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Biomedical subjects

C Y Hsu

Publications and source records attributed to C Y Hsu.

At least 163 records · Page 9Linked to original sources
PubMed1996

Preliminary report of outpatient weekly adjuvant chemotherapy for high-risk nasopharyngeal carcinoma.

Distant metastasis has become the most frequent failure site-more so than locoregional relapse-after adequate radiotherapy in nasopharyngeal carcinoma (NPC). A prospective study was initiated to test the role of postradiation adjuvant chemotherapy using a weekly schedule for selected patients with high-risk NPC (N3, T4N2b-2c, and N2b-2c, with one of nodal size > 4 cm, or residual disease after radiotherapy). Through July 1993 to August 1994, a total of 20 patients were entered into the study: 16 men and four women, with a median age of 49 years and age range of 27-75 years. Pathology showed WHO type I:II:III = 2:13:5. Previous treatment consisted of concurrent chemoradiotherapy (16 patients), radiotherapy alone (two), and neoadjuvant chemotherapy followed by radiotherapy (two). Postradiation adjuvant chemotherapy was usually started 2 months after radiotherapy, using a weekly FP schedule (5-fluorouracil 1,250 mg/m2 + cisplatin 25 mg/m2, mixed in 100 ml saline, 24 h continuous i.v. infusion) for 18 weeks. The treatment of five patients was at 5, 6, 10, 14, and 15 weeks because of leukopenia-induced mortality, sudden death unrelated to adjuvant chemotherapy, a patient's refusal, and distant metastasis (the last two cases) during adjuvant chemotherapy. The major toxicity was leukopenia (grade I, 20%; grade II, 45%; grade III, 15%; and grade IV, 10%). Ten patients (50%) developed distant metastasis after a median follow-up time of 20 months. Our preliminary data indicate that postradiation adjuvant chemotherapy with a weekly FP regimen at our dosage is not recommended for high-risk NPC.

Adult↗
PubMed1996

Very delayed infarction after mild focal cerebral ischemia: a role for apoptosis?

The temporal evolution of cerebral infarction was examined in rats subjected to transient occlusion of both common carotid arteries and the right middle cerebral artery. After severe (90-min) ischemia, substantial right-sided cortical infarction was evident within 6 h and fully developed after 1 day. After mild (30-min) ischemia, no cortical infarction was present after 1 day. However, infarction developed after 3 days; by 2 weeks, infarction volume was as large as that induced by 90-min ischemia. These data suggest that infarction after mild focal ischemia can develop in a surprisingly delayed fashion. Some evidence of neuronal apoptosis was present after severe ischemia, but only to a limited degree. However, 3 days after mild ischemia, neurons bordering the maturing infarction exhibited prominent TUNEL staining, and DNA prepared from the periinfarct area of ischemic cortex showed internucleosomal fragmentation. Furthermore, pretreatment with 1 mg/kg cycloheximide markedly reduced infarction volume 2 weeks after mild ischemia. These data raise the possibility that apoptosis, dependent on active protein synthesis, contributes to the delayed infarction observed in rats subjected to mild transient focal cerebral ischemia.

Animals↗
PubMed1996

Detection of human T lymphotropic virus type I proviral DNA in patients with diffuse panbronchiolitis.

In Japan a number of reported cases of diffuse panbronchiolitis (DPB) have been associated with human T lymphotropic virus type I (HTLV-I) infection. In this study the hypothesis that HTLV-I proviral DNA may be prevalent in DPB was examined using polymerase chain reaction (PCR) for the region of env or the two-step PCR for the pX region of this virus. The presence of HTLV-I proviral DNA was studied in the peripheral blood mononuclear cells (PBMC) obtained from 10 patients with DPB. The presence of proviral DNA in PBMC in 12 patients with chronic obstructive pulmonary disease (COPD), eight patients with idiopathic interstitial pneumonia (IIP), four patients disease were also studied as relevant controls. The lung tissue obtained from 11 patients with DPB, 12 patients with diffuse aspiration bronchiolitis (DAB) at autopsy, and the surgical lung samples obtained from 12 patients with bronchogenic cancer were also studied. Peripheral blood mononuclear cells obtained from one DPB patient and one bronchogenic carcinoma patient were positive for the HTLV-I pX region. The presence of the pX region was also found in the lung tissue of three DPB patients (27.3%) and one DAB patient (8.3%). None of other subjects were positive for HTLV-I proviral DNA, In conclusion, HTLV-I is not the causative virus in the pathogenesis of COPD, IIP, bronchiectasis and bronchogenic carcinoma. There is a likelihood that HTLV-I infection is associated with some cases of DPB; however this association needs further verification.

