PubMed Health⌕ Search

Biomedical subjects

J C Yu

Publications and source records attributed to J C Yu.

At least 19 recordsLinked to original sources
PubMed2006

Intrapericardial isolation of the inferior vena cava through a transdiaphragmatic pericardial window for tumor resection without sternotomy or thoracotomy.

AIMS: The prognosis for patients with advanced tumors invading the inferior vena cava (IVC) is dismal and surgical treatments for these tumors are challenging. A surgical approach that avoids sternotomy and thoracotomy for tumors invading the IVC even to the level of the hepatocaval junction would be extremely helpful. METHODS: The intrapericardial IVC was isolated via a transdiaphragmatic pericardial window using a transabdominal approach. Hepatectomy was then applied via an anterior approach until the IVC was seen. Total hepatic vascular exclusion was achieved by clamping the portal triad, intrapericardial IVC and infrahepatic IVC. We removed the primary tumor, the liver portion involved and the tumor thrombi, with segmental resection of the IVC. Vascular continuity was reestablished using a 20-mm-diameter polytetrafluoroethylene graft. RESULTS: Four patients with tumors invading the IVC were treated with this method. All underwent gross en-bloc tumor resections and all survived. CONCLUSION: This method for the resection of IVC tumors could avoid emboli dislodging from the tumor thrombi, prevent the complications of sternotomy, cardiopulmonary bypass and shorten operative times.

Adrenal Cortex Neoplasms↗
PubMed2006

Comparison of clinical staging systems in predicting survival of hepatocellular carcinoma patients receiving major or minor hepatectomy.

AIM: To compare the utility of seven commonly used staging systems in the prediction of survival among patients with hepatocellular carcinoma (HCC) undergoing major or minor hepatectomy. METHODS: All patients were classified by the Okuda, the TNM, the CLIP, the BCLC, the CUPI, the JIS and the MELD classifications to estimate the probabilities of survival. Survival curves were calculated using the Kaplan-Meier method and were examined using log-rank testing. The overall predictive power for patient survival with each staging system was evaluated using linear trend chi(2) tests and from the area under the receiver operating characteristic (ROC) curve. RESULTS: In our patient cohort, the log-rank test and the linear trend chi(2) test of the CLIP and JIS systems gave better results than did the other staging systems. The discriminatory ability of the CLIP and JIS staging for death, evaluated by ROC curve areas, was also better. In the subgroups of major hepatectomy patients with a non-cirrhotic liver or minor hepatectomy patients with a cirrhotic liver, the CLIP and JIS systems showed similar better performances in these three tests. The discriminatory ability of the CLIP system was the best in major hepatectomy patients with a non-cirrhotic liver while JIS score discriminated best in minor hepatectomy patients with a cirrhotic liver. CONCLUSION: Among the seven staging systems, the CLIP and JIS systems perform better than do the others. While the CLIP system should be considered to stage major hepatectomy patients, the JIS system could be chosen to stage minor hepatectomy patients.

Carcinoma, Hepatocellular↗
PubMed2005

An alternative technique for totally implantable central venous access devices. A retrospective study of 1311 cases.

AIM: The aim of the present study was to report our experience of totally implantable central venous access devices (TICVAD) implantation using two techniques and attempt to define the better technique. MATERIALS AND METHODS: From January 1998 to September 2003, 1131 patients were reviewed and divided into two groups with implantation by cephalic vein cut-down (group A) done by general surgeons and subclavian vein puncture with the Seldinger technique (group B) done by vascular surgeons. The operative time, early and late complications of these two groups were compared. Data were analysed by Student's t-test. RESULTS: The average of operative time was 43 min in group A (35-70 min) and 40 min in group B (35-60 min) (P>0.05). No post-operative pneumothorax, hemothorax and fragmentation occurred in group A; the incidence of peri-operative complication was higher in group B. The overall and early complications of group A were significantly lower than that of group B (P<0.0001). CONCLUSION: This retrospective study showed that the cephalic vein cut-down approach for TICVAD placement avoided the risks of pneumothorax, hemothorax and catheter fragmentation.

Blood Vessel Prosthesis Implantation↗
PubMed2005

Prediction of the risk of hepatic failure in patients with portal vein invasion hepatoma after hepatic resection.

