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Biomedical subjects

C L Li

Publications and source records attributed to C L Li.

At least 37 records · Page 2Linked to original sources
PubMed2001

Epidemiology of type 2 diabetes in Taiwan.

In the face of the growing worldwide prevalence of type 2 diabetes, effective methods of preventing further increases in prevalence are needed. In this paper, we review the community-based epidemiologic studies of diabetes in Taiwan published during the last decade, and look at the effectiveness of a two-stage screening protocol for identifying subjects at risk for progression to type 2 diabetes. The results of these studies indicate that the age-adjusted prevalence rate of undiagnosed diabetes in Taiwan is stable, at around 4.0%, while the annual incidence rate is about 1.8%. The results of several studies strongly suggest that a two-step screening strategy, in which only subjects with a fasting plasma glucose level of 5.6-7.8 mmol/l receive the oral glucose tolerance test, may be an effective means of identifying diabetics and persons at high risk for progression to type 2 diabetes and, ultimately, slowing the increase in the prevalence of this disease.

Diabetes Mellitus, Type 2↗
PubMed2001

Functional heterogeneity within rhodamine123(lo) Hoechst33342(lo/sp) primitive hemopoietic stem cells revealed by pyronin Y.

OBJECTIVE: The aim of this study was to determine the function of primitive hematopoietic stem cells (PHSC) at phases G(0) and G(1) of the cell cycle. MATERIALS AND METHODS: A combination of supravital dyes rhodamine123 (Rh), Hoechst33342 (Ho), and pyronin (PY) was used to isolate the G(0) and G(1) subsets of PHSC. A competitive repopulation assay was used to evaluate their in vivo function. RESULTS: We confirmed that the Rh(lo)Lin(-)Kit(+)Sca-1(+) PHSC were relatively quiescent when compared with the more mature Rh(hi)Lin(-)Kit(+)Sca-1(+) HSC and Rh(hi)Lin(-)Kit(+)Sca-1(-) progenitors. In addition, cells with Rh(lo)Lin(-)Kit(+)Sca-1(+), Rh(lo)Ho(lo)Lin(-)Sca-1(+), or Rh(lo)Ho(sp)Lin(-)Sca-1(+) phenotypes identified the same cell population. We further subfractionated the Rh(lo)Ho(lo/sp)Lin(-)Sca-1(+) PHSC using PY into PY(lo) and PY(hi) subsets. Limiting dilution analysis revealed that the frequency of long-term in vivo competitive repopulating units (CRU) of the PY(lo)Rh(lo)Ho(lo/sp) PHSC was 1 in 10 cells, whereas there was at least a three-fold lower frequency in those isolated at the G(1) phase (PY(hi)). We found a dose-dependent PY-mediated cytotoxicity that at moderate concentration affected most of the murine hematopoietic compartment but spared the early HSC compartment. CONCLUSION: Our data confirm that the HSC compartment is hierarchically ordered on the basis of quiescence and further extend this concept to PY-mediated cytotoxicity. PY supravital dye can be used to reveal functional heterogeneity within the Rh(lo)Ho(lo/sp) PHSC population but is of limited use in dissecting the relatively more mature hematopoietic stem/progenitor cell population.

Animals↗
PubMed2001

Tetracaine topical anesthesia for myringotomy.

OBJECTIVES/HYPOTHESIS: To study the efficacy and safety of topical tetracaine anesthesia for office myringotomy and myringotomy with a tube. STUDY DESIGN: Retrospective review of patients undergoing office myringotomy, with or without tube insertion, performed over a 4-year period. METHODS: A topical solution of 8% tetracaine base in 70% isopropyl alcohol was used in 381 ears. Five to 10 drops of the solution were applied to the tympanic membrane for 10 to 15 minutes and aspirated. Myringotomy was performed either with a myringotomy knife or with a CO(2) laser (OtoLAM). RESULTS: Topical tetracaine was used in all 231 ears (100%) undergoing myringotomy without a tube and 150 of 212 ears (71%) undergoing myringotomy with a tube. Tetracaine alone was effective in providing tympanic membrane anesthesia in 95% of myringotomy without a tube (220 ears) and in 93% of myringotomy with a tube (139 ears). There were six complications, including five cases of severe vertigo and one unusual prolonged, transient facial nerve weakness. CONCLUSION: Topical tetracaine is efficacious and safe for use in office myringotomy.

