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C P Hsu

Publications and source records attributed to C P Hsu.

At least 19 recordsLinked to original sources

Pre-tracheal lymph node metastasis in squamous cell carcinoma of the thoracic esophagus.

AIMS: To clarify the incidence of pre-tracheal lymph node metastasis in squamous cell carcinoma of the esophagus, and their impact on survival. METHODS: A cohort of 101 patients with squamous cell carcinoma of the thoracic esophagus who underwent esophagectomy together with 2-field lymphadenectomy including the pre-tracheal region was analysed, retrospectively. The p-TNM staging included stage I in 9, stage IIa in 33, stage IIb in 4, stage III in 43, and stage IV in 12 cases. RESULTS: Nodal metastases were identified in 56 patients (55.4%). Subcarinal lymph node and pre-tracheal lymph-node metastases were found in 24 patients (23.8%) and 15 patients (14.9%), respectively. The 5-year cumulative survival rates were 26.5 and 2.5% in nodal negative and nodal positive patients, respectively. Patients with pre-tracheal nodal metastasis all died within 2 years. Cox proportional hazards model in patients with nodal involvement revealed T-factor (p=0.0017), pre-tracheal nodal involvement (p=0.0055) and distant metastasis (p=0.0024) as independent prognostic factors. CONCLUSIONS: Our findings suggest that pre-tracheal lymph node metastasis indicates a dismal prognosis. Its occurrence is not unusual, especially in tumour of upper or middle thoracic esophagus. The subcarinal node cannot be regarded as a sentinel node of the pre-tracheal nodal station. Complete lymphadenectomy excluding the pre-tracheal lymph nodes in treating esophageal cancers is only a myth.

Adult↗

Suppression of proline-directed protein kinase F(A) potentiates apoptotic induction and greatly enhances chemosensitivity in human acute lymphoblastic leukemia cells.

BACKGROUND: Previously, the authors reported that specific antisense suppression of overexpressed proline-directed protein kinase (PDPK) F(A) enhances the chemosensitivity of various clinical anticancer drugs up to > 100-fold in human prostate carcinoma cells, suggesting an association of PDPK F(A) with drug resistance in human malignancies. METHODS: In this report, by using a similar approach, the authors demonstrate further that the suppression of PDPK F(A) enhances even more dramatically the chemosensitivity of clinically used anticancer drugs in various types of human acute lymphoblastic leukemia (ALL) cells. RESULTS: Compared with parental and control transfected cells, transduced ALL cells (both Jurkat and CCRF-CEM cells) with low levels of PDPK F(A) displayed an enhanced sensitivity to vincristine, vinblastine, paclitaxel, methotrexate, doxorubicin, and daunorubicin. Estimation of the 50% inhibitory concentration (IC(50)) index further revealed that the transduced cells displayed up to > 3000-fold drug sensitivity, and there was a correlation between suppressed levels of PDPK F(A) and drug sensitivity. A mechanistic study further revealed that the enhanced chemosensitivity in transduced ALL cells was due mainly to the potentiation of apoptotic induction. CONCLUSIONS: Taken together, the results demonstrate that the suppression of overexpressed PDPK F(A) greatly enhances the chemosensitivity of various clinical anticancer drugs in both types of human ALL cells, providing initial evidence for an important role of this PDPK in controlling multidrug resistance of ALL.

Antineoplastic Agents↗

Suppression of proline-directed protein kinase F(A) systemically inhibits the growth of human acute leukemia cells.

Initial studies revealed that proline-directed protein kinase F(A) (PDPK F(A)) was overexpressed in various cancerous tissues relative to normal controls. However, the functional role of overexpressed PDPK F(A) in cancer remains to be established. In this report, we explore the potential role of PDPK F(A) in leukemia cell growth by investigating the effects of partial inhibition of this kinase on human acute promyelocytic leukemia (HL-60) and acute lymphoblastic leukemia (Jurkat) cells. Cloning of PDPK F(A) cDNA and its recombinant antisense expression vector and antibody were successfully developed. Several stable antisense clones of HL-60 and Jurkat cells were subcloned, which expressed a low level of PDPK F(A) when compared with the control-transfected clone in immunoblot analysis. Moreover, these antisense clones potently inhibited cell growth, clonogenic growth in soft agar and serum-independent growth. The results taken together demonstrate that suppression of PDPK F(A) is able to interfere with the growth of HL-60 and Jurkat cells, suggesting an essential role of this PDPK in human acute leukemia cell growth.