AIM: Hepatic failure can develop after curative hepatectomy in patients with a hepatocellular carcinoma (HCC) invading the portal vein, because of cirrhosis and excessive tissue loss. This study aimed to identify the risk factors for hepatic failure in such patients. METHOD: Forty patients with an HCC invading the portal vein underwent curative hepatectomy from January 1995 to June 2003. Eight patients developed hepatic failure and died within 3 months. Possible risk factors for this were analysed using univariate and multivariate regression. These included the liver function index, surgical blood loss, tumour pattern, portal hypertension, estimated residual liver volume measured by computed tomography (ERLV(CT)) and estimated residual liver volume using the indocyanine green (ICG) retention rate at 15 min (ERLV(ICG15)). RESULTS: The ERLV(CT) smaller than the ERLV(ICG15) and presence of portal hypertension were independent risk factors for post-hepatectomy hepatic failure. CONCLUSION: Having portal vein invasion HCC with portal hypertension or an ERLV(CT) less than an ERLV(ICG15) are significant predictors of post-hepatectomy hepatic failure. These factors are important considerations for patients with portal vein invasion HCC who could undergo curative hepatic resection.

Carcinoma, Hepatocellular↗
PubMed2005

Preparation of stable porous nickel and cobalt oxides using simple inorganic precursor, instead of alkoxides, by a sonochemical technique.

Porous nickel and cobalt oxides were prepared using NiSO4.6H2O and anhydrous Co(CH3COO)2, a precursor other than alkoxides and cetyltrimethylammonium bromide as organic surfactant. The sonication method has been used for such synthesis. The surfactants were removed by calcination, as well as by solvent extraction and it is extent was examined by IR spectroscopy. The trend of removal of surfactant was followed by TGA studies and the change in phases by DSC. The products were identified by XRD. Peak in low angle XRD indicates the porous nature of the oxides. The morphology of the pores was studied by transmission electron microscopy. The pores were found less ordered, having an average size of 4-6 nm. The Brunauer-Emmet-Teller surface areas of the as-prepared, as well as the treated samples are reported having H2 and H4 type hysteresis for Ni and Co, respectively.

Journal Article↗
PubMed2004

Abnormality of the DNA double-strand-break checkpoint/repair genes, ATM, BRCA1 and TP53, in breast cancer is related to tumour grade.

The role of the DNA double-strand-break (DSB) checkpoint/repair genes, ATM, BRCA1 and TP53, in sporadic breast cancer requires clarification, since ATM and BRCA1 mutations are rare in sporadic tumours. In an attempt to explain this phenomenon, we postulated that (i) in addition to genetic deletion, abnormal expression of DSB checkpoint/repair proteins might abolish the function of these genes and (ii) there might be a combined effect of individual defective genes during breast cancer pathogenesis. Using a largely homogenous group of 74 specimens of early-onset (< or =35 years of age) infiltrating ductal carcinomas, we examined associations between pathological grade and genetic deletion and/or abnormal protein expression of ATM, BRCA1 and TP53. The results showed that high-grade tumours displayed a high frequency of loss of heterozygosity (LOH) at, and/or abnormal expression of, ATM, BRCA1 and TP53. Multigenetic analysis showed abnormalities in BRCA1 to be independently associated with high-grade tumours. ATM and TP53 appeared to play an assistant role, abnormalities in these genes significantly increasing the possibility of poor differentiation in tumours with abnormalities in BRCA1. Furthermore, a higher number of abnormalities (LOH or abnormal expression) in these three genes correlated with poor tumour differentiation. Thus, this study suggests that combined changes in several DSB checkpoint/repair genes belonging to a common functional pathway are associated with breast cancer pathogenesis.

Adult↗
PubMed2004

Tbx2 represses expression of Connexin43 in osteoblastic-like cells.

Tbx2 belongs to a family of developmental transcription regulatory factors. We evaluated whether the gap junction protein Connexin43 (Cx43), an important regulator of osteoblast function and bone development, may be a downstream target gene regulated by Tbx2. The Cx43 promoter contains direct repeats of the consensus T-box binding motif, TCACAC, and moreover, Tbx2 and Cx43 show overlapping expression domains in precursors to bone and in osteoblasts. In vitro analysis showed that the Cx43 promoter contains two Tbx2 binding sites, and this binding was dependent on the TCACAC consensus sequence. Transient transfection analysis with a Cx43 promoter-driven lacZ reporter construct revealed negative regulation mediated by these two Tbx2 binding sites in osteoblast-like cells. Thus, downregulation of Tbx2 led to de-repression of wild-type Cx43 promoter activity, whereas a promoter construct with mutated binding sites showed no de-repression. In stably transfected osteosarcoma cells in which expression of the endogenous Tbx2 gene was downregulated with a Tbx2 antisense construct, a marked de-repression of the endogenous Cx43 gene was observed. This was accompanied by a marked increase in the abundance of Cx43 gap junctions and increased functional gap junction-mediated cell-cell communication. Analysis of lacZ expression in transgenic mice containing the mutated Cx43 promoter-driven lacZ construct further suggested de-repression of the Cx43 promoter in limb buds, a region destined to give rise to long bones of the limbs. Taken together, these findings indicate that the promoter of Cx43 is repressible by Tbx2, both in cultured osteoblast-like cells in vitro and likely in the developing embryo.

