Biomedical subjects

C H Fang

Publications and source records attributed to C H Fang.

At least 19 recordsLinked to original sources

PubMed2006

Qualitative identification of tea categories by near infrared spectroscopy and support vector machine.

Near-infrared (NIR) spectroscopy has been successfully utilized for the rapid identification of green, black and Oolong tea. The spectral features of each tea category are reasonably differentiated in the NIR region, and the spectral differences provided enough qualitative spectral information for the identification of tea. Support vector machine (SVM) as the pattern recognition was applied to identify three tea categories in this study. The top five principal components (PCs) were extracted as the input of SVM classifiers by principal component analysis (PCA). The RBF SVM classifiers and the polynomial SVM classifiers were studied comparatively in this experiment. The best experimental results were obtained using the radial basis function (RBF) SVM classifier with sigma=0.5. The accuracies of identification were all more than 90% for three tea categories. Finally, compared with the back propagation artificial neural network (BP-ANN) approach, SVM algorithm showed its excellent generalization for identification results. The overall results show that NIR spectroscopy combined with SVM can be efficiently utilized for rapid and simple identification of the tea categories.

Pattern Recognition, Automated↗

PubMed2006

Feasibility study on identification of green, black and Oolong teas using near-infrared reflectance spectroscopy based on support vector machine (SVM).

Near-infrared (NIR) spectroscopy has been successfully utilized for the rapid identification of green, black and Oolong teas. The spectral features of each category are reasonably differentiated in the NIR region, and the spectral differences provided enough qualitative spectral information for identification. Support vector machine as a pattern recognition was applied to attain the differentiation of the three tea categories in this study. The top five latent variables are extracted by principal component analysis as the input of SVM classifiers. The identification results of the three tea categories were achieved by the RBF SVM classifiers and the polynomial SVM classifiers in different parameters. The best identification accuracies were up to 90%, 100% and 93.33%, respectively, when training, while, 90%, 100% and 95% when test. It was obtained using the RBF SVM classifier with sigma=0.5. The overall results ensure that NIR spectroscopy combined with SVM discrimination method can be efficiently utilized for rapid and simple identification of the different tea categories.

Feasibility Studies↗

PubMed2006

Three dimensional reconstruction of the pancreas based on the virtual Chinese human--female number 1.

OBJECTIVE: To study the three dimensional (3D) reconstruction and 3D visualisation of the pancreas and create anatomy of the digitalised visual pancreas so as to construct a concrete basis for virtual operation and surgical operation on pancreas. METHODS: The digital imaging data of pancreas, duodenum, common bile duct, arteries, and veins were obtained from the virtual Chinese human--female 1 (VCH-F1). The image data were investigated and 380 images ascertained of pancreas picked up from images numbers 2617 to 2996. Finally, the images from number 2574 to 3017 were adopted to segment and processed using ACDSee and Photoshop so as to reconstruct 3D pancreas digitally. The data of pancreatic surfaces were transformed into Visualization Toolkit (VTK). The GUI program written with VC+ was used to display this VTK file and realise 3D visualisation of the pancreas. RESULTS: 3D reconstruction and visualisation of the pancreas and the peri-pancreatic structures (the duodenum, the common bile duct,the inferior vena cava, the portal vein vessels, the aorta, the coeliac trunk vessels) was successful. The 3D and visualised pancreas manifested itself with its complete structure as well as its adjacency to other tissues. CONCLUSION: The 3D reconstruction and 3D visualisation of the pancreas based on the digital data of VCH-F1 produces a digitally visualised pancreas, which promises a novel method for virtual operation on the pancreas, clinical operation on the pancreas, and anatomy of 3D visualised pancreas.

Arteries↗

PubMed2001

Intestinal permeability is reduced and IL-10 levels are increased in septic IL-6 knockout mice.

