• Title/Summary/Keyword: CDH3

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Quantitative Assessment of the Diagnostic Role of CDH13 Promoter Methylation in Lung Cancer

  • Zhong, Yun-Hua;Peng, Hao;Cheng, Hong-Zhong;Wang, Ping
    • Asian Pacific Journal of Cancer Prevention
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    • v.16 no.3
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    • pp.1139-1143
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    • 2015
  • In order to explore the association between cadherin 13 (CDH13) gene promoter methylation and lung carcinoma (LC) risk, we carried out a meta-analysis with searching of PubMed, Web of Science. Ultimately, 17 articles were identified and analysised by STATA 12.0 software. Overall, we found a significant relationship between CDH13 promoter methylation and LC risk (odds ratio=6.98, 95% confidence interval: 4.21-11.56, p<0.001). Subgroup analyses further revealed that LC risk was increased for individuals carrying the methylated CDH13 compared with those with unmethylated CDH13. Hence, our study identified a strong association between CDH13 gene promoter methylation and LC and highlighted a promising potential for CDH13 methylation in LC risk prediction.

Induction of Cyclohexanol Dehydrogenase in Acinetobacter calcoaceticus C10 (Acinetobacter calcoaceticus C10에 의한 Cyclohexanol Dehydrogenase의 유도)

  • Park, Heui-Dong;Choi, Sun-Taek;Rhee, In-Koo
    • Applied Biological Chemistry
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    • v.29 no.3
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    • pp.304-310
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    • 1986
  • A. calcoaceticus C10 grown on cyclohexanol as sole source of carbon and energy produced cyclohexanol dehydrogenase(CDH) and glucose dehydrogenase (GDH) concomitantly. CDH and GDH were different in coenzyme, induction and electrophoretic patterns. CDH depended for activity on $NAD^+$ only, while GDH required $NAD^+$ or $NADP^+$ alternatively. CDH was produced in the medium added cyclohexanol, but GDH was produced in various media such as LB, LB added 0.2% glucose or cyclohexanol and cyclohexanol medium. Productivity of CDH in A. calcoaceticus C10 was enhanced about 8 times by the addition of 0.2% cyclohexanol to LB medium after 4 hours as much as LB medium only. Production of CDH was induced by cyclohexanol, cyclohexanone, cyclohexan-1,2-diol and cyclohexene oxide, but not induced by ${\varepsilon}-caprolactone$ and adipate.

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PROMOTER METHYLATION OF THE CDH-13 GENE IN THE ORAL SQUAMOUS CELL CARCINOMA (구강 편평상피암종에서 CDH-13 유전자의 promoter methylation에 대한 연구)