Cell Division↗

Experiences in thoracoscopic sympathectomy for axillary hyperhidrosis and osmidrosis: focusing on the extent of sympathectomy.

HYPOTHESIS: A more selective sympathectomy can improve the outcome of axillary hyperhidrosis and osmidrosis and minimize the potential sequelae. DESIGN: Retrospective cohort. SETTING: Tertiary care center. PATIENTS: Between July 1, 1996, and May 30, 2000, 171 patients with axillary hyperhidrosis and osmidrosis were studied. INTERVENTIONS: T3-4 sympathectomies were performed in 40 patients (group 1), T4 sympathectomies were performed in 56 patients (group 2), and T4-5 sympathectomies were performed in 75 patients (group 3). MAIN OUTCOME MEASURES: The surgical outcomes were evaluated by direct patient interview in the outpatient clinic or by telephone or mail questionnaires. The results were categorized as excellent (significant or complete disappearance of symptoms), good (>/=50% improvement), or poor (<50% improvement). RESULTS: There were no surgical mortalities in this study. Twenty-eight group 1 patients (70%), 16 group 2 patients (29%), and 22 group 3 patients (29%) developed compensatory perspiration (P<.001). Six group 1 patients (15%), 1 group 2 patient (2%), and 1 group 3 patient (1%) developed dry hands (P =.02). In the group 1 patients, the surgical outcomes were excellent in 21 (52%), good in 6 (15%), and poor in 13 (32%). In the group 2 patients, the surgical outcomes were excellent in 29 (52%), good in 10 (18%), and poor in 17 (30%). In the group 3 patients, the surgical outcomes were excellent in 53 (71%), good in 11 (15%), and poor in 11(15%) (P =.04). (Percentages may not sum to 100 because of rounding.) CONCLUSION: T4-5 sympathectomies provide higher patient satisfaction rates in treating axillary hyperhidrosis and osmidrosis, with fewer sequelae.

Adolescent↗

Prediction of prognosis by the extent of lymph node involvement in squamous cell carcinoma of the thoracic esophagus.

OBJECTIVES: Current criteria of the N-category in the TNM staging system for carcinoma of the esophagus needs further subgrouping due to its simplicity in mixing together patients with different prognosis. METHOD: A retrospective cohort study of 186 patients (176 men and ten women; mean age, 59.9 years) with squamous cell carcinoma (SCC) of the thoracic esophagus who underwent esophagectomy followed by two-field lymphadenectomy and cervical lymph node sampling between 1992 and 1999 was conducted. A proposed N-category which involved dividing the nodal status into N0 (no nodal involvement), N1 (< or =4 nodes or < or =20% nodal involvement), and N2 (>4 nodes, or >20%, or non-regional nodal involvement) subgroups was used for survival analysis. RESULTS: The overall 5-year cumulative survival rate was 27%. Lymph node metastases were identified in 101 (54.3%) patients. Cumulative survival rates were 46% at 4 years in the N0 group and 21% at 4 years in the N1 group, whereas no patients in N2 group survived longer than 3 years (P<0.01). A multivariable analysis revealed that independent prognostic factors included the depth of tumor invasion (P<0.01), nodal involvement (P<0.01), and organ metastasis (P<0.01). CONCLUSION: In addition to the location of nodes, the extent of nodal involvement in SCC of the thoracic esophagus also plays an important role in prognosis prediction.

Adult↗

Study of anticipation in Chinese families with schizophrenia.

The anticipation phenomenon is an important aspect in several genetic disorders in which the age at onset (AAO) decreases and the severity of illness increases in successive generations. This phenomenon has been reported in several schizophrenic family studies, and expanded repeat mutations are implicated. In the present study, we investigate the anticipation phenomenon in Chinese schizophrenic families. We compare the AAO between two generations of 38 unilinear schizophrenic families. Intergenerational comparisons show that the AAO was significantly earlier in the offspring generation (mean AAO, 22.2 years) than that in the parental generation (mean AAO, 31.0 years) (P < 0.001). When only including the offspring generation who married, the AAO difference between the two generations was not significant (28.4 years vs 31.0 years, P = 0.151). Our findings suggest that a selection bias in the parental group might greatly impact the study of anticipation in schizophrenia. Other unavoidable biases associated with these analyses are discussed in the text.

