Biomedical subjects

H C Hsu

Publications and source records attributed to H C Hsu.

At least 91 records · Page 5Linked to original sources

PubMed2000

Exercise shifts the platelet aggregation modulatory role from native to mildly oxidized low-density lipoprotein.

PURPOSE: The role of low-density lipoprotein (LDL) lipid peroxides in strenuous exercise-induced changes in platelet function was studied in 30 patients (male/female = 22/8) aged 30-62 yr (mean +/- SD = 508). METHODS: All subjects were subjected to a treadmill exercise test, using the standard Bruce protocol. Blood samples were collected pre-, peak, and 10 min postexercise to assess hematological and biochemical parameters and platelet aggregation. Ex vivo whole blood platelet aggregation during treadmill exercise was assessed in 10 subjects by adding mildly oxidized LDL. RESULTS: Preexercise, a correlation existed between plasma thromboxane (TX) levels and plasma LDL cholesterol or beta-thromboglobulin (beta-TG) levels (r = 0.48, P < 0.05: r = 0.47, P < 0.05, respectively), whereas, at peak exercise, TX and beta-TG levels increased, but no correlation was seen. At peak exercise, platelets showed hyperaggregability in terms of maximal amplitude and reaction slope (P < 0.001 and P < 0.01, respectively). In contrast to the increase in plasma lipid peroxide levels seen during peak exercise (P < 0.05), LDL lipid peroxides decreased during exercise, this decrease reaching a statistical significance at 10 min postexercise (P < 0.05). In addition, the ex vivo addition of mildly oxidized LDL (10 mg protein x L(-1)) to peak exercise blood resulted in a significant attenuation of platelet aggregation and a decrease in TX release. At 10 min postexercise, a correlation was seen between LDL lipid peroxides and TX levels (r = 0.78, P < 0.001) or beta-TG levels (r = 0.68, P < 0.005). CONCLUSION: These results suggest that LDL lipid peroxides play a role in modulating and attenuating platelet aggregation during strenuous exercise.

Adult↗

PubMed2000

Antigen presenting cells expressing Fas ligand down-modulate chronic inflammatory disease in Fas ligand-deficient mice.

We assessed the effect of modified antigen presenting cells (APCs) expressing high levels of Fas ligand (APC-FasL) on post-viral chronic inflammatory disease. FasL-deficient B6-gld/gld mice infected with murine cytomegalovirus (MCMV) cleared the virus from their lungs, kidneys, and livers within 2 weeks of infection. However, inflammation persisted in these organs for more than 8 weeks, with a chronically increased T-cell response to MCMV-infected APCs and production of autoantibodies. Administration of APC-AdFasL at 4 weeks suppressed this inflammation and diminished the T-cell response and autoantibody production. APC-AdFasL that had been transfected with ultraviolet-irradiated MCMV were more effective than uninfected APC-AdFasL in ameliorating the chronic inflammation. APC-AdFasL migrated preferentially to the spleen, where they triggered apoptosis of lymphocytes in the marginal zone of the spleen. These results confirm that Fas-mediated apoptosis is not required for clearance of virus, but is required for down-modulation of the virally induced chronic inflammatory response. This organwide effect of APC-AdFasL appears to be mediated by elimination of activated T lymphocytes in the spleen before their emigration to the target organs.

Adenoviridae↗

PubMed2000

Negative regulation of the antimetastatic gene Nm23-H1 by thyroid hormone receptors.