Blotting, Southern↗
PubMed1996

Antiarrhythmic and electrophysiologic effects of intravenous ibutilide and sotalol in the canine sterile pericarditis model.

INTRODUCTION: Atrial arrhythmias are a frequent clinical complication following open heart surgery. We compared the Class III agents d,l-so-talol and ibutilide fumarate in an intravenous cross-over study using the canine atrial sterile pericarditis model. METHODS AND RESULTS: We studied pacing-induced sustained atrial flutter over a 7-day post-surgical period in conscious dogs, alternating analysis of ibutilide (1.0 to 30.0 micrograms/kg) and d,l-sotalol (0.1 to 3.0 mg/kg). Ibutilide significantly increased atrial flutter cycle length (AFL CL) 11 +/- 2 msec and atrial effective refractory period (AERP) 13 +/- 2 msec, and terminated atrial flutter in all cases (n = 12) following a mean dose of 6 +/- 2 micrograms/kg. Plasma concentrations of ibutilide were 53 +/- 13 ng/mL. Ventricular effective refractory period (VERP) was not significantly affected (4 +/- 2 msec). Following termination with ibutilide, atrial flutter could be reinitiated in 1 of 12 trials, and was nonsustained (40-sec duration). Sotalol significantly increased AFL CL 23 +/- 3 msec and terminated atrial flutter in 8 of 12 trials following a mean dose of 1.5 +/- 0.4 mg/kg. AERP and VERP were significantly increased 20 +/- 6 and 12 +/- 2 msec, respectively. The incidence of reinduced atrial flutter was 9 of 12 trials (P < or = 0.05 vs ibutilide) (7 nonsustained 57 +/- 7 sec duration, and 2 sustained). Sotalol failed to terminate atrial flutter in two dogs on days 1 and 5, despite increases in AFL CL (21 +/- 8 msec) and AERP (16 +/- 9 msec), whereas on day 3, ibutilide (20 +/- 7 micrograms/kg) terminated atrial flutter in those two dogs while increasing AFL CL and AERP 18 +/- 6 and 15 +/- 0 msec, respectively. CONCLUSION: Both sotalol and ibutilide terminate atrial flutter in this model. Ibutilide converted atrial flutter in dogs in which sotalol was not successful. Following atrial flutter termination, ibutilide had a lower incidence of reinduced arrhythmias compared to sotalol. Ibutilide produced atrial antiarrhythmic effects while having no significant electrophysiologic effects on the ventricle.

Animals↗
PubMed1996

DNA damage and repair in central nervous system injury: National Institute of Neurological Disorders and Stroke Workshop Summary.

BACKGROUND AND PURPOSE: DNA damage and repair are areas of research with important implications for stroke and cerebral trauma. DNA damage is present in central nervous system (CNS) injury, and defects in repair mechanisms are associated with neurodegenerative disease. METHODS: A workshop, DNA Damage and Repair in CNS Injury, was organized by the National Institute of Neurological Disorders and Stroke in Bethesda, Md, on September 11, 1995. The objective of this workshop was to promote inquiry and to foster application of research in DNA damage and repair after stroke and trauma. RESULTS: The participants discussed the connection between the fields of DNA damage and repair and stroke and trauma and identified gaps in knowledge to be filled to expand research of DNA damage and repair in CNS injury. Specific recommendations were made targeting research opportunities in the areas of DNA repair and damage in stroke and trauma. CONCLUSIONS: Research in the science of DNA injury and repair will likely provide new and important information on mechanisms of cell damage and provide opportunities for the development of novel and effective therapies to reduce CNS injury in stroke and trauma.

Animals↗
PubMed1996

Automated measurement of infarct size with scanned images of triphenyltetrazolium chloride-stained rat brains.