Administration, Topical↗
PubMed2001

Mutations of PTEN/MMAC1 in primary prostate cancers from Chinese patients.

PTEN/MMAC1 is a putative tumor suppressor gene located on 10q23, one of the most frequently deleted chromosomal regions in human prostate cancer. Although mutations of PTEN have often been detected in metastases of prostate cancer, localized tumors have shown lower rates of mutation, which have varied from 0 to 20% among different studies. It is unknown whether the rate of PTEN mutations is different in prostate cancer from Asian men compared with Western men. To further clarify the role of PTEN in prostate cancer and to examine the gene for mutations in Asian men, we analyzed 32 cases of primary prostate cancers from Chinese patients, each of whom was not diagnosed by screening with serum prostate-specific antigen, for PTEN mutations using the methods of tissue microdissection, single-strand conformational polymorphism, and direct DNA sequencing. Seventy % of the tumors were Gleason scores 8-10, whereas the remainder were Gleason score 7. Six metastases of prostate cancer from American patients were also analyzed. Five of 32 (16%) primary prostate cancers from Chinese men and two of six metastases from American men showed mutations in a total of 10 codons of PTEN, which involved exons 1, 2, 5, 8, and 9. Two of the mutations were truncation type, whereas the rest were missense mutations. The mutation frequency in these cases from Asian patients was higher than that in our previous study of cases in radical prostatectomy specimens from American men, in which the 40 primary tumors were lower grade and had been detected by serum prostate-specific antigen test. We conclude that mutation of PTEN occurs more often in primary prostate cancers of Chinese men, whose tumors are high grade and reflective of an unscreened population.

Aged↗
PubMed2001

[Clonning and identification of the gene encoding specific IgE antibody-related antigen of Schistosoma japonicum].

OBJECTIVE: To obtain the gene encoding specific IgE-related antigen of Schistosoma japonicum from the cDNA library of adult Schistosoma japonicum. METHODS: The pooled sera from 15 individuals with high levels of specific IgE antibody against SWAP were absorbed with Protein-G and used for screening of IgE-related antigen from the adult worm cDNA library of Schistosoma japonicum. The inserted cDNA was amplified by PCR and sequenced. According to the first reading frame of the sequence, a pair of new probes, in which EcoR I and Not I sites were incorporated respectively, were designed and used to amplify the target gene. Then, the gene was cloned into vector pGEM-T and subcloned into expression vector pGEX-6p-1. The fusion protein was expressed, analysed by SDS-PAGE and identified by Western blotting with the specific IgE antibody, respectively. RESULTS: The inserted cDNA fragment from the positive clone was about 1,200 bp, with the ORF of 507 bp which encoded 169 amino acids. The deduced molecular weight of the recombinant protein was 19.3 kDa. The homology between the target gene (Sj43B) and other known DNA sequences was less than 40%. The fusion protein expressed by the recombinant vector pGEX-6p-1/Sj43B could be recognized by schistosome specific IgE antibody. CONCLUSION: Sj43B may encode the specific IgE-related antigen of Schistosoma japonicum. The successful construction of recombinant plasmid pGEX-6p-1/Sj43B lay the groundwork for further studies on immunological characteristics and protection immunity of the recombinant protein.

Animals↗
PubMed2001

[Histological evaluation of the biocompatibility of PDLLA membranes].

OBJECTIVE: To evaluate the histological response and biocompatibility of implanted domestic bio-degradable PDLLA membranes in vivo. METHODS: The domestic biodegradable PDLLA membranes and non-degradable ePTFE membranes were in pairs placed subcutaneously in surgical incision made in the dorsum of rats. The tissue responses to these materials were observed histologically at 1, 2, 4, 8 and 12 weeks after placement. RESULTS: The tissue responses of the two kinds of materials were similar to the non-specific reaction mainly infiltrated with lymphocytes, plasmocytes, macrophages, and foreign body giant cells. The polymorphonuclears and foreign body giant cells infiltrated round the ePTFE membranes existed for a relatively long period, in contrast to that of PDLLA membranes. CONCLUSION: Domestic PDLLA membranes with good biocompatibility will be adapted to making GTR into a single step procedure.