Metastasis of various malignant cells is inversely related to the abundance of the Nm23-H1 protein. The possible role of thyroid hormones in tumor metastasis has now been investigated by examining the effect of T3 on the expression of the Nm23-H1 gene. Human hepatoma HepG2 cells, in which endogenous thyroid hormone receptor subtype alpha1 (TRalpha1) is expressed at a low level, were stably transfected, either with expression plasmids encoding wild-type TRalpha1 or a dominant negative mutant of TRalpha1, or with the empty vector (yielding HepG2-Wt, HepG2-Mt, and HepG2-Neo cells, respectively). Immunoblot analysis revealed that exposure of HepG2-Wt and HepG2-Neo cells, but not HepG2-Mt cells, to T3-induced time-dependent decreases in the abundance of Nm23-H1 messenger RNA and protein, with the extent of these effects correlating with the level of expression of TRalpha1. An in vitro assay also revealed that T3 induced a marked increase in the invasive activity of HepG2-Wt cells; it induced a smaller increase in that of HepG2-Neo cells but had no effect on that of HepG2-Mt cells. Finally, the promoter region of Nm23-H1 spanning nucleotides -471 to -437 (relative to the transcriptional initiation site) inhibited the expression of a downstream reporter gene, in a T3-dependent manner, in COS-1 cells also transfected with an expression plasmid encoding TRalpha1 or TRbeta1. The DNA binding domain of TRbeta1 was required for this inhibitory effect. These results indicate that T3, acting through TRs, inhibits transcription of Nm23-H1, and that this effect is mediated by a negative regulatory element in the promoter region of the gene. Thus, it is possible that T3 promotes tumor metastasis by inducing down-regulation of Nm23-H1 expression.

Base Sequence↗

PubMed2000

Angiotropic lymphoma manifesting as a solitary adrenal tumor in a case of ankylosing spondylitis.

Angiotropic lymphoma is an extremely rare disease characterized by intravascular accumulation of large neoplastic lymphocytes, with the clinical manifestations of fever, skin lesions and neurologic deficits. We report a patient who developed angiotropic lymphoma after a 10-year history of ankylosing spondylitis. The clinical disease manifested as a unilateral, solitary adrenal tumor, fever and body weight loss. The fever subsided after surgical removal of the adrenal tumor. Systemic chemotherapy was administered postoperatively. The patient was leading an uneventful life 44 months after the initial diagnosis. To our knowledge, this is the first case of angiotropic lymphoma associated with ankylosing spondylitis. It is also the second reported case manifesting with a unilateral solitary adrenal tumor without systemic involvement.

Adrenal Gland Neoplasms↗

PubMed2000

Septo-optic dysplasia with unilateral optic nerve hypoplasia: case report.

Septo-optic dysplasia (de Morsier syndrome) is a well-described entity that includes optic nerve hypoplasia and the absence of the septum pellucidum with or without pituitary abnormalities. We describe a case with unilateral optic nerve hypoplasia and absence of a septum pellucidum. A 6-year-old boy was referred to our clinic because of poor visual acuity. His best-corrected visual acuity was counting fingers at 15 cm in the right eye and 1.0 in the left eye. Extraocular muscle movements were normal, and exotropia of 30 prism diopters by Hirschberg test in the right eye was present. The pupils were equal and reactive to light with a mild Marcus Gunn pupillary response in the right eye. Perimetry revealed small visual fields in the superior quadrants of the right eye, while the left eye was normal. Ophthalmoscopic examination showed a small pale optic disc in the right eye; the optic disc of the left eye was normal. Magnetic resonance imaging showed the absence of the septum pellucidum. Endocrine studies revealed no evidence of pituitary insufficiency.

Child↗

PubMed1999

Studies on effective PCR screening strategies for white spot syndrome virus (WSSV) detection in Penaeus monodon brooders.