Animals↗
PubMed2002

Degradation of azo dye Procion Red MX-5B by photocatalytic oxidation.

The photocatalytic oxidation (PCO) of a monoazo dye Procion Red MX-5B under various physico-chemical conditions was investigated. Degradation of the dye by PCO was enhanced by augmentation in UV intensity, titanium dioxide and hydrogen peroxide concentrations but was inhibited by increase in initial dye concentration. The PCO process was affected by pH in a peculiar way. In the presence of 100 mg/l of TiO2 and the absence of H2O2, the highest reaction rate was observed when the initial pH was 10. With 500 mg/l of TiO2 and 10 mM of H2O2, the reaction was the fastest at initial pH of 3-5. The optimal conditions for the degradation of the dye, at an UV intensity of 17 mW/cm2, were determined to be: TiO2 concentration, 500 mg/l; initial H2O2 concentration, 10 mM; initial pH, 5.0. Monitoring of TOC loss showed that the dye was mineralized by 90% within 80 min under these conditions. Nevertheless, the persistence of a low level of TOC indicated that mineralization was not complete and dead-end product(s) which was (were) resistant to PCO might have accumulated.

Azo Compounds↗
PubMed2001

Mechanisms of inactivation of E-cadherin in breast carcinoma: modification of the two-hit hypothesis of tumor suppressor gene.

Loss of heterozygosity (LOH) allows the expression of recessive mutation in tumor suppressor genes (TSG). Therefore, on the basis of Knudson's 'two-hit' hypothesis for TSG inactivation, the detection of a high LOH frequency in a chromosomal region is considered critical for TSG localization. One of these LOH regions in breast cancer is 16q22.1, which has been suggested to reflect the involvement of E-cadherin (E-cad), a cell-cell adhesion molecule. To confirm the tumorigenic role of E-cad, 81 sporadic invasive ductal carcinomas (IDCs) of the breast were tested for the 'two hits' required to inactivate this gene. A high frequency (37.3%) of LOH was detected in 67 informative tumors, but no mutation was found. To examine the possibility that transcriptional mechanisms serve as the second hit in tumors with LOH, specific pathways, including genetic variant and hypermethylation at the promoter region and abnormal expression of positive (WT1) and negative (Snail) transcription factors, were identified. Of these, promoter hypermethylation and increased expression of Snail were found to be common (>35%), and to be strongly associated with reduced/negative E-cad expression (P<0.05). However, unexpectedly, a significantly negative association was found between the existence of LOH and promoter hypermethylation (P<0.05), which contradicts the 'two-hit' model. Instead, since they coexisted in a high frequency of tumors, hypermethylation may work in concert with increased Snail to inactivate E-cad expression. Given that E-cad is involved in diverse mechanisms, loss of which is beneficial for tumors to invade but may also trigger apoptosis, this study suggests that maintaining a reversible mechanism, either by controlling the gene at the transcriptional level or by retaining an intact allele subsequent to LOH, might be important for E-cad in IDC and may also be common in TSGs possessing diverse functions. These findings provide clues to explain why certain TSGs identified by LOH cannot fulfil the two-hit hypothesis.

Adaptor Proteins, Signal Transducing↗
PubMed2001

Determination of lead in fine particulates by slurry sampling electrothermal atomic absorption spectrometry.

A simple method for determining lead in fine particulates (PM2.5) by using electrothermal atomic absorption spectrometry (ETAAS) has been developed. Particulates collected on Nuclepore filter by using a dichotomous sampler were suspended in diluted nitric acid after ultrasonic agitation. The dislodging efficiency is nearly 100% after agitation for 5 min. In order to study the suspension behavior of PM2.5 in solvents, a Brookhaven ZetaPlus Particle Size Analyzer was used to determine the particle size distribution and suspension behavior of air particulates in the solvent. The pre-digestion and modification effect of nitric acid would be discussed. Palladium was added as a chemical modifier and the temperature program of ETAAS was changed in order to improve the recovery. The slurry was introduced directly into a graphite tube for atomization. The metal content in the sample was determined by the standard addition method. In addition, a conventional acid digestion procedure was applied to verify the efficiency of the slurry sampling method. It offers a quick and efficient alternative method for heavy metal characterization in fine particulates.

Environmental Pollution↗
PubMed2001

Carcinoid tumor of the spleen: report of a case.

