OMFS training revisited.
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Clinical Competence↗
Biomedical subjects
K Fan
Publications and source records attributed to K Fan.
Anomalous decrease in groundwater radon before the Taiwan M6.8 Chengkung earthquake.
On December 10, 2003, an earthquake of magnitude (M) 6.8, the strongest since 1951, occurred near the Chengkung area in eastern Taiwan. Approximately 65 d prior to the 2003 Chengkung earthquake, precursory changes in the groundwater radon concentration were observed at the Antung radon-monitoring station located 20 km from the epicenter. The radon anomaly was a decrease from a background level of 28.9 BqL(-1) to a minimum of 12.2 BqL(-1). Observations at the Antung hot spring suggest that the groundwater radon, when observed under suitable geological conditions, can be a sensitive tracer for strain changes in the crust preceding an earthquake.
Disasters↗
Hypertrophic cardiomyopathy with mid ventricular obstruction, apical infarction and aneurysm formation.
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Aged↗
Colonic epithelial cell proliferation decreases with increasing levels of serum 25-hydroxy vitamin D.
Epidemiological evidence suggests a potential role for vitamin D in colon cancer prevention. Vitamin D, absorbed from the intestine or derived from solar ultraviolet light, is metabolized in the liver to 25-hydroxyvitamin D (25-OH D(3)). Previous studies examining effects of vitamin D upon carcinogenesis have focused upon the active metabolite 1,25-dihydroxyvitamin D [1,25-(OH)(2) D(3)], which interacts with nuclear vitamin D receptors in several organs. Until recently, the metabolism of 25-OH D(3) to 1,25-(OH)(2) D(3) was believed to occur only in the kidney, but more recent studies have shown that 25-OH D(3) conversion to 1,25-(OH)(2) D(3) can occur in other tissues. We examined the association between fasting levels of 25-OH D(3), 1,25-(OH)(2) D(3), and BsmI polymorphism of the vitamin D receptor (VDR) gene with indices of colonic epithelial cell proliferation and differentiation in a chemoprevention study, after giving vitamin D or calcium and taking rectal biopsies that were incubated with bromodeoxyuridine. Vitamin D receptor polymorphism was determined by genotyping of the 3' BsmI polymorphism in intron eight of the VDR gene. No significant changes in cell proliferation or in differentiation were found in subjects between study start and end. However, fasting serum levels of 25-OH D(3) showed a highly significant decrease with whole crypt labeling index and the size of the proliferative compartment (phi h). There was no correlation between serum levels of 1,25-(OH)(2) D(3) and the proliferative parameters. Calcium supplementation induced a significant effect upon the relationship between serum 25-OH D(3) and rectal epithelial cell labeling index and phi h when studied by covariance analysis without a relationship with 1,25-(OH)(2) D(3) levels. VDR genotype did not influence the effects of serum 25-OH D(3) or serum 1,25-(OH)(2) D(3) levels upon proliferation. These data suggest that there might be a local effect of 25-OH D(3) on colonic epithelial cells through conversion of 25-OH D(3) to 1,25-(OH)(2) D(3). Subsequent studies have demonstrated the presence of 1alpha-hydroxylase mRNA in normal colorectal epithelium and in colorectal cancer. Thus, vitamin D may have an important role in determining the effects of calcium on colorectal epithelial proliferation and may explain some of the discrepancies found previously in studies that examine the direct role of calcium on the colorectal epithelium.
Adult↗
The distinct spectra of tumor-associated Apc mutations in mismatch repair-deficient Apc1638N mice define the roles of MSH3 and MSH6 in DNA repair and intestinal tumorigenesis.
