This experiment was carrid out to investigate the interaction between boilelr strains and nutrition levels, and the performances of four broiler strains such as Han Hyup 603, Hubbard, Anak and Filch when they were fed by four different nutrition levels (High Protein and energy; HP. HE., Medium Protein and energy; MP. ME., Low Protein ana energy; LP. LE., and low protein and energy; LLP. LLE.). The data used in this study were obtained from a total of 1200 broiler type chicks in Poultry Testing Station, Korean Poultry Association from June 16, to August 11, 1978. Differences of all characters among four nutrition levels were significant except viability and carcass rate. HP. HE and MP. ME treatments showed nearly the same performances in body weight, feed efficiency and point, spread but they were significantly superior to those of LP. LE and LLP. LLE. There were not significant differences among four strains in feed efficiency and viability but other characters, body weight, point spread and carcass rate were observed that the performance of the best strain B was significantly superior to strain D but it was not recognized significance compared with strain A, C in tile result of statisticel analysis. In the interaction between strains and nutrition levels, body weight at high and levels showed significantly differences but at low and low nutrition levels were nearly same among four strains. Therefore this study demonstrated that comparision of body weights between strains should be performed at medium nutrition level or above. Also point spread calculated as index of body weight and feed efficiency was observed that strain B at low nutrition level is excellently higher than other strains and there were little differences at low nutrition level among all strains. It was found that ]it tie differences between performances of high arid medium levels seemed to be as the reason of high fat addition for energy source to high mutrition feed, and in general superior strain showed good performance at all the nutrition levels in$.$all characters but in body weight and point spread there were significantly different responses with different nutrition level, The most superior strain B among four strains earned the most profit per bird, Although performances of high and medium nutrition levels were nearly the same, medium nutrition level also showed the most profit because the feed cost of high nutrition level was higher than that of medium nutrition level.
To determine the effect of chemical structure of linear amine curing agents on thermal and mechanical properties, standard epoxy resin DGEBA was cured with diaminodiphenyl methane (DDM), diaminodiphenyl sulphone (DDS) in a stoichiometrically equivalent ratio. From this work, the effect of aromatic amine curing agents. In contrast, the results show that the DGEBA/DDS cure system having the sulfone structure between the benzene rings had higher values in the conversion of epoxide, density, shrinkage (%), glass transition temperature, tensile modulus and strength, flexural modulus and strength than the DGEBA/DDM cure system having methylene structure between the benzene rings, whereas the DGEBA/DDM cure system presented higher values in the maximum exothermic temperature, thermal expansion coefficient, and thermal stability. These results are caused by the relative effects of sulfone group having strong electronegativity and methylene group having (+) repulsive property and stem from the effect of the conversion ratio of epoxide group. The result of fractography shows that the each grain size of the DDM/DGEBA system with feather-like structure is larger than that of the DDS/DGEBA system.
Purpose : The human genetic disorder ataxia-telangiectasia (AT) is a multisystem disease characterized by extreme radiosensitivity. The recent identification of the gene mutated in AT, ATM, and the demonstration that it encodes a homologous domain of phosphatidylinositol 3-kinase (PI3-K), the catalytic subunit of an enzyme involved in transmitting signals from the cell surface to the nucleus, provide support for a role of this gene in signal transduction. Although ionizing radiation was known to induce c-fos transcription, nothing is known about how ATM or PKCI mediated signal transduction pathway modulates the c-fos gene transcription and gene expression. Here we have studied the effect of PKCI on radiation sensitivity and c-fos transcription in normal and AT cells. Materials and Methods: Normal (LM217) and AT (AT5BIVA) cells were transfected with PKCI expression plasmid and the overexpression and integration of PKCI was evaluated by northern blotting and polymerase chain reaction, respectively. 5 Gy of radiation was exposed to LM and AT cells transfected with PKCI expression plasmid and cells were harvested 48 hours after radiation and investigated apoptosis with TUNEL method. The c-fos transcription activity was studied by performing CAT assay of reporter gene after transfection of c-fos CAT plasmid into AT and LM cells. Results: Our results demonstrate for the first time a role of PKCI on the radiation sensitivity and c-fos expression in LM and AT cells. PKCI increased radiation induced apoptosis in LM cells but reduced apoptosis in AT cells. The basal c-fos transcription activity is 70 times lower in AT cells than that in LM cells. The c-fos transcription activity was repressed by overexpression of PKCI in LM cells but not in AT cells. After induction of c-fos by Ras protein, overexpression of PKCI repressed c-fos transcription in LM cells but not in AT cells Conclusion: Overexpression of PKCI increased radiation sensitivity and repressed c-fos transcription in LM cells but not in AT cells. The results may be a. reason of increased radiation sensitivity of AT cells. PKCI may be involved in an ionizing radiation induced signal transduction pathway responsible for radiation sensitivity and c-fos transcription. The data also provided evidence for novel transcriptional difference between LM and AT cells.