We re-tested stored (frozen) DNA samples in 5 independent polymerase chain reaction (PCR) replicates and confirmed that equivocal test results from a previous study on white spot syndrome virus (WSSV) in brooders and their offspring arose because amounts of WSSV DNA in the test samples were near the sensitivity limits of the detection method. Since spawning stress may trigger WSSV replication, we also captured a fresh batch of 45 brooders for WSSV PCR testing before and after spawning. Replicates of their spawned egg batches were also WSSV PCR tested. For these 45 brooders, WSSV prevalence before spawning was 67% (15/45 1-step PCR positive, 15/45 2-step PCR positive and 15/45 2-step PCR negative). Only 27 (60%) spawned successfully. Of the successful spawners, 56% were WSSV PCR positive before spawning and 74% after. Brooders (15) that were heavily infected (i.e. 1-step PCR positive) when captured mostly died within 1 to 4 d, but 3 (20%) did manage to spawn. All their egg batch sub-samples were 1-step PCR positive and many failed to hatch. The remaining 30 shrimp were divided into a lightly infected group (21) and a 2-step PCR negative group (9) based on replicate PCR tests. The spawning rates for these 2 groups were high (81 and 78%, respectively). None of the negative spawners (7) became WSSV positive after spawning and none gave egg samples positive for WSSV. In the lightly infected group (21), 6 brooders were 2-step WSSV PCR negative and 15 were 2-step WSSV PCR positive upon capture. However, all of them were WSSV PCR positive in replicate tests and after spawning or death. Four died without spawning. The remaining 17 spawned but only 2 gave egg samples PCR negative for WSSV. The other 15 gave PCR positive egg samples, but they could be divided into 2 spawner groups: those (7) that became heavily infected (i.e. 1-step PCR positive) after spawning and those (8) that remained lightly infected (i.e. became or remained 2-step PCR positive only). Of the brooders that became heavily infected after spawning, almost all egg sample replicates (91 %) tested 2-step PCR positive. One brooder even gave heavily infected (i.e. 1-step PCR positive) egg samples. For the brooders that remained lightly infected after spawning, only 27% of the egg sample replicates were 2-step PCR positive. Based on these results, we recommend that to avoid false negatives in WSSV PCR brooder tests screening tests should be delayed until after spawning. We also recommend, with our PCR detection system, discarding all egg batches from brooders that are 1-step PCR positive after spawning. On the other hand, it may be possible with appropriate monitoring to use eggs from 2-step PCR positive brooders for production of WSSV-free or lightly infected postlarvae. These may be used to stock shrimp ponds under low-stress rearing conditions.

Animals↗

PubMed1999

Expression of mutant thyroid hormone nuclear receptors in human hepatocellular carcinoma cells.

To understand the expression and role of thyroid hormone nuclear receptors (TRs) in hepatocarcinogenesis, we characterized the TRs in 16 human hepatocellular carcinoma (HCC) specimens. The full-length cDNAs for the two TR subtypes, alpha1 and beta1, were cloned from several tumors by reverse transcription-polymerase chain reaction. Southern blot analysis indicated that, in addition to the full-length cDNA, truncated TRalpha1 and TRbeta1 cDNAs were present in nine tumors (53%). In addition, point mutations detected by the mismatch RNase cleavage assay in TRalpha1 and TRbeta1 were found in 65% and 76% of the tumors, respectively. The mutations were confirmed by DNA sequencing. Interestingly, most of the TRalpha1 mutations were in amino acid codons 209-228 and 245-256, two hot-spots in HCC patients. However, no hot-spot was detected in TRbeta1. The expression of TRalpha1 and TRbeta1 proteins was determined in the tissue extracts by western blotting. TRbeta1 protein was expressed or elevated in 10 tumors but not in normal livers, whereas the expression of TRalpha1 was variable among tumors. The mutant TR proteins were translated in vitro, and their hormone- and DNA-binding activities were evaluated. Abnormal binding to the thyroid hormone response elements was observed. The proteins' DNA binding activity was either partially impaired or completely lost. The high prevalence of TR mutations found in the tumors of patients with hepatocellular carcinoma suggests that mutant TRs could play an important role in liver carcinogenesis.

Adult↗

PubMed1999

Lipoprotein (a) level in the population in Taiwan: relationship to sociodemographic and atherosclerotic risk factors.