Adolescent↗

Correlation between epithelial cell permeability of cephalexin and expression of intestinal oligopeptide transporter.

The proton-coupled oligopeptide transporter (PEPT1) has been shown to mediate mucosal cell transport of di- and tripeptide, and some peptidomimetic drugs. In this study, we determined the correlation between PEPT1 protein expression and the permeability of cephalexin, a substrate of PEPT1, in human PEPT1 (hPEPT1)-overexpressed Caco-2 cells (Caco-2/hPEPT1 cells) and rat jejunum. Caco-2/hPEPT1 cells with various levels of hPEPT1 expression were established by an adenoviral transfection system. The effective intestinal permeability (P(eff)) in rat jejunum was evaluated using a single pass in situ perfusion method. The level of PEPT1 in Caco-2/hPEPT1 cells and rat intestinal mucosal samples was quantitated by densitometry after immunoblotting and enhanced chemiluminescence detection. In Caco-2/hPEPT1 cells, an excellent correlation was observed between cephalexin uptake and hPEPT1 expression (R2 = 0.96, P < 0.005). This demonstrates that cephalexin uptake is directly proportional to hPEPT1 expression. In the rat perfusion study, the mean P(eff) +/- S.D. (n = 15) of cephalexin was 3.89 +/- 1.63 x 10(-5) cm/s. A very significant correlation between PEPT1 expression and cephalexin permeability with an R2 = 0.63 (P < 0.001) was observed. This indicates that the variation in PEPT1 expression is one of the major factors accounting for variable intestinal cephalexin absorption. To our knowledge, this is the most direct evidence that variation of PEPT1 expression is correlated with absorption permeability variation of peptide-like compounds in vitro and in vivo.

Algorithms↗

Ascending aorta to lower limbs revascularization for reoperation via ministernotomy.

The extra-anatomic bypasses, femorofemoral or axillofemoral, have been performed in selected patients for lower extremity revascularization of aortoiliac occlusion. However, significant graft occlusion rate does exist and reoperation constitutes an increasing proportion of vascular surgery practice. We presented our experience in a high-risk patient who received bypass surgery for the third time using the ascending aorta as the source of inflow with good result.

Aged↗

Effects of verapamil on coronary vascular resistance in rabbits: measurement with pulsed Doppler velocimetry.

BACKGROUND: Verapamil is an effective vasodilator. The purpose of this study was to investigate the in vivo effect of verapamil on coronary blood flow velocity and vascular resistance in anesthetized, open-chest rabbits. METHODS: Twenty-one male New Zealand white rabbits were anesthetized, and a 3-mm suction-type pulsed Doppler velocimeter probe was applied to the proximal part of the left anterior descending coronary artery after median sternotomy. The rabbits received intravenous bolus infusion of 4 different doses of verapamil (0.01 mg/kg, n = 5; 0.1 mg/kg, n = 5; 1 mg/kg, n = 5, and 10 mg/kg, n = 6). The percent changes in coronary blood flow velocity and coronary vascular resistance were examined. RESULTS: There was 10.0+/-1.6% increase in coronary blood flow (CBF) and 12.5+/-1.9% reduction in coronary vascular resistance (CVR) after infusion of 0.01 mg/kg of verapamil. The CBF increased 23.0+/-9.5% and CVR decreased 24.2+/-5.2% after infusion of 0.1 mg/kg of verapamil. Infusion of 1 mg/kg of verapamil induced 34.8+/-10.5% increase in CBF and 32.6+/-2.5% reduction in CVR. The CBF increased 41.1+/-14.8% and CVR decreased 45.1+/-5.4% after infusion of 10 mg/kg of verapamil. CONCLUSIONS: Compared with baseline condition, all doses of verapamil increased coronary blood flow velocity and decreased coronary vascular resistance significantly in anesthetized, open-chest rabbits.

