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Biomedical subjects

L Yin

Publications and source records attributed to L Yin.

At least 19 recordsLinked to original sources
PubMed2001

Butyrate suppression of colonocyte NF-kappa B activation and cellular proteasome activity.

Butyrate is derived from the microbial metabolism of dietary fiber in the colon where it plays an important role in linking colonocyte turnover and differentiation to luminal content. In addition, butyrate appears to have both anti-inflammatory and cancer chemopreventive activities. Using confocal microscopy and cell fractionation studies, butyrate pretreatment of a human colon cell line (HT-29 cells) inhibited the tumor necrosis factor-alpha (TNF-alpha)-induced nuclear translocation of the proinflammatory transcription factor NF-kappaB. Butyrate inhibited NF-kappaB DNA binding within 30 min of TNF-alpha stimulation, consistent with an inhibition of nuclear translocation. IkappaB.NF-kappaB complexes extracted from butyrate-treated cells were relatively resistant to in vitro dissociation by deoxycholate, suggesting a change in cellular IkappaB composition. Butyrate treatment increased p100 expression, an IkappaB that was not degraded upon TNF-alpha treatment. Butyrate also reduced the extent of TNF-alpha-induced IkappaB-alpha degradation and enhanced the presence of ubiquitin-conjugated IkappaB-alpha. The suppression of IkappaB-alpha degradation corresponded with a reduction in cellular proteasome activity as determined by in vitro proteasome assays and the increased presence of ubiquitin-conjugated proteins. The butyrate suppression of IkappaB-alpha degradation and proteasome activity may derive from its ability to inhibit histone deacetylases since the specific deacetylase inhibitor trichostatin A had similar effects. These results suggest a potential mechanism for the anti-inflammatory activity of butyrate and demonstrate the interplay between short chain fatty acids and cellular proteasome activity.

Active Transport, Cell Nucleus↗
PubMed2001

The epidermal growth factor receptor regulates interaction of the human DF3/MUC1 carcinoma antigen with c-Src and beta-catenin.

The DF3/MUC1 mucin-like, transmembrane glycoprotein is aberrantly overexpressed in most human carcinomas. The MUC1 cytoplasmic domain interacts with the c-Src tyrosine kinase and thereby increases binding of MUC1 and beta-catenin. In the present work, coimmunoprecipitation studies demonstrate that MUC1 associates constitutively with the epidermal growth factor receptor (EGF-R) in human ZR-75-1 breast carcinoma cells. Immunofluorescence studies show that EGF-R and MUC1 associate at the cell membrane. We also show that the activated EGF-R phosphorylates the MUC1 cytoplasmic tail on tyrosine at a YEKV motif that functions as a binding site for the c-Src SH2 domain. The results demonstrate that EGF-R-mediated phosphorylation of MUC1 induces binding of MUC1 to c-Src in cells. Moreover, in vitro and in vivo studies demonstrate that EGF-R increases binding of MUC1 and beta-catenin. These findings support a novel role for EGF-R in regulating interactions of MUC1 with c-Src and beta-catenin.

Antigens, Neoplasm↗
PubMed2001

The homeodomain proteins PBX and MEIS1 are accessory factors that enhance thyroid hormone regulation of the malic enzyme gene in hepatocytes.

Triiodothyronine (T3) stimulates a robust increase (>40-fold) in transcription of the malic enzyme gene in chick embryo hepatocytes. Previous work has shown that optimal T3 regulation of malic enzyme transcription is dependent on the presence of an accessory element (designated as region E) that immediately flanks a cluster of five T3 response elements in the malic enzyme gene. Here, we have analyzed the binding of nuclear proteins to region E and investigated the mechanism by which region E enhances T3 responsiveness. In nuclear extracts from hepatocytes, region E binds heterodimeric complexes consisting of the homeodomain proteins PBX and MEIS1. Region E contains four consecutive PBX/MEIS1 half-sites. PBX-MEIS1 heterodimers bind the first and second half-sites, the third and fourth half-sites, and the first and fourth half-sites. The configuration conferring the greatest increase in T3 responsiveness consists of the first and fourth half-sites that are separated by 7 nucleotides. Stimulation of T3 response element functions by region E does not require the presence of additional malic enzyme sequences. In pull-down experiments, PBX1a and PBX1b specifically bind the nuclear T3 receptor-alpha, and this interaction is enhanced by the presence of T3. A T3 receptor-alpha region containing the DNA binding domain plus flanking sequences (amino acids 21-157) is necessary and sufficient for binding to PBX1a and PBX1b. These results indicate that PBX-MEIS1 complexes interact with nuclear T3 receptors to enhance T3 regulation of malic enzyme transcription in hepatocytes.