Impaired insulin secretion from pancreatic beta-cells in response to glucose is an important feature in the pathology of non-insulin-dependent diabetes mellitus (NIDDM). In the course of screening for useful insulin secretagogues, we have isolated and identified YHB-2017 (Genistein) as a insulin secretion potentiator from fermentation broths of our in-house microbial library. The insulinotropic activity of YHB-2017 in isolated rat pancreatic islets was exerted only at high concentration of glucose (8.3-16 mM) but not at low concentration of glucose (3.3-5.5 mM). Also, in perifusion study with isolated rat pancreatic islets, YHB-2017 stimulated insulin secretion in a time-dependent manner when YHB-2017 was added to KRB buffer containing 16 mM glucose. In the presence of $200\;{\mu}M$ diazoxide and 35 mM KCI, which stimulates maximum $Ca^{2+}$ influx independently of KATP channel, YHB-2017 enhanced KATP channel-independent insulin secretion at high concentration glucose (16 mM). To elucidate the mechanisms of the glucose-dependent potentiation effect of YHB-2017, pharmacologic inhibitors for protein kinase A, protein kinase C and calcium/calmodulin kinase II were pre-treated and then the potentiation effect of YHB-2017 on insulin secretion was investigated. Pre-treatment of H89 as a PKA inhibitor had a significant inhibitory effect on YHB-2017-induced potentiation effect. Furthermore, western immunoblotting analyses revealed that YHB-2017 increased phosphorylation of PKA substrates and cAMP response element-binding protein (CREB) under high concentration of glucose. These results demonstrated that the insulinotropic effect of YHB-2017 is mediated through PKA signal pathway and activated amplifying $K_{ATP}$ channel-independent insulin secretion pathway.
In order to produce high concentration of sodium gluconate, optimization of the fermentation conditions, such as glucose concentration, inoculum size, dissolved oxygen concentration and glucose feeding method, was examined. When the glucose concentration was maintained in the range of 30∼50 g/L during the batch fermentation, glucose conversion yield and productivity were 92.2% and 6.0 g/L/hr, respectively. In the case of the low concentration below 30 g/L, the yield decreased by about 25%. As the inoculum size increased above 20%(w/v), lag phase was shortened but the productivity decreased. The dissolved oxygen level of 60∼70% was shown to be the threshold point for 75% of increase in the productivity of sodium gluconate. Finally, optimal glucose feeding rate was determined using various feeding methods such as exponential feeding, feeding based on the average glucose consumption rate and was determined using various feeding methods such as exponential feeding, feeding based on the average glucose consumption rate and on the oxygen uptake rate and etc. Our result shows that glucose feeding, based on the oxygen uptake rate is a very simple, efficient and robust method, especially when oxygen is consumed as a substrate for the bioconversion. Using the above glucose feeding strategy under the optimized condition, 255 g/L of sodium gluconate concentration, 12 g/L/hr of productivity and 95% of glucose conversion yield were achieved with A. niger ACM53.
