Quality of Care for Lung Cancer in Taiwan: A Pattern of Care Based on Core Measures in the Taiwan Cancer Database Registry

Background/Purpose: To investigate the quality of care (QOC) for lung cancer in Taiwan, as measured by pattern of care (POC) variation. Methods: Based on core measures in the Taiwan Cancer Database (TCDB) registry, QOC for lung cancer was measured as variation in POC for 16 selected core measures for different hospital characteristics. Statistical significance in variation was evaluated by the χ2 test. Results: Among the 26 participating hospitals (one excluded as an outlier), 6624 cases of lung cancer were reported in 2004. Among the 16 core measures (6 in the diagnostic and 10 in the therapeutic domain), no significant variation in POC was noted in 12 in northern and non-northern hospitals. However, significant variation in POC was noted for most (5/6) of the core measures in the diagnostic domain for other hospital characteristics (large vs. small, medical center vs. regional hospital, public vs. private). Increasing utilization of tissue diagnosis, diagnostic computed tomography (CT), and CT or magnetic resonance imaging for staging advanced non-small cell lung cancer was noted in the four participating hospitals from 2002 to 2004. Conclusion: It is very likely that significant variation in QOC for lung cancer in Taiwan exists among different types but not locations of hospitals, at least in the diagnostic domain. The introduction of internal benchmarking (TCDB and core measures) was associated with some changes, at least in some diagnostic domains, which may lead to improvement in QOC for lung cancer in Taiwan

Arabidopsis RGLG2, Functioning as a RING E3 Ligase, Interacts with AtERF53 and Negatively Regulates the Plant Drought Stress Response1[W][OA]

Transcriptional activities of plants play important roles in responses to environmental stresses. ETHYLENE RESPONSE FACTOR53 (AtERF53) is a drought-induced transcription factor that belongs to the AP2/ERF superfamily and has a highly conserved AP2 domain. It can regulate drought-responsive gene expression by binding to the GCC box and/or the dehydration-responsive element in the promoter of downstream genes. Overexpression of AtERF53 driven by the cauliflower mosaic virus 35S promoter resulted in an unstable drought-tolerant phenotype in T2 transgenic Arabidopsis (Arabidopsis thaliana) plants. Using a yeast two-hybrid screen, we identified a RING domain ubiquitin E3 ligase, RGLG2, which interacts with AtERF53 in the nucleus. The copine domain of RGLG2 exhibited the strongest interacting activity. We also demonstrated that RGLG2 could move from the plasma membrane to the nucleus under stress treatment. Using an in vitro ubiquitination assay, RGLG2 and its closest sequelog, RGLG1, were shown to have E3 ligase activity and mediated AtERF53 ubiquitination for proteasome degradation. The rglg1rglg2 double mutant but not the rglg2 or rglg1 single mutant exhibited a drought-tolerant phenotype when compared with wild-type plants. AtERF53-green fluorescent proteins expressed in the rglg1rglg2 double mutants were stable. The 35S:AtERF53-green fluorescent protein/rglg1rglg2 showed enhanced AtERF53-regulated gene expression and had greater tolerance to drought stress than the rglg1rglg2 double mutant. In conclusion, RGLG2 negatively regulates the drought stress response by mediating AtERF53 transcriptional activity in Arabidopsis

Effect of implant designs on insertion torque and implant stability quotient (ISQ) value

Statement of problem. Primary implant stability has long been identified as a prerequisite to achieve osseointegration. So the application of a simple, clinically applicable noninvasive test to assess implant stability and osseiointegratation are considered highly desirable. Purpose. The purpose of this study was to evaluate the ISQ value and the insertion torque of the 3 different implant system, then to evaluate whether there was a correlation between ISQ value and insertion torque; and to determine whether implant design has an influence on either insertion torque or ISQ value. Material and method. The experiment was composed of 3 groups: depending on the implant fixture design. Group1 was Branemark type parallel implant in 3.75x7 mm. Group2 was Oneplant type straight implant in 4.3x8.5mm . Group3 was Oneplant type tapered implant in 4.3x8.5mm. Depending on the density of the bone, 2 types of bone were used in this experiment. Type I bone represented for cortical bone, type II bone represented for cancellous bone. With the insertion of the implant in type I and type II bone, the insertion torque was measured, then the ISQ value was evaluated, and then the correlation between insertion torque and ISQ value was analyzed Result and conclusion. Within the limitations of this study, the following conclusions were drawn. 1. Within the 3 different implants, the insertion torque value and ISQ value were higher in type I bone, when compared with type II bone.(p0.05) 4. Significant linear correlation was found in type parallel implant:3.75x7mm in type II bone.This study was supported by a grant of the Korea Health 21 R & D Project. Ministry of Health & Welfare. Republic of Kore