BACKGROUND AND PURPOSE: The extent of brain infarction after local cerebral ischemia is frequently assessed with the mitochondrial activity indicator 2,3,5-triphenyltetrazolium chloride (TTC). We describe an automated procedure for analysis of infarct size in TTC-stained rat brains. METHODS: Rats were subjected to middle cerebral artery occlusion and killed after 24 to 36 hours, and their brains were processed for TTC staining. Digital images of coronal sections from these brains (n > 50) were acquired with a desktop color scanner. The resulting images were divided into red, blue, and green component images. Total brain and infarct areas were automatically determined on the basis of total pixel intensity and area after segmentation of the red and green images, respectively. Automated measurements were compared with those made with a video camera-based image acquisition system that required manual tracing of lesion boundaries. RESULTS: The spatial resolution of scanned brain images (approximately equal to 200 microns) was comparable to that of the camera-based system and provided sufficient detail to recognize infarct boundaries and neuroanatomical features. Scanner-based acquisition and analysis were faster than with the camera-based method. The green component image accurately distinguished infarcted from normal brain, and the red component image represented total brain dimensions. Infarct measurements obtained by the automated method correlated closely with those from conventional apparatus (R2 = .89, P < .001). Intraobserver reliability with the automated method (R2 = 1.00) was higher than with the conventional method (R2 = .77). CONCLUSIONS: Infarct size after middle cerebral artery occlusion in the rat can be rapidly and reproducibly assessed with inexpensive scanning equipment and automated image analysis of TTC-stained brains.

Animals↗
PubMed1996

Immediate early gene expression in response to cerebral ischemia. Friend or foe?

BACKGROUND: Cerebral ischemia is a potent modulator of gene expression. Immediate early genes undergo rapid induction after both global and focal cerebral ischemia. Many immediate early genes code for transcription factors. Additional genes, including those encoding for neurotrophic factors and neurotransmitter systems, are induced in a delayed fashion after cerebral ischemia. The functional significance of early and late gene regulation after cerebral ischemia requires further investigation. These changes may be beneficial (friend) or detrimental (foe). Many of the genes are likely neuroprotective and important for recovery, but others may be involved in ischemic cell death mediated by apoptosis. SUMMARY OF REVIEW: We review evidence that supports the hypothesis that cell death after cerebral ischemia occurs through the dual pathways of ischemic necrosis and apoptosis. CONCLUSIONS: Gene regulation, including immediate early genes, is required for programmed neuronal death after trophic factor deprivation and is predicted to be involved in apoptosis triggered by cerebral ischemia. Novel therapies following cerebral ischemia may be directed at genes mediating either recovery or apoptosis.

Animals↗
PubMed1996

Adenosquamous carcinoma and schneiderian papilloma-like lesion in a mature cystic teratoma of the ovary: a case report.

Malignant transformation is uncommon in the mature cystic teratoma of ovary, in which adenosquamous carcinoma is even rarer. It seldom combines with papillary lesion, like schneiderian papilloma of upper airway. We report such a rare case of mature cystic teratoma undergoing malignant change, with the pictures of both adenosquamous carcinoma and schneiderian papilloma.

Carcinoma, Adenosquamous↗
PubMed1996

Use of recombinant Epstein-Barr virus early antigen for detection of antibody in patients with nasopharyngeal carcinoma.

BACKGROUND: Nasopharyngeal carcinoma (NPC) is one of the most common cancers in southern China and Taiwan. Serological studies revealed the close-relationship between NPC and Epstein-Barr virus (EBV). Elevated serum and saliva levels of anti-EBV antibodies are detected in patients with NPC. Therefore, Development Center for Biotechnology prepared the EBV-early antigen (EA-D) by recombinant DNA technique for screening the serum and throat washing samples from patients with head and neck cancers. METHODS: The BMRF1 gene for EBV early antigen (EA-D) was placed into the plasmid pDB18, then transformed into an Escherichia coli strain containing the lambda cI857 temperature-sensitive repressor. Heat treatment of the transformant, at exponential growth phase, inactivated the cI protein and induced an over-expression of the EA-D protein. Next, the EA-D was purified by chromatography and characterized as a protein of molecular weight 47 kDa, by sodium dodecyl sulfate-polyacry lamide gel electrophoresis (SDS-PAGE) and Western blot analysis using monoclonal anti-EA antibody and sera from patients with nasopharyngeal carcinoma (NPC). Enzyme-linked immunosorbent assay (ELISA) with the purified EA-D antigen was used to screen 129 serum and throat washing (TW) samples from patients with head and neck tumors, 24 from patients with a nonmalignant disease and 44 from normal donors. RESULTS: Experimental results indicated significantly higher positive rates of EA-D IgA (69%) and EA-D IgG (91%) in NPC sera than in the sera of patients with other head and neck tumors and normal controls. TW samples from patients with NPC also showed a higher positive rate (34%) than the other groups (7-20%). CONCLUSIONS: Results in this study demonstrate that the bacterially expressed EA-D antigen could be recognized by sera from patients with NPC and monoclonal anti-EA antibody. Thus, it has potential use in ELISA for screening EBV-related diseases such as NPC.

