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Biomedical subjects

T C Liu

Publications and source records attributed to T C Liu.

At least 37 records · Page 2Linked to original sources
PubMed2000

Loudness discomfort levels in patients with conductive and mixed hearing loss.

OBJECTIVE: The purpose of this study is to investigate the effects of conductive component on the loudness discomfort level (LDL) judgments. The relation between LDL value and the magnitude of air-bone gap in such subjects was also assessed. METHODS: LDLs were obtained from 100 ears of 50 hearing-impaired subjects. Twenty five subjects (50 ears) had either conductive or mixed hearing loss for both ears. Another 25 subjects (50 ears) with bilateral sensorineural hearing loss served as control. LDL measurements were performed using the method reported by Hawkins et al. in 1987. LDL data were plotted and analyzed as a function of hearing loss for three stimulus frequencies (0.5, 1.0 and 2 kHz). Also, LDL values were plotted as a function of air-bone gap in the conductive group. RESULTS: LDLs were significantly higher in subjects with conductive or mixed hearing loss for all three tested frequencies. There is a significant positive correlation between LDL value and the magnitude of air-bone gap for all three test frequencies. Considerable intersubject variability was found in LDLs obtained from subjects with conductive component which prevented the accurate prediction of LDLs from threshold data for such patients. CONCLUSION: The large intersubject variation in LDL data strongly suggests the need for individualized LDL measurements in patients with conductive or mixed hearing loss. Higher LDLs indicates that higher maximal power output can be prescribed for such patients without worrying about loudness intolerance.

Adult↗
PubMed2000

Histological rearrangement in the facial nerve and central nuclei following immediate and delayed hypoglossal-facial nerve anastomosis.

The timing of hypoglossal-facial nerve anastomosis is controversial. The present study was performed to clarify the influence of the timing of hypoglossal-facial nerve anastomosis on histological changes in the facial nerve and central nuclei using guinea pigs. The facial nerve was transected first at the labyrinthine portion, and then transected again at the stylomastoid foramen. Hypoglossal-facial nerve anastomosis was carried out immediately or 3 months later. Nerve regeneration and survival of the neurons in the facial and hypoglossal nuclei were evaluated by toluidine blue staining and horseradish peroxidase (HRP). Immediate anastomosis resulted in better nerve regeneration of the facial nerve, but the numbers of surviving neurons in the facial and hypoglossal nuclei were almost the same in both the immediate and delayed anastomosis groups.

Anastomosis, Surgical↗
PubMed2000

Clinical implications of aberrant TSG101 transcripts in acute myeloblastic leukemia.

Tsg101 is a mouse tumor suppressor gene whose homozygous deletion produces transformation of NIH3T3 cells and leads to metastases in nude mice. The human homologue of the gene, TSG101, is localized in chromosome 11p15.1-p15.2. Reduced TSG101 expression may cause the defect of the cell cycle checkpoint that leads to genetic instability and consequently to the progression of neoplasia. Aberrant TSG101 transcript have been identified in many types of cancers, and the relaxation of RNA splicing fidelity may be an onco-developmental marker in cancers and could play a general role in tumorigenesis. In our previous study, smaller TSG101 transcripts were found in AML specimens, hematopoietic cell lines and normal controls. The aberrant transcripts occurred more frequently in the AML cases and cell lines. The patients with aberrant TSG101 transcripts had higher initial white cell count, lower LDH level, and lower complete remission rate after induction chemotherapy. However, further multivariate analysis of clinical data revealed that there was no relationship to the TSG101 aberrant transcripts. The clinical significance of TSG101 aberrant transcript in AML needs further evaluation.

3T3 Cells↗
PubMed2000

Aberrant transcripts of FHIT, TSG101 and PTEN/MMAC1 genes in normal peripheral mononuclear cells.

Aberrant transcripts of FHIT and TSG101 using nested RT-PCR were reported in many human tumours. The role of these aberrant transcripts in tumourigenesis is not clear. We, therefore, analyzed the aberrant transcripts of FHIT, TSG101 and PTEN/MMAC1 in peripheral mononuclear cells of normal individuals using nested RT-PCR to explore the role of these genes in cancer development. The results showed that there are at least five types of aberrant transcripts: type I is the deletion at junction located in-between normal exon and intron; type II has deletion of some bases and subsequent insertion of several bases in the deletion area; type III accommodates splicing donor or acceptor site-like sequence; type IV has homologous sequences near the deleted junction; and type V comprises the homologous sequences at the deletion junction. A normal healthy person can have more than one aberrant transcripts of FHIT, TSG101 and PTEN/MMAC1 genes. The size and the number of the transcripts vary and the diversity is unconstrained. It is not depended on the time, condition of the reaction, or the isolation method. From these results, we suggested that the aberrant transcripts of FHIT, TSG101 and PTEN/MMAC1 genes may be the imperfect products of splicesome which occur one in every thousands, ten thousands or more. As a result, these data implied no direct association between the aberrant transcripts and tumourigenesis.