  • Lee, Moon-Joo;Han, Se-Jin;Kim, Kyung-Wook
    • Journal of the Korean Association of Oral and Maxillofacial Surgeons
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    • v.34 no.5
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    • pp.525-531
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    • 2008
  • CDH-13(T-cadherin), which is one of a kind among the 20 cadherins, can be found mainly in wall of aorta, neuron, spleen, blood vessel etc. It is also called H-cadherin. This structural difference can explain that CDH-13 is thought to play a key role in maintaining mutual relation between extra and intra-cellular environment rather than in cell adhesion. The main function of CDH-13 is to participate in blood vessel function. Additionally, it is known to regulate cell growth and cell contact inhibition. When cells are proliferating, cell surface perceives other cells so that substance such as CDH-13 can inhibit their growth or proliferation resulting in homeostasis without endless proliferation or invasion of connective tissue boundaries. However, tumor cell itself appears to be different from normal cells' growth, invasion or transmission. Therefore, it can be diagnosed that these characteristics are closely related to expression of CDH-13 in tumor cells. This study is to investigate expression of CDH-13 in SCC and its correlation with promoter methylation. 20 of tissue species for the study are excised and gathered from 20 patients who are diagnosed as SCC in department of OMS, dental hospital, dankook university. To find development of CDH-13 in each tissue samples, immunohistochemical staining, RT-PCR gene analysis and methylation specific PCR are processed. The results are as follows. 1.Immunohistochemical staining: In normal oral squamous epithelial tissue, strong expression of CDH-13 was found in cell plasma membrane of basal cell layer. On the other hand, in case of low-differentiated oral SCC, development of CDH-13 was hardly seen. 2.The development of CDH-13 gene: In 9 of samples, expression of CDH-13 gene could be seen and 2 of them showed low expression compared to the others. And rest of the 11 samples showed no expression of CDH-13 gene. 3.Methylation of CDH-13 gene: Among 9 samples which expressed CDH-13 gene, 7 of them showed unmethylation. In addition, among 11 samples without CDH-13 gene expression, 10 showed methylation. According to the results stated above, promoter methylation were found in 13 samples(65%) among 20 of oral SCC samples. In low-differentiated SCC, suppression of gene expression could be seen accompanying promoter methylation. These phenomenon of gene expression was proved by immunohistochemical investigation. Finally, for development of oral SCC, conclusions can be made that suppression of CDH-13 played a main role and suppression of gene expression was originated from promoter methylation. Considering this, it is expected that suppression of CDH-13 from promoter methylation to be utilized as a good diagnostic marker of oral SCC.

Design and decoration of heparin on porous nanosilica via reversible disulfide linkages for controlled drug release

  • Nguyen, Dai Hai
    • Journal of IKEEE
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    • v.21 no.3
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    • pp.320-330
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    • 2017
  • Porous nanosilica (PNS) has been identified as a potential candidate for controlled drug delivery. However, unmodified PNS-based carriers exhibited an initial release of loaded bioactive agents, which may limit their potential clinical applications. In this study, the surface of PNS was functionalized with adamantylamine (ADA) via disulfide bonds (-S-S-), PNS-S-S-ADA, which was then modified with cyclodextrin (CD)-heparin (Hep) (CD-Hep), PNS-S-S-CDH, for redox triggered rhodamine B (RhB) delivery. The obtained samples were then characterized by proton nuclear magnetic resonance ($^{1}H\;NMR$), Fourier transform infrared (FTIR), and transmission electron microscope (TEM). These results showed that PNS-S-S-CDH was successfully formed with spherical shape and average diameter of $45.64{\pm}2.33nm$. In addition, RhB was relatively encapsulated in the PNS-S-S-CDH (RhB@PNS-S-S-CDH) and slowly released up to 3 days. The release of RhB, in particular, was triggered due to the cleavage of -S-S- in the presence of dithiothreitol (DTT). It might be anticipated that the modified PNS can be used as redox-responsive drug delivery system in cancer therapy.

Loss of Expression and Aberrant Methylation of the CDH1 (E-cadherin) Gene in Breast Cancer Patients from Kashmir