To examine the lipoprotein(a) (Lp(a)) level in the Taiwanese population and its association with cardiovascular risk factors, 1703 men and 1899 women aged 35 years and above were enrolled in a community-based study cohort established between 1990 and 1991. The distributions of Lp(a) levels were skewed to the right, and females were more likely than males to have Lp(a) levels greater than 30 mg/dl (14.3% versus 11.6%, P < 0.05). The Lp(a) level increased with age. Socioeconomic status did not seem to have consistent influence on the level of Lp(a). Smoking and alcohol use also had no effect on Lp(a) levels. Multivariate analysis indicated that older age and high level of low-density-lipoprotein cholesterol corresponded to an elevated Lp(a) level, while hypertriglyceridemia, low high-density-lipoprotein cholesterol level, obesity and high insulin resistance corresponded to a lower Lp(a) level. In univariate analysis, hyperinsulinemia was negatively associated with Lp(a) level (-0.107, P < 0.01) only in males. In females, use of oral contraceptive lowered Lp(a) levels, but menopause did not change Lp(a) levels. We also found that different correlation patterns existed for selected coagulation profiles between sexes. There was a significant correlation between Lp(a) and fibrinogen levels in males (0.154, P < 0.001) but not in females (0.007, P > 0.05). These data provided clues for investigating atherosclerotic risk factors and coagulation parameters for the Taiwanese population.

Adult↗

PubMed1999

Circulating levels of thrombopoietic and inflammatory cytokines in patients with clonal and reactive thrombocytosis.

The regulation of megakaryocytopoiesis and thrombopoiesis appears to be under the control of an array of hematopoietic growth factors. To determine the relationship between endogenous cytokine levels and circulating platelet counts, we measured the serum levels of both thrombopoietic and inflammatory cytokines in the peripheral blood and bone marrow samples from 70 patients with clonal thrombocytosis (CT) caused by myeloproliferative disorders, 28 patients with reactive thrombocytosis (RT), and 35 normal control subjects. The levels of thrombopoietin (TPO), interleukin-6 (IL-6), soluble IL-6 (sIL-6) receptor, IL-11, stem cell factor (SCF), IL-3, and IL-8 were determined by enzyme-linked immunosorbent assay (ELISA). Platelet counts were significantly higher in both CT and patients with RT (699+/-399x10(9)/L, P<.001; 642+/-200 x 10(9)/L, P<.001; respectively) as compared with the normal control subjects (240+/-47x10(9)/L). The concentrations of cytokines in the bone marrow correlated well with those in the peripheral blood. The endogenous levels of TPO, IL-6, and sIL-6 receptor were significantly higher in both CT and patients with RT than those in normal control subjects. The median level of IL-6 was significantly higher in patients with RT than in patients with CT (40 pg/mL vs. 5 pg/mL; P<.001); however, there was no detectable difference in TPO and sIL-6 receptor levels between the two groups. Significantly higher levels of SCF and IL-8 were also found in patients with CT as compared with those found in normal control subjects (median 2460 pg/mL vs 1995 pg/mL, P<.05; 20 ng/mL vs. 5 ng/mL, P = .001; respectively). Finally, IL-11 and IL-3 levels were undetectable in most patients with thrombocytosis. Our results reveal that the endogenous levels of TPO, IL-6, sIL-6 receptor, IL-8, and SCF are elevated in patients with CT or RT. These cytokines appear to be active mediators involved in the regulation of thrombopoiesis during clonal and reactive thrombocytosis.

Adult↗

PubMed1999

The role of vitamin E on the anti-atherosclerotic effect of fish oil in diet-induced hypercholesterolemic rabbits.

