• Journal of Animal Science and Technology
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• v.46 no.4
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• pp.585-592
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• 2004

Our previous studies demonstrated that relaxin in concert with estrogen promotes development of the mammary parenchyma during the last third of gestation in gilts, and the specific relaxin-binding sites were present in the mammary gland. This study was conducted to determine if relaxin-binding sites in the mammary gland were functional relaxin receptors. Three cycling cross-bred gilts were bilaterally ovariectomized on day 0 of the experiment. Beginning on day 15 and continuing through day 29 post-surgery, the gilt received an im. injection of estradiol benzoate at 12-hr intervals. Beginning on day 22 post-surgery, highly purified porcine relaxin was administered(lug/hr) into the left fourth mammary gland from the anterior end via miniature osmotic pump. Physiological saline was administered to the right fourth mammary gland. The gilt was sacrificed on day 29 post-surgery and histological characteristics of the mammary parenchyma were examined. The mammary glands treated locally with saline showed little, if any, lobulo-alveolar development, whereas the mammary glands treated with relaxin showed not only marked lobulo-alveolar development but also prominent secretions in the alveoli. The saline-treated glands were characterized by relatively dense and highly organized collagen fiber bundles. Whereas, in the relaxin-treated mammary glands, collagen fiber bundles were dispersed and loosely organized. In conclusion, relaxin-binding sites in the mammary gland are functional relaxin receptors and relaxin acts directly on the pig mammary gland to promote development of the alveoli and remodeling of the extracellular matrix.

• Journal of Life Science
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• v.29 no.5
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• pp.570-579
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• 2019

Diabetes is one of the serious chronic metabolic diseases caused by Westernized eating habits, and the goal of diabetes treatment is to keep blood glucose at a normal level and prevent diabetic complications. This study was designed to investigate the anti-diabetic effects of a mealworm (Tenebrio molitor larva) extract (MWE) on hyperglycemia in an animal model with type 2 diabetes. Diabetic C57BL/Ksj-db/db mice were divided into three groups: diabetic control, rosiglitazone, and MWE. The mice supplemented with MWE showed significantly lower blood levels of glucose and glycosylated hemoglobin when compared with the diabetic control mice. The homeostatic index of insulin resistance was significantly lower in mice supplemented with MWE than in diabetic control mice. MWE supplementation significantly stimulated the phosphorylation of insulin receptor substrate-1 and Akt, and activation of phosphatidylinositol 3-kinase in insulin signaling pathway of skeletal muscles. Eventually, MWE increased the expression of the plasma membrane glucose transporter 4 (GLUT4) via PI3K/Akt activation. These findings demonstrate that the increase in plasma membrane GLUT4 expression by MWE promoted the uptake of blood glucose into cells and relieved hyperglycemia in skeletal muscles of diabetic C57BL/Ksj-db/db mice. Therefore, mealworms are expected to prove useful for the prevention and treatment of diabetes, and further studies are needed to improve type 2 diabetes in the future.

• Korean Journal of Food Science and Technology
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• v.45 no.2
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• pp.148-155
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• 2013

Sulfoxaflor is a new active ingredient within the sulfoximine insecticide class that acts via a unique interaction with the nicotinic receptor. The MRLs (maximun residue limit) of sulfoxaflor in apple and pear are set at 0.4 mg/kg and that in pepper is set at 0.5 mg/kg. The purpose of this study was to develop an analytical method for the determination of sulfoxaflor residues in agricultural commodities using HPLC-UVD and LC-MS. The analysis of sulfoxaflor was performed by reverse phase-HPLC using an UV detector. Acetone and methanol were used for the extraction and aminopropyl ($NH_2$) cartridge was used for the clean-up in the samples. Recovery experiments were conducted on 7 representative agricultural products to validate the analytical method. The recoveries of the proposed method ranged from 82.8% to 108.2% and relative standard deviations were less than 10%. Finally, LC-MS with selected ion monitoring was also applied to confirm the suspected residues of sulfoxaflor in agricultural commodities.