Animals↗
PubMed2001

Defective lymphotoxin-beta receptor-induced NF-kappaB transcriptional activity in NIK-deficient mice.

The role of NF-kappaB-inducing kinase (NIK) in cytokine signaling remains controversial. To identify the physiologic functions of NIK, we disrupted the NIK locus by gene targeting. Although NIK-/- mice displayed abnormalities in both lymphoid tissue development and antibody responses, NIK-/- cells manifested normal NF-kappaB DNA binding activity when treated with a variety of cytokines, including tumor necrosis factor (TNF), interleukin-1 (IL-1), and lymphotoxin-beta (LTbeta). However, NIK was selectively required for gene transcription induced through ligation of LTbeta receptor but not TNF receptors. These results reveal that NIK regulates the transcriptional activity of NF-kappaB in a receptor-restricted manner.

Animals↗
PubMed2001

Divergent N-terminal sequences of a deubiquitinating enzyme modulate substrate specificity.

Ubiquitin-specific processing proteases (UBPs) are characterized by a conserved core domain with surrounding divergent sequences, particularly at the N-terminal end. We previously cloned two isoforms of a testis UBP, UBP-t1 and UBP-t2, which contain identical core regions but distinct N termini that target the two isoforms to different subcellular locations (Lin, H., Keriel, A., Morales, C. R., Bedard, N., Zhao, Q., Hingamp, P., Lefrancois, S., Combaret, L., and Wing, S. S. (2000) Mol. Cell. Biol. 20, 6568-6578). To determine whether the N termini also influence the biochemical functions of the UBP, we expressed UBP-t1, UBP-t2, and the common core domain, UBP core, in Escherichia coli. The three isoforms cleaved branched triubiquitin at >20-fold faster rates than linear diubiquitin, suggesting that UBP-testis functions as an isopeptidase. Both N-terminal extensions inhibited the ability of UBP-core to generate free ubiquitin when linked in a peptide bond with itself, another peptide, or to small adducts. The N-terminal extension of UBP-t2 increased the ability of UBP-core to cleave branched triubiquitin. UBP-core removed ubiquitin from testis ubiquitinated proteins more rapidly than UBP-t2 and UBP-t1. Thus, UBP enzymes appear to contain a catalytic core domain, the activities and specificities of which can be modulated by N-terminal extensions. These divergent N termini can alter localization and confer multiple functions to the various members of the large UBP family.

Amino Acid Sequence↗
PubMed2001

Thyroid hormone stimulates acetyl-coA carboxylase-alpha transcription in hepatocytes by modulating the composition of nuclear receptor complexes bound to a thyroid hormone response element.

Triiodothyronine (T3) stimulates a 7-fold increase in transcription of the acetyl-CoA carboxylase-alpha (ACCalpha) gene in chick embryo hepatocytes. Here, we characterized an ACCalpha T3 response element (ACCalpha-T3RE) with unique functional and protein binding properties. ACCalpha-T3RE activated transcription both in the absence and presence of T3, with a greater activation observed in the presence of T3. In nuclear extracts from hepatocytes incubated in the absence of T3, ACCalpha-T3RE bound protein complexes (complexes 1 and 2) containing the liver X receptor (LXR) and the retinoid X receptor (RXR). In nuclear extracts from hepatocytes incubated in the presence of T3 for 24 h, ACCalpha-T3RE bound a different set of complexes. One complex contained LXR and RXR (complex 3) and another contained the nuclear T3 receptor (TR) and RXR (complex 4). Mutations of ACCalpha-T3RE that inhibited the binding of complexes 1 and 2 decreased transcriptional activation in the absence of T3, and mutations of ACCalpha-T3RE that inhibited the binding of complexes 3 and 4 decreased transcriptional activation in the presence of T3. The stimulation of ACCalpha transcription caused by T3 was closely associated with changes in the binding of complexes 1-4 to ACCalpha-T3RE. These data suggest that T3 regulates ACCalpha transcription by a novel mechanism involving changes in the composition of nuclear receptor complexes bound to ACCalpha-T3RE. We propose that complexes containing LXR/RXR ensure a basal level of ACCalpha expression for the synthesis of structural lipids in cell membranes and that complexes containing LXR/RXR and TR/RXR mediate the stimulation of ACCalpha expression caused by T3.

