Biomedical subjects

Y Huang

Publications and source records attributed to Y Huang.

At least 199 records · Page 11Linked to original sources

PubMed2001

Variations in transmembrane Ca2+ gradient and apoptosis of macrophages induced by oxidized low density lipoprotein.

While Ca2+ has been proposed to be a messenger in OxLDL-induced cell death, few studies have addressed the possibility that it may influence the occurrence of apoptosis and necrosis of macrophages induced by OxLDL in virtue of change of transmembrane Ca2+ gradient including that across plasma membrane and intracellular organelle membranes. In this paper, various lipophilic Ca2+ fluorescent indicators and specific organelle markers were used to study the relationship between the changes of the transmembrane Ca2+ gradients and the OxLDL induced apoptosis of macrophages. Our results showed that following exposure of low dose OxLDL to macrophages, the transmembrane Ca2+ gradient across the plasma membrane, as well as the membrane-proximal Ca2+ gradient, the transnuclear, and the transmitochondrial membrane Ca2+ gradient were all changed significantly. These data suggested that changes in transmembrane Ca2+ gradients might be involved in the apoptosis of macrophages induced by OxLDL.

Animals↗

PubMed2001

Molecular cloning and characterization of a novel Dehydrogenase/reductase (SDR family) member 1 genea from human fetal brain.

Short-chain dehydrogenases/reductases (SDR) constitute a large protein family of NAD(P)(H)-dependent oxidoreductase. They are defined by distinct, common sequence motifs and show a wide range of substrate specialisms. By large-scale sequencing analysis of a human fetal brain cDNA library, we isolated a novel human SDR-type dehydrogenase/reductase gene named Dehydrogenase/reductase (SDR family) member 1 (DHRS1). The DHRS1 cDNA is 1411 base pair in length, encoding a 314-amino-acid polypeptide which has a SDR motif. Northern blot reveals two bands, of about 0.9 and 1.4 kb in size. These two forms are expressed in many tissues. The DHRS1 gene is localized on chromosome 14q21.3. It has 9 exons and spans 9.2 kb of the genomic DNA.

Amino Acid Sequence↗

PubMed2001

A novel human hydroxysteroid dehydrogenase like 1 gene (HSDL1) is highly expressed in reproductive tissues.

We report the cloning and characterization of a novel human hydroxysteroid dehydrogenase like gene (HSDL1) located on human chromosome 16q24.2. The HSDL1 cDNA is 3407 base pair in length, encoding a 309 amino acid polypeptide related to human 17beta-HSD3. Northern blot reveals that the HSDL1 is highly expressed in testis and ovary. In situ hybridization indicates that the expression of HSDL1 is predominantly increased in the prostate cancer tissue compared with the normal prostate tissue, which suggests that the gene expression is important to the arising of prostate cancer.

Amino Acid Sequence↗

PubMed2001

Familial deletion of (8)(q24.13q24.22) associated with a normal phenotype.

We report a familial deletion of (8q) detected in amniocytes of a fetus with a normal ultrasound and in the phenotypically normal mother, who has now had three pregnancy losses. Chromosome analysis of amniocytes and maternal peripheral blood cells showed an interstitial deletion of (8)(q24.13q24.22), which is distal to the region associated with Langer-Giedion syndrome (LGS) or trichorhinophalangeal (TRP) syndrome. This deletion was confirmed by fluorescence in situ hybridization with a c-myc cosmid clone and chromosome 8 painting library.

Adult↗

PubMed2001

Doc-2/hDab2 expression is up-regulated in primary pancreatic cancer but reduced in metastasis.