Animals↗

Expression of apoptosis-regulating proteins p53, Bcl-2, and Bax in primary resected esophageal squamous cell carcinoma.

Apoptosis plays a key role in the pathogenesis, aggressiveness, and therapy responsiveness of cancer. Proteins of the Bcl-2 family as well as p53 are important regulators of apoptosis. The present study retrospectively examines the expression of apoptosis-regulating proteins in primary resected esophageal squamous cell carcinoma (ESCC) and the correlation between the outcome of patients' treatment and the expression of the proteins. We used antibodies specific for the human p53, Bcl-2 and Bax proteins to examine the expression of these apoptosis-regulating proteins in 40 archival specimens of patients with primary resected esophageal squamous cell carcinoma. The overall expression of p53, Bcl-2, and Bax was 73%, 18%, and 100%, respectively. No significant correlations were found between the expression of p53, Bcl-2, and Bax. The expression of Bcl-2 had a negative influence on survival in this population of primary resected ESCC patients (p=0.03). But no differences in survival were observed in relation to the expression of p53 or Bax. In conclusion, Bcl-2 expression may provide additional and prognostic information for the clinical course of the disease and therefore to be developed as a prognostic indicator for primary resected esophageal squamous cell carcinoma.

Apoptosis↗

Femtosecond dynamics of the forbidden carotenoid S1 state in light-harvesting complexes of purple bacteria observed after two-photon excitation.

Time-resolved excited-state absorption intensities after direct two-photon excitation of the carotenoid S(1) state are reported for light-harvesting complexes of purple bacteria. Direct excitation of the carotenoid S(1) state enables the measurement of subsequent dynamics on a fs time scale without interference from higher excited states, such as the optically allowed S(2) state or the recently discovered dark state situated between S(1) and S(2). The lifetimes of the carotenoid S(1) states in the B800-B850 complex and B800-B820 complex of Rhodopseudomonas acidophila are 7+/-0.5 ps and 6+/-0.5 ps, respectively, and in the light-harvesting complex 2 of Rhodobacter sphaeroides approximately 1.9+/-0.5 ps. These results explain the differences in the carotenoid to bacteriochlorophyll energy transfer efficiency after S(2) excitation. In Rps. acidophila the carotenoid S(1) to bacteriochlorophyll energy transfer is found to be quite inefficient (phi(ET1) <28%) whereas in Rb. sphaeroides this energy transfer is very efficient (phi(ET1) approximately 80%). The results are rationalized by calculations of the ensemble averaged time constants. We find that the Car S(1) --> B800 electronic energy transfer (EET) pathway ( approximately 85%) dominates over Car S(1) --> B850 EET ( approximately 15%) in Rb. sphaeroides, whereas in Rps. acidophila the Car S(1) --> B850 EET ( approximately 60%) is more efficient than the Car S(1) --> B800 EET ( approximately 40%). The individual electronic couplings for the Car S(1) --> BChl energy transfer are estimated to be approximately 5-26 cm(-1). A major contribution to the difference between the energy transfer efficiencies can be explained by different Car S(1) energy gaps in the two species.

Carotenoids↗

Suppression of proline-directed protein kinase F(A) expression potentiates erythroid differentiation of human myeloid leukemia cells.

BACKGROUND: Initial clinic studies revealed that the overexpression of proline-directed protein kinase F(A) (PDPK F(A)) is associated conversely with various stages of tumor tissue differentiation. However, the role of overexpressed PDPK F(A) in tumor cell differentiation remains unknown and needs to be established. In this report, the authors explore the potential role of PDPK F(A) in cellular differentiation by investigating the effects of partial inhibition of this kinase on erythroid differentiation of chronic myeloid leukemia cells (K562). METHODS: PDPK F(A) antisense expression vector and its specific antibody were developed successfully. Two stable, transfected antisense clones of human myeloid leukemia cells were subcloned that expressed approximately 80% and approximately 50% of the total PDPK F(A) existing in control-transfected clones, as determined by both immunoprecipitate activity assay and immunoblot analysis. In sharp contrast, the PDPK F(A) antisense clones expressed no significant suppression of any other related PDPK members' expression, demonstrating the specificity of these two antisense clones. RESULTS: The antisense clones proportionally induced spontaneous erythroid differentiation up to approximately 30% of the total K562 cells. Moreover, antisense suppression of PDPK F(A) expression appeared to potentiate sodium butyrate/hemin-induced erythroid differentiation of K562 cells to a more complete stage compared with the control. CONCLUSIONS: The results demonstrate that specific antisense suppression of overexpressed PDPK F(A) in human myeloid leukemia cells is sufficient to potentiate both spontaneous and drug-induced erythroid differentiation, indicating that PDPK F(A) is an important negative regulator in controlling the erythroid differentiation of human myeloid leukemia cells.