Acid Anhydride Hydrolases↗
PubMed2000

Mutation analysis of PTEN/MMAC 1 in sporadic thyroid tumors.

Recently, a putative tumor suppressor gene, PTEN/MMAC1, has been identified at chromosome 10q23.3. This gene encodes a 403 amino acid dual specificity phosphatase containing a region of homology to tensin and auxillin. Somatic mutations of the PTEN/MMAC1 gene have been found in a number of cancer cell lines and primary cancers. Cowden disease, an autosomal dominant harmartoma syndrome associated with thyroid and breast tumors, has been found to be associated with mutations of PTEN/MMAC1 gene. To evaluate the role of the PTEN/MMAC1 gene in sporadic thyroid tumors, we studied 17 sporadic thyroid tumors, of which 12 were papillary thyroid carcinomas, 1 was follicular thyroid carcinoma, 1 was medullary thyroid carcinoma and 3 were thyroid adenomas. Direct sequencing of PCR-amplified products was performed for all nine exons of PTEN/MMAC1. No mutations of PTEN/MMAC1 gene were observed in any of the sporadic thyroid tumors. Our results indicate that the PTEN/MMAC1 gene may not play a major role in sporadic thyroid tumors.

Genes, Tumor Suppressor↗
PubMed2000

Myelodysplastic syndrome with monosomy 7 and pulmonary aspergillosis.

A 43-year-old man with no past history presented with symptoms of fever, cough and dyspnoea arising from invasive pulmonary aspergillosis and was found to have myelodysplastic syndrome with monosomy 7. Before initiation of chemotherapy, he deteriorated rapidly, developing multi-organ failure requiring mechanical ventilation, and he eventually succumbed despite amphotericin B treatment. The importance of monosomy 7 in determining immune function in patients with myelodysplastic syndrome is emphasised.

Adult↗
PubMed2000

Molecular basis of Lewis blood type in Taiwanese.

The Lewis (Le) histo-blood group system comprises two major antigens, Le(a) and Le(b) which are determined by alpha (1,2)-fucosyltransferase (FUT2) and alpha (1,3/1,4)-fucosyltransferase (FUT3). In this study, we analyzed the mutations of FUT2 and FUT3 genes in 101 Taiwanese by molecular biology method and compared them with their serologic phenotypes to explore their relationship. There is at least one wild allele of FUT2 and FUT3 genes in phenotype of Le (a-b+). The phenotypes of Le (a+b-) and Le (a+b+) are caused by mutations of both alleles of FUT2 gene and at least one wild allele of FUT3 gene. The genotypes of Le (a+b-) and Le (a+b+) are the same. Twenty cases are phenotype of Le (a-b-), which are caused by mutations of both alleles of FUT 2 gene and/or FUT 3 gene. Twelve cases were caused by both alleles mutations of FUT 3 gene only, while three cases were caused by mutations of both alleles of FUT2 gene and the rest of the cases were caused by mutations of both alleles of FUT2 and FUT3 genes. Our findings confirm that the Le histo-blood group is determined by the interaction of FUT 2 and FUT 3 genes. Our report is the first study of FUT 2 gene and FUT 3 gene in a Taiwanese population. We suggest that the genetic analysis of Le blood group should include FUT 2 and FUT 3 genes together.

Fucosyltransferases↗
PubMed1999

Site-directed mutagenesis of human dihydrolipoamide dehydrogenase: role of lysine-54 and glutamate-192 in stabilizing the thiolate-FAD intermediate.