The role of vitamin E on the anti-atherosclerotic effect of fish oil in diet-induced hypercholesterolemic rabbits was studied in male New Zealand white rabbits. The animals were randomly divided into six groups of 14 each according to the chow given them. Group I, control, rabbits were fed regular laboratory rabbit chow. In addition to the regular chow, Group II rabbits were fed a high (1%) cholesterol-enriched diet. Group III had the same diet as Group II plus 450 mg vitamin E/1000 g chow. Group IV also had the same diet as Group II plus 10% fish oil, but without vitamin E. Group V's diet contained 1% cholesterol, 10% fish oil, and 450 mg vitamin E/1000 g chow. Group VI had the same diet as Group V, but with 150 mg vitamin E/1000 g chow. At the end of a 6-week feeding, the ascending aorta from seven rabbits from each group was harvested for the analysis of prostanoid production, thiobarbituric acid reactive substances (TBARS), superoxide dismutase activity, and cholesterol and vitamin E levels; the same tissue from the other seven rabbits from each group was obtained for the delineation of atherosclerotic lesions by planimetry after the Sudan IV stain. The high cholesterol diet-treated rabbits had worse prostanoid synthesis and higher TBARS levels, which paralleled the severity of the atherosclerosis. Vitamin E or fish oil supplementation in a high cholesterol diet had beneficial prostanoid production, reduced aortic TBARS levels, and attenuated atherosclerotic lesions; these effects were potentiated when vitamin E and fish oil were combined together. The atherosclerotic lesion reduction in rabbits treated with high cholesterol plus fish oil and 450 mg vitamin E/1000 g chow reached statistical significance (P < 0.05) compared to high cholesterol and the same dose of vitamin E-treated rabbits. The rabbits treated with high cholesterol plus fish oil, but without vitamin E or with 150 mg vitamin E/1000 g chow showed an increased plasma creatine kinase activity at 4 (P < 0.01 and 0.05, respectively) and 6 (P < 0.001 and 0.01, respectively) week of feeding. These results suggest that vitamin E and/or fish oil attenuate atherosclerosis in high cholesterol-fed rabbits; vitamin E and fish oil potentiated the effect of each other. Furthermore, without sufficient vitamin E supplementation, rabbits treated with high cholesterol plus fish oil will show an elevation of plasma creatine kinase activity.

Animals↗

PubMed1999

Investigation of chromosomal aberrations in hepatocellular carcinoma by fluorescence in situ hybridization.

Molecular cytogenetic approaches have been applied only rarely in the characterization of hepatocellular carcinoma (HCC). The aim in this study was to evaluate aberrations, particularly deletions, of specific chromosomal regions in HCC. Dual-color fluorescence in situ hybridization (FISH) was performed on intact nuclei from touch preparations of 17 HCCs and 1 hepatic adenoma. Each touch preparation was hybridized with a digoxigenin-labeled centromere probe and a biotin-labeled unique sequence probe from the same chromosome. This approach permitted the simultaneous evaluation of ploidy changes and chromosome arm deletions. Eight noncentromeric chromosome regions, 3p14, 4q21, 6q14, 6q21, 8p12, 8p22, 9p21, and 9p24 were selected for study on the basis of their having been implicated as tumor suppressor regions in HCC or other common types of carcinoma. Together with the 5 corresponding centromeric probes on chromosomes 3, 4, 6, 8, and 9, a total of 13 chromosome loci were evaluated. All cases of hepatocellular carcinoma showed at least one deletion or aneuploidy. The hepatic adenoma was all diploid. Chromosome 4q21 showed the highest rate of deletion (76.5%) and aneusomy (88%). The second and the third were chromosome 8p22 and 6q14, which showed 59% and 47% of deletion, respectively. A 4q21 deletion is also the most frequent single chromosome aberration. Prominent tumor heterogeneity and variable deletion patterns were noted. Interphase FISH was an efficient means for evaluating numerical and structural chromosome aberrations in HCCs. Most HCCs contained deletions of known tumor suppressor regions (4q and 8p), and a novel deletion hotspot was demonstrated on chromosome band 6q14.

Adult↗

PubMed1999

Infant arousal in an en-face exchange with a new partner: effects of prematurity and perinatal biological risk.