In mammalian cells, mismatch recognition has been attributed to two partially redundant heterodimeric protein complexes of MutS homologues, MSH2-MSH3 and MSH2-MSH6. We have conducted a comparative analysis of Msh3 and Msh6 deficiency in mouse intestinal tumorigenesis by generating Apc1638N mice deficient in Msh3, Msh6 or both. We have found that Apc1638N mice defective in Msh6 show reduced survival and a 6-7-fold increase in intestinal tumor multiplicity. In contrast, Msh3-deficient Apc1638N mice showed no difference in survival and intestinal tumor multiplicity as compared with Apc1638N mice. However, when Msh3 deficiency is combined with Msh6 deficiency (Msh3(-/-)Msh6(-/-)Apc1638N), the survival rate of the mice was further reduced compared to Msh6(-/-)Apc(1638N) mice because of a high multiplicity of intestinal tumors at a younger age. Almost 90% of the intestinal tumors from both Msh6(-/-)Apc1638N and Msh3(-/-)Msh6(-/-)Apc1638N mice contained truncation mutations in the wild-type Apc allele. Apc mutations in Msh6(-/-)Apc1638N mice consisted predominantly of base substitutions (93%) creating stop codons, consistent with a major role for Msh6 in the repair of base-base mismatches. However, in Msh3(-/-)Msh6(-/-)Apc1638N tumors, we observed a mixture of base substitutions (46%) and frameshifts (54%), indicating that in Msh6(-/-)Apc1638N mice frameshift mutations in the Apc gene were suppressed by Msh3. Interestingly, all except one of the Apc mutations detected in mismatch repair-deficient intestinal tumors were located upstream of the third 20-amino acid beta-catenin binding repeat and before all of the Ser-Ala-Met-Pro repeats, suggesting that there is selection for loss of multiple domains involved in beta-catenin regulation. Our analysis therefore has revealed distinct mutational spectra and clarified the roles of Msh3 and Msh6 in DNA repair and intestinal tumorigenesis.
Animals↗
Modeling two-state cooperativity in protein folding.
A protein model with the pairwise interaction energies varying as the local environment changes, i.e., including some kind of collective effect between the contacts, is proposed. Lattice Monte Carlo simulations on the thermodynamical characteristics and free energy profile show a well-defined two-state behavior and cooperativity of folding for such a model. As a comparison, related simulations for the usual G&o model, where the interaction energies are independent of the local conformation, are also made. Our results indicate that the evolution of interactions during the folding process plays an important role in the two-state cooperativity in protein folding.
Biophysics↗
A model of interfacial inactivation for papain in aqueous organic biphasic systems.
A model was proposed to describe the effects of the main factors in aqueous-organic two-liquid-phase media on the stability of papain. The relationships between the half-life of papain activity and these factors including interfacial tension, stirring rate, phase volume ratio and temperature were investigated. The results showed that these factors had notable effects on papain stability except temperature. The correlation coefficient between the model and the experimental data were 0.829, which indicated the model is practicable.
Journal Article↗
Transcatheter closure of atrial septal defect using Amplatzer septal occluder in Chinese adults.
Amplatzer septal occluder (AGA Med. Co., USA) is a novel device for occlusion of atrial septal defect. We present our experience of transcatheter closure of atrial septal defects using Amplatzer septal occluder in 45 adult Chinese patients (age range 18-69 years). The size of atrial septal defect varied from 14-28 (23 +/- 4) mm. Cardiac catheterization revealed a pulmonary-to-systemic shunt ratio ranging from 1.4-2.8 (mean 2.0 +/- 0.4). The procedure was successful in 44 (98%) patients. Displacement of the device requiring surgical removal occurred in one (2%) patient and minor wound complication occurred in two (4%) patients. Total procedure time was 67 +/- 16 minutes and the fluoroscopy time was 25 +/- 8 min. Immediate post-procedure and pre-discharge echocardiography revealed complete abolition of shunt in 42 (93%) and trivial residual shunt in 3 (7%) patients. The average follow-up period was 16 +/- 6 months (range 2 months to 3 years) months. None of the patients had developed other major complication at follow-up. Cathet Cardiovasc Intervent 2001;52:373-377.
Adolescent↗
A Western-style diet induces benign and malignant neoplasms in the colon of normal C57Bl/6 mice.