  • Asiaf, Asia;Ahmad, Shiekh Tanveer;Aziz, Sheikh Aejaz;Malik, Ajaz Ahmad;Rasool, Zubaida;Masood, Akbar;Zargar, Mohammad Afzal
    • Asian Pacific Journal of Cancer Prevention
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    • v.15 no.15
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    • pp.6397-6403
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    • 2014
  • Background: Aberrant promoter hypermethylation has been recognized in human breast carcinogenesis as a frequent molecular alteration associated with the loss of expression of a number of key regulatory genes and may serve as a biomarker. The E-cadherin gene (CDH1), mapping at chromosome 16q22, is an intercellular adhesion molecule in epithelial cells, which plays an important role in establishing and maintaining intercellular connections. The aim of our study was to assess the methylation pattern of CDH1 and to correlate it with the expression of E-cadherin, clinicopathological parameters and hormone receptor status in breast cancer patients of Kashmir. Materials and Methods: Methylation specific PCR (MSP) was used to determine the methylation status of CDH1 in 128 invasive ductal carcinomas (IDCs) paired with the corresponding normal tissue samples. Immunohistochemistry was used to study the expression of E-cadherin, ER and PR. Results: CDH1 hypermethylation was detected in 57.8% of cases and 14.8% of normal adjacent controls. Reduced levels of E-cadherin protein were observed in 71.9% of our samples. Loss of E-cadherin expression was significantly associated with the CDH1 promoter region methylation (p<0.05, OR=3.48, CI: 1.55-7.79). Hypermethylation of CDH1 was significantly associated with age at diagnosis (p=0.030), tumor size (p=0.008), tumor grade (p=0.024) and rate of node positivity or metastasis (p=0.043). Conclusions: Our preliminary findings suggest that abnormal CDH1 methylation occurs in high frequencies in infiltrating breast cancers associated with a decrease in E-cadherin expression. We found significant differences in tumor-related CDH1 gene methylation patterns relevant to tumor grade, tumor size, nodal involvement and age at diagnosis of breast tumors, which could be extended in future to provide diagnostic and prognostic information.

Respiratory Severity Score as a Predictive Factor for the Mortality of Congenital Diaphragmatic Hernia

  • Ahn, Ja-Hye;Jung, Young Hwa;Shin, Seung Han;Kim, Hyun-Young;Kim, Ee-Kyung;Kim, Han-Suk
    • Neonatal Medicine
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    • v.25 no.3
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    • pp.102-108
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    • 2018
  • Purpose: Congenital diaphragmatic hernia (CDH) is rare but potentially fatal. The overall outcome is highly variable. This study aimed to identify a simple and dynamic parameter that helps predict the mortality of CDH patients in real time, without invasive tests. Methods: We conducted a retrospective chart review of 59 CDH cases. Maternal and fetal information included the gestational age at diagnosis, site of defect, presence of liver herniation, and lung-to-head ratio (LHR) at 20 to 29 weeks of gestational age. Information regarding postnatal treatment, including the number of days until surgery, the need for inhaled nitric oxide (iNO), the need for extracorporeal membrane oxygenation (ECMO), and survival, was collected. The highest respiratory severity score (RSS) within 24 hours after birth was also calculated. Results: Statistical analysis showed that a younger gestational age at the initial diagnosis (P<0.001), a lower LHR (P=0.001), and the presence of liver herniation (P=0.003) were prenatal risk factors for CDH mortality. The RSS and use of iNO and ECMO were significant factors affecting survival. In the multivariate analysis, the only remaining significant risk factor was the highest preoperative RSS within 24 hours after birth (P=0.002). The area under the receiver operating characteristic curve was 0.9375, with a sensitivity of 91.67% and specificity of 83.87% at the RSS cut-off value of 5.2. The positive and negative predictive values were 82.14% and 92.86%, respectively. Conclusion: Using the RSS as a prognostic predictor with simple calculations will help clinicians plan CDH management.

Outcomes after Extracorporeal Membrane Oxygenation in Neonates with Congenital Diaphragmatic Hernia: A Single-Center Experience