Acetyl-CoA Carboxylase↗
PubMed2001

Cooking oil fume-induced cytokine expression and oxidative stress in human lung epithelial cells.

Epidemiological studies have shown an association between exposure to indoor air pollution from Chinese-style cooking and risk of lung cancer among Chinese females. Several toxic substances have been identified in cooking oil fumes (COF) collected from heated rapeseed oil. In this study, we examined the biological effects of COF on CL3 human lung epithelial cells. Exposure to 200 microg/ml COF significantly reduced cell growth within 4 days. In addition, we examined the effect of COF on TGFbeta1, TGFbeta2, IL-6, IL-8, and IFN-gamma gene expressions with the RT-PCR method. We found that TGFbeta1 mRNA levels increased after exposure to 200 microg/ml COF for 24 h. Similarly, exposure to 10 microM benzo[a]pyrene or 100 nM 12-O-tetradecanoylphorbol-13-acetate increased TGFbeta1 mRNA levels at 24 h. The mRNA levels of TGFbeta2, IL-6, IL-8, and IFN-gamma did not increase after treatment with COF, benzo[a]pyrene, or 12-O-tetradecanoylphorbol-13-acetate. COF-induced TGFbeta1 production was confirmed by quantification of TGFbeta1 in conditioned medium with enzyme-linked immunosorbent assay. Exposure to 200 microg/ml COF significantly increased TGFbeta1 secretion in a time-dependent and dose-dependent manner. It has been demonstrated that reactive oxygen intermediates induce TGFbeta1 gene expression. When CL3 cells were exposed to 200 microg/ml COF for 15 min, there was an increase in intracellular peroxide formation with the dichlorofluorescein method. Furthermore, treatment with 200 microg/ml COF for 12 h also significantly induced lipid peroxidation in CL3 cells. Our results show that exposure to COF inhibits cell growth, increases TGFbeta1 secretion, and induces oxidative stress in CL3 lung epithelial cells. This suggests that TGFbeta1 and oxidative stress play a role in the biological effects of COF on lung epithelial cells.

Air Pollution, Indoor↗
PubMed2001

The two-in-one model: a new variation of the arteriovenous malformation model in swine.

We report a new variation of the well-established experimental arteriovenous malformation (AVM) model in swine. To provide high flow through the rete mirabile (nidus, RM) and thereby to reduce the rate of spontaneous thrombosis of the AVM, we performed an end-to-end anastomosis of the left common carotid artery (CCA) and the external jugular vein (EJV) microsurgically in three micropigs. After 1 and 4 months the animals underwent angiograms of the CCA and vertebral artery (VA). In all cases the diversion of the blood through the RM was patent, up to the 4 months follow-up. We observed an arteriovenous fistula (arteriovenous pseudomalformation, pAVF) between the VA and the EJV in each case at both 1 and 4 months. This modification of the well-known AVM model in the micropig could be used to monitor long-term changes after embolisation, avoiding the naturally high rate of spontaneous thrombosis. This two-in-one model is thus well suited for preclinical testing of embolic materials.

Animals↗
PubMed2001

Cysteine proprotease colocalizes with vitellogenin in compound granules of the cockroach fat body.