SUMMARY: DOC-2/hDab2 (DOC-2) has tumor suppressive functions in ovarian cancer and choriocarcinoma. In these tumors, it negatively influences mitogenic signal transduction of growth factors and blocks ras activity. Pancreatic cancer exhibits a high frequency of K-ras gene mutations; however, it is not known whether DOC-2 expression is altered in these tumors. Therefore, we investigated DOC-2 expression in 22 pancreatic adenocarcinomas and in 6 pancreatic cancer cell lines. Findings in human tumors were compared with normal controls and correlated with clinicopathological data. Additionally, the influence of K-ras on DOC-2 transcription was investigated. Northern blot and Western blot analyses both demonstrated an increase of DOC-2 mRNA and protein levels in primary pancreatic cancers in comparison with normal controls. In situ hybridization showed DOC-2 mRNA expression in the majority of cancer cells of primary tumors, as well as in chronic pancreatitis-like lesions surrounding the cancer mass. Immunohistochemistry mirrored the in situ hybridization findings. In contrast, levels of expression of DOC-2 in lymph node metastases were markedly decreased in comparison with levels in primary tumors. In addition, in 5 metastatic pancreatic cancer cell lines, DOC-2 mRNA and protein levels were low, whereas quantitative RT-PCR demonstrated relatively higher levels in a nonmetastatic pancreatic cancer cell line. In conclusion, DOC-2 is overexpressed in primary pancreatic adenocarcinoma but down-regulated in metastatic disease, suggesting a tumor suppressor function of DOC-2 in the late steps of pancreatic carcinogenesis.

Adaptor Proteins, Signal Transducing↗

PubMed2001

Cloning and characterization of a novel gene (C17orf25) from the deletion region on chromosome 17p13.3 in hepatocelular carcinoma.

Using a combination of hybridization of PAC to a cDNA library and RACE technique, we isolated a novel cDNA, designated as C17orf25 (Chromosome 17 open reading frame 25, previously named it HC71A), from the deletion region on chromosome 17p13.3. The cDNA encodes a protein of 313 amino acids with a calculated molecular mass of 34.8 kDa. C17orf25 is divided into 10 exons and 9 introns, spanning 23 kb of genomic DNA. Northern blot analysis showed that the mRNA expression of C17orf25 was decreased in hepatocellular carcinoma samples as compared to adjacent noncancerous liver tissues from the same patients. The transfection of C17orf25 into the hepatocellular carcinoma cell SMMC7721 and overexpression could inhibit the cell growth. The above results indicate that C17orf25 is a novel human gene, and the cloning and preliminary characterization of C17orf25 is a prerequisite for further functional analysis of this novel gene in human hepatocellular carcinoma.

Amino Acid Sequence↗

PubMed2001

Insulin-like growth factor I and truncated keratinocyte growth factor accelerate healing of left-sided colonic anastomoses.

BACKGROUND: Human full-length keratinocyte growth factor (KGF) promotes healing of colon anastomoses in rats through mechanisms other than enhancement of collagen synthesis. Since insulin-like growth factor (IGF) I increases matrix synthesis, the aim of this study was to evaluate the effect of systemic truncated KGF (tKGF), IGF-I and combined tKGF-IGF-I administration on the healing of colonic anastomoses in rats. METHODS: Rats underwent laparotomy, division of the left colon, and sigmoidosigmoidostomy. tKGF (1 mg/kg), IGF-I (1 mg/kg), tKGF-IGF-I (both 1 mg/kg) or vehicle was administered intraperitoneally in four groups (n = 18 per group) 12 h before surgical intervention, and then once daily until killing (six animals per group; 2, 4 and 6 days after surgery). Bursting pressure measurements, histological evaluation, morphometric analysis, mucin and collagen staining, and 5-bromo-2'-deoxyuridine (BrdU) immunohistochemistry of the anastomotic site were undertaken. RESULTS: Administration of tKGF, IGF-I and the combination of both growth factors significantly increased anastomotic bursting pressure at postoperative day 2 (63, 71 and 113 per cent respectively), day 4 (68, 83 and 80 per cent) and day 6 (48, 43 and 43 per cent) compared with the control group. No intergroup differences were found. Histological examination, mucin and BrdU staining, and measurement of colonic crypt depth indicated less inflammation, increased acidic mucin content, a higher crypt cell proliferation rate and thickened mucosal layer in the growth factor-treated animals than in controls. Enhanced collagen staining was observed only in IGF-treated animals. CONCLUSION: tKGF and IGF-I markedly accelerate the healing of colonic anastomoses in rats. However, combined administration of the two growth factors does not show additional benefit. Both growth factors may be acting to accelerate host reparative processes as well as to enhance protection of the anastomotic wound bed.