  • Choi, Wooseok;Cho, Won Chul;Choi, Eun Seok;Yun, Tae-Jin;Park, Chun Soo
    • Journal of Chest Surgery
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    • v.54 no.5
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    • pp.348-355
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    • 2021
  • Background: Congenital diaphragmatic hernia (CDH) is a rare disease often requiring mechanical ventilation after birth. In severe cases, extracorporeal membrane oxygenation (ECMO) may be needed. This study analyzed the outcomes of patients with CDH treated with ECMO and investigated factors related to in-hospital mortality. Methods: Among 254 newborns diagnosed with CDH between 2008 and 2020, 51 patients needed ECMO support. At Asan Medical Center, a multidisciplinary team approach has been applied for managing newborns with CDH since 2018. Outcomes were compared between hospital survivors and nonsurvivors. Results: ECMO was established at a median of 17 hours after birth. The mean birth weight was 3.1±0.5 kg. Twenty-three patients (23/51, 45.1%) were weaned from ECMO, and 16 patients (16/51, 31.4%) survived to discharge. The ECMO mode was veno-venous in 24 patients (47.1%) and veno-arterial in 27 patients (52.9%). Most cannulations (50/51, 98%) were accomplished through a transverse cervical incision. No significant between-group differences in baseline characteristics and prenatal indices were observed. The oxygenation index (1 hour before: 90.0 vs. 51.0, p=0.005) and blood lactate level (peak: 7.9 vs. 5.2 mmol/L, p=0.023) before ECMO were higher in nonsurvivors. Major bleeding during ECMO more frequently occurred in nonsurvivors (57.1% vs. 12.5%, p=0.007). In the multivariate analysis, the oxygenation index measured at 1 hour before ECMO initiation was identified as a significant risk factor for in-hospital mortality (odds ratio, 1.02; 95% confidence interval, 1.01-1.04; p=0.05). Conclusion: The survival of neonates after ECMO for CDH is suboptimal. Timely application of ECMO is crucial for better survival outcomes.

Extracorporeal Membrane Oxygenation in Neonates with Congenital Diaphragmatic Hernia: a Preliminary Experience (체외막 산소화 요법을 적용한 선천성 횡격막탈장 치료의 초기 경험)

  • Kim, Tae-Hoon;Cho, Min-Jeng;Park, Jeong-Jun;Kim, Dae-Yeon;Kim, Seong-Chul;Kim, In-Koo
    • Advances in pediatric surgery
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    • v.17 no.2
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    • pp.133-138
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    • 2011
  • Extracorporeal membrane oxygenation (ECMO) has been utilized in congenital diaphragmatic hernia (CDH) patients with severe respiratory failure unresponsive to conventional medical treatment. We retrospectively reviewed 12 CDH patients who were treated using ECMO in our center between April 2008 and February 2011. The pre ECMO and on ECMO variables analyzed included gestational age, sex, birth weight, age at the time of ECMO cannulation, arterial blood gas analysis results, CDH location, timing of CDH repair operation, complications and survival. There were 9 boys and 3 girls. All patients were prenatally diagnosed. Mean gestational age was $38.8{\pm}1.7$ weeks and mean birth weight was $3031{\pm}499$ gram. Mean age at the time of ECMO cannulation was $29.9{\pm}28.9$ hours. There were 4 patients who survived. Survivors showed higher 5 min Apgar scores ($8.25{\pm}0.96$ vs. $7.00{\pm}1.20$, p=0.109), higher pre ECMO mean pH ($7.258 {\pm}0.830$ vs. $7.159{\pm}0.986$, p=0.073) and lower pre ECMO $PaCO_2$ ($48.2{\pm}7.9$ vs. $64.8{\pm}16.1$, p=0.109) without statistical significance. The hernia was located on the left side in 10 patients and the right side in 2 patients. The time interval from ECMO placement to operative repair was about 3~4 days in 5 early cases and around 24 in the remaining cases. There were 3 cases of post operative bleeding requiring re operation and 2 cases of abdominal compartment syndrome requiring abdominal fascia reopening. ECMO catheter reposition was required in 4 cases. Three cases of arterial or venous thrombosis were detected and improved with follow up. Our data suggests that ECMO therapy could save the lives of some neonates with CDH who can not be maintained on other treatment modalities. Protocolized management and accumulation of case experience might be valuable in improving outcomes for neonates with CDH treated with ECMO.