• Korean Journal of Plant Resources
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• v.35 no.5
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• pp.652-658
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• 2022

This study was conducted to induce somatic embryogenic callus (SEC) derived from petals in rose. The petal explants of 3 cultivars ('Ice Wing', 'Orange Eye' and 'Pink Beauty') with different flower colors were placed on three types media (MS, SH and WPM) supplemented with 11 mg/L 2,4-D, respectively, and then cultured in the dark for 47 days. Calluses were formed at explants of all three cultivars. Also, 'Ice Wing', which were cultured in the SH as the basal medium, showed the highest callus formation rate. However, somatic embryos were generated from only petal-derived callus of 'Ice Wing', which were induced on the WPM as the basal medium, transferred it to SH basal medium supplemented with 3 mg/L 2,4-D, and 300 mg/L L-proline, and cultured for 5 weeks. The SEC has been proliferated every four weeks at the subculture interval. In addition, as a results of making a comparison of expression of RhSERK3 and RhSERK4, which is used as signal for generation of somatic embryo from callus in rose, between the SEC and petal-derived callus from 'Ice Wing' by RT-qPCR, the former showed 10 times higher RhSERK3 expression and 700 times higher RhSERK4 expression than the latter.

• Journal of Life Science
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• v.25 no.9
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• pp.993-999
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• 2015

The beetle Popillia flavosellata has been no reported its functional effects. In this study, we investigated the anti-inflammatory effect of P. flavosellata ethanol extract (PFE) on RAW 264.7 mouse macrophage cells treated with lipopolysaccharide (LPS) for the induction of inflammation. First, we examined the cytotoxicity of PFE in the RAW 264.7 cells at a concentration of 2,000 μg/ml or less. To evaluate the anti-inflammatory effects of PFE, we investigated the expression levels of proinflammatory cytokines, such as tumor necrosis factor (TNF)-α and interleukin (IL)-6, and proinflammatory enzymes, such as inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) in LPS-induced RAW 264.7 cells. In addition, we examined whether PFE inhibited the translocation of nuclear factor kappa B (NF-κB) p65 into the nucleus in the LPS-induced RAW 264.7 cells. We found that the protein levels of TNF-α and IL-6 were decreased in the LPS-induced RAW 264.7 cells after the treatment with PFE in a dose-dependent manner. In addition, we confirmed that PFE inhibited the translocation of NF-κB p65 into the nucleus, as well as the protein expression levels of iNOS and COX-2. Accordingly, we propose that PFE exerts an anti-inflammatory effect through the down-regulation of NF-κB p65, TNF-α, IL-6, iNOS, and COX-2 via the toll like receptor (TLR)-4 inflammatory signaling pathway.

• Journal of Chest Surgery
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• v.23 no.3
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• pp.452-464
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• 1990