Antibodies, Viral↗
PubMed1995

Alteration of transcription factor binding activities in the ischemic rat brain.

Transient focal ischemia-reperfusion in the cerebral cortex caused regional alteration of DNA-binding activities of transcription factors AP-1, CREB, Sp-1, and NF-kB. The changes were time-dependent. During the first 24 hr of reperfusion after 90 min ischemia, there was an increase in the binding activity of AP-1 only in the region surrounding the ischemic cortex. Five days after ischemia, an increase in the binding activities of CREB, Sp-1, and NF-kB, but not AP-1, was noted in the ischemic cortex, and to a lesser extent, Sp-1 and NF-kB, in the surrounding region. The binding activities of these transcription factors were reduced by hydrogen peroxide but could be restored by dithiothreitol and 2-mercaptoethanol. These results are the first demonstration of ischemia-induced differential regulation of transcription factor binding activities which are time-, region-, and redox state dependent.

Animals↗
PubMed1995

Toxicity of cephalosporins to fatty acid metabolism in rabbit renal cortical mitochondria.

UNLABELLED: Cephaloglycin (Cgl) and cephaloridine (Cld) are acutely toxic to the proximal renal tubule, in part because of their cellular uptake by a contraluminal anionic secretory carrier and in part through their intracellular attack on the mitochondrial transport and oxidation of tricarboxylic acid (TCA) cycle anionic substrates. Preliminary studies with Cgl have provided evidence of a role of fatty acid (FA) metabolism in its nephrotoxicity, and work with Cld has shown it to be a potent inhibitor of renal tubular cell and mitochondrial carnitine (Carn) transport. Studies were therefore done to examine the effects of Cgl and Cld on the mitochondrial metabolism of butyrate, the anion of a short-chain FA that does not require the Carn shuttle to enter the inner matrix, and the effects of Cgl on the metabolism of palmitoylcarnitine (PCarn), the Carn conjugate of a long-chain FA that does enter the mitochondrion by the Carn shuttle. The following was found: (1) Cgl reduced the oxidation and uptake of butyrate after in vitro (2000 micrograms/mL, immediate effect) and after in vivo (300 mg/kg body weight, 1 hr before killing) exposure; (2) Cld caused milder in vitro toxicity, and no significant in vivo toxicity, to mitochondrial butyrate metabolism; (3) like Cld, Cgl reduced PCarn-mediated respiration after in vivo exposure, but, unlike Cld, it did not inhibit respiration with PCarn in vitro; (4) the Carn carrier was stimulated slightly by in vitro Cgl but was unaffected by in vivo Cgl; (5) in vivo Cgl had no effect on mitochondrial free Carn or long-chain acylCarn concentrations in the in situ kidney; (6) Cgl increased the excretion of Carn minimally compared with the effect of Cld; and (7) cephalexin, a nontoxic cephalosporin, caused mild reductions of respiration with butyrate and PCarn during in vitro exposure, but stimulated respiration with both substrates after in vivo exposure. CONCLUSIONS: Cgl has essentially the same patterns of in vitro and in vivo toxicity against mitochondrial butyrate uptake and oxidation that both Cgl and Cld have against TCA-cycle substrates. Cld has little or no in vivo toxicity to mitochondrial butyrate metabolism, whereas in vivo Cgl is as toxic as Cld to respiration with PCarn. The greater overall in vivo toxicity of Cgl to mitochondrial FA metabolism, with lower cortical concentrations and AUCs than those of Cld, supports earlier evidence that Cld is less toxic than Cgl at the molecular level.