Journal of the Korean Association of Oral and Maxillofacial Surgeons
/
v.27
no.3
/
pp.214-220
/
2001
The clinical application of the three-dimensional radiographic technique had been limited to standard Broadbent-Bolton cephalometer with biplanar stereoradiography. We developed a new method for compensating the error of head position in ordinary non-biplanar cephalostat. It became to possible to use the three dimensional cephalogram commonly in clinical bases. 1. The method of methemetical compensation of head positioning error in non-biplanar condition was evaluated with dry skull. The error of the method of first and the second trial was $0.46{\pm}1.21$, $0.33{\pm}0.90mm$, which means the error of the head positioning correction in conventional cephalogram was within clinical acceptance. 2. The reproducibility of this system for clinical application was 0.54 mm ($-2.99{\sim}2.26mm$) which defines the absolute mean difference of the first and second trial. Compare to the The landmark identification error $1.2{\pm}1.6mm$, the error of the measurement was within the range of landmark identification error. The result indicates the adequate clinical accuracy of the computation of three-dimensional coordinates by compensation of the error of the head position in ordinary non-biplanar cephalostat.
Rhim, Byung-Yong;Kim, Chi-Dae;Kim, Dong-Heon;Biancani, Piero;Behar, Jose
The Korean Journal of Pharmacology
/
v.32
no.1
/
pp.67-74
/
1996
Cholecystokinin octapeptide (CCK-8), acetylcholine (ACh) and KCl caused a dose dependent contraction in muscle cells enzymatically digested from cat gallbladder. Maximal contraction was obtained at concentration of $10^{-9}M$ for CCK-8, $10^{-5}M$ for ACh and 20mM for KCl. CCK-8 induced contraction was unaffected in calcium free physiological salt solution (PSS) and was completely blocked by strontium substitution for calcium (p<0.001). In contrast, KCl evoked contraction was blocked in calcium free PSS (p<0.01) but was unaffected by strontium replacement of calcium. The contraction elicited by ACh was only slightly reduced in calcium free PSS (p<0.05) and was unaltered by strontium. Muscle cells permeabilized with saponin contracted in response to inositol 1,4.5-trisphosphate $(IP_3)$ and CCK-8. The contraction was blocked by the calmodulin antagonist CGS 9343B (p<0.001), whereas heparin completely blocked the effect of $IP_3$ (p<0.001). The protein kinase C (PKC) antagonist H7 had no effect on either agonist. We conclude that CCK-8 induced gallbladder muscle contraction is mediated by $IP_3$ dependent intracellular calcium release from intracellular stores and a calmodulin dependent pathway; ACh may utilize both extracellular and intracellular calcium. KCl causes muscle contracrion through influx of extracellular calcium and a calmodulin independent machanism.
Stimulation of mast cells through the high affinity IgE receptor (Fc${\varepsilon}$RI) induces degranulation, lipid mediator release, and cytokine secretion leading to allergic reactions. Although various signaling pathways have been characterized to be involved in the Fc${\varepsilon}$RI-mediated responses, little is known about the precious mechanism for the expression of tumor necrosis factor-${\alpha}$ (TNF-${\alpha}$) in mast cells. Here, we report that rapamycin, a specific inhibitor of mammalian target of rapamycin (mTOR), reduces the expression of TNF-${\alpha}$ in rat basophilic leukemia (RBL-2H3) cells. IgE or specific antigen stimulation of RBL-2H3 cells increases the expression of TNF-${\alpha}$ and activates various signaling molecules including S6K1, Akt and p38 MAPK. Rapamycin specifically inhibits antigeninduced TNF-${\alpha}$ mRNA level, while other kinase inhibitors have no effect on TNF-${\alpha}$ mRNA level. These data indicate that mTOR signaling pathway is the main regulation mechanism for antigen-induced TNF-${\alpha}$ expression. TNF-${\alpha}$ mRNA stability analysis using reporter construct containing TNF-${\alpha}$ adenylate/uridylate-rich elements (AREs) shows that rapamycin destabilizes TNF-${\alpha}$ mRNA via regulating the AU-rich element of TNF-${\alpha}$ mRNA. The antigen-induced activation of S6K1 is inhibited by specific kinase inhibitors including mTOR, PI3K, PKC and $Ca^{2+}$chelator inhibitor, while TNF-${\alpha}$ mRNA level is reduced only by rapamycin treatment. These data suggest that the effects of rapamycin on the expression of TNF-${\alpha}$ mRNA are not mediated by S6K1 but regulated by mTOR. Taken together, our results reveal that mTOR signaling pathway is a novel regulation mechanism for antigen-induced TNF-${\alpha}$ expression in RBL-2H3 cells.