English Abstract↗
PubMed2000

NF-kappa B regulates the LPS-induced expression of interleukin 12 p40 in murine peritoneal macrophages: roles of PKC, PKA, ERK, p38 MAPK, and proteasome.

NF-kappa B plays a critical role in coordinating the control of gene expression during monocyte/macrophage activation. In this report we describe our investigation of the mechanisms of LPS-induced NF-kappa B activation and IL-12 expression in murine peritoneal suppressor macrophages. Treatment of these macrophages with LPS induced I kappa B alpha degradation and NF-kappa B activation. EMSAs demonstrated that NF-kappa B bound to a cis-acting element located in the murine IL-12 p40 promoter. LPS signal transduction has been shown to involve a variety of signal pathways. The results in this paper indicate that LPS-induced NF-kappa B binding activity was independent of PKC, PKA, ERK, and p38 MAPK, but was regulated by proteasome. Furthermore, Proteasome Inhibitor I abolished the LPS-induced mRNA expression of IL-12 p35 and p40, and SB203580 reduced these mRNA levels, whereas the blockade of PKC, PKA, and ERK had little effect. These data demonstrate that the LPS-induced activation of proteasome. I kappa B. NF-kappa B and p38 MAPK signal pathways regulate the IL-12 expression in murine peritoneal suppressor macrophages.

Animals↗
PubMed2000

Establishment of human prostate carcinoma skeletal metastasis models.

BACKGROUND: Prostate carcinoma progression from an androgen dependent (AD) state to an androgen independent (AI) state occurs clinically in patients who undergo hormonal therapy. In their laboratory, the authors developed two human prostate carcinoma skeletal metastasis models, the LNCaP progression model and the ARCaP model, to investigate phenotypic and genotypic changes of prostate carcinoma cells during disease progression and to understand molecular pathways for potential therapeutic targeting. METHODS: LNCaP or ARCaP cells were inoculated in athymic mice and were exposed to selective hormonal conditions both in vivo and in vitro. The effects of various hormonal treatment regimens on tumor volumes and distant metastasis and the effects of bone stromal cells on prostate specific antigen (PSA) expression by prostate carcinoma cells were evaluated. RESULTS: The authors propose that prostate carcinoma progression from the AD state to the AI state assumes three AI phenotypes: AI that remains androgen responsive, AI that is unresponsive to androgen stimulation, and AI that is suppressed by or hypersensitive to androgen. AI prostate carcinoma cells interacted reciprocally with osteoblasts to produce enhanced tumor growth and osteoblastic reaction when they are deposited in bone. Bone stromal cell conditioned media stimulated prostate carcinoma cell growth and suppressed its PSA expression, as also evidenced by androgen receptor-mediated transactivation of PSA promoter reporter activity. Conditioned media obtained from prostate carcinoma cells also stimulated osteoblastic cell growth in vitro. A novel gene therapy strategy is being developed to target prostatic tumor epithelium and its supporting stroma using tissue specific and tumor-restricted, promoter-directed toxic gene expression in both cellular compartments. In addition, new strategies are being designed to target the tumor endothelial system in the stroma and tumor cell-extracellular matrix interaction mediated by isotype specific integrins. CONCLUSIONS: Prostate carcinoma skeletal metastasis models may prove useful in developing a new targeting strategy for the prevention and treatment of patients with prostate carcinoma.

Animals↗
PubMed2000

Expression of the Wilms' tumor suppressor gene, WT1, reduces the tumorigenicity of the leukemic cell line M1 in C.B-17 scid/scid mice.