Anastomosis, Surgical↗

PubMed2001

Differential judgement of static facial expressions of emotions in three cultures.

Judging facial expressions of emotions has important clinical value in the assessment of psychiatric patients. Judging facial emotional expressions in foreign patients however, is not always easy. Controversy has existed in previous reports on cultural differences in identifying static facial expressions of emotions. While it has been argued that emotional expressions on the face are universally recognized, experimental data obtained were not necessarily totally supportive. Using the data reported in the literature, our previous pilot study showed that the Japanese interpreted many emotional expressions differently from USA viewers of the same emotions. In order to explore such discrepancies further, we conducted the same experiments on Chinese subjects residing in Beijing. The data showed that, similar to the Japanese viewers, Chinese viewers also judged many static facial emotional expressions differently from USA viewers. The combined results of the Chinese and the Japanese experiments suggest a major cross-cultural difference between American and Asian viewers in identifying some static facial emotional expressions, particularly when the posed emotion has negative connotations. The results have important implications for cross-cultural communications when facial emotional expressions are presented as static images.

Adult↗

PubMed2001

t-PA promotes glomerular plasmin generation and matrix degradation in experimental glomerulonephritis.

BACKGROUND: In addition to its well-known role in degrading fibrin, recent evidence suggests that plasmin degrades matrix proteins and activates prometalloproteinases. Plasmin is generated from plasminogen by tissue plasminogen activator (t-PA). We hypothesized that t-PA treatment increases plasmin generation in nephritic glomeruli and degrades pathological matrix leading to a therapeutic reduction in matrix accumulation. METHODS: Anti-Thy-1 nephritis was induced by injection of OX-7 antibody. Rats were given twice daily intravenous injections of saline (disease control group) or human recombinant t-PA (rt-PA; 1 mg/kg body weight) on days 3 through 5. Proteinuria, glomerular matrix protein staining, and glomerular mRNA levels for transforming growth factor-beta 1 (TGF-beta 1), fibronectin, and plasminogen activator inhibitor type 1 (PAI-1) were evaluated at day 6. Localization of rt-PA, plasmin generation by glomeruli in vitro, and glomerular production and content of active TGF-beta1 were also investigated. RESULTS: Compared with disease control animals, proteinuria and staining score for periodic acid-Schiff (2.75 +/- 0.17 vs. 1.41 +/- 0.09), fibronectin-EDA+ (19 +/- 2 vs. 14 +/- 1), laminin (35 +/- 2 vs. 25 +/- 2), type I collagen (33 +/- 1 vs. 21 +/- 3), and type IV collagen (27 +/- 2 vs. 23 +/- 1) were significantly reduced in treated rats (P < 0.01). Glomerular TGF-beta 1, fibronectin, and PAI-1 mRNA levels were unchanged. rt-PA colocalized with fibrin along glomerular capillary walls and in the mesangium. Nephritic glomeruli in vitro had decreased plasmin activity, which was elevated by an in vivo presacrifice injection of rt-PA. Glomerular production and content of active TGF-beta 1 were unchanged by the rt-PA injection. CONCLUSIONS: : These results show that injected rt-PA binds to fibrin in nephritic glomeruli, thus increasing plasmin generation and promoting pathological matrix degradation without activating latent TGF-beta. Agents that increase plasmin generation, such as t-PA, may have potential as antifibrotic therapies.

Animals↗

PubMed2001

Current status of pain management in China: an overview.