Decreased dietary intakes of calcium, vitamin D and folic acid have been suggested as risk factors for human colon cancer. We previously fed a Western-style diet (WD) containing reduced calcium, vitamin D and increased fat content to normal C57/Bl6 mice: hyperproliferation, hyperplasia and whole crypt dysplasias developed in the colon following WD administration. Utilizing the same diet, we now also decreased the levels of several nutrients that are required for biochemical reactions involving methyl group inadequacy, i.e. folic acid, methionine, choline and vitamin B(12). Dietary levels of these nutrients were reduced to nutrient-density levels approximating those consumed by large segments of human Western populations. This further modification of the WD resulted in adenoma and carcinoma development in normal mouse colon (P < 0.04 compared with AIN-76A diet). The results indicate, for the first time, that a semi-purified rodent diet designed to mimic the human Western diet can induce colonic tumors in normal mice without carcinogen exposure.
Adenoma↗
Expression of fas ligand in metastatic prostatic carcinoma: suggestive of possible clonal expansion of subpopulation with metastatic potential.
Fas ligand (FasL) is a type II transmembrane tumor necrosis factor family protein, known to trigger apoptosis in cells that bear the FasL receptor, Fas. The authors found that normal prostate, benign hyperplasia, and most prostatic carcinoma cells at the primary site did not express FasL, whereas metastatic prostatic carcinoma cells in lymph nodes and bone marrow displayed almost uniform, immunohistochemically detectable, FasL expression. However, small foci of FasL-positive prostatic carcinoma cells amid a vast majority of FasL-negative tumor cells were noted at the primary sites in patients with distant metastases. Analysis of the FasL gene and its mRNA by polymerase chain reaction and reverse transcriptase-polymerase chain reaction, respectively, suggested that the expression of immunohistochemically detectable FasL in metastatic tumor cells was not due to mutation in the FasL gene with resulting overexpression. Further, FasL expression was detectable in the acinar epithelial cells of prostates with morphologic atrophic changes, suggesting that FasL also plays a role in the physiologic apoptosis process of noncancerous prostate. The current data suggest that a subpopulation of prostate carcinoma cells clonally expresses FasL, and this subpopulation may have metastatic potential. Evaluation of FasL expression in the primary tumor thus may provide a useful parameter for predicting metastatic potential of the tumor.
Bone Marrow↗
Clinicopathologic study of mucosa-associated lymphoid tissue lymphoma of the salivary gland.
OBJECTIVE: To study the histopathologic features and pathogenesis of mucosa-associated lymphoid tissue lymphoma (MALT-oma) of salivary glands. METHODS: Clinical data, paraffin-embedded sections, immunohistochemical slides (SP method) and electron microscopic features of surgical specimens of 32 cases of salivary gland MALT-oma were studied. RESULTS: The patients were 27 males and 5 females, with a mean age of 54.76 years. The lesions were located in the parotid area in 17 cases, and in the submandibular gland in the remaining 15 cases. Much of the MALT-oma was replaced by infiltration of a great amount of centrocyte-like cells (CCL) as background and occasional large cells (centroblast- or immunoblast-like). In MALT-omas "lymphoepithelial lesions" were present. Immunohistochemically, CD20 expression was found to be positive and CD45RO expression was negative in all MALT-omas. CONCLUSION: Most of the MALT-omas are low grade malignant tumors and have a "homing back" phenomenon. The cases were managed by surgery and chemotherapy. In a few MALT-omas which turned into high grade malignant tumors, the prognosis was poor. Acquired MALT may develop as a reaction to autoimmune disease and infection. Hyper-immune reaction and MALT hyperplasia under stimulation may result in myoepithelial sialadenitis and lead to MALT-oma of the salivary gland.
Adolescent↗
Effects of biatrial pacing in prevention of postoperative atrial fibrillation after coronary artery bypass surgery.
