• Food Science and Preservation
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• v.16 no.6
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• pp.875-883
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• 2009

We investigated the effects of manufacturing method on the quality of beef jerky using electron micrography. Six types of beef jerky were prepared by the addition of sugar (A), licorice (B), one of three kinds of spice extract (clove: C, fennel fruit: D, and Chungyang green pepper extract: E), or a mixture of all spice extracts (F). Microstructural changes in beef jerky during preparation by drying, with respect to drying method and the nature of the added spice extract, were observed by scanning electron micrography (SEM) and transmission electron micrography (TEM). The latter technique showed that the microstructure of fresh meat showed actin and myosin in myofibril lines, and also mitochondria and inner membranes. Beef muscle structure was broken at many myofibril lines and decomposition of inner membrane material was evident after seasoning. SEM of air-blast dried beef jerky with added medicinal herb extracts showed both large spaces and regular myofibrils, whereas hot air-dried beef jerky had no spaces and the muscle myofibrils were still evident. After review of all available micrographs from SEM and TEM, we concluded that use of medicinal herb extracts could be helpful in preserving the muscle myofibril structure during drying, and the air-blast drying method is recommended to optimize the textural quality characteristics of beef jerky.

• Tuberculosis and Respiratory Diseases
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• v.44 no.1
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• pp.183-190
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• 1997

Tocolytics are agents widely used in the treatment of premature labor to inhibit uterine contractions. Ritodrine is most commonly used tocolytic agent and acts by increasing intracellular cyclic adenosine monophosphate, which decreases the activity of myosin light-chain kinase, the rate-limiting enzyme in the signal network leading to contraction. Physiologic effects associated with the use of ritodrine are due to their effect on bera-l as well as beta-2 receptors. Some of maternal complications of therapy are rachycardia, hyperglycemia, hypokalemia, lactic acidosis, myocardial ischemia, and pulmonary edema. Tocolytics induced pulmonary edema is a serious complication that can lead to marternal death, although infrequent, The incidence varies from 0.5% to 5% of those receiving these agents. Predisposing factors include the concommitant use of corticosteroid, twin gestation, fluid overload (particularly with saline), and anemia. Several mechanisms have been postulated, but the pathogenesis is uncertain. It is suggested that both types of mechanism, hydrostatic and permeability induced, might be involved. The association of tocolytic therapy with pulmonary edema appears to be unique to the pregnant state, because this complication has never been reported in asthmatic patients exposed to high dosages. We report a case of tocolytic induced pulmonary edema developed in 24 hours after delivery.

• Molecules and Cells
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• v.43 no.11
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• pp.909-920
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• 2020

Cytosolic Ca²⁺ levels ([Ca²⁺]_c) change dynamically in response to inducers, repressors, and physiological conditions, and aberrant [Ca²⁺]_c concentration regulation is associated with cancer, heart failure, and diabetes. Therefore, [Ca²⁺]_c is considered as a good indicator of physiological and pathological cellular responses, and is a crucial biomarker for drug discovery. A genetically encoded calcium indicator (GECI) was recently developed to measure [Ca²⁺]_c in single cells and animal models. GECI have some advantages over chemically synthesized indicators, although they also have some drawbacks such as poor signal-to-noise ratio (SNR), low positive signal, delayed response, artifactual responses due to protein overexpression, and expensive detection equipment. Here, we developed an indicator based on interactions between Ca²⁺-loaded calmodulin and target proteins, and generated an innovative GECI sensor using split nano-luciferase (Nluc) fragments to detect changes in [Ca²⁺]_c. Stimulation-dependent luciferase activities were optimized by combining large and small subunits of Nluc binary technology (NanoBiT, LgBiT:SmBiT) fusion proteins and regulating the receptor expression levels. We constructed the binary [Ca²⁺]_c sensors using a multicistronic expression system in a single vector linked via the internal ribosome entry site (IRES), and examined the detection efficiencies. Promoter optimization studies indicated that promoter-dependent protein expression levels were crucial to optimize SNR and sensitivity. This novel [Ca²⁺]_c assay has high SNR and sensitivity, is easy to use, suitable for high-throughput assays, and may be useful to detect [Ca²⁺]_c in single cells and animal models.