A cysteine proprotease has been identified in developing embryos of the cockroach Blattella germanica and found to be a maternally encoded gene product that is transferred endocytically to the oocyte. The present study aims at establishing how this maternally derived proprotease is synthesized, packaged, and secreted during vitellogenesis. To this end, proprotease was localized immunocytochemically in the fat body of postmating females and its localization compared with that of vitellogenin over the same developmental periods. Fat bodies in cockroaches are comprised of two different cell types: trophocytes and bacteriocytes. Data show that proprotease and vitellogenin come to colocalize in compound granules of the fat body trophocytes. While synthesis of vitellogenin can be traced back to granules resulting from the coalescence of Golgi-derived vesicles in the trophocyte cytoplasm, proprotease appears to be localized predominantly on the cytolysosomes of both trophocytes and bacteriocytes. When probed with an anti-proprotease antiserum, bacteria are also positively labeled, regardless of whether they are segregated inside the cytolysosomes or free in the bacteriocyte cytoplasm. Since vitellogenin and proprotease colocalize within the same cell organelle, it is assumed that Golgi-derived vesicles, which contain vitellogenin, may fuse with cytolysosomes bearing proprotease to yield compound secretory granules. To account for the present observations, the origin and role of proprotease are discussed in relation to the turnover of bacteria in the fat body and to the requirements of endosymbiosis.

Animals↗
PubMed2001

A hierarchical storage management (HSM) scheme for cost-effective on-line archival using lossy compression.

A hierarchical storage management (HSM) scheme for cost-effective on-line archival of image data using lossy compression is described. This HSM scheme also provides an off-site tape backup mechanism and disaster recovery. The full-resolution image data are viewed originally for primary diagnosis, then losslessly compressed and sent off site to a tape backup archive. In addition, the original data are wavelet lossy compressed (at approximately 25:1 for computed radiography, 10:1 for computed tomography, and 5:1 for magnetic resonance) and stored on a large RAID device for maximum cost-effective, on-line storage and immediate retrieval of images for review and comparison. This HSM scheme provides a solution to 4 problems in image archiving, namely cost-effective on-line storage, disaster recovery of data, off-site tape backup for the legal record, and maximum intermediate storage and retrieval through the use of on-site lossy compression.

Algorithms↗
PubMed2001

Skin premature aging induced by tobacco smoking: the objective evidence of skin replica analysis.

Epidemiological studies have showed that heavy smoking causes premature skin aging. Using a silicone rubber replica combined with computerized image processing, an objective measurement of skin's topography, we investigated the association between wrinkle formation and tobacco smoking in this study. The replica analysis was used to study the changes in the surface furrows of the volar forearm in 63 volunteers. Results confirmed that the depth (Rz) and variance (Rv) of furrows were increased and lines of furrows (Rl) were decreased with age. The replica analytic results showed that Rz and Rv in subjects with a smoking history > or =35 pack-years were significantly higher than non-smokers (P<0.05). Rl in subjects with a smoking history were significantly lower than non-smokers (P<0.05). In addition, the present results gave a good correlation between the parameters from the computerized replica analysis with the clinical grading assessment of wrinkles, which further confirmed that skin replica technique is an objective and efficacious tool in evaluation of skin premature aging.

Aged↗
PubMed2001

Skin aging induced by ultraviolet exposure and tobacco smoking: evidence from epidemiological and molecular studies.