EFFECT OF IMPLANT DESIGNS ON INSERTION TORQUE AND IMPLANT STABILITY QUOTIENT (ISQ) VALUE

Statement of problem. Primary implant stability has long been identified as a prerequisite to achieve osseointegration. So the application of a simple, clinically applicable noninvasive test to assess implant stability and osseiointegratation are considered highly desirable. Purpose. The purpose of this study was to evaluate the ISQ value and the insertion torque of the 3 different implant system, then to evaluate whether there was a correlation between ISQ value and insertion torque; and to determine whether implant design has an influence on either insertion torque or ISQ value. Material and method. The experiment was composed of 3 groups: depending on the implant fixture design. Group1 was Branemark type parallel implant in . Group2 was Oneplant type straight implant in . Group3 was Oneplant type tapered implant in . Depending on the density of the bone, 2 types of bone were used in this experiment. Type I bone represented for cortical bone, type II bone represented for cancellous bone. With the insertion of the implant in type I and type II bone, the insertion torque was measured, then the ISQ value was evaluated, and then the correlation between insertion torque and ISQ value was analyzed Result and conclusion. Within the limitations of this study, the following conclusions were drawn. 1. Within the 3 different implants, the insertion torque value and ISQ value were higher in type I bone, when compared with type II bone.(p0.05) 4. Significant linear correlation was found in type parallel implant: in type II bone.This work was supported by a grant from the Korea Health 21 R&D Project, Ministry of Health and Welfare, Requblic of Korea (02-PJ3-PG6-EV11-002

Macrophage CARD9 mediates cardiac injury following myocardial infarction through regulation of lipocalin 2 expression

Abstract Immune cell infiltration in response to myocyte death regulates extracellular matrix remodeling and scar formation after myocardial infarction (MI). Caspase-recruitment domain family member 9 (CARD9) acts as an adapter that mediates the transduction of pro-inflammatory signaling cascades in innate immunity; however, its role in cardiac injury and repair post-MI remains unclear. We found that Card9 was one of the most upregulated Card genes in the ischemic myocardium of mice. CARD9 expression increased considerably 1 day post-MI and declined by day 7 post-MI. Moreover, CARD9 was mainly expressed in F4/80-positive macrophages. Card9 knockout (KO) led to left ventricular function improvement and infarct scar size reduction in mice 28 days post-MI. Additionally, Card9 KO suppressed cardiomyocyte apoptosis in the border region and attenuated matrix metalloproteinase (MMP) expression. RNA sequencing revealed that Card9 KO significantly suppressed lipocalin 2 (Lcn2) expression post-MI. Both LCN2 and the receptor solute carrier family 22 member 17 (SL22A17) were detected in macrophages. Subsequently, we demonstrated that Card9 overexpression increased LCN2 expression, while Card9 KO inhibited necrotic cell-induced LCN2 upregulation in macrophages, likely through NF-κB. Lcn2 KO showed beneficial effects post-MI, and recombinant LCN2 diminished the protective effects of Card9 KO in vivo. Lcn2 KO reduced MMP9 post-MI, and Lcn2 overexpression increased Mmp9 expression in macrophages. Slc22a17 knockdown in macrophages reduced MMP9 release with recombinant LCN2 treatment. In conclusion, our results demonstrate that macrophage CARD9 mediates the deterioration of cardiac function and adverse remodeling post-MI via LCN2

Detection Rate, Distribution, Clinical and Pathological Features of Colorectal Serrated Polyps