The Wilms' tumor suppressor gene, WT1, encodes a transcription of the Cys2-His2 zinc finger type. Loss of WT1 gene function has been implicated in the development of malignancies including Wilms' tumor and acute leukemias. We have shown previously that ectopic expression of WT1 +KTS isoforms in murine M1 leukemic cells spontaneously induces monocytic differentiation without the requirement for external differentiation-inducing stimuli. To determine whether these observed effects in vitro corresponded to a reduction in tumorigenicity in vivo, parental M1, control M1.Neo, and M1.WT1 +KTS cells were transplanted into C.B-17 scid/scid mice, and the growth and metastatic behavior of the cell lines were monitored for a period of 20 weeks. Mice inoculated either s.c. on the flank or directly into the peritoneal cavity, with M1 cells stably expressing WT1 +KTS isoforms exhibited a marked decrease in tumor formation compared with control groups. Moreover, tumors arising in mice after the injection of M1.WT1 +KTS cells exhibited a loss in ectopic WT1 protein expression. Confirmation that the tumors arose from M1.WT1 +KTS cells was achieved by the amplification of the introduced transgene from tumor samples and indicates that the tumorigenicity of leukemic M1 cells in these animals correlates with a loss in WT1 expression. This investigation is the first to demonstrate the tumor-suppressive effects of WT1 expression in a leukemic cell line, further advancing the notion that WT1 acts as a differentiation-promoting gene during hematopoiesis and that loss of functional WT1 expression may contribute to leukemogenesis in vivo.

Animals↗
PubMed2000

Community-based epidemiological study of glucose tolerance in Kin-Chen, Kinmen: support for a new intermediate classification.

In this population-based survey, we investigated the prevalence of varying degrees of glucose tolerance among residents of Kin-Chen, Kinmen, as well as the association of glucose tolerance status with potential risk factors for type 2 diabetes and cardiovascular disease (CVD). We focused particularly on subjects with normal 2-h postload glucose level (<7.8 mmol/l) but persistent fasting hyperglycemia (PFH) (5.6-7.8 mmol/l), to examine whether PFH represents an intermediate state between normal glucose tolerance (NGT) and impaired glucose tolerance (IGT). The target population comprised 6346 residents aged 30 years and older. A total of 4354 subjects could be classified into categories of NGT, PFH, IGT, new diabetes, and known diabetes according to medical history, fasting plasma glucose levels, and the results of a 75-g oral glucose tolerance test (OGTT). The potential cardiovascular risk factors assessed included age, obesity (general and central), systolic blood pressure, and fasting levels of insulin, C-peptide, triglyceride, cholesterol, and high-density lipoprotein cholesterol (HDL-C). The age-standardized prevalences of PFH, IGT, new diabetes, and known diabetes were 2.9%, 3.5%, 4.0%, and 3.0%, respectively. Among nondiabetic subjects, the cardiovascular risk factor profiles worsened with decreasing glucose tolerance, with most values differing significantly among the NGT, PFH, and IGT groups. Subjects with PFH, who would be classified as having NGT according to conventional WHO criteria, had physical and biochemical features between those of the NGT and IGT groups. These findings support our previous observation that PFH may be a transition state between NGT and IGT in the progression toward type 2 diabetes.

Adult↗
PubMed2000

Oral bioavailability and pharmacokinetics of elimination of 9-hydroxybenzo[a]pyrene and its glucoside and sulfate conjugates after administration to male and female American lobsters, Homarus americanus.

The pharmacokinetics of [(3)H]-9-hydroxybenzo[a]pyrene (9-OH-BaP), a highly lipophilic primary metabolite of benzo(a)pyrene, were examined after intrapericardial (iv) or oral doses of 50 or 200 microg/kg to intermolt American lobsters, Homarus americanus. Combining data for all lobsters, the average terminal elimination half-life of parent 9-OH-BaP was 97.3 h after iv and 56.5 h after oral administration, considerably less than found previously for benzo(a)pyrene (720 h). The oral bioavailability of parent 9-OH-BaP, calculated from the area under the hemolymph concentration curve, was 15.9%. The low bioavailability and variable elimination rates were attributed to extensive first-pass conjugation and sequestration in the hepatopancreas. BaP-9-sulfate was the major metabolite. Hemolymph concentrations of BaP-9-sulfate increased up to one day after the dose, and then decreased, with a terminal elimination half-life of 45 h. BaP 9-beta-D-glucoside was a minor metabolite in most hemolymph and tissue samples; an exception was hemolymph from the iv high-dose group. Concentrations of 9-OH-BaP and metabolites in the edible muscle tissue were similar to those in hemolymph, and 9-OH-BaP residues at 10 to 16 days after the dose were 3 to 12 ng/g muscle. Sulfotransferase and UDP-glucosyltransferase (UGT) activities with 9-OH-BaP were found in the antennal gland, intestinal mucosa, and hepatopancreas (UGT only). Sulfatase activity with BaP-9-sulfate, found in both the hepatopancreas and the antennal gland, was thought to contribute to metabolite cycling. These studies showed that 9-OH-BaP was readily conjugated to sulfate and glucose in the lobster, and that despite their high lipophilicity, 9-OH-BaP and conjugates were excreted from the lobster hemolymph and tissues much more rapidly than benzo[a]pyrene.