The roles of lysine-54 (K54) and glutamate-192 (E192) of human dihydrolipoamide dehydrogenase (E3) in stabilizing the thiolate-FAD intermediate during electron transfer were investigated by site-directed mutagenesis. Recombinant human E3s, wild-type, K54E, S53K54-K53S54 (SK-KS), and E192Q, were overexpressed, purified, and characterized. Only K54E and SK-KS E3s had about 25% less bound FAD compared to wild-type, implicating that K54 is crucial for the protein-FAD interaction. The specific activities of all mutant E3s were markedly decreased (<5% wild-type). In the case of K54E E3, the Km for lipoamide in the reverse reaction was increased by about twofold. Surprisingly, for both SK-KS and E192Q E3s, the Kms for both dihydrolipoamide (forward reaction) and lipoamide (reverse reaction) were markedly reduced. The catalytic rate constants (kcat/Km) for both reactions for SK-KS E3 were significantly lower than wild-type, indicating that K54 is crucial for the catalytic efficiency of the enzyme. Fluorescence spectral analyses showed that the FAD in E3s were reduced by the addition of dihydrolipoamide, and that its reoxidation by NAD+ in the mutant E3s was slower than wild-type E3. Interestingly, in K54E E3 dihydrolipoamide reduced FAD efficiently only when NAD+ was present, indicating that K54 stabilizes the thiolate-FAD interaction. The lack of the formation of thiolate-FAD intermediate in the absence of NAD+ in K54E E3 was also confirmed by CD spectra. The SK-KS mutation demonstrates that the correct sequence of residues is as critical as the nature of the amino acid residues. These results suggest that K54 plays an important role in stabilizing the thiolate-FAD intermediate during the electron transfer in the reaction, and E192 is involved in maintaining correct orientation of K54 during catalysis.

Base Sequence↗
PubMed1999

Molecular characterization of secretor type alpha(1, 2)-fucosyltransferase gene deficiency in the Philippine population.

We analyzed the seven mutations which are responsible for the deficiency of the secretor type alpha(1,2)-fucosyltransferase gene product, Se enzyme, in the Philippine population. One hundred and one unrelated Filipinos in Taiwan were studied. A new mutation, a 3-base pair deletion from nt 688 through 690, was found in two (0. 1%) of 202 chromosomes. The frequencies of six other mutated alleles were as follows: 71/202 (35.2%) were cDNA 385 A-->T missensed mutation (se2), 28/202 (13.9%) were C571T nonsense mutation (se3), 16/202 (7.9%) were G849A nonsense mutation (se4), 4/202 (1.9%) were G428A nonsense mutation (se1), and 81/202 (40.1%) were wild-type allele (Se). No C628T nonsense mutations (se5) or fusion genes of pseudogene and FUT2 gene (se 6) were found in this population. For the molecular basis of phenotype Le(a+ b-): eight cases had se2/se2, six cases had se2/se3, two cases had se3/se4, one case was homozygous of se4, one case was se3/se1, and two cases were se2/se7. For the Le(a+ b+) phenotype: four cases had se2/se2, two cases had se2/se3, one case was se3/se3, and one case was se2/se4. For the Le(a- b+) phenotype: 16 cases were Se/Se, 21 cases were Se/se2, six cases were Se/se3, five cases were Se/se4, and two cases had Se/se1. Our results suggest that the genotypes of the alpha(1, 2)-fucosyltransferase gene in phenotypes Le(a+ b+) and Le(a+ b-) are the same. Other factors that play important roles may cause the differences between these two phenotypes. Several hotspot mutations in the alpha(1,2)-fucosyltransferase gene are responsible for the nonsecretor phenotype.

Fucosyltransferases↗
PubMed1999

External ear resonance in patients with tympanic membrane perforations.

This study investigated the effects of a tympanic membrane perforation on the external ear resonance. Measurements of external ear resonance using a probe-tube microphone system were performed in 14 patients who had medium to large unilateral tympanic membrane perforations. The contralateral normal ears of these 14 patients served as control. The results showed that there were no significant differences in the peak frequency, peak amplitude and peak sharpness between perforated and normal ears. However, intersubject variability in the resonant frequency was greater in the perforated group. In addition, the resonance curves of these two groups were substantially different. In 10 out of the 14 patients in the perforated group, the resonance curves showed 2-3 prominent peaks separated by valleys of about 10 dB reduced gain. In addition, in 11 out of 14 perforated ears, reduced responses (3.8 dB in average) occurred consistently in the lower frequency region (0.3-2 kHz). Clinically, the abnormal external ear resonance and the larger intersubject variation must be taken into consideration in fitting hearing aids for this group of patients.

Acoustic Stimulation↗
PubMed1999

Molecular analysis of secretor type alpha(1,2)-fucosyltransferase gene mutations in the Chinese and Thai populations.