BACKGROUND: Atrial fibrillation (AF) is common after coronary artery bypass surgery (CABG) and results in prolonged hospitalization. The purpose of this study was to evaluate the efficacy of biatrial pacing in preventing post-CABG AF compared with single-site atrial pacing. METHODS AND RESULTS: A total of 132 patients who had no history of AF and who underwent CABG were randomized to 1 of the following 4 groups: biatrial pacing (BiA), left atrial pacing (LA), right atrial pacing (RA), or no pacing (control) in postoperative period. Overdrive atrial pacing was performed for 5 days. The incidence of AF was significantly reduced in the BiA group (12.5%) compared with the other 3 groups (LA, 36.4%; RA, 33.3%; control, 41. 9%; P<0.05). The mean length of hospital stay was significantly reduced in the BiA group. At baseline, the mean P-wave duration (P(dur)) and dispersion (P(dis)) were not prolonged. BiA pacing resulted in the most significant percentage of reduction in P(dis) when compared with the LA or RA groups (BiA, 42+/-8%; LA, 13+/-6%; RA, 10+/-9%; P<0.05 for BiA versus LA or RA). No significant differences existed in mean P(dur) and P(dis) between patients who developed AF and those who remained in sinus rhythm at baseline. However, only those patients who remained in sinus rhythm had a significant reduction in mean P(dur) and P(dis) after pacing therapy. CONCLUSIONS: Biatrial overdrive pacing is more effective in preventing post-CABG AF than single-site atrial pacing; this therapy also results in a shortened hospital stay. The overall reduction in atrial activation time with BiA pacing was reflected in the reduction in P(dis).
Aged↗
The DNA mismatch repair genes Msh3 and Msh6 cooperate in intestinal tumor suppression.
Repair of mismatches in DNA in mammalian cells is mediated by a complex of proteins that are members of two highly conserved families of genes referred to as MutS and MutL homologues. Germline mutations in several members of these families, MSH2, MSH6, MLH1, and PMS2, but not MSH3, are responsible for hereditary non-polyposis colorectal cancer. To examine the role of MSH3, we generated a mouse with a null mutation in this gene. Cells from Msh3-/- mice are defective in repair of insertion/ deletion mismatches but can repair base-base mismatches. Msh3-/- mice develop tumors at a late age. When the Msh3-/- and Msh6-/- mutations are combined, the tumor predisposition phenotype is indistinguishable from Msh2-/- or Mlh1-/- mice. These results suggest that MSH3 cooperates with MSH6 in tumor suppression.
Animals↗
Instability studies of porcine somatotropin in aqueous solutions and the possible reagents for its stabilization.
The instability of porcine somatotropin (pST) in various solutions and possible stabilization of the hormone by sugars and mild detergents were studied. Aggregation and decomposition of the hormone molecules in various pH solutions and under presence of sugar or detergent were monitored by gel permeation chromatography (GPC) or ultraviolet spectroscopy (UV). The pST is a very unstable hormone in an aqueous environment. It was found in this project that the peptide hormone underwent aggregation or decomposition quickly in acidic and alkaline solutions but slowly in neutral pH solutions. High losses of pST monomers were seen in concentrated solutions of the hormone. On the other hand, pST monomers were stabilized to a certain degree in glucose solutions and at a low concentration of urea. These results should facilitate the development of efficient controlled-release systems which are essential for commercializing porcine somatotropin.
Animals↗
Chemoprevention studies of the flavonoids quercetin and rutin in normal and azoxymethane-treated mouse colon.
In this study we investigated the chemopreventive effects of quercetin and rutin when added to standard AIN-76A diet and fed to normal and azoxymethane (AOM)-treated mice. Early changes in colonic mucosa were analyzed, including colonic cell proliferation, apoptotic cell death, cyclin D(1) expression and focal areas of dysplasia (FAD). The findings show that the number of colonic epithelial cells per crypt column increased (P: < 0.01) in each normal mouse group fed the flavonoids; AOM administration increased colonic crypt cell proliferation and resulted in a marked rise of bromodeoxyuridine-labeled cells in the lower proliferative zone of the crypt. Both supplementary dietary quercetin and rutin increased the apoptotic index and caused a redistribution of apoptotic cells along the crypt axis in normal mice fed a standard AIN-76A diet. The number of apoptotic cells/column and apoptotic indices markedly increased (P: < 0.01) in the AOM-treated group compared with untreated animals; apoptotic cells expanded throughout the colonic crypts after flavonoid supplementation and AOM administration. Positive cyclin D(1) expression was detected in mice on diets supplemented either with quercetin (P: < 0.01) or rutin (P: < 0.05). AOM administration resulted in the formation of FAD. Both the number of mice exhibiting FAD and the total numer of FAD observed were significantly reduced (P: < 0.01) in AOM-treated animals fed flavonoids compared with mice maintained on the standard AIN-76A diet. Surprisingly, however, quercetin alone was able to induce FAD in 22% of normal mice fed the standard AIN-76A diet.