Antisense Elements (Genetics)↗

Suppression of proline-directed protein kinase F(A) expression inhibits the growth of human chronic myeloid leukaemia cells.

Initial studies revealed that proline-directed protein kinase F(A) (PDPK F(A)) was overexpressed in various cancerous tissues relative to normal controls. However, the functional role of overexpressed PDPK F(A) in cancer remains to be established. In this report, we explore the potential role of PDPK F(A) in leukaemia cell growth by investigating the effects of partial inhibition of this kinase on the malignant phenotype of human chronic myeloid leukaemia cells (K562). Cloning of PDPK F(A) cDNA and its recombinant antisense expression vector and PDPK F(A)-specific antibody were successfully developed. Two stable antisense clones of K562 cells were subcloned which expressed 70% and 45% of PDPK F(A) respectively, compared with control-transfected clone in both immunoprecipitate activity assay and immunoblot analysis. In sharp contrast, these two antisense clones expressed no significant suppression of any other related PDPK family members, indicating the specificity of these two antisense clones. Moreover, these antisense clones proportionally and potentially exhibited cell growth retardation, poor clonogenic growth in soft agar and loss of serum independence. The results demonstrate that specific antisense suppression of PDPK F(A) is sufficient to interfere with the growth of K562 cells, indicating that PDPK F(A) is essential for human chronic myeloid leukaemia cell growth.

Amino Acid Sequence↗

Antisense suppression of proline-directed protein kinase FA enhances chemosensitivity in human prostate cancer cells.

Initial clinic studies revealed that proline-directed protein kinase FA (PDPK FA) is overexpressed manyfold in various human cancerous tissues relative to the normal control. However, the role of overexpressed PDPK FA in cancers remains unknown and needs to be established. To determine whether PDPK FA is associated with drug sensitivity, we investigated the effects of partial inhibition of this kinase on the human prostate carcinoma cell line (PC-3). PDPK FA antisense expression vector and its specific antibody were successfully developed. Two stable transfected antisense clones (PA7 and PA3) of human prostate carcinoma cell were subcloned, and they expressed approximately 75% and approximately 35% of the total PDPK FA existing in the control-transfected clone as determined by both immunoprecipitate activity assay and immunoblot analysis. In sharp contrast, the PDPK FA antisense clones expressed no significant suppression of any other related proline-directed protein kinase member expression, demonstrating the specificity of these two antisense clones. When compared with parental or control-transfected cells, the low-PDPK FA-expressing antisense clones displayed an enhanced sensitivity to carboplatin, 5-fluorouracil, paclitaxel, and hydroxyurea. Estimation of the IC50 index further revealed that the antisense clones displayed up to > 100-fold drug sensitivity, and there was a correlation between suppressed levels of PDPK FA and drug sensitivity. Taken together, the results demonstrate that specific antisense suppression of overexpressed PDPK FA in human prostate cancer cells is sufficient to enhance various drug sensitivity, indicating that PDPK FA is an important regulator in controlling multiple drug resistance of human prostate cancer cells.

Antineoplastic Agents↗

Surgical repair of postinfarction ventricular septal defect.