Administration, Oral↗
PubMed2000

[Protein kinase B and its role in the signal transduction pathway mediated by phosphoinositide 3-kinase].

Protein kinase B (PKB) is the expression product of a proto-oncongen (c-akt), which is involved in the signaling pathways initiated by some growth factors and mediated by phosphoinositide 3-kinase (PI3K). PKB is a direct target of PI3K. Similar to many protein kinases, PKB has a specific AH/PH domain which can mediate the interaction between signaling molecules. The lipid second messengers, PI-3, 4-P2 and PI-3,4,5-P3 produced by PI3K, can bind to the AH/PH domain of PKB and of PDK (phosphoinositide dependent protein kinase). This binding translocates PKB and PDK to the plasma membrane, and activates them. PKB is also activated via phosphorylation by PDK and, in turn, will activate the anti-apoptotic machinery, glucose metabolism (glycogen synthesis, glycolysis and glucose uptake) and protein synthesis. All these lead to cell growth and proliferation.

3-Phosphoinositide-Dependent Protein Kinases↗
PubMed1999

Loss of heterozygosity and lack of mutations of the XPG/ERCC5 DNA repair gene at 13q33 in prostate cancer.

BACKGROUND: Three regions of chromosome 13 were previously identified for having loss of heterozygosity (LOH) in human prostate cancer. One of them, at 13q33, was defined by LOH at markers D13S158 and D13S280. The XPG/ERCC5 gene, a DNA repair gene that when mutated in the germline leads to xeroderma pigmentosum, has been mapped to 13q33, within one megabase of D13S158 and D13S280. This paper describes LOH and mutational analysis of the XPG gene in human prostate cancers, in order to determine whether the XPG gene is involved in the development of prostate cancer. METHODS: LOH of the XPG gene was analyzed in 40 primary prostate cancers and 14 metastases by using the microsatellite assay, and its mutations were examined in 5 cell lines, 14 metastases, and 8 tumors with LOH at 13q33 by using the single-strand conformation polymorphism (SSCP)-direct DNA sequencing analysis. RESULTS: Four of the 29 (14%) informative primary tumors and 4 of 8 (50%) metastases showed LOH for the XPG gene. Analysis of the 8 tumors with LOH at the 13q33 region, 14 metastases, and 5 cell lines of prostate cancer revealed two polymorphisms but no mutation of the gene. The polymorphism in exon 2 did not change the amino-acid sequence of the XPG protein, but the exon 15 polymorphism altered codon 1104 from histidine to aspartic acid. The two polymorphisms also occurred in individuals without prostate cancer. CONCLUSIONS: LOH at XPG in prostate cancer supports the conclusion that the 13q33 region contains a gene important in the development of prostate cancer, while lack of mutations of the gene suggests that XPG is not the target gene involved.

Adult↗
PubMed1999

Structural and functional abnormalities in the spleen of an mFtz-F1 gene-disrupted mouse.

The spleen has two main functions. The first is to provide a proper microenvironment to lymphoid and myeloid cells, whereas the second involves clearance of abnormal erythrocytes. Ad4BP/SF-1, a product of the mammalian FTZ-F1 gene (mFTZ-F1), was originally identified as a steroidogenic, tissue-specific transcription factor. Immunohistochemical examination of the mammalian spleens confirmed the expression of Ad4BP/SF-1 in endothelial cells of the splenic venous sinuses and pulp vein. In mFtz-F1 gene-disrupted (KO) mice, several structural abnormalities were detected in the spleen, including underdevelopment and nonuniform distribution of erythrocytes. Examination of the spleen of KO fetuses showed failure of development of certain tubular structures during embryogenesis. These structures are normally assembled by Ad4BP/SF-1 immunoreactive cells, and most likely form the vascular system during later stages of development. Other structural abnormalities in the spleen of the KO mice included defects in the tissue distribution of type-IV collagen, laminin, c-kit, and vimentin. These morphologic defects in the vascular system were associated with a decrease in the proportion of hematopoietic cells, although differentiation of these cells was not affected significantly. A high number of abnormal red blood cells containing Howell-Jolly bodies were noted in the KO mice, indicating impaired clearance by the splenic vascular system. We also detected the presence of an mRNA-encoding cholesterol side-chain cleavage P450 in the spleen, resembling the findings in steroidogenic tissues such as the gonads and adrenal cortex. The mRNA transcript was not involved in splenic structural defects as it was detected in the spleens of both normal and KO mice, indicating that the regulatory mechanism of the P450 gene in the spleen is different from that in steroidogenic tissues. Our results indicate that a lack of the mFtz-F1 gene in mice is associated with structural and functional abnormalities of the splenic vascular system.