Sepsis is associated with increased intestinal permeability, but mediators and mechanisms are not fully understood. We examined the role of interleukin (IL)-6 and IL-10 in sepsis-induced increase in intestinal permeability. Intestinal permeability was measured in IL-6 knockout (IL-6 -/-) and wild-type (IL-6 +/+) mice 16 h after induction of sepsis by cecal ligation and puncture or sham operation. In other experiments, mice or intestinal segments incubated in Ussing chambers were treated with IL-6 or IL-10. Intestinal permeability was assessed by determining the transmucosal transport of the 4.4-kDa marker fluorescein isothiocyanate conjugated dextran and the 40-kDa horseradish peroxidase. Intestinal permeability for both markers was increased in septic IL-6 +/+ mice but not in septic IL-6 -/- mice. Treatment of nonseptic mice or of intestinal segments in Ussing chambers with IL-6 did not influence intestinal permeability. Plasma IL-10 levels were increased in septic IL-6 -/- mice, and treatment of septic mice with IL-10 resulted in reduced intestinal permeability. Increased intestinal permeability during sepsis may be regulated by an interaction between IL-6 and IL-10. Treatment with IL-10 may prevent the increase in mucosal permeability during sepsis.

Animals↗

PubMed2000

Degradation of methoxysuccinyl-phe-leu-phe-7-amido-4-trifluoromethyl coumarin (FLF) in cultured myotubes and HepG2 cells is proteasome- and calpain/calcium-dependent.

During recent years, it has become increasingly clear that the ubiquitin-proteasome proteolytic pathway regulates intracellular protein degradation in various physiological and pathophysiological conditions. Substrates specifically degraded by the proteasome are important tools to assess the involvement of the proteasome in cellular proteolysis. It was recently proposed that the membrane permeable substrate methoxysuccinyl-phenylalanine-leucine-phenylalanine-7-amido-4- trifluoromethyl coumarin (FLF) is degraded specifically by the proteasome. The role of other proteolytic pathways in the degradation of FLF, however, is not fully understood. In the present study, we tested the role of different proteolytic pathways in the degradation of FLF in cultured myotubes and HepG2 cells by treating the cells with inhibitors of lysosomal, calpain and proteasome activity. In addition, we tested the hypothesis that insulin blocks proteasome-dependent degradation of FLF in myotubes and HepG2 cells. Results suggest that degradation of FLF in both myotubes and HepG2 cells is regulated by proteasome and calpain activity but not by lysosomal activity. Insulin inhibited proteasome-dependent but not calpain-dependent degradation of FLF in both myotubes and HepG2 cells. The results are important because they suggest that FLF degradation does not specifically reflect proteasome activity.

Animals↗

PubMed2000

Insulin-like growth factor I reduces ubiquitin and ubiquitin-conjugating enzyme gene expression but does not inhibit muscle proteolysis in septic rats.

We examined the effect of insulin-like growth factor I (IGF-I), administered in vivo, on protein turnover rates and gene expression of the ubiquitin-proteasome proteolytic pathway in skeletal muscle of septic rats. Sepsis was induced by cecal ligation and puncture. Other rats were sham-operated. Miniosmotic pumps were implanted sc, and groups of rats received IGF-I (7 mg/kg x 24 h) or saline. Protein synthesis and breakdown rates were determined in incubated extensor digitorum longus muscles. Messenger RNA levels for ubiquitin and the ubiquitin-conjugating enzyme E2(14k) were determined by Northern blot analysis. Sepsis resulted in an approximately 30% reduction of muscle protein synthesis, and this effect of sepsis was blunted in rats treated with IGF-I. In contrast, IGF-I did not prevent the sepsis-induced increase in total and myofibrillar muscle protein breakdown. Ubiquitin and E2(14k) messenger RNA levels were increased several fold in muscle from septic rats, and this effect of sepsis was abolished in IGF-I treated rats. The results suggest that administration of IGF-I may improve sepsis-induced muscle cachexia by stimulating protein synthesis. However, because muscles were resistant to IGF-I, with regard to regulation of protein breakdown, the use of IGF-I to treat muscle cachexia during sepsis remains unclear. An additional important implication of the present study is that changes in messenger RNA levels for ubiquitin and the ubiquitin-conjugating enzyme E2(14k) do not always reflect changes in muscle protein breakdown rates.