Animals↗
Reversal of left ventricular remodeling by synchronous biventricular pacing in heart failure.
Synchronous biventricular pacing is a new nonpharmacological supplemental treatment of advanced heart failure associated with electromechanical conduction delay. However, the role of pacing on left ventricular remodeling is unknown. Eleven patients with New York Heart Association Class III to IV heart failure, a left ventricular ejection fraction < 35%, and a QRS duration > or = 140 ms received a biventricular dual chamber pacemaker. Serial echocardiography, 6-minute hall walk, and Minnesota Living with Heart Failure quality-of-life (QOL) questionnaire were performed before and after up to 3 months of pacing. At 3 months there was a significant increase in fractional shortening (P < 0.001), ejection fraction (P < 0.001), and cardiac output (P < 0.05). The left ventricular end-diastolic volume (245 +/- 70 vs 185 +/- 37 mL, P < 0.05), end-systolic volume (209 +/- 69 vs 140 +/- 44 mL P < 0.05), and mitral regurgitation were reduced (P < 0.05), and diastolic filling time was lengthened (P < 0.05). There were also improvements in heart failure symptoms, an increase in 6-minute walk distance, and a decrease in QOL scores. Synchronous biventricular pacing for 3 months was associated with hemodynamic improvements, reversal of left ventricular remodeling, and increase in left ventricular systolic function, and a decrease in secondary mitral regurgitation.
Cardiac Pacing, Artificial↗
Prevention of ventricular fibrillation by pacing in a man with Brugada syndrome.
The unique ECG appearance of Brugada syndrome is caused by failure of the dome of the action potential to develop. It occurs when the outward currents (mainly Ito) overwhelm the inward currents (mainly Ica) at the end of phase 1 of the action potential. Because Ito becomes less prominent at a faster rate, increased heart rate is associated with decreased ST segment elevation on ECG and probably decreased incidence of ventricular arrhythmia. We present the first report on prevention of ventricular fibrillation in a man with Brugada syndrome by overdrive pacing from his dual chamber implantable cardioverter defibrillator.
Adult↗
Treatment of in-stent coronary restenosis with excimer laser angioplasty.
OBJECTIVE: To evaluate the efficacy and safety of excimer laser coronary angioplasty (ELCA) with adjunctive balloon angioplasty in patient with in-stent restenosis. METHODS: ELCA was performed in 20 patients of instent restenosis. All patients were symptomatic and had class III-IV angina. ELCA was performed with the Spectranetics CVX-300 System. The laser catheter of Vittesse C (concentric) and E (eccentric) with diameter of 1.4-2.0 mm was used. RESULTS: Laser catheter crossed all stenotic stents without difficulty. The lesion length was 4.6-51.2 mm, mean 20.7 +/- 13.7 mm, including 14 lesions > 10 mm. Laser treatment alone increased minimal lumen diameter (MLD) from 0.3 +/- 0.3 mm to 1.4 +/- 0.3 mm (P < 0.0001) and improved the diameter stenosis from 88.8% +/- 10.0% to 46.0% +/- 8.0% (P < 0.0001). Adjunctive balloon angioplasty further increased minimal lumen diameter to 2.3 +/- 0.7 mm and reduced diameter stenosis to 14.2% +/- 8.2% (P < 0.0001). At follow-up (1-17 months, mean 8.9 +/- 5.7 months), 17 (85%) patients had remained asymptomatic, 3 (15%) patients had mild to moderate exertional angina, 1 (5%) patient received CABG. CONCLUSION: ELCA with adjunctive percutaneous transluminal coronary angioplasty (PTCA) is an efficient and safe technique to debulk tissue in the patient with in-stent restenosis. The incidence of procedural related complication was low and ELCA may be used as a good method for in-stent restenosis treatment.
Aged↗