BACKGROUND: The human Lewis histo-blood group system belongs to a family of structurally related oligosaccharides. The mutations of fucosyltransferase genes alpha(1,2)-fucosyltransferase (FUT2 or Se) and alpha(1,3/1,4)-fucosyltransferase (FUT3 or Le), are responsible for the polymorphism of Lewis blood group phenotypes. However, a population study of the FUT2 mutation in Chinese and Thais has not yet been done, and there is some controversy about the phenotypes of Le(a+b+) and Le(a+b-). STUDY DESIGN AND METHODS: One hundred twentyfour Chinese and 70 Thais were phenotyped for Lea and Le(b). DNA samples were studied by polymerase chain reaction and then by a restriction enzyme digestion method to distinguish wild-type and six known mutations. Direct sequencing was done for controls and some uncertain cases. RESULTS: A new mutation, C302T mutation, was found in 2 of 136 chromosomes in the Thai population; none were discovered in Chinese. The frequencies of the normal and six mutant alleles among Chinese and Thais, respectively, were as follows: 134 (54.0%) of 248 and 58 (41.4%) of 140 were wild-type (Se); 0 of 248 and 2 of 140 (both 1.4%) had the G428A mutation; 120 (48.4%) of 248 and 75 (53.6%) of 140 had the A385T mutation; 2 (0.81%) of 248 and 0 of 140 had the C571T mutation; and 1 (0.4%) of 248 and 3 (2.2%) of 140 had the G849A mutation. Only 1 Chinese (0.4%) of 248 had the C628T mutation, and none had fusion gene mutation. CONCLUSION: The FUT2 genes encoding for the phenotypes Le(a+b+) and Le(a+b-) are the same. The function and character of the mutant enzyme may play an important role in the phenotype. The methods used in this study are clinically applicable in population studies of the FUT2 gene polymorphism to explore relationships among different ethnic groups and correlations between phenotype and genotype.

China↗
PubMed1999

Muscarinic regulation of basal versus thyrotropin-releasing hormone-induced prolactin secretion in rat anterior pituitary cells. differential roles of nitric oxide and intracellular calcium mobilization.

Acetylcholine (ACh), synthesized in the pituitary, can act locally to modulate pituitary function. We used rat primary anterior pituitary (AP) cells to investigate how ACh affects pituitary prolactin (PRL) secretion in the presence or absence of known PRL regulators: thyrotropin-releasing hormone (TRH), 17beta-estradiol (E(2)) and triiodothyronine (T(3)). Cultured AP cells were prepared from ovariectomized rats and pretreated with diluent, 0.6 nM E(2), 10 nM T(3), or E(2) plus T(3) for 5 days, then challenged with various doses of ACh or muscarinic receptor agonists (oxotremorine or carbachol) and TRH (100 nM) for 20 min. Significant ACh (10(-5) M) suppression of both basal and TRH-induced PRL secretion was not evident in diluent-, E(2)- or T(3)-pretreated cells, but observed only in cells pretreated with both E(2) and T(3). Moreover, in E(2) plus T(3)-pretreated cells, oxotremorine and carbachol, like ACh (10(-7)-10(-5) M), suppressed both responses in a dose- related manner. Pertussis toxin (PTX; 100 ng/ml) as well as atropine (a muscarinic receptor antagonist; 1 mM) blocked these effects of cholinomimetics. ACh also inhibited both PRL responses elicited by drugs elevating intracellular cAMP (10 microM forskolin) or Ca(2+) (1 microM Bay K-8644) in a PTX-sensitive manner. ACh inhibition of basal PRL secretion was unaltered by intracellular Ca(2+) mobilization blockers, TMB-8 (100 microM) and thapsigargin (1 microM), but abrogated by the nitric oxide synthase inhibitor (300 microM L-NAME). ACh inhibition of TRH-induced PRL secretion was accentuated by TMB-8 and alleviated by thapsigargin or L-NAME. In summary, muscarinic inhibition of either basal or TRH-induced PRL secretion was augmented by E(2) and T(3), and involved the PTX-sensitive cAMP/Ca(2+) pathways. Furthermore, nitric oxide mediated the basal rather than TRH-induced PRL response to ACh, whereas the intracellular Ca(2+) mobilization concerned the TRH-induced rather than the basal PRL response to ACh. Thus, ACh synthesized in the AP appears to inhibit basal vs. TRH-induced PRL secretion via different mechanisms.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1999

Allogeneic bone marrow transplantation of chronic myeloid leukemia from an HLA-matched unrelated donor with the beta-thalassemic trait.

We report a chronic myeloid leukemia patient who underwent allogeneic bone marrow transplantation from an HLA-matched unrelated donor with the beta-thalassemic trait. The donor was a heterozygote for the -28 A-->G mutation. We examined the recipient's bone marrow and peripheral blood using the polymerase chain reaction (PCR) method to detect the -28 G-->A mutation of the donor type and monitored the sustained engraftment. This case suggests that a donor with the thalassemic trait can be a candidate for matched unrelated bone marrow transplantation for hematological malignancies and that PCR based genetic examination of the thalassemic mutation is a useful tool to detect early engraftment.