China is a large country with a huge population. It is estimated that 1.8 million patients suffer initially from cancer and 1.4 million patients die from it each year in Mainland China. Cancer ranks as the primary reason for death among the common diseases in cities and the second in rural areas. The management of pain is still a critical issue in the care of patients both with cancer and non-cancer pain. A national survey suggested that the fear of addicting patients was still a major barrier for medical professionals in prescribing opioid analgesics. The major reasons for poor management or negative factors of pain relief came from patients' own reasons including their over-concern about addiction to opioid analgesics, their reluctance to report pain and their resistance to use opioid analgesics. Oral long-acting opioids are the most commonly used drugs for third ladder pain management. With policy support from the government, the consumption of morphine for medical purposes has increased significantly for the first time in recent Chinese history as this new cancer pain relief policy has been developed in the country. As a result, the three-step analgesic ladder of the World Health Organization (WHO) has been gradually accepted by medical personnel and patients. Although pain management has been improved since the WHO's strategy of the three-step approach was implemented in China, variations still exist in different regions of the Mainland. Currently the three main aspects of work on pain measurement are going to be undertaken including (1) continuous support from government policy; (2) consistent education and training; and (3) better availability of drugs for medical use throughout the whole country.

Analgesics, Opioid↗

PubMed2001

Effect of inflammatory cytokines on the metabolism of low-density lipoproteins by human vascular endothelial cells.

Cytokines have been shown to activate multiple, varied metabolic pathways in endothelial cells. Little information is available concerning the effects of inflammatory cytokines on lipoprotein metabolism by vascular endothelial cells. Human umbilical vein endothelial cells (HuECs) and bovine aortic endothelial cells (BAECs) were incubated with the inflammatory cytokines recombinant human interleukin-1beta (IL-1), tumor necrosis factor alpha (TNF), interferon gamma (gamma-IF), and interferon beta (beta-IF) at increasing concentrations (0.1 to 1,000 U/mL), for increasing periods (6 to 72 hours). After the incubation period, the media were removed and replaced with serum-free media containing radiolabeled native or acetylated low-density lipoprotein (Ac-LDL) and the rates of degradation and accumulation of radiolabeled LDL were determined. The degradation and accumulation of 125I-LDL were significantly increased (P < .02) in HuECs preincubated with IL-1 (100 U/mL) compared with control incubations without the cytokine or incubations containing gamma-IF, beta-IF, or TNF. This resulted from a 38% increase in LDL receptor protein in cells incubated with IL-1. The increased rate of LDL catabolism by HuECs incubated with IL-1 was accompanied by a significant increase (P < .05) in the rate of cholesteryl ester synthesis in the cells. Cholesteryl ester synthesis rates in HuECs preincubated with gamma-IF, beta-IF, or TNF did not differ significantly from the rates in control incubations. The effect of preincubation with cytokine on the activity of the scavenger receptor was also determined. There were no significant differences in the rate of degradation or accumulation of radiolabeled Ac-LDL in control incubations compared with cultures preincubated with IL-1, gamma-IF, beta-IF, or TNF. There also were no significant differences in the rate of catabolism of native LDL or Ac-LDL in BAECs preincubated with cytokines. Although cytokines have been shown previously to alter the binding of monocytes to endothelial cells, there was no significant increase in the binding of monocytes to cultures incubated with IL-1 plus LDL compared with IL-1 alone. In summary, we now demonstrate that cytokines, specifically IL-1, may alter LDL metabolism by human vascular endothelial cells and alter endothelial cell cholesterol metabolism. These changes in endothelial cell metabolism provide additional evidence supporting the critical role of cytokines in atherogenesis.

Animals↗

PubMed2001

Relaxing effects of Ligstrum purpurascens extract and purified acteoside in rat aortic rings.