• The Korean Journal of Physiology and Pharmacology
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• v.5 no.4
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• pp.343-351
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• 2001

This study was undertaken to investigate the mechanism of lipopolysaccharide (LPS) and nitric oxide (NO) as a regulator of vascular smooth muscle cell (VSMC) proliferation. VSMC was primarily cultured from rat aorta and confirmed by the immunocytochemistry with anti-smooth muscle myosin antibody. The number of viable VSMCs were counted, and lactate dehydrogenase (LDH) activity was measured to assess the degree of cell death. Concentrations of nitrite in the culture medium were measured as an indicator of NO production. LPS was introduced into the medium to induce the inducible nitric oxide synthase (iNOS) in VSMC, and Western blot for iNOS protein and RT-PCR for iNOS mRNA were performed to confirm the presence of iNOS. Inhibitors of iNOS and soluble guanylate cyclase (sGC), sodium nitroprusside (SNP) and L-arginine were employed to observe the action of LPS on the iNOS-NO-cGMP signalling pathway. LPS and SNP decreased number of VSMCs and increased the nitrite concentration in the culture medium, but there was no significant change in LDH activity. A cell permeable cGMP derivative, 8-Bromo-cGMP, decreased the number of VSMCs with no significant change in LDH activity. L-arginine, an NO substrate, alone tended to reduce cell count without affecting nitrite concentration or LDH level. Aminoguanidine, an iNOS specific inhibitor, inhibited LPS-induced reduction of cell numbers and reduced the nitrite concentration in the culture medium. LY 83583, a guanylate cyclase inhibitor, suppressed the inhibitory actions of LPS and SNP on VSMC proliferation. LPS increased amounts of iNOS protein and iNOS mRNA in a concentration-dependent manner. These results suggest that LPS inhibits the VSMC proliferation via production of NO by inducing iNOS gene expression. The cGMP which is produced by subsequent activation of guanylate cyclase would be a major mediator in the inhibitory action of iNOS-NO signalling on VSMC proliferation.

• The Korean Journal of Pharmacology
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• v.12 no.1
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• pp.23-29
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• 1976

Aconiti tuber butanol fraction has been recently known to have stimulatory effect on myocardial contractility. In the present study, the possibility that the Aconiti tuber butanol fraction acts directly on contractile proteins of myocardium has been investigated using natural actomyosin extracted from dog heart. It revealed that Aconiti tuber butanol fraction in concentrations from $10^{-2}{\sim}10^{-7}\;gm/ml$ had no stimulatory effect on either the $Mg^{++}$ or $Ca^{++}$-activated adenosinetriphosphatase activity of cardiac actomyosin. And no direct $Ca^{++}$-like action of the drug on cardiac actomyosin was also found. Aconiti tuber butanol fraction in concentrations above $10^{-4}\;gm/ml$, however, was somewhat stimulatory on superprecipitation of actomyosin and markedly inhibited the membrane bound $Na^+-K^+$-activated ATPase activity. In these connections, the positive inotropic action of Aconiti tuber butanol fraction on myocardium thus does not seem to reflect a direct interaction with contractile proteins, but the drug seem to stimulate myocardial contractility through the actions on the membrane transport of $Ca^{++}$.