Very low birth weight (VLBW) infants of higher (n = 18) and lower (n = 29) perinatal biological risk were contrasted at 4 months adjusted age with healthy full-term infants (n = 32) in their arousal during a standardized peekaboo game with an examiner. VLBW infants showed less positive arousal, more negative arousal, and 3 mixtures of behavioral cues across the peekaboo game seldom seen for full-term infants-strong cues of both positive and negative arousal, strong cues of negative arousal alone, and no strong cues of either positive or negative arousal. Contrary to expectations, perinatal biological risk did not strongly predict variations in arousal within the VLBW group. Possible changes in how internal and external sources of arousal are integrated provide one explanation for the presence of strong relationships between perinatal biological risk and social responsiveness near term age and their disappearance by 4 months of age.

Analysis of Variance↗

PubMed1999

The integration of laughter and speech in vocal communication: a dynamic systems perspective.

Laughter in infant-directed speech was examined in 13 mother-infant pairs to investigate the possible co-occurrence of speech and laughter. Contrary to previous findings in adult-adult social interaction, all mothers produced speech simultaneously with laughter in up to 50% of laughs. In most of these speech-laughs the onset of laugh and speech was simultaneous. Laughter occurred on both function and content words and was more likely to occur on approximately 2 words and on utterances that were statements rather than questions or exclamations. Laughter and speech are different outcomes produced from a reorganization of the same vocal/anatomical parameters. A 3rd outcome is possible in the form of speech-laughs utilizing features from both laughter and speech. In speech-laughs, the duration of the vocalization was more likely to increase, and the changes in the utterance were likely to include 1 or more of the features of vowel elongation, syllabic pulsation, breathiness, and pitch change. These findings and individual variations in the resulting vocal output are discussed from a dynamic systems perspective. It is argued that neither speech nor laughter is dominant when both are combined, but that this is a more complex vocal outcome produced with idiosyncratic flexibility within stable temporal and physiological constraints.

Communication↗

PubMed1999

Case report: portal vein thrombosis associated with hereditary protein C deficiency: a report of two cases.

Protein C deficiency is one of the causes of curable or preventable portal vein thrombosis. We report two patients of portal vein thrombosis associated with hereditary protein C deficiency. The first patient presented with continuous right upper quadrant pain and high fever. The abdominal sonography revealed normal liver parenchyma but portal vein and superior mesenteric vein thrombosis. Based on a 55% (normal 70-140%) plasma protein C level, he was diagnosed as having protein C deficiency. A trace of his family history showed that his elder brother also had protein C deficiency with a 50% plasma C level. Both patients received anticoagulant therapy. The younger brother showed good response. Unfortunately, the elder one suffered from recurrent episodes of variceal bleeding and received a life-saving splenectomy and devascularization. We herein remind clinicians that early screening and therapy are helpful in preventing late complications of protein C deficiency with portal vein thrombosis.

Abdomen, Acute↗

PubMed1999

Herpes simplex virus type 2 infection induced apoptosis in peritoneal macrophages independent of Fas and tumor necrosis factor-receptor signaling.

Freshly isolated macrophages from mature mice are poorly or nonpermissive for infections with HSV. However, despite lack of significant viral replication, HSV infection has been demonstrated to induce substantial cell death among macrophages. To determine if HSV-induced cytotoxicity of macrophages is due to apoptosis, peritoneal macrophages were obtained from C57BL/6 (B6) mice, and apoptosis was analyzed following HSV-2 infection in vitro. Macrophages underwent apoptosis upon HSV-2 infection indicated by annexin V staining, labeling of DNA strand breaks and electronmicroscopy. Apoptosis was associated with macrophage activation demonstrated by upregulation of MHC class II and Mac-1 surface expression. Though there was also an upregulation of Fas (Apo-1/CD95) and tumor necrosis factor (TNF)-receptor 1 (TNF-R1) pathways, inhibition of Fas by soluble Fas and blocking of TNF-alpha using a TNF-binding protein did not prevent HSV-induced apoptosis. Moreover, apoptosis was not impaired in HSV-2 infected macrophages from Fas-deficient B6-lpr/lpr mice suggesting involvement of other apoptosis pathways, or activation of Fas or TNF-R pathways downstream of the receptor level. The present results demonstrate that HSV-2 infection leads to activation and subsequent apoptosis in peritoneal macrophages independent of Fas or TNF-R1 signaling.