The present study describes the effects of an extract obtained from the leaves of Ligstrum purpurascens and acteoside purified from the extract on the contractile response to various agonists in rat isolated aortic rings. L. purpurascens extract relaxed 9,11-dideoxy-11 alpha,9 alpha-epoxymethanoprostaglandin F2 alpha (U46619)-preconstricted rings in a concentration-dependent manner (IC50: 0.14 +/- 0.01 mg/ml with endothelium and 0.16 +/- 0.01 mg/ml without endothelium). The extract also reduced contraction induced by 35 mM K+ or by 1 microM phorbol 12,13-diacetate (PDA) in endothelium-intact rings. The extract (0.1-0.3 mg/ml) reduced the concentration-response to U46619 in normal Krebs solution or to CaCl2 in 35 mM K(+)-containing solution. Acteoside accounts for 2.05% of total L. purpurascens extract in weight. Acteoside induced relaxation of rings preconstricted by U46619 (IC50: 0.22 +/- 0.01 mg/ml) but it caused an increase in 35 mM K(+)-induced tone. Removal of endothelium enhanced the relaxing effect of acteoside. Besides, pretreatment with acteoside inhibited endothelium/nitric oxide-mediated relaxation induced by acetylcholine. These results indicate that acteoside is unlikely the major ingredient responsible for the vasodilator effect of L. purpurascens extract. The extract relaxed the preconstricted aortic rings probably through multiple mechanisms by acting on smooth muscle cells. The inhibitory effect on endothelial nitric oxide-mediated relaxation suggests that acteoside could also act on the endothelial cells to reduce nitric oxide release.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗

PubMed2001

Purification of phenylethanoids from Brandisia hancei and the antiproliferative effects on aortic smooth muscle.

The present study describes the isolation and purification of acteoside, 2'-acetylacteoside, poliumoside and brandioside, four phenylethanoid glycosides from Brandisia hancei. We examined their effects on the proliferation of cultured A7r5 rat aortic smooth muscle cells. The proliferative response was measured from the [(3)H]-thymidine incorporation into DNA. All four glycosides suppressed the proliferative response in the presence of 2 % or 5 % fetal bovine serum in a concentration-dependent manner. The rank order of effectiveness for inhibition of cell proliferation was: brandioside > or = poliumoside > 2'-acetylacteoside > or = acteoside. The acetyl group at position 2' of glucose does not seem necessary for the anti-proliferative effects of acteoside and 2'-acetylacteoside, while the hydroxy groups of the aromatic rings appear to play a role. Inhibition of smooth muscle cell proliferation by phenylethanoids indicates that these compounds may have preventative effects on arteriosclerosis.

Animals↗

PubMed2001

The smooth muscle cell membrane during atherogenesis: a potential target for amlodipine in atheroprotection.

BACKGROUND: Atherosclerotic disease has been present in the human population apparently from the beginning of time. However, it has only been in the 20th century that improvements in the control of infectious diseases have allowed the average life span to increase to the point where atherosclerosis has been able to affect the general population. By the middle of the 20th century, atherosclerosis had reached epidemic levels, and it is currently pandemic and increasing worldwide. Despite its growing significance to health care, we still know relatively little about the cellular basis for plaque genesis in the vessel wall. Current thinking holds that atherosclerosis is caused by an unchecked chronic inflammatory process involving the cells of the arterial wall and their interaction with LDL and various inflammatory cells. Considerable evidence suggests that the principal insults underlying atherogenesis are serum dyslipidemias and oxidative stress mediated primarily by oxidized LDL. However, just how these insults alter the cell biology of vascular cells and lead to the atherosclerotic phenotype is still under intense investigation. Moreover, recent clinical trials have provided evidence that certain classes of drugs, including newer calcium channel blockers (CCBs), can remodel the arterial smooth muscle cell (SMC) membrane and inhibit the progression of atherosclerotic disease. METHODS: This review summarizes our current thinking on atherogenesis in the arterial SMC and considers recent developments regarding alterations in the SMC membrane during the very early period of atherogenesis. We also discuss how certain CCBs might operate to produce atheroprotection. RESULTS: The SMC membrane becomes enriched in unesterified cholesterol soon after the development of serum hypercholesterolemia. With excess membrane cholesterol, the membrane becomes thicker and develops distinct cholesterol domains. These alterations in the membrane increase the permeability of SMC to calcium and induce a variety of alterations in SMC function that contribute to cellular atherogenic processes during plaque genesis. Amlodipine, a third-generation CCB, markedly inhibits the progression of lesions. The explanation of this novel action may lie in the effects of this drug on various potential cellular targets. CONCLUSIONS: Evidence is accumulating that excess membrane cholesterol may contribute to the cellular defects responsible for the transformation of the SMC to the atherosclerotic phenotype. Amlodipine, which has membrane-remodeling properties, is emerging as an important atheroprotective drug.