It is well known that extracellular Calcium plays a very important role in several steps of smooth muscle excitability and contractility, and there have been many concerns about factors influencing the distribution of extracellular Ca++ and the Ca++ flux through the cell membrane of the smooth muscle. Based on the assumption that Mg++ may also play an important role in the excitation and contraction processes of the smooth muscle by taking part in affecting Ca++ distribution and flux, many researches are being performed about the exact role of Mg++, especially in the vascular smooth muscle. But yet the effect of Mg++ in the smooth muscle activity is not clarified, and moreover the mechanism of Mg++ action is almost completely unknown. Present study attempted to clarify the effect of Mg++ on the excitability and contractility in the multiunit and unitary smooth muscle, and the mechanism concerned in it. The preparations used were the guinea-pig aortic strip as the experimental material of the multiunit smooth muscle and the rat uterine strip as the one of the unitary smooth muscle. The tissues were isolated from the sacrificed animal and were prepared for recording the isometric contraction. The effects of Mg++ and Ca++ were examined on the electrically driven or spontaneous contraction of the preparations. And the effects of these ions were also studied on the K+ or norepinephrine contracture. All experiments were performed in tris-buffered Tyrode solution which was aerated with 100% 02 and kept at 35oC. The results obtained were as follows: 1] Mg++ suppressed the phasic contraction induced by electrical field stimulation dose-dependently in the guinea-pig aortic strip, while the high concentration of Ca++ never recovered the decreased tension. These phenomena were not changed by the a - or b - adrenergic blocker. 2]Mg++ played the suppressing effect on the low concentration [20 and 40 mM] of K+-contracture in the aortic muscle, but the effect was not shown in the case of 100mM K+-contracture. 3] Mg++ also suppressed the contracture induced by norepinephrine in the aortic preparation. And the effect of Mg++ was most prominent in the contracture by the lowest [10 mM] concentration of norepinephrine. 4] In both the spontaneous and electrically driven contractions of the uterine strip, Mg++ decreased the amplitude of peak tension, and by the high concentration of Ca++ the amplitude of tension was recovered unlike the aortic muscle. 5] The frequency of the uterine spontaneous contraction increased as the [Ca++] / [Mg++] ratio increased up to 2, but the frequency decreased above this level. 6] Mg++ decreased the tension of the low[20 and 40mM] K+-contracture in the uterine smooth muscle, but the effect did not appear in the 100mM K+-contracture. From the above results, the following conclusion could be made. 1] Mg++ seems to suppress the contractility directly by acting on the smooth muscle itself, besides through the indirect action on the nerve terminal, in both the aortic and uterine smooth muscles. 2] The fact that the depressant effect of Mg++ on the K+-contracture is in inverse proportion to an increase of K+ concentration appears resulted from the extent of the opening state of the Ca++ channel. 3] Mg++ may play a depressant role on both the potential dependent and the receptor-operated Ca++ channels. 4] The relationship between the actions of Mg++ and Ca++ seems to be competitive in uterine muscle and non-competitive in aortic strip.

• Development and Reproduction
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• v.10 no.1
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• pp.55-61
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• 2006

There is growing concern that dietary soy intake is associated with protection of breast cancer. However, questions persist on the potential adverse effects of the main soy constituent genistein(GS) on female reproductive physiology. In this study, we examined whether prepubertal exposure to GS affected on the onset of puberty and the associated reproductive parameters such as hormone receptor expressions in female rats. GS(100mg/kg/day) was administrated daily from postnatal day 25(PND 25) to the day when the first vaginal opening(VO) was observed, and the animals were sacrificed on the day after VO occurred. Gross anatomy and tissue weight were compared to test the GS's effect on the cell proliferation. Furthermore, histological studies were performed to assess the structural alterations in tissues. Specific radioimmunoassay(RIA) were carried out to measure serum LH levels. To determine the transcriptional changes in progesterone receptors(PR), total RNAs were extracted from ovary and uterus and were applied to semi-quantitative reverse transcription polymerase chain reaction(RT-PCR). As a results, advanced VO was shown in the GS group(PND $31.2{\pm}0.6$) compared to the vehicle group (PND $35.3{\pm}0.7$). GS treatment significantly increased wet weight of ovaries and uteri compared to the vehicle group. Increased serum LH levels were also shown in the GS group. Graafian follicles and corpora lutea(CL) were observed only in the ovaries from GS treated animals. Similarly, hypertrophy of luminal and glandular uterine epithelium were found only in the GS group. Collectively, these effects were probably due to the estrogenic effects of GS. In the semi-quantitative RT-PCR studies, the transcriptional activities of PR in both ovary and uterus from GS-treated group were significantly higher than those from the vehicle group. The present studies demonstrated that acute exposure to GS, at levels comparable to the ranges of human exposure, during the critical period of prepubertal stage activates the reproductive system resulting precocious puberty in immature female rats.