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Lamellar Body Counts in Fetal Rabbits' Experimental Diaphragmatic Hernia and Tracheal Ligation (기도결찰을 시행한 토끼 태자의 실험적 횡격막탈장에서 Lamellar body counts)

  • Chun, Yong-Soon;Jung, Soo-Jin;Lee, Jeong-Nyeo
    • Advances in pediatric surgery
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    • v.17 no.2
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    • pp.179-187
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    • 2011
  • Experimental tracheal ligation (TL) has been shown to reverse the pulmonary hypoplasia associated with congenital diaphragmatic hernia (CDH) and to normalize gas exchange. The purpose of this study was to determine whether the TL would correct the surfactant deficiency present in the fetal rabbit model of CDH by using lamellar body count. Lamellar bodies are synthesized and secreted by the type II pneumocytes of fetal lung. The phospholipids present in these bodies constitute the major component of pulmonary surfactant. Twenty-one pregnant New Zealand rabbits underwent hysterotomy and fetal surgery on gestational day 24. Two fetuses of each pregnant rabbit were operated. In the fetus of one end of bicornuate uterus, left DH was created by excision of fetal diaphragm through open thoracotomy (DH Group). In the fetus of the other end of bicornuate uterus, left DH and TL were created (TL Group). The fetuses were delivered by Cesarean section on gestational day 31. Fourteen in control group, 12 in the DH group and 13 in TL group were born alive. En bloc excision of lungs, bronchi and trachea was done in all newborn rabbits. A five Fr catheter was inserted through trachea and repeated irrigations with 10 cc normal saline were done. The irrigated fluid was centrifuged at $280{\times}g$ for 5 minutes and the lamellar bodies were counted with the upper level fluid in platelet channel of electronic cell counter. The average lamellar body counts were $37.1{\pm}14.2{\times}10^3/{\mu}L$ in control group, $11.5{\pm}4.4 {\times}10^3/{\mu}L$ in DH group, and $6.5{\pm}0.9{\times}10^3/{\mu}L$ in TL group. Lamellar body count in DH group was lower than in control group and did not increase after TL. This study shows TL has no therapeutic effect on decreased surfactant level of CDH and the pregnant rabbit is appropriate for the animal model of CDH.

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Roles of E-Cadherin (CDH1) Genetic Variations in Cancer Risk: a Meta-analysis

  • Deng, Qi-Wen;He, Bang-Shun;Pan, Yu-Qin;Sun, Hui-Ling;Xu, Ye-Qiong;Gao, Tian-Yi;Li, Rui;Song, Guo-Qi;Wang, Shu-Kui
    • Asian Pacific Journal of Cancer Prevention
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    • v.15 no.8
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    • pp.3705-3713
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    • 2014
  • E-Cadherin (CDH1) genetic variations may be involved in invasion and metastasis of various cancers by altering gene transcriptional activity of epithelial cells. However, published studies on the association of CDH1 gene polymorphisms and cancer risk remain contradictory, owing to differences in living habits and genetic backgrounds. To derive a more better and comprehensive conclusion, the present meta-analysis was performed including 57 eligible studies of the association between polymorphisms of CDH1 gene promoter -160 C>A, -347 G>GA and 3'-UTR +54 C>T and cancer risk. Results showed that these three polymorphisms of CDH1 were significantly associated with cancer risk. For -160 C>A polymorphism, -160A allele carriers (CA and CA+AA) had an increased risk of cancer compared with the homozygotes (CC), and the similar result was discovered for the -160A allele in the overall analyses. In the subgroup analyses, obvious elevated risk was found with -160A allele carriers (AA, CA, CA+AA and A allele) for prostate cancer, while a decreased colorectal cancer risk was shown with the AA genotype. For the -347 G>GA polymorphism, the GAGA genotype was associated with increased cancer risk in the overall analysis with homozygous and recessive models. In addition, results of subgroup analysis indicated that the elevated risks were observed in colorectal cancer and Asian descendants. For +54 C>T polymorphism, a decreased risk of cancer was found in heterozygous, dominant and allele models. Moreover, +54T allele carriers (CT, CT+TT genotype and T allele) showed a potential protective factor in gastric cancer and Asian descendants.