Animals↗

PubMed2000

Burn injury upregulates the activity and gene expression of the 20 S proteasome in rat skeletal muscle.

There is evidence that burn injury stimulates ubiquitin-proteasome-dependent protein breakdown in skeletal muscle. In this proteolytic pathway, protein substrates are conjugated to multiple molecules of ubiquitin, whereafter they are recognized, unfolded and degraded by the multicatalytic 26 S protease complex. The 20 S proteasome is the catalytic core of the 26 S protease complex. The influence of burn injury on the expression and activity of the 20 S proteasome has not been reported. We tested the hypothesis that burn injury increases 20 S proteasome activity and the expression of mRNA for the 20 S proteasome subunits RC3 and RC7. Proteolytic activity of isolated 20 S proteasomes, assessed as activity against fluorogenic peptide substrates, was increased in extensor digitorum longus muscles from burned rats. Northern-blot analysis revealed that the expression of mRNA for RC3 and RC7 was increased by 100% and 80% respectively following burn injury. Increased activity and expression of the 20 S proteasome in muscles from burned rats support the concept that burn-induced muscle cachexia is at least, in part, regulated by the ubiquitin-proteasome proteolytic pathway.

Animals↗

PubMed1998

Treatment of burned rats with insulin-like growth factor I inhibits the catabolic response in skeletal muscle.

Thermal injury is associated with a pronounced catabolic response in skeletal muscle, reflecting inhibited protein synthesis and increased protein breakdown, in particular myofibrillar protein breakdown. Administration of insulin-like growth factor I (IGF-I) has a nitrogen-sparing effect after burn injury, but the influence of this treatment on protein turnover rates in skeletal muscle is not known. In the present study, we examined the effect of IGF-I on muscle protein synthesis and breakdown rates following burn injury in rats. After a 30% total body surface area burn injury or sham procedure, rats were treated with a continuous infusion of IGF-I (3. 5 or 7 mg . kg-1 . 24 h-1) for 24 h. Protein synthesis and breakdown rates were determined in incubated extensor digitorum longus muscles. Burn injury resulted in increased total and myofibrillar protein breakdown rates and reduced protein synthesis in muscle. The increase in protein breakdown rates was blocked by both doses of IGF-I and the burn-induced inhibition of muscle protein synthesis was partially reversed by the higher dose of the hormone. IGF-I did not influence muscle protein turnover rates in nonburned rats. The results suggest that the catabolic response to burn injury in skeletal muscle can be inhibited by IGF-I.

Amino Acids↗

PubMed1998

The molecular regulation of protein breakdown following burn injury is different in fast- and slow-twitch skeletal muscle.

We compared the effect of burn injury on the energy-ubiquitin-dependent proteolytic pathway in the fast-twitch extensor digitorum longus (EDL) and the slow-twitch soleus muscle in rats. Rats were subjected to a 30% total body surface area full-thickness burn or sham procedure. At various time points after injury, total and myofibrillar protein breakdown rates were determined in incubated EDL and soleus muscles. The energy-dependent component of protein break-down was determined by incubating muscles in energy-depleting medium. Messenger RNA levels for ubiquitin and RC3, a 20S proteasome subunit, were measured by Northern blot analysis. Burn injury resulted in an approximately 50% increase in total protein breakdown and a 3-4 fold increase in myofibrillar protein breakdown in EDL muscles, and this response reflected increased energy-dependent protein breakdown. In contrast, protein breakdown rates were not significantly influenced by the burn injury in soleus muscles. Ubiquitin mRNA levels were increased almost 10-fold in EDL and approximately 4.5-fold in soleus muscles following burn injury. Burn injury resulted in a 2-fold increase in RC3 mRNA in EDL with no significant changes noted in soleus muscles. The results suggest that the more pronounced effect of burn injury on protein breakdown in fast-twitch than in slow-twitch muscle may reflect different regulation of proteolysis at the molecular level.

Animals↗

PubMed1998

Proteasome blockers inhibit protein breakdown in skeletal muscle after burn injury in rats.