• Korean Journal of Microbiology
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• v.46 no.1
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• pp.15-20
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• 2010

Xenotransplantation of pig organs is complicated by the existence of polytropic replication-competent porcine endogenous retroviruses (PERV) capable of infecting human cells. Two classes of infectious human-tropic replication-competent PERVs (PERV-A and PERV-B) and one class of ecotropic PERV-C are known. The potential for recombination between ecotropic PERV-C and human-tropic PERVs adds another level of infectious risk. A recombinant PERV-A/C (PERV-A14/220) virus is 500-fold more infectious than PERV-A. Two determinants of this high infectivity was identified; one was isoleucine-to-valine substitution at position 140 in RBD (receptor binding domain), and the other lies within the PRR (proline rich region) of the envelope protein. To examine whether the effects of the cytoplasmic tail of the PERV-C Env on fusogenesity also influences infectivity, we constructed a pseudotype retroviral vectors containing MoMLV core protein and PERV envelopes. Pseudotyping experiments with the PERV envelope glycoproteins indicated that recombinant PERV-A/C virus is 10-fold more infectious than PERV-A by lacZ staining. This result supports the suggestion that viral transduction of PERV-A/C is enhanced by a membrane-proximal cytoplasmic amphiphilic ${\alpha}$-helix in PERV-C Env tail.

• The Korean Journal of Pharmacology
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• v.28 no.1
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• pp.61-74
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• 1992

Influence of the blockade of the three major pressor systems-sympathetic nervous system (SNS), renin-angiotensin system (RAS) and vasopressin system-on the pressor responsiveness to norepinephrine (NE), angiotensin II (AII), and vasopressin (VP) as well as on basal blood pressure (BP) levels was investigated in urethane-anesthetized rabbits. To block the SNS and RAS, chlorisondamine (CS) and pirenzepine (PZ), sympathetic ganglionic blockers, and enalapril (ENAL), an inhibitor of angiotensin converting enzyme, respectively were used. And for suppressing the VP system bremazocine (BREM), a kappa opiate receptor agonist shown to suppress plasma levels of VP, was employed. Each of CS (0.4 mg/kg), ENAL (2 mg/kg), and BREM (0.25 mg/kg) produced almost same levels of steady hypotensive state. The hypotensive effect of BREM was significantly attenuated by desmopressin, a synthetic VP-like analogue, suggesting the hypotension being at least in part due to suppression of plasma levels of VP. CS, ENAL and BREM elicited further fall of the BP which had been lowered by ENAL or BREM, CS or BREM, and CS or ENAL, respectively. The hypotension produced by both CS and PZ together with either of ENAL or BREM was more marked than that produced by the three drugs other than CS. CS potentiated the pressor response not only to NE but to AII and VP. The pressor effect of AII was increased by ENAL and BREM, too. The pressor response to VP was also enhanced by BREM. Blockade of ${\alpha}-adrenergic$ receptors with phentolamine or phenoxybenzamine potentiated the pressor response to AII and that to VP. The results on basal BP levels indicate that the three major pressor systems are all participating in control of BP, but SNS has the greatest potential for supporting BP. The finding that blockade of one of the pressor systems induced enhanced pressor responsiveness to the pressor hormone of that particular system as well as to the pressor hormone(s) of the other systems(s) provides evidence for important interactions among the three major pressor systems.

• Applied Microscopy
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• v.41 no.4
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• pp.235-248
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• 2011

Traumatic brain injury (TBI) is one of the leading causes of death and disability in children and adults and is a major risk factor for the development of posttraumatic epilepsy (PTE). Recent studies have provided significant insight into the pathophysiological mechanisms underlying the development of epilepsy. Although the link between brain trauma and epilepsy is well recognized, the complex biological mechanisms that result in PTE following TBI have not been fully elucidated. Therefore, this study investigated in order to identify whether or not the abnormal expression of calcium-binding proteins in the lesioned hippocampus plays a role in neuronal damage by brain trauma and whether or not the expressions may change in the contralateral hippocampus during the adaptive stage as early time point following TBI. During early time point following TBI, both parvalbumin (PV) and calbindin D-28k (CB) immunoreactivities were decreased with in the lesioned hippocampus. However, these expressions were recovered to control levels as depend on time courses. On the other hand, PV immunoreactivity in contralateral hippocampus was transiently reduced as compared to the control levels, whereas CB expression was unchanged. These findings indicate that the alterations of the calcium-binding proteins, especially PV and CB, may contribute to the neuronal death and/or damage induced by abnormal inhibitory neurotransmission at early time period following brain trauma and the development of epileptogenesis in patients with traumatic brain injury.