• The Korean Journal of Physiology and Pharmacology
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• v.14 no.1
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• pp.29-35
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• 2010

We have shown that myosin light chain kinase (MLCK) was required for the off-contraction in response to the electrical field stimulation (EFS) of feline esophageal smooth muscle. In this study, we investigated whether protein kinase C (PKC) may require the on-contraction in response to EFS using feline esophageal smooth muscle. The contractions were recorded using an isometric force transducer. On-contraction occurred in the presence of $N^G$-nitro-L-arginine methyl ester (L-NAME), suggesting that nitric oxide acts as an inhibitory mediator in smooth muscle. The excitatory composition of both contractions was cholinergic dependent which was blocked by tetrodotoxin or atropine. The on-contraction was abolished in $Ca^{2+}$-free buffer but reappeared in normal $Ca^{2+}$-containing buffer indicating that the contraction was $Ca^{2+}$ dependent. 4-aminopyridine (4-AP), voltage-dependent $K^+$ channel blocker, significantly enhanced on-contraction. Aluminum fluoride (a G-protein activator) increased on-contraction. Pertussis toxin (a $G_i$ inactivator) and C3 exoenzyme (a rhoA inactivator) significantly decreased on-contraction suggesting that Gi or rhoA protein may be related with $Ca^{2+}$ and $K^+$ channel. ML-9, a MLCK inhibitor, significantly inhibited on-contraction, and chelerythrine (PKC inhibitor) affected on the contraction. These results suggest that endogenous cholinergic contractions activated directly by low-frequency EFS may be mediated by $Ca^{2+}$, and G proteins, such as Gi and rhoA, which resulted in the activation of MLCK, and PKC to produce the contraction in feline distal esophageal smooth muscle.

• Journal of Microbiology and Biotechnology
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• v.13 no.6
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• pp.841-845
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• 2003

In order for engineered tissues to find clinical utility, the engineered tissues must function appropriately. However, smooth muscle (SM) tissues engineered in vitro with a conventional tissue engineering technique may not exhibit contractile functions, because smooth muscle cells (SMCs) cultured in vitro typically revert from a contractile, differentiated phenotype to a synthetic, nondifferentiated phenotype and lose their ability to contract. SMCs in vivo typically reside in mechanically dynamic environments. We hypothesized that cyclic mechanical stretch induces the features of SMCs in in vitro engineered tissues to be similar to those of SMCs in native tissues. To test the hypothesis, aortic SMCs were seeded onto elastic, three-dimensional scaffolds and cultured in vitro under a cyclic mechanical stretching condition for 4 weeks. A significant cell alignment in a direction parallel to the cyclic stretching direction was found in the SM tissues exposed to cyclic stretching. The cellular alignment and alignment direction were consistent with those of native vascular SM tissues, in which SMCs in vivo align in the radial direction (parallel to stretching direction). In control tissues (SM tissues engineered without stretching), cells randomly aligned. The expression of SM ${\alpha}-actin$ and SM myosin heavy chain, phenotypic markers of SMCs in a contractile state, was upregulated in the stretched tissues by 2.5- and 2.0-fold, respectively, compared to SMCs in the control tissues. The cellular features of alignment and contractile phenotype of SMCs in the SM tissues engineered under a mechanically dynamic environment could allow the engineered SM tissues to exhibit contractile functions.

• Journal of Animal Science and Technology
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• v.52 no.4
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• pp.329-336
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• 2010

Myogenic satellite cells (MSCs) are mononuclear, multipotent progenitors of adult skeletal muscle possessing a capacity of forming adipocyte-like cells (ALC). To identify the skeletal muscle type-specific myogenic and adipogenic genes during MSCs differentiation, total RNA was extracted from bovine MSCs, myotube-formed cell (MFC), and ALC from each of Beef shank, Longissimus dorsi, Deep pectoral, and Semitendinosus. DNA microarray analysis (24,000 oligo chip) comparing MSCs with MFC and ALC, respectively, revealed 135 differentially expressed genes (> 4 fold) among four cuts. Real-time PCR confirmed expression of 29 genes. Furthermore, the whole tissue sample RNAs analysis showed 6 differentially expressed genes in Beef shank. Among which, 1 gene in MSCs, 4 in MFC, and 1 in ALCs were highly expressed. This study will provide an insight for better understanding the molecular mechanism of differentiation of skeletal muscle type-specific MSCs. The identified genes may be used as marker to distinguish skeletal muscle types.