1. Burn injury stimulates ubiquitin-dependent protein breakdown in skeletal muscle. The 20S proteasome is the proteolytic core of the 26S proteasome that degrades ubiquitin conjugates. We examined the effects of the proteasome inhibitors N-acetyl-L-leucinyl-L-leucinal-L-norleucinal (LLnL), lactacystin and beta-lactone on protein breakdown in muscles from burned rats. 2. A full-thickness burn of 30% total body surface area was inflicted on the back of rats. Control rats underwent a sham procedure. After 24 h, extensor digitorum longus muscles were incubated in the absence or presence of 20S proteasome blocker and protein turnover rates and ubiquitin mRNA levels were determined. 3. LLnL resulted in a dose- and time-dependent inhibition of total protein breakdown in incubated muscles from burned rats. Lactacystin and beta-lactone blocked both total and myofibrillar muscle protein breakdown. In addition to inhibiting protein breakdown, LLnL increased ubiquitin mRNA levels, possibly reflecting inhibited proteasome-associated RNase activity. 4. Inhibited muscle protein breakdown caused by LLnL, lactacystin and beta-lactone supports the concept that the ubiquitin-proteasome pathway plays a central role in burn-induced muscle proteolysis. Because the proteasome has multiple important functions in the cell, in addition to regulating general protein breakdown, further studies are needed to test the role of proteasome blockers in the treatment or prevention of muscle catabolism.

Acetylcysteine↗

PubMed1997

Cytokines block the effects of insulin-like growth factor-I (IGF-I) on glucose uptake and lactate production in skeletal muscle but do not influence IGF-I-induced changes in protein turnover.

There is evidence that proinflammatory cytokines are involved in the regulation of muscle protein breakdown in various catabolic conditions but the mechanisms are not fully understood. Previous studies suggest that cytokines reduce circulating and tissue levels of insulin-like growth factor-I (IGF-I) and may block the anabolic effects of the hormone in certain cell types and tissues. We tested the hypothesis that a mixture of tumor necrosis factor alpha, interleukin-1 alpha, and interferon-gamma block the anabolic effects of IGF-I in skeletal muscle. Muscles from burned or unburned rats were incubated in the absence or presence of 1 microgram/mL of IGF-I with or without the addition of the cytokines. As expected, IGF-I stimulated protein synthesis and inhibited protein breakdown in incubated muscles. The cytokines did not influence protein turnover rates in muscles incubated with or without IGF-I. In additional experiments, the effects of IGF-I on glucose uptake and lactate production were tested. IGF-I increased glucose uptake approximately 2.5-fold and stimulated lactate production approximately 5-fold. These effects of the hormone were significantly inhibited by the cytokine mixture. The results suggest that cytokines do not induce protein catabolism by directly inhibiting the anabolic effects of IGF-I in muscle tissue. The inhibitory effects of the cytokines on IGF-I-stimulated glucose transport and lactate production suggest that the lack of effect of cytokines on protein metabolism was not due to a metabolic unresponsiveness of the incubated muscles to the cytokines.

Animals↗

PubMed1996

Linkage of aerobic glycolysis to sodium-potassium transport in rat skeletal muscle. Implications for increased muscle lactate production in sepsis.

Although a linkage between aerobic glycolysis and sodium-potassium transport has been demonstrated in diaphragm, vascular smooth muscle, and other cells, it is not known whether this linkage occurs in skeletal muscle generally. Metabolism of intact hind-leg muscles from young rats was studied in vitro under aerobic incubation conditions. When sodium influx into rat extensor digitorum longus (EDL) and soleus muscles was facilitated by the sodium ionophore monensin, muscle weight gain and production of lactate and alanine were markedly stimulated in a dose-dependent manner. Although lactate production rose in both muscles, it was more pronounced in EDL than in soleus. Monensin-induced lactate production was inhibited by ouabain or by incubation in sodium-free medium. Preincubation in potassium-free medium followed by potassium re-addition also stimulated ouabain-inhibitable lactate release. Replacement of glucose in the incubation medium with pyruvate abolished monensin-induced lactate production but exacerbated monensin-induced weight gain. Muscles from septic or endotoxin-treated rats exhibited an increased rate of lactate production in vitro that was partially inhibited by ouabain. Increases muscle lactate production in sepsis may reflect linked increases in activity of the Na+, K+-ATPase, consumption of ATP and stimulation of aerobic glycolysis.