Carcinoid tumors are uncommon tumors of the neuroendocrine system. They grow slowly and may remain silent for years before presenting with carcinoid syndrome. A diagnosis of asymptomatic carcinoid tumor is difficult. Wide resection of the primary tumor and metastatic lesions is the first choice of treatment. Primary carcinoid is sometimes distributed throughout the entire body, but it is rare in the spleen. We herein present a rare case of a symptomless carcinoid tumor that predominantly invaded the spleen with liver metastasis.

Aged↗
PubMed2001

Extrinsic tension results in FGF-2 release, membrane permeability change, and intracellular Ca++ increase in immature cranial sutures.

There are numerous studies cataloging the temporal profiles of the various growth factors during the morphogenesis of cranial sutures. There are also many clearly documented mutations of the receptors of some of these growth factors such as fibroblast growth factor (FGF)R-2 and FGFR-3 in clinical craniosynostosis. It is obvious, and often concluded, that growth factors play a role or are involved in craniofacial development. However, precisely what that role is, what causes the changes in the growth factor levels, and why these changes occur in the particular temporal and spatial patterns observed remains elusive. Using simple physics, we applied a plasma membrane disruption model and the principles of complex adaptive systems to arrive at a conjecture of calvarial morphogenesis. The purpose of this article is to introduce the concept of complex adaptive systems, to propose our conjecture, and to provide experimental proof of some key steps in this conjecture: tension induces rapid and demonstrable physiological responses in some cells within the immature cranial sutures. These responses include increases of intracellular Ca++, plasma membrane permeability, and the release of growth factors, e.g., FGF-2. Paired coronal sutures from 1-week-old Sprague-Dawley rat pups were subjected to either 0.59 N of tensile force or no force for 5 minutes in a protein-free medium. FGF-2 levels in the media were measured by slot blot analysis. Western blot analysis was used to determine FGF-2 levels in the sutures. To determine cell membrane permeability changes, fluorescein-conjugated dextran, with a molecular weight of 10 kd, was added to the media during the 5 minutes with or without tensile force. Laser confocal microscopy was used to compare the amount of entry of this impermeant tracer and the pattern of permeability change at the tissue level. To determine the intracellular pCa++, the sutures were first loaded with a calcium indictor, FURA-2 AM, and then subjected isotonically to 0.059 N of tension. The intracellular pCa++ was expressed as ratio of Ca++-bound FURA-2 to Ca++-free FURA-2. The experimental findings were as follows: 1) Sutures, in response to tension, release FGF-2. 2) Sutures contain higher levels of FGF-2 when strained. 3) There is an increase in the sutural cell membrane permeability as a result of tensile strain. 4) The cells along the leading edges of the ossification fronts (at the insertion sites of Sharpey's fibers) demonstrated the maximum permeability increase. 5) There was an immediate (within seconds) increase in intracellular Ca++. and 6) This increase in intracellular Ca++ caused by tension was reversible and independent of the extracellular Ca++ ion availability. In summary, these data support, in part, the conjecture that growth of the brain places strain on the cells within the immature sutures, which causes the iteration of a set of cellular subroutines. These subroutines integrate to generate the emergent property of directed cranial expansion with dissipation of the initiating strains.

Adaptation, Physiological↗
PubMed2001

Efficacy of the novel selective platelet-derived growth factor receptor antagonist CT52923 on cellular proliferation, migration, and suppression of neointima following vascular injury.

Exaggerated or inappropriate signaling by the platelet-derived growth factor receptor (PDGFR) tyrosine kinase has been implicated in a wide variety of diseases. Thus, a series of piperazinyl quinazoline compounds were identified as potent antagonists of the PDGFR by screening chemical libraries. An optimized analog, CT52923, was shown to be an ATP-competitive inhibitor that exhibited remarkable specificity when tested against other kinases, including all members of the closely related PDGFR family. The PDGFRs and stem cell factor receptor were inhibited with an IC(50) of 100 to 200 nM, while 45- to >200-fold higher concentrations of CT52923 were required to inhibit fms-like tyrosine kinase-3 and colony-stimulating factor-1 receptor, respectively. Other receptor tyrosine kinases, cytoplasmic tyrosine kinases, serine/threonine kinases, or members of the mitogen-activated protein kinase pathway were not significantly inhibited at 100- to 1000-fold higher concentrations. In addition, this compound also demonstrated specificity for inhibition of cellular responses. Platelet-derived growth factor-induced smooth muscle cell migration or fibroblast proliferation was found to be blocked by CT52923 with an IC(50) of 64 and 280 nM, respectively, whereas 50- to 100-fold higher concentrations were required to inhibit these responses when induced with fibroblast growth factor. To investigate the effect of CT52923 on PDGFR signaling, in vivo studies demonstrated that CT52923 could significantly inhibit neointima formation following carotid artery injury by oral administration in the rat. Therefore, PDGFR antagonism by CT52923 could be a viable strategy for the prevention of clinical restenosis or the treatment of other human diseases involving PDGFR signaling.