BACKGROUND: Tobacco smoking, similar to ultraviolet (UV) A radiation exposure, has previously been identified as an important factor contributing to premature aging of human skin. OBJECTIVE AND DESIGN: To investigate the relationship between these two environmental factors, we have conducted a cross-sectional study of 83 subjects (48 males, 35 females, age range 23-95), in which sun exposure, pack-years of smoking history and potential confounding variables were assessed by questionnaire. Facial wrinkles were quantified using the Daniell score. In order to study the molecular mechanism by which smoking caused wrinkle formation, in vitro studies were conducted to assess the alteration of matrix metalloproteinase-1 (MMP-1) mRNA expression in human fibroblasts stimulated with tobacco smoke extract or/and UVA. RESULTS: Logistic statistic analysis of the data revealed that age [odds ratio (OR)=7.5, 95% confidence interval (CI)=1.87-30.161, pack-years (OR=5.8, 95% CI=1.72-19.87), and sun exposure (OR=2.65, 95% CI=1.0-7.0) independently contributed to facial wrinkle formation. When excessive sun exposure (>2 h/day) and heavy smoking (35 pack-years) occurred together, the risk for developing wrinkles was 11.4 times higher than that of non-smokers and those with less sun exposure (<2 h/day) at the same age. The in vitro studies revealed that MMP-1 expression was significantly increased in fibroblasts after the stimulation with either tobacco smoke extract or UVA. Maximum induction was observed when cells were treated with tobacco smoke extract plus UVA, indicating that the two factors act in an additive manner. MMP-1 induction was significantly higher in the low glutathione (GSH) content fibroblast compared to that in the high GSH fibroblast, indicating that the differences in glutathione content define the susceptibility of fibroblasts towards UV- or tobacco smoking-induced MMP-1 expression. CONCLUSION: Tobacco smoke and UVA cause wrinkle formation independently of each other. We propose that both factors cause aging of human skin through additive induction of MMP-1 expression.

Adult↗
PubMed2001

Intravascular ultrasound Doppler measurement of blood flow velocity.

BACKGROUND AND PURPOSE: The authors investigated the feasibility and accuracy of intravascular Doppler sonography (IVDS) with a newly developed microprobe. METHODS: The known method to determine blood flow velocity by transcutaneous Doppler sonography was transferred to an intravascular usable Doppler probe. With the improved technique, a microprobe measuring 0.3 mm in diameter can be advanced through a 5F catheter used in routine diagnostic angiography to perform intravascular Doppler sonography. In a first step, the conditions for application and measurement were studied in a flow tube model and were transferred in a second step to patients undergoing routine angiography and patients with arterial stenoses. RESULTS: Measurements with nondegassed liquids showed a high intensive acoustic signal, but no echo effect could be recorded in degassed liquids. IVDS of healthy vessels in 40 patients showed the same typical flow pulse curve as seen in transcutaneous measurements. The optimal position of the microprobe with respect to the contact of the vessel wall, the diastolic and systolic phase, and the distance to the tip of the catheter could be evaluated. In 95.6% of the 40 patients with healthy vessels, IVDS was successful. Fourteen patients with arterial stenotic diseases were investigated before and after percutaneous transluminal angioplasty, and the results of these investigations correlated well with the angiographical results. CONCLUSIONS: For percutaneously directly reachable vessels, the transcutaneous Doppler sonography is the choice for easy noninvasive and inexpensive measurement of blood flow velocity. However, for vessels that are difficult or impossible to reach percutaneously, intravascular measurement is a valid procedure.

Angiography↗
PubMed2001

Vasospasm after subarachnoid hemorrhage: interest in diffusion-weighted MR imaging.

BACKGROUND AND PURPOSE: Vasospasm secondary to subarachnoid hemorrhage (SAH) is responsible for severe ischemic complications. Although effective, angioplasty must be performed at a very early stage to produce any clinical recovery. Diagnostic investigations to assess arterial narrowing (transcranial Doppler, angiography) or cerebral perfusion (xenon CT, single-photon emission CT) do not provide evidence of the extent of parenchymal ischemia. In stroke, diffusion-weighted MR imaging (DWI) appears to be the most sensitive procedure to detect cerebral ischemia. We studied asymptomatic vasospasm in patients with aneurysmal SAH to assess whether DWI provides predictive markers of silent ischemic lesions and/or progression toward symptomatic ischemia. METHODS: Seven asymptomatic vasospasm patients (average blood velocity rates >120 cm/s), 3 patients with symptomatic vasospasm, and 4 patients with SAH but without vasospasm were studied at regular intervals by DWI, and their apparent diffusion coefficients (ADCs) were calculated. RESULTS: All patients with vasospasm including those without symptoms presented abnormalities on DWI with a reduction of the ADC prevalently in the white matter. No such abnormalities were observed in patients without vasospasm. The abnormalities on DWI resolved completely in 4 of the 7 patients, with no parenchymal lesion. Resolution was partial in 3 patients whose white matter still presented residual round, focal ischemic lesions. CONCLUSIONS: Being able to correlate abnormalities on DWI with parenchymal involvement in asymptomatic patients would be of considerable clinical significance. It is hoped that larger studies will be undertaken to determine whether the ADC has a reversibility threshold, because this would facilitate patient management.