Animals↗
PubMed1995

Neuronal apoptosis: current understanding of molecular mechanisms and potential role in ischemic brain injury.

Apoptosis is a rediscovered mechanism of cell death crucial in normal development. Recent exploration of the genetic mechanisms of apoptosis has broadened our insight into the regulation of cell death in development as well as disease states. We present an overview on current understanding of the genetic molecular events in apoptosis in all, or most cell types, with emphasis on events observed in a well-characterized model of neuronal death in vitro. The second part of this article reviews recent studies in in vivo stroke models on the mechanism of cell death relevant to apoptosis after cerebral ischemia. Further delineation of the mechanisms of cell death, especially those that trigger apoptosis, is likely to redirect our approaches in the development of new therapeutic interventions for ischemic stroke.

Animals↗
PubMed1995

Neoadjuvant chemotherapy for advanced nasopharyngeal carcinoma.

Between October 1990 and November 1991, a total of 16 male patients with advanced nasopharyngeal carcinoma were treated by neoadjuvant chemotherapy before conventional radiotherapy. They belonged to the AJCC stage IV with multiple bulky neck nodes metastases. The chemotherapy consisted of bleomycin, epirubicin, and cisplatin. Six patients completed 3 cycles, 9 patients finished 2 cycles, and 1 patient received 1 cycle of chemotherapy. Seven of the 16 patients (44%) were in complete response, and 50% (8/16) achieved partial response. The overall response rate was 94%. The major toxicities consisted of leucopenia (12/37 cycles had grade III-IV), nausea/vomiting, alopecia. Aplastic marrow developed in 1 patient, and one died of bleomycin-induced pneumonitis. Subsequent radiation therapy was well tolerated. After a minimal follow-up time of 24 months, the 2-year actuarial survival rate was 56%. Although we confirmed the impressively high response rate of this regimen, the toxicities were high and most patients failed at distant site(s). The efficacy of neoadjuvant chemotherapy for advanced nasopharyngeal carcinoma is doubtful and should be further studied in prospective randomized trials.

Actuarial Analysis↗
PubMed1995

Evaluation of tissue perfusion by the Xe-133 washout method in lower limbs of patients with noninsulin-dependent diabetes mellitus.

Ischemia is thought to be a major component in the pathogenesis of foot problems. The authors use the Xe-133 washout method to evaluate the blood perfusion of muscle tissue in the lower legs of patients with noninsulin-dependent diabetes mellitus (NIDDM). Eighty-five male patients with NIDDM ranging in age from 51 years to 79 years (mean, 66.5 years) and 47 nondiabetic control males with a matched age ranging from 52 years to 82 years (mean, 64.5 years) were included in this study. None of the diabetics had a history or presentation of peripheral vascular disease in the lower limbs. The patients were separated into groups according to the duration of the disease and condition of blood sugar control. The Xe-133 washout method was performed in the anterior tibial muscle of all the subjects. According to a Student's t-test, the tissue perfusion were of significant difference between 1) NIDDM and normal controls (1.98 +/- 1.39 ml/100 g/minute versus 2.85 +/- 1.35 ml/100 g/minute), 2) good and poor blood sugar control (2.36 +/- 1.58 versus 1.51 +/- 0.94), and 3) long and short disease durations (1.50 +/- 0.78 versus 2.35 +/- 1.63). It is concluded that the tissue perfusion in the lower legs of patients with NIDDM is significantly decreased and related to the duration of the disease and condition of blood sugar control. This may contribute to the high incidence of foot gangrene and limb loss in patients with NIDDM.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1995

Effects of inhalation of steroids on lung permeability in patients with asthma.

This study evaluated the effect of inhalation of steroids on lung permeability in patients with asthma by measuring the clearance of Tc-99m DTPA aerosol from the alveolar to vascular space. Twenty patients with asthma were studied in the supine position with a gamma camera and the clearance half time (T 1/2) was calculated. The base line lung permeability study was performed before treatment with inhalation of 100 micrograms beclomethasone dipropionate four times daily for 1 week, then the study was repeated. After treatment with inhalation of steroid, there was a change in T 1/2 from 76.4 +/- 37.4 minutes to 86.6 +/- 48.2 minutes (P = 0.08). This preliminary study suggests that lung permeability is not altered by inhaled steroid therapy.

Administration, Inhalation↗