BACKGROUND: Rupture of the interventricular septum complicates 1% to 2% of all acute myocardial infarction patients and its natural course is ominous. The purpose of this study is to present our experience with surgical ventricular septal defect (VSD) repair and examine the possible risk factors and explanations for surgical mortality. METHODS: Fourteen patients underwent repair of postinfarction VSD from 1996 to 1998 at the Taipei Veterans General Hospital. Thirteen patients were in New York Heart Association (NYHA) Functional Class IV and one was in Functional Class III. Eleven patients were in cardiogenic shock with intra-aortic balloon pumps (IABPs) prior to surgery. The operative techniques for VSD repair range from extensive infarctectomy with reconstruction of the septum and the right and left ventricular free walls using single or double patches, to minimal or no infarctectomy with closure of the VSD by excluding the infarcted muscle from the left ventricular cavity and leaving the right ventricle intact. RESULTS: Overall surgical mortality occurred in four patients. All deaths occurred in patients with cardiogenic shock, two with anterior VSD and two with posterior VSD. Three late survivors had limited exercise tolerance with NYHA Functional Class II to III. Left ventricular function was moderately impaired in most patients with a mean nuclear scan ejection fraction of 0.32. However, all patients were elderly and adapted to their residual symptoms without significant life-style changes. CONCLUSIONS: The surgical mortality for treating patients with postinfarction VSD has decreased with improvements in surgical technique. Rapid diagnosis, appropriate preoperative management and delicate surgical repair improve the overall results and help to attain long-term survival.

Aged↗

Surgical management of substernal goiter.

PURPOSE: We describe the clinical results and complications associated with different surgical approaches to the treatment of substernal goiter. METHODS: We retrospectively reviewed the medical records of 56 patients treated for substernal goiter from 1983 through 1999. Eight had undergone previous thyroidectomy. Posterior mediastinal goiter was diagnosed in eight patients, hyperthyroidism in seven, acute respiratory failure in three, and superior vena cava syndrome in two. All but one of the patients underwent thyroidectomy. RESULTS: Thyroid scan revealed that 88% of patients had substernal goiter. A cervical incision alone was used in 46 of 55 patients. Nine patients underwent thyroidectomy via a thoracic approach. Both lobes were resected in 16 patients. Two deaths occurred: one patient suffered a stroke and another patient developed pneumonia after surgery. The most frequent complication was recurrent laryngeal nerve injury, followed by removal of a normal parathyroid gland and pneumonia. Multinodular goiter occurred in 52 patients. Resected goiter with occult malignancy was found in three patients, two of whom underwent lobectomy only. These three patients had survived at 5, 7, and 11 years postoperatively, respectively. All patients with tracheal lumen narrowing showed a normal sized tracheal lumen 2 to 3 months postoperatively. CONCLUSION: Our data indicate that the presence of a substernal goiter should be considered an indication for resection based on risk of acute respiratory distress, risk of malignancy, and lower surgical morbidity. Most secondary substernal goiters can be simply resected through cervical incision and curation.

Adult↗

Serotonin-6 receptor variant (C267T) and clinical response to clozapine.

Clozapine is an effective atypical antipsychotic that has high affinity for serotonin type 6 receptors (5HT6). We tested the hypothesis that clinical response to clozapine in patients refractory to typical antipsychotic treatment is related to the genetic variant (C267T) of the 5HT6 receptors. Ninety-nine schizophrenic patients with a history of non-response to typical antipsychotics were included in the study. The results demonstrated a modest but significant relationship between presence of the variant of the 5HT6 receptors and the response to clozapine in these patients. Patients with homogenous 267T/T genotype had a better response than other patients. Although replication is required, these results suggest that the 5HT6 receptor C267T polymorphism may be involved in clozapine response, especially in patients with anxious or depressed symptoms.

Antipsychotic Agents↗

No evidence for association of serotonin-2A receptor variant (102T/C) with schizophrenia or clozapine response in a Chinese population.

The serotonin hypothesis in schizophrenia had regained interest with the superior efficacy of clozapine in the refractory schizophrenic patients. Among the serotonin receptors, the serotonin 2A (5HT2A) receptor subtype is the most widely studied. Previous studies on the association between a silent mutation polymorphism of the 5HT2A gene (102T/C) and schizophrenia or clozapine response have yielded conflicting findings. Therefore, we investigated whether these genetic variants of the 5HT2A receptor are associated with schizophrenia or with response to clozapine treatment in a Chinese population. Ninety-seven schizophrenic patients and 101 control subjects were included in the study. The receptor variants were found at similar frequencies in schizophrenic patients and healthy control subjects. Also, we did not find the variants to influence the response to clozapine in schizophrenic patients. We suggest that the assessment method of clozapine response and the ethnicity may influence the result.

Adult↗