Animals↗

PubMed1999

Massive ascites caused by peritoneal extramedullary hematopoiesis as the initial manifestation of myelofibrosis.

An 83-year-old man presented with massive ascites. Cytological examination of the ascites revealed primitive hematopoietic cells. The specimen of bone marrow biopsy disclosed diffuse fibrosis, which suggested myelofibrosis with extramedullary hematopoiesis as the cause of ascites. His symptoms resolved dramatically after administration of hydroxyurea. Ascites formation in myelofibrosis is often attributed to presinusoidal portal hypertension and occurs in the context of well-established disease. This case demonstrates that myelofibrosis may manifest as massive ascites caused by peritoneal implants of myeloid tissues. Extramedullary hematopoiesis should be included in the differential diagnosis of ascites.

Aged↗

PubMed1999

In vitro effect of granulocyte-colony stimulating factor and all-trans retinoic acid on the expression of inflammatory cytokines and adhesion molecules in acute promyelocytic leukemic cells.

Differentiation therapy with all-trans retinoic acid (ATRA) represents a landmark approach in the treatment of acute promyelocytic leukemia (APL). However, a potentially fatal complication of retinoic acid (RA) syndrome occurs in about a quarter of patients and its pathophysiology is still unclear. In order to investigate whether or not the treatment with ATRA leads to increased elaboration of inflammatory cytokines and adhesion molecules by the APL cells, the expression of interleukin (IL)-1beta, tumor necrosis factor (TNF)-alpha, IL-8, L-selectin and intercellular adhesion molecule-1 (ICAM-1) was examined in the APL cells after induction of differentiation with ATRA in the presence or absence of granulocyte-colony stimulating factor (G-CSF) or IL-3 in the present study. Cytokine elaboration by the treated cells was detected using both Northern blotting and enzyme-linked immunosorbent assay. Our results have shown that ATRA induces an increased expression of IL-8, IL-1beta, TNF-alpha and ICAM-1 in APL cells, which can be amplified by the addition of G-CSF. These data imply that the induction of inflammatory cytokines in APL cells may play an important role in the pathogenesis of RA syndrome. Furthermore, G-CSF, through its potent differentiating activity, may increase the risk of such complications during ATRA treatment.

Antineoplastic Agents↗

PubMed1999

Infrequent p53 mutations in patients with areca quid chewing-associated oral squamous cell carcinomas in Taiwan.

Mutations in the conserved regions (exons 5-9) of the p53 gene were investigated in 37 untreated human primary oral squamous cell carcinomas (SCCs) using polymerase chain reaction-single strand conformation polymorphism and DNA sequencing analyses. P53 mutations were detected in 2 of 37 (5.4%) oral SCC cases. One tumor sample (case 23) showed a mis-sense point mutation at codon 177, changing CCC to CTC, which resulted in a substitution of proline to leucine in the p53 protein. The other tumor (case 33) had a point mutation at codon 266, changing GGA to AGA and causing a substitution of glycine to arginine in the p53 protein. These two patients with p53 mutations did not have an areca quid chewing habit. These results suggest that mutations in the p53 gene may not play a role in the pathogenesis of human oral SCCs in Taiwan. Recently, we have shown that positive p53 staining was observed in 47 of 81 (58%) cases of oral SCC. The discrepancies between positive p53 protein staining and the low prevalence of p53 mutation in oral SCCs indicate that other mechanism(s) are involved in p53 overexpression.

Adult↗