Adult↗
PubMed1998

Nitric oxide enhances the growth of U937 human leukemic cells through a cyclooxygenase-mediated pathway.

The mechanisms of exogenous nitric oxide (NO)-enhanced growth of the U937 human myeloid leukemic cells were examined using sodium nitroprusside (SNP) as a NO donor. Treatment with 0.1 mM SNP for 72 h caused a 45 +/- 2% increase in U937 cell growth with significantly increased S/G2+M-phase and decreased G0/G1-phase of the cell cycle. The growth-enhancing effect of SNP was blocked by indomethacin, a cyclooxygenase inhibitor, but not by H7, a broad spectrum kinase inhibitor, or PD98059, a mitogen-activated protein kinase inhibitor. SNP treatment resulted in a dose-dependent increase in prostaglandin E2 (PGE2) production. Furthermore, the addition of exogenous PGE2 not only enhanced U937 cell growth but restored the indomethacin-inhibited mitogenic effect of SNP. We suggest that NO can enhance cell growth through activating the cyclooxygenase pathway and that PGE2 may be an effector molecule for NO-regulated cell proliferation. Our data provide a mechanistic insight into the regulatory role of NO in myelopoiesis.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1998

Aberrant TSG101 transcripts in acute myeloid leukaemia.

Recently, a tumour susceptibility gene, TSG101, has been identified at chromosome 11p15. A large intragenic deletion of this gene has been demonstrated in primary breast tumours. To evaluate the role of the TSG101 gene in leukaemia, bone marrow and/or peripheral blood from 68 acute myeloid leukaemia patients, five haemopoietic cell lines (HL60, U937. Raji, KG-1, K562) and 30 normal controls were analysed by reverse transcription of the TSG101 mRNA, followed by PCR amplification and sequencing of the products. The results showed aberrant TSG101 transcripts in 24/68 (35%) acute myeloid leukaemia (AML) patients, all of the cell lines (100%) and 3/30 (10%) normal controls. Our study indicated that the abnormal transcripts may have resulted from aberrant RNA splicing as evidenced by these aberrant transcripts. Also, normal full-length transcripts were present in all specimens examined. The aberrant transcript occurred more frequently in the AML and cell lines. However, because aberrant transcripts of TSG101 were also found in the normal controls, the role of TSG101 as a tumour suppressor gene should be evaluated carefully.

Acute Disease↗
PubMed1998

Structuring a safer donor-replacement program.

BACKGROUND: Replacement donors are more likely than volunteer donors to have positive or abnormal tests for transfusion-transmissible disease. In an effort to increase the donor pool, workers sought to identify a safer replacement-donor subgroup that may be acceptable for routine donations. STUDY DESIGN AND METHODS: In a retrospective review and cohort study, the replacement-donor effect was separated from the new-donor effect. The relative effect the replacement donor has on the risk of transfusion-transmissible diseases, donor retention, and frequency of returning donations was then quantified by comparison against the effect of repeat volunteer donors. RESULTS: The replacement donor had 3.1 times the risk and 0.72 times the donor retention rate and made 0.81 times as many returning donations as the repeat volunteer donor. The figures for the new-donor effect were similar. The two risks were additive, making a new replacement donor particularly hazardous. If replacement donations only from repeat replacement donors were considered, the donor risk and the number of donations per returning donor were made comparable to those for the general (combined) volunteer donor. CONCLUSION: The negative effect of the replacement donor is similar in magnitude to that of the new volunteer donor. A replacement-donation program targeting repeat replacement donors has an acceptable risk profile and may be a valuable adjunct to the collection of blood from general volunteer donors.

Blood Donors↗
PubMed1998

Donor leukocyte infusion as salvage therapy in an adult with relapsed acute lymphoblastic leukemia after allogeneic bone marrow transplantation.

Relapse of malignancy after allogeneic bone marrow transplantation remains the major cause of treatment failure in patients with leukemia. While donor leukocyte infusion (DLI) has been used to treat such patients, its use in patients with acute lymphoblastic leukemia is seldom reported. We describe a 35-year-old woman who suffered relapse of acute lymphoblastic leukemia after allogeneic bone marrow transplantation. She received DLI twice as salvage therapy. This patient achieved complete remission following DLI and has remained in remission for more than 11 months without further chemotherapy. We suggest DLI can be used as an initial salvage therapy, without significant toxicity, for patients with relapsed acute lymphoblastic leukemia following bone marrow transplantation.

Adult↗