Aerobiosis↗

PubMed1996

Ciliary neurotrophic factor is catabolic and shares with IL-6 the capacity to induce an acute phase response.

Ciliary neurotrophic factor (CNTF), a member of the interleukin-6 (IL-6) superfamily, has recently been shown to induce several inflammatory responses when administered to healthy animals, including induction of fever and a hepatic acute phase protein response. In the present report, 250 micrograms.kg body wt-1.day-1 of recombinant rat CNTF or murine IL-6 were repeatedly administered to healthy mice over a 7-day period in an effort to compare biological responses. In addition to its in vivo capacity to elicit a hepatic acute phase response, administration of CNTF, but not IL-6, produced profound anorexia and lean tissue wasting in mice. In C57B1/6 mice, 7 days of CNTF administration led to a 21% loss in carcass protein content, resulting from carcass protein breakdown rates being increased 218% over freely fed controls (both P < 0.01). Protein synthesis rates in carcass protein were also increased in CNTF-treated mice compared with both freely fed animals and mice pair-fed equivalent quantities of food. In contrast, administration of equivalent quantities of murine IL-6 had no effect on food intake or body weight in mice, although IL-6 produced a similar hepatic acute phase response, as determined by increases in serum amyloid P and seromucoid fraction and increases in total hepatic protein synthesis. However, when CNTF was coincubated with extensor digitorum longus muscles from juvenile rats in vitro, rates of total muscle and myofibrillar protein degradation and muscle protein synthesis were unchanged. We conclude that CNTF can regulate in vivo both skeletal muscle remodeling as well as the distant anorexia and hepatic acute phase protein responses. In the case of skeletal muscle, these actions are both indirect and independent of the associated anorexia. These properties of CNTF are distinct from IL-6, which when administered to the mouse at these doses is neither anorexigenic nor cachexia producing.

Acute-Phase Proteins↗

PubMed1996

Activation of factor X by factor VIIa complexed with human-mouse tissue factor chimeras requires human exon 3.

In an attempt to define sequence elements in human and mouse tissue factor (TF) that are responsible for the species specificity observed in their interaction with human factor VIIa (HVIIa), we constructed human-mouse chimeric TF cDNAs, inserted them into plasmid vectors, and induced their expression in E. coli. Assays for procoagulant activity were carried out with the resulting E. coli lysates using (HVIIa) human and mouse (MVIIa). The ratio of the procoagulant activities, HVIIa/MVIIa, revealed that human TF exon 3 was essential for activity when the TF:VIIa complex was formed with HVIIa. By ligating the maltose binding protein (MBP) gene to TF cDNAs it was possible to construct, express and purify MBP-TF chimeras as well as to estimate their specific activities. With selected MBP-TF chimeras and HVIIa we determined kinetic parameters for the activation of human factor X. Replacement of exon 3 in human TF cDNA with the corresponding exon from mouse TF cDNA resulted in both lower affinity for HVIIa and failure to convert bound HVIIa into a potent protease.

Amino Acid Sequence↗

PubMed1995

Burn injury stimulates multiple proteolytic pathways in skeletal muscle, including the ubiquitin-energy-dependent pathway.