Animals↗
PubMed1999

Evaluation of endothelial function in hypertensive elderly patients by high-resolution ultrasonography.

BACKGROUND: Multiple investigations, both in experimental models and in middle-aged patients with essential hypertension, demonstrate impaired endothelium-dependent vasodilatation. HYPOTHESIS: We attempted to determine whether hypertension still exerts additional negative effect on endothelial function of large arteries in hypertensive elderly patients who may already be affected by endothelial dysfunction due to aging. METHODS: We compared 13 elderly patients with hypertension [69 +/- 9 years, (mean +/- standard deviation)] with 13 matched healthy elderly subjects (72 +/- 6 years) as controls. Using high-resolution vascular ultrasound, we measured brachial artery responses to reactive hyperemia (with increased flow causing endothelium-dependent dilatation) and sublingual nitroglycerin (causing endothelium-independent dilatation). RESULTS: Flow-mediated dilatation correlated inversely with age (r = -0.60, p = 0.03) in the controls. Flow-mediated dilatation was significantly impaired in hypertensive elderly patients (6.7 +/- 3.3 vs. 13.3 +/- 1.8% in controls, p < 0.0001). No significant difference could found in nitroglycerin-induced dilatation between controls (12.1 +/- 4.9%) and hypertensive elderly patients (10.2 +/- 6.8%, p = 0.5). On multivariate analysis, flow-mediated dilatation in hypertensive elderly patients was inversely related to aging (r = -0.37, p = 0.04) and mean blood pressure (r = -0.57, p = 0.03). CONCLUSIONS: Our study showed decreased flow-mediated dilatation with aging even in the healthy controls, and further decline in flow-mediated dilatation in hypertensive elderly patients compared with controls. This impairment of flow-mediated dilatation in hypertensive elderly patients was related to age and mean blood pressure, indicating that aging and hypertension may independently impair endothelial function in the brachial artery of these patients.

Aged↗
PubMed1999

Comparison of the results between two diagnostic criteria by ADA and WHO among subjects with FPG 5.6-7.8 mmol/l in Kin-Hu and Kin-Chen, Kinmen, 1991-94.

The objective of this study was to compare the results between two diagnostic criteria by ADA (1997) and WHO (1985) among those with fasting plasma glucose (FPG) level 5.6-7.8 mmol/l from a community-based survey in Kin-Hu and Kin-Chen, Kinmen conducted in 1991-94. According to official household registry, 10,797 residents aged over 30 were eligible for screening. 7580 had completed FPG screening and 1855 with FPG 5.6-7.8 mmol/l were invited to receive a 75-g oral glucose tolerance test (OGTT). 78.5% (1456/1855) had completed OGTT. The prevalence of impaired fasting glucose (IFG, by ADA) was 15.7%; the prevalence of impaired glucose tolerance (IGT, by WHO) was 22.7%; the prevalence of undiagnosed diabetes was 7.4% by ADA criteria and 10.9% by WHO criteria. It should be noticed that, among subjects with FPG 5.6-7.8 mmol/l, 50.3% of individuals with undiagnosed diabetes and 67.6% of individuals with IGT by WHO criteria would be missed by ADA criteria. Based on the above findings, the two-step screening strategy using FPG as the first line screening and OGTT for high-risk group (FPG 5.6-7.8 mmol/l) only was recommended in epidemiological study and case finding in consideration of feasibility and validity.

Adult↗