• Asian-Australasian Journal of Animal Sciences
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• v.31 no.2
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• pp.301-308
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• 2018

Objective: This study compared the meat quality, muscle fiber characteristics, and fatty acids between Jinjiang yellow cattle (JJ) and F1 Simmental${\times}$Jinjiang yellow cattle (SJ) which were offered the same diet. Methods: Six JJ and six SJ individuals were reared and fattened from 10 to 26 months of age. After feeding, the highrib (HR), ribeye (RB), and tenderloin (TL) samples were taken from the carcass for meat quality evaluations. Results: The results showed that growth performance of SJ was higher than that of JJ (higher live weight and average daily gain), and the hot carcass weight of SJ was higher than that of JJ (p<0.05). pH of JJ was higher than that of SJ in TL (p<0.05); the color of $a^{\ast}$ of SJ was higher than that of JJ in TL and RB (p<0.05); the cooking loss of SJ was significantly lower than that of JJ in TL and RB (p<0.05); the shear force value was significantly lower in SJ compared to JJ (p<0.05); the muscle fiber diameter was higher and the fiber density was lower in SJ compared to JJ in HR and TL (p<0.05); compared to SJ, the muscles of JJ had higher saturated fatty acid (SFA) composition; the sum of monounsaturated fatty acid and polyunsaturated fatty acid (PUFA) were lower in the muscle of JJ; the mRNA expressions of myosin heavy chain-I (MyHC-I) and MyHC-IIa were higher in SJ compared to JJ in muscle of HR and RB; the mRNA expressions of MyHC-IIx and MyHC-IIb were lower in SJ compared to JJ in HR and RB (p<0.05). Conclusion: Meat quality and fatty acid profile differed between SJ and JJ; the muscle of SJ had higher $a^{\ast}$ and SFA; SJ had lower cooking loss, shear force and PUFA compared to the muscle of JJ. In addition, the type and development characteristics of the muscle fiber had some difference between SJ and JJ; these might be factors which caused the differences in meat quality and fatty acid profile between SJ and JJ.

• The Korean Journal of Pain
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• v.29 no.4
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• pp.229-238
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• 2016

Background: The goal of this in vitro study was to investigate the effect of lipid emulsion on vasodilation caused by toxic doses of bupivacaine and mepivacaine during contraction induced by a protein kinase C (PKC) activator, phorbol 12,13-dibutyrate (PDBu), in an isolated endothelium-denuded rat aorta. Methods: The effects of lipid emulsion on the dose-response curves induced by bupivacaine or mepivacaine in an isolated aorta precontracted with PDBu were assessed. In addition, the effects of bupivacaine on the increased intracellular calcium concentration ($[Ca^{2+}]_i$) and contraction induced by PDBu were investigated using fura-2 loaded aortic strips. Further, the effects of bupivacaine, the PKC inhibitor GF109203X and lipid emulsion, alone or in combination, on PDBu-induced PKC and phosphorylation-dependent inhibitory protein of myosin phosphatase (CPI-17) phosphorylation in rat aortic vascular smooth muscle cells (VSMCs) was examined by western blotting. Results: Lipid emulsion attenuated the vasodilation induced by bupivacaine, whereas it had no effect on that induced by mepivacaine. Lipid emulsion had no effect on PDBu-induced contraction. The magnitude of bupivacaine-induced vasodilation was higher than that of the bupivacaine-induced decrease in $[Ca^{2+}]_i$. PDBu promoted PKC and CPI-17 phosphorylation in aortic VSMCs. Bupivacaine and GF109203X attenuated PDBu-induced PKC and CPI-17 phosphorylation, whereas lipid emulsion attenuated bupivacaine-mediated inhibition of PDBu-induced PKC and CPI-17 phosphorylation. Conclusions: These results suggest that lipid emulsion attenuates the vasodilation induced by a toxic dose of bupivacaine via inhibition of bupivacaine-induced PKC and CPI-17 dephosphorylation. This lipid emulsion-mediated inhibition of vasodilation may be partly associated with the lipid solubility of local anesthetics.