BACKGROUND: Burn injury is associated with increased muscle protein breakdown. However, the role of different intracellular proteolytic pathways in burn-induced muscle proteolysis is not known. STUDY DESIGN: A 30 percent total body surface area burn injury was inflicted on rats. Total and myofibrillar proteolysis was determined in incubated extensor digitorum longus muscles as release of tyrosine and 3-methylhistidine, respectively. Lysosomal proteolysis was assessed by using the lysosomotropic agents leupeptin and methylamine. Calcium-dependent proteolysis was determined by incubating muscles in the absence or presence of calcium or by blocking the calcium-dependent proteases calpain I and II. Energy-dependent proteolysis was determined in muscles depleted of adenosine triphosphate (ATP) by 2-deoxyglucose and 2,4-dinitrophenol. Muscle ubiquitin messenger RNA (mRNA) was determined by Northern blot analysis to assess ATP-ubiquitin-dependent proteolysis. RESULTS: Calcium-dependent total protein breakdown was stimulated in muscles from burned rats. However, the sensitivity to calcium in vitro was not increased after burn. The lysosomal and energy-dependent components of total protein breakdown were doubled in muscles from burned rats and the energy-dependent myofibrillar protein breakdown was increased almost seven-fold. Ubiquitin mRNA was increased in muscles from burned rats. CONCLUSIONS: Burn injury stimulates multiple proteolytic pathways in skeletal muscle. The ubiquitin-energy-dependent pathway may be particularly important for the breakdown of myofibrillar proteins.

Animals↗

PubMed1995

Influence of burn injury on protein metabolism in different types of skeletal muscle and the role of glucocorticoids.

BACKGROUND: Negative nitrogen balance after burn injury mainly indicates muscle catabolism, but the exact influence of burn on protein synthesis and breakdown in different types of skeletal muscle and the role of glucocorticoids in this metabolic response are unknown. STUDY DESIGN: A 30 percent body surface area flame burn was inflicted on rats. Protein turnover rates were measured in vitro in the white fast-twitch extensor digitorum longus (EDL) muscle and the red slow-twitch soleus muscle. To test the role of glucocorticoids, groups of rats were treated with the glucocorticoid receptor antagonist RU 38486 or vehicle. RESULTS: Burns resulted in reduced protein synthesis and stimulated protein breakdown, in particular myofibrillar protein breakdown, and the changes were substantially more pronounced in the EDL than in the soleus muscle. A burn-induced increase in muscle proteolysis was abolished by treatment with RU 38486, whereas the reduced protein synthesis was not affected by the glucocorticoid receptor antagonist. CONCLUSIONS: The results suggest that the white fast-twitch muscle is more sensitive to the effects of burn injury than the red slow-twitch muscle. Burn-induced muscle proteolysis may be mediated, at least in part, by glucocorticoids, whereas protein synthesis is probably regulated by other mechanisms.

Animals↗

PubMed1993

[The effects of bFGF on the contraction of composite skin grafts].

The authors previously reported that a composite skin graft (CSG) consisting of allodermis graft overlaid with an isogenic epidermis accomplished permanent coverage of a full-thickness skin defect in one operation setting in a rat model. However, the CSG contracted more than the isogenic epidermis alone, presumably due to patchy necrosis of the CSG caused by inadequate blood supply to the isografts. The present study was designed to determine the effects of bFGF on CSG take and its contraction. Rats were divided into two groups. In the tested group the allodermis of CSG was treated with bFGF prior to grafting, while in the control group no treatment was administered. The results showed that the incidence of ischemic necrosis of the isograft was lowered and the area of necrotic patches was lessened in the bFGF group than the control (P < 0.05), and that the contraction of the CSG in the treated group was much less severe than the control as well (P < 0.001). It was found that the extent of necrosis of the CSG was negatively correlated with the resultant area of contraction (r = -0.450, P < 0.05). The study suggests that the ideal results may be obtained when the CSG contracts less than the simple isogenic epidermis graft, provided an optimum treatment modality of CSG by bFGF should be found.

Animals↗

PubMed1991

[Clinical experience of the treatment of ipsilateral femoral shaft fractures after hip arthroplasty].

Femoral shaft fracture after hip arthroplasty is a rate problem. Between January 1983 and January 1989, twelve cases were admitted to Taichung Veteran General Hospital. The causes of the fractures were due to (1) a weakening of the bone stock secondary to stress risers from prior surgery, (2) prefracture evidence of loosening, and (3) high velocity trauma. The twelve cases were treated with different methods and were followed up within an average time of 21.6 months (ranging from 12 to 66 months). After the treatment, it was showed that 83.3% of the patients had satisfactory results (33.3% of the patients has good results and 50% of the patients had fair results.) A comparison of the superiority of different treatment methods and the short term results of this study was presented.

Adult↗