Amlodipine↗

PubMed2001

Identification of choroidal ovotransferrin as a potential ocular growth regulator.

PURPOSE: In an effort to identify choroidal factors potentially involved in the regulation of ocular growth, proteins released into culture medium of organ-cultured choroids were compared between control eyes and eyes recovering from form deprivation myopia. METHODS: The choroids were obtained from the posterior poles of control and recovering chick eyes, and placed into organ culture containing ( 35)S-methionine/(35)S-cysteine. Culture medium was collected after 24 hours and proteins were separated and identified by SDS-polyacrylamide gel electrophoresis (SDS-PAGE), fluorography, immunoprecipitation, western blot analysis and by amino acid sequencing. Choroidal proteins were tested for their effect on scleral proteoglycan synthesis by measuring (35)SO( 4) incorporation into scleral glycosaminoglycans (GAG) in vitro. Choroidal thickness and axial elongation were measured in control and recovering eyes using high frequency A-scan ultrasound. RESULTS: The synthesis of an 80 kD protein was greatly increased in the choroids of recovering eyes compared with those of control eyes. Amino acid sequencing and immunoprecipitation indicated that the newly synthesized 80 kD protein was ovotransferrin (transferrin, conalbumin). Ovotransferrin release into the culture medium by isolated recovering choroids was associated with a decrease in the rate of axial elongation in recovering eyes. When tested in vitro, ovotransferrin (500 ng/micro) inhibited scleral proteoglycan synthesis in the sclera by 62% in a dose-dependent manner. CONCLUSIONS: Chick choroids of recovering eyes synthesize and release ovotransferrin during the recovery from form deprivation myopia. Ovotransferrin significantly inhibited proteoglycan synthesis by the sclera, indicating that ovotransferrin may play a role in slowing the rate of vitreous chamber elongation and facilitating the recovery from induced myopia.

Amino Acid Sequence↗

PubMed2001

Accumulation and apparent oxidation of cis,trans-18 : 2 isomers relative to linoleic acid in rats.

Dietary cis,trans-18 : 2 isomers impair desaturation and elongation of linoleic acid (Delta9cis,12cis-18 : 2), but little is known of their proportional partitioning between accumulation and oxidation. The present study was therefore designed to assess the accumulation and apparent oxidation of cis,trans-18 : 2 isomers compared with that of trans-18 : 1 isomers and Delta9cis,12cis-18 : 2 in rats. Accumulation is defined as whole-body increase in a fatty acid during a given period (i.e. final body content-initial body content). The apparent oxidation (disappearance) is defined as whole-body utilization of a fatty acid relative to its intake for a given period (intake-excretion-accumulation-longer-chain products)/intakex100). The animals were fed on a diet containing 15 % (w/w) partially hydrogenated rapeseed oil with 1.72 % energy as cis,trans-18 : 2 isomers and varying amounts of Delta9cis,12cis-18 : 2. The apparent oxidation of total cis,trans-18 : 2 isomers (72-76 % dietary intake) was greater than that of Delta9cis,12cis-18 : 2 (38-51 % dietary intake) but it was similar to that of total trans-18 : 1 isomers (78-82 % dietary intake). Among the four isomers, the apparent oxidation of Delta9trans,12trans-18 : 2 was greater than that of the other isomers including Delta9trans,12cis-18 : 2, Delta9cis,12trans-18 : 2 and Delta9cis,13trans-18 : 2. Accumulation of Delta5cis,8cis,11cis,15trans-20 : 4 and Delta5cis,8cis,11cis,14trans-20 : 4 derived from chain-elongation and desaturation of Delta9cis,13trans-18 : 2 and Delta9cis,12trans-18 : 2 was decreased when the dietary Delta9cis,12cis-18 : 2 supply was increased.