Purpose: Thyroglobulin (Tg) is a valuable and sensitive tool as a marker for diagnosis and follow-up for several thyroid disorders, especially, in the follow-up of patients with differentiated thyroid cancer (DTC). Often, clinical decisions rely entirely on the serum Tg concentration. But the Tg assay is one of the most challenging laboratory measurements to perform accurately owing to antithyroglobulin antibody (Anti-Tg). In this study, we have compared the degree of Anti-Tg effects on the measurement of Tg between availale Tg measuring kits. Materials and Methods: Measurement of Tg levels for standard Tg solution was performed with two different kits commercially available (A/B kits) using immunoradiometric assay technique either with absence or presence of three different concentrations of Anti-Tg. Measurement of Tg for patient's serum was also performed with the same kits. Patient's serum samples were prepared with mixtures of a serum containing high Tg levels and a serum containg high Anti-Tg concentrations. Results: In the measurements of standard Tg solution, presence of Anti-Tg resulted in falsely lower Tg level by both A and B kits. Degree of Tg underestimation by h kit was more prominent than B kit. The degree of underestimation by B kit was trivial therefore clinically insignificant, but statistically significant. Addition of Anti-Tg to patient serum resulted in falsely lower Tg levels with only A kit. Conclusion: Tg level could be underestimated in the presence of anti-Tg. Anti-Tg effect on Tg measurement was variable according to assay kit used. Therefore, accuracy test must be performed for individual Tg-assay kit.
Background : Phospholipase C(PLC) plays an important role in cellular signal transduction and is thought to be critical in cellular growth, differentiation and transformation of certain malignancies. Two second messengers produced from the enzymatic action of PLC are diacylglycerol (DAG) and inositol 1, 4, 5-trisphosphate (IP3). These two second messengers are important in down stream signal activation of protein kinase C and intracellular calcium elevation. In addition, functional domains of the PLC isozymes, such as Src homology 2 (SH2) domain, Src homology 3 (SH3) domain, and pleckstrin homology (PH) domain play crucial roles in protein translocation, lipid membrane modificailon and intracellular memrane trafficking which occur during various mitogenic processes. We have previously reported the presence of PLC-${\gamma}1$, ${\gamma}2$, ${\beta}1$, ${\beta}3$, and ${\delta}1$ isozymes in normal human lung tissue and tyrosine-kinase-independent activation of phospholipase C-${\gamma}$ isozymes by tau protein and AHNAK. We had also found that the expression of AHNAK protein was markedly increased in various mstologic types of lung can∞r tissues as compared to the normallungs. However, the report concerning expression of various PLC isozymes in lung canærs and other lung diseases is lacking. Therefore, in this study we examined the expression of PLC isozymes in the paired surgical specimens taken from lung cancer patients. Methods : Surgically resected lung cancer tissue samples taken from thirty seven patients and their paired normal control lungs from the same patients, The expression of various PLC isozymes were studied. Western blot analysis of the tissue extracts for the PLC isozymes and immunohistochemistry was performed on typical samples for localization of the isozyme. Results : In 16 of 18 squamous cell carcinomas, the expression of PLC-${\gamma}1$ was increased. PLC-${\gamma}1$ was also found to be increased in all of 15 adenocarcinoma patients. In most of the non-small cell lung cancer tissues we had examined, expression of PLC-${\delta}1$ was decreased. However, the expression of PLC-${\delta}1$ was markedly increased in 3 adenocarcinomas and 3 squamous carcinomas. Although the numbers were small, in all 4 cases of small cell lung cancer tissues, the expression of PLC-${\delta}1$ was nearly absent. Conclusion : We found increased expression of PLC-${\gamma}1$ isozyme in lung cancer tissues. Results of this study, taken together with our earlier findings of AHNAK protein-a putative PLD-${\gamma}$, activator-over-expression, and the changes observed in PLC-${\delta}1$ in primary human lung cancers may provide a possible insight into the derranged calcium-inositol signaling pathways leading to the lung malignancies.
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