clinically significant portal hypertension (CSPH) are limited. Herein, we developed a new non-invasive model for predicting CSPH in patients with compensated cirrhosis and investigated whether carvedilol can prevent hepatic decompensation in patients with high-risk CSPH stratified using the new model. Methods: Non-invasive risk factors of CSPH were identified via systematic review and meta-analysis of studies involving patients with hepatic venous pressure gradient (HVPG). A new non-invasive model was validated for various performance aspects in three cohorts, i.e., a multicenter HVPG cohort, a follow-up cohort, and a carvediloltreating cohort. Results: In the meta-analysis with six studies (n=819), liver stiffness measurement and platelet count were identified as independent risk factors for CSPH and were used to develop the new “CSPH risk” model. In the HVPG cohort (n=151), the new model accurately predicted CSPH with cutoff values of 0 and –0.68 for ruling in and out CSPH, respectively. In the follow-up cohort (n=1,102), the cumulative incidences of decompensation events significantly differed using the cutoff values of <–0.68 (low-risk), –0.68 to 0 (medium-risk), and >0 (high-risk). In the carvediloltreated cohort, patients with high-risk CSPH treated with carvedilol (n=81) had lower rates of decompensation events than non-selective beta-blockers untreated patients with high-risk CSPH (n=613 before propensity score matching [PSM], n=162 after PSM). Conclusions Treatment with carvedilol significantly reduces the risk of hepatic decompensation in patients with high-risk CSPH stratified by the new model.

Background: s/Aims: Non-invasive models stratifying clinically significant portal hypertension (CSPH) are limited. Herein, we developed a new non-invasive model for predicting CSPH in patients with compensated cirrhosis and investigated whether carvedilol can prevent hepatic decompensation in patients with high-risk CSPH stratified using the new model. Methods: Non-invasive risk factors of CSPH were identified via systematic review and meta-analysis of studies involving patients with hepatic venous pressure gradient (HVPG). A new non-invasive model was validated for various performance aspects in three cohorts, i.e., a multicenter HVPG cohort, a follow-up cohort, and a carvediloltreating cohort. Results: In the meta-analysis with six studies (n=819), liver stiffness measurement and platelet count were identified as independent risk factors for CSPH and were used to develop the new “CSPH risk” model. In the HVPG cohort (n=151), the new model accurately predicted CSPH with cutoff values of 0 and –0.68 for ruling in and out CSPH, respectively. In the follow-up cohort (n=1,102), the cumulative incidences of decompensation events significantly differed using the cutoff values of <–0.68 (low-risk), –0.68 to 0 (medium-risk), and >0 (high-risk). In the carvediloltreated cohort, patients with high-risk CSPH treated with carvedilol (n=81) had lower rates of decompensation events than non-selective beta-blockers untreated patients with high-risk CSPH (n=613 before propensity score matching [PSM], n=162 after PSM). Conclusions Treatment with carvedilol significantly reduces the risk of hepatic decompensation in patients with high-risk CSPH stratified by the new model.

Background: s/Aims: Non-invasive models stratifying clinically significant portal hypertension (CSPH) are limited. Herein, we developed a new non-invasive model for predicting CSPH in patients with compensated cirrhosis and investigated whether carvedilol can prevent hepatic decompensation in patients with high-risk CSPH stratified using the new model. Methods: Non-invasive risk factors of CSPH were identified via systematic review and meta-analysis of studies involving patients with hepatic venous pressure gradient (HVPG). A new non-invasive model was validated for various performance aspects in three cohorts, i.e., a multicenter HVPG cohort, a follow-up cohort, and a carvediloltreating cohort. Results: In the meta-analysis with six studies (n=819), liver stiffness measurement and platelet count were identified as independent risk factors for CSPH and were used to develop the new “CSPH risk” model. In the HVPG cohort (n=151), the new model accurately predicted CSPH with cutoff values of 0 and –0.68 for ruling in and out CSPH, respectively. In the follow-up cohort (n=1,102), the cumulative incidences of decompensation events significantly differed using the cutoff values of <–0.68 (low-risk), –0.68 to 0 (medium-risk), and >0 (high-risk). In the carvediloltreated cohort, patients with high-risk CSPH treated with carvedilol (n=81) had lower rates of decompensation events than non-selective beta-blockers untreated patients with high-risk CSPH (n=613 before propensity score matching [PSM], n=162 after PSM). Conclusions Treatment with carvedilol significantly reduces the risk of hepatic decompensation in patients with high-risk CSPH stratified by the new model.