Analysis of Variance↗

PubMed2001

Differential effect of PKC isoform on insulin- and phorbol ester-stimulated glucose uptake mechanism in rat adipocytes.

Insulin stimulates glucose uptake in association with phosphatidylinositol (PI) 3-kinase activation mechanisms in rat adipocytes. Insulin stimulated glucose uptake to 6.5-fold, and 12-o-tetradecanoyl phorbol 13-acetate (TPA) also stimulated glucose uptake to 4.5-fold in rat adipocytes. We examined these differences in glucose uptake, PKCzeta activation, and PI 3-kinase activation after stimulation with insulin and TPA. TPA stimulated PI 3-kinase activity and increased the p85 subunit of PI 3-kinase immunoreactivity in anti-phosphotyrosine antibody-immunoprecipitated protein. Insulin and TPA provoked increases in membrane PKCzeta immunoreactivity. The PI 3-kinase inhibitor, wortmannin, suppressed insulin-induced increases in glucose uptake, PI 3-kinase activity, and PKCzeta activation. Wortmannin also suppressed TPA-induced PI 3-kinase activity and PKCzeta activation but suppressed TPA-induced glucose uptake to only a small extent. The PKC inhibitor, Go6976, which only inhibits conventional PKCalpha and _, suppressed TPA-induced glucose uptake, but suppressed insulin-induced glucose uptake to only a small extent. On the other hand, the PKC inhibitor, RO32-0432, which inhibits conventional, novel, and atypical PKCs, markedly suppressed both insulin- and TPA-induced glucose uptake. These results suggest that insulin-induced glucose uptake is mainly mediated by PI 3-kinase-PKCzeta signaling, whereas phorbol ester-induced glucose uptake is mainly mediated by conventional PKC despite PI 3-kinase and PKCzeta activations.

Adipocytes↗

PubMed2001

Quantitative magnetic resonance first-pass perfusion analysis: inter- and intraobserver agreement.

Magnetic resonance first-pass (MRFP) imaging awaits longitudinal clinical trials for quantification of myocardial perfusion. The purpose of this study was to assess inter- and intraobserver agreement of this method. Seventeen MRFP studies (14 rest and 3 under adenosine-induced hyperemia) from 14 patients were acquired. Two observers visually graded study quality. Each study was subdivided into eight regions. Both observers analyzed all 17 studies (8 x 17 = 136 regions) for interobserver agreement. Each observer then analyzed 10 of the 17 studies a second time (2 x 8 x 10 = 160 regions) for intraobserver agreement. Signal intensity curves were obtained with Argus software (Siemens, Iselin, NJ). The maximum amplitude of the impulse response function (Rmax) and the change of signal intensity (deltaSImax) of the contrast bolus were determined. Intraclass correlation coefficient was used to determine intra- and interobserver agreement. The quality was good or excellent in 14 studies. Intraobserver agreement of Rmax and deltaSImax were good (0.85 and 0.80, n = 160). Interobserver agreement of Rmax was fair (0.55, n = 136) but improved after exclusion of poor-quality studies (0.88, n = 112). Interobserver agreement of deltaSImax was good (0.73) and improved less than Rmax with study quality (0.83). Interobserver agreement for Rmax in individual myocardial regions before and after exclusion of studies with poor quality changed most markedly in lateral and posterior regions (0.69 and 0.65 vs. 0.97 and 0.94), where signal-to-noise ratios were reduced compared with anteroseptal regions (p < 0.01). Analysis of MRFP images provides good intraobserver agreement. Interobserver agreement of the quantitative perfusion analysis is good under the premise of good image quality.

Adult↗