Adult↗
PubMed2001

[Study of EEG processing system and EEG wavelet transform].

In this paper are reported our studies on the time and frequency characteristics of wavelet transform, the EEG signals processing through wavelet transform, the EEG analysis and reconstruction results. The related EEG processing system design and implementation are given in detail. This system may be applied to EEG feedback research and EEG monitoring.

Computers↗
PubMed2000

Thyroid hormone, glucagon, and medium-chain fatty acids regulate transcription initiated from promoter 1 and promoter 2 of the acetyl-CoA carboxylase-alpha gene in chick embryo hepatocytes.

High-carbohydrate feeding and triiodothyronine (T3) increase the abundance of acetyl-CoA carboxylase-alpha (ACC alpha) mRNA in avian hepatocytes, whereas starvation, glucagon, and medium-chain fatty acids decrease the abundance of ACC alpha mRNA. These changes in ACC alpha mRNA levels are mediated by alterations in the rate of transcription of the ACC alpha gene. In liver, ACC alpha transcription is initiated from two promoters, promoter 1 and promoter 2, resulting in transcripts that contain heterogeneity in their 5'-untranslated regions. Here, we investigated the role of promoter 1 and promoter 2 in mediating nutrient- and hormone-induced changes in ACC alpha mRNA abundance by measuring the level of transcripts expressed from promoter 1 and promoter 2 using a ribonuclease protection assay. The results indicated that both promoter 1 and promoter 2 were regulated by starvation/refeeding in livers of intact chicks and by T3, glucagon, and medium-chain fatty acids in chick embryo hepatocyte cultures and that alterations in the activity of promoter 2 accounted for a greater proportion of the changes in total ACC alpha mRNA abundance caused by nutrient and hormone treatment. Five DNase-hypersensitive sites were also identified between -500 and +1 bp relative to the transcription start site of promoter 2 in livers of intact chicks and in chick embryo hepatocyte cultures. In transient transfection analyses, this region of DNase hypersensitivity conferred regulation of transcription by T3, glucagon, and medium-chain fatty acids in chick embryo hepatocytes. Data from this study demonstrate that diet-induced changes in the activities of promoter 1 and promoter 2 in livers of intact chicks are mimicked in chick embryo hepatocyte cultures by manipulating the concentrations of T3, glucagon and medium-chain fatty acids in the culture medium and that cis-acting sequences mediating the effects of nutrients and hormones on promoter 2 activity are located immediately upstream of the transcription start site of this promoter.

Acetyl-CoA Carboxylase↗
PubMed2000

NF-kappa B regulates transcription of the mouse telomerase catalytic subunit.

Expression of the telomerase catalytic subunit (TERT) is the rate-limiting determinant of telomerase activity in most cells. Analysis of the mouse TERT promoter revealed a potential NF-kappaB binding site 350 base pairs upstream from the translational start site. An oligonucleotide from this region of the TERT promoter bound to proteins in a nuclear extract prepared from a mouse hepatoma cell line. These proteins were identified as NF-kappaB by a number of criteria: 1) the protein complex formed on the TERT oligonucleotide had an electrophoretic mobility similar to that formed on an NF-kappaB consensus oligonucleotide; 2) protein binding to this site was enhanced by NF-kappaB activators tumor necrosis factor-alpha, phorbol 12-myristate 13-acetate, and interleukin-1beta; and 3) the complex was specific and could be supershifted with antibodies against the p50 or p65 NF-kappaB subunits. The NF-kappaB binding site from the mouse TERT promoter activated transcription when fused to a basal SV40 promoter and enhanced the activity of the native TERT promoter in mouse hepatoma cells stimulated with phorbol 12-myristate 13-acetate. Transcriptional activation by the TERT NF-kappaB site could also be enhanced by co-transfection with an NF-kappaB1 expression vector. NF-kappaB may therefore contribute to the activation of TERT expression observed in mouse tissue.

Animals↗