Angioplasty, Balloon↗
PubMed2000

Genome-wide search for loss of heterozygosity using laser capture microdissected tissue of breast carcinoma: an implication for mutator phenotype and breast cancer pathogenesis.

Breast cancer is considered to display a high degree of intratumor heterogeneity, without any obvious morphological and pathological steps to define sequential evolution, and its progression may vary among individual tumors. In an attempt to elucidate these etiological and phenotypic complexities, the present study, based on the fundamental concept that genomic instability is the engine of both tumor progression and tumor heterogeneity, was conducted to test the hypothesis that breast cancer pathogenesis is driven by double-strand break (DSB)-initiated chromosome instability (CIN). The rationale underlying this hypothesis is derived from the clues provided by family breast cancer syndromes, in which susceptibility genes, including p53, ATM, BRCA1 and BRCA2, are involved within the common functional pathway of DSB-related checkpoint/ repair. Because genomic deletion caused by DSB is reflected in the genetic mechanism of loss of heterozygosity (LOH), this genome-wide LOH study was conducted, using 100 tumors and 400 microsatellite markers. To minimize the effect of heterogeneity within tumors, the experimental technique of laser capture microdissection was used to ensure that genetic and phenotypic examinations were based on the same tumor cells. Support for our hypothesis comes from the observations that: (a) the extent of DSB-initiated CIN in tumors significantly increased as tumors progressed to poorer grades or later stages; (b) in the sequential steps toward CIN, the loci of p53 and ATM, the key checkpoint genes against DSB, were lost at the earliest stage; and (c) many loci identified to be important in breast tumorigenesis were the genomic sites possibly harboring the genes involved in DSB-related checkpoint/repair (including RAD51, RAD52, and BRCA1) or CIN (including FA-A, FA-D, and WRN), and a higher number of these loci showing LOH was significantly associated with increased level of DSB-initiated CIN (P < 0.0001). Breast cancers are thus considered to be sequentially progressive with CIN. However, CIN might also cause genetic heterogeneity, which was revealed by the findings that LOH at some markers was observed only in the component of ductal carcinoma in situ but not in the invasive component of the same tumors. In addition, some markers were found to preferentially lose at specific tumor grades, implying their contribution to genetic heterogeneity during tumor development. Therefore, this study suggests that breast cancer progression is clonal with regard to CIN, but different breast cancers would present distinct molecular profiles resulting from genetic heterogeneity caused by CIN.

Adult↗
PubMed2000

Microsatellite alterations on human chromosome 11 in in situ and invasive breast cancer: a microdissection microsatellite analysis and correlation with p53, ER (estrogen receptor), and PR (progesterone receptor) protein immunoreactivity.

BACKGROUND AND OBJECTIVES: Microsatellite instability (MSI) has been documented in a subset of sporadic tumors. Loss of heterozygosity (LOH) on chromosome 11 loci in breast cancer is a frequent event. The purpose of the present study is to examine the incidence of microsatellite alterations in in situ and invasive human breast carcinoma and to clarify their significance in regulating the dynamics of cancer progression. METHODS: Four highly polymorphic (CA)n repeat microsatellites were used to determine microsatellite alterations in ten ductal carcinoma in situ (DCIS) and 19 invasive ductal carcinoma (IDC). To investigate the expression of p53, ER (estrogen receptor), and PR (progesterone receptor) association with MSI, immunohistochemistry staining was applied. RESULTS: MSI were detected in 20% (2/10) of DCIS and in 47.4% (9/19) of IDC. The frequency of MSI in IDC was significantly higher than that in DCIS (P < 0.001). Also, the MSI seemed to correlate with clinical stage (P = 0.0001) and tumor size (P = 0.004) but not histological grade or age. In addition, we found that 27% of the tumors showed LOH at 11q23.3-24 region between loci D11S934 and D11S912. Seven of nine MSI cases demonstrated low or no expression of p53. However, there was significantly reduced expression of PR, but not ER in MSI cases. CONCLUSIONS: Our results suggest that breast cancer acquires the RER phenotype (replication-error phenotype) in the relatively late stages, and that the RER phenotype is associated with aggressiveness of IDC (infiltrative duct carcinoma). The result also implicated that mismatch repair failure can alter the expression of PR but not ER and p53.

Adult↗