Background: Colorectal serrated polyp is considered as histologically heterogeneous lesions with malignant potential in western countries. However, few Asian studies have investigated the comprehensive clinical features of serrated polyps in symptomatic populations. The aim of the study was to evaluate the features of colorectal serrated polyps in a Chinese symptomatic population. Methods: Data from all consecutive symptomatic patients were documented from a large colonoscopy database and were analyzed. Chi-square test or Fisher′s exact test and logistic regression analysis were used for the data processing. Results: A total of 9191 (31.7%) patients were detected with at least one colorectal polyp. The prevalence of serrated polyps was 0.53% (153/28,981). The proportions of hyperplastic polyp (HP), sessile serrated adenoma/polyp (SSA/P), and traditional serrated adenoma (TSA) of all serrated polyps were 41.2%, 7.2%, and 51.6%, respectively, which showed a lower proportion of HP and SSA/P and a higher proportion of TSA. Serrated polyps appeared more in males and elder patients while there was no significant difference in the subtype distribution in gender and age. The proportions of large and proximal serrated polyps were 13.7% (21/153) and 46.4% (71/153), respectively. In total, 98.9% (89/90) serrated adenomas were found with dysplasia. Moreover, 14 patients with serrated polyps were found with synchronous advanced colorectal neoplasia, and large serrated polyps (LSPs) (odds ratio: 3.446, 95% confidence interval: 1.010-11.750, P < 0.05), especially large HPs, might have an association with synchronous advanced neoplasia (AN). Conclusions: The overall detection rate of colorectal serrated polyps in Chinese symptomatic patient population was low, and distribution pattern of three subtypes is different from previous reports. Moreover, LSPs, especially large HPs, might be associated with an increased risk of synchronous AN

AMP-activated Protein Kinase alpha 2 Protects against Liver Injury from Metastasized Tumors via Reduced Glucose Deprivation-induced Oxidative Stress

Chinese Ministry of Science and Technology [2009CB522205, 2012AA02A201]; National Natural Science Foundation of China [81230006, 31090363, 81000871]Background: AMPK senses energetic changes and regulates glucose metabolism. Results: AMPK 2 deficiency aggravated the glucose deprivation and necrosis of the hepatocytes via increased ROS production and decreased mitophagy. Conclusion: AMPK 2 is essential for attenuation of liver injury during tumor metastasis. Significance: This is the first time to reveal the mechanism by which glucose/energy competition induced tissue damage in tumor. It is well known that tumors damage affected tissues; however, the specific mechanism underlying such damage remains elusive. AMP-activated protein kinase (AMPK) senses energetic changes and regulates glucose metabolism. In this study, we examined the mechanisms by which AMPK promotes metabolic adaptation in the tumor-bearing liver using a murine model of colon cancer liver metastasis. Knock-out of AMPK 2 significantly enhanced tumor-induced glucose deprivation in the liver and increased the extent of liver injury and hepatocyte death. Mechanistically, we observed that AMPK 2 deficiency resulted in elevated reactive oxygen species, reduced mitophagy, and increased cell death in response to tumors or glucose deprivation in vitro. These results imply that AMPK 2 is essential for attenuation of liver injury during tumor metastasis via hepatic glucose deprivation and mitophagy-mediated inhibition of reactive oxygen species production. Therefore, AMPK 2 might represent an important therapeutic target for colon cancer metastasis-induced liver injury

AMP-activated protein kinase α2 protects against liver injury from metastasized tumors via reduced glucose deprivation-induced oxidative stress

It is well known that tumors damage affected tissues; however, the specific mechanism underlying such damage remains elusive. AMP-activated protein kinase (AMPK) senses energetic changes and regulates glucose metabolism. In this study, we examined the mechanisms by whichAMPKpromotes metabolic adaptation in the tumor-bearing liver using a murine model of colon cancer liver metastasis. Knock-out of AMPK α2 significantly enhanced tumor-induced glucose deprivation in the liver and increased the extent of liver injury and hepatocyte death. Mechanistically, we observed that AMPK α2 deficiency resulted in elevated reactive oxygen species, reduced mitophagy, and increased cell death in response to tumors or glucose deprivation in vitro. These results imply that AMPK α2 is essential for attenuation of liver injury during tumor metastasis via hepatic glucose deprivation and mitophagy-mediated inhibition of reactive oxygen species production. Therefore, AMPK α2 might represent an important therapeutic target for colon cancer metastasis-induced liver injury. ? 2014 by The American Society for Biochemistry and Molecular Biology, Inc