• The Korean Journal of Physiology
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• v.20 no.1
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• pp.1-7
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• 1986

It has been well documented that the peripheral autonomic nervous system plays an important role in exocrine pancreatic secretion. However, the role of the central nervous system in pancreatic function is still obscure even though the central nervous system has been known to control gastrointestinal functions through the autonomic nervous system. Since the reticular formation in the mesencephalone seems to integrate the autonomic function, the present study was undertaken to investigate a possible influence of the reticular formation upon the exocrine pancreatic secretion. Twenty·two albino rats fasted for 24 hours were anesthetized by intraperitoneal injection of urethane in a dose of 1 g/kg, The pancreatic duct was cannulated to collect pancreatic juice and bile juice was diverted to the jejunum. The gastroduodenal junction was ligated to Prevent passage of gastic juice into the duodenum. A pair of electrodes were bilaterally inserted in the reticualr formation of the mesencephalone with aid of a stereotaxic apparatus. When the volume of pancreatic juice secreted for 10 min became constant, the reticular formation was electrically stimulated for 10 min. Parameters of the electical stimulation was 1.3V, 40 Hz and 2 msec. When the pancreatic secretion returned to the level before the electrical stimulation, cervical vagotomy (11 rats) or administration of propranolol (11 rats) in a dose of 0.1 mg/kg through the jugular vein was carried out. Ten minutes after the treatment, the electrical stimulation of the reticular formation was repeated. The brain was fixed by perfusion of 10% formaline solution through the heart, and then placement of the electrode tip was examined histologically. Protein concentration and amylase activity in samples of Pancreatic secretion were measured. The electrical stimulation of the reticular formation significantly increased in volume $({\mu}l/10\;min)$, Protein output $({\mu}g/10\;min)$ and amylase output (U/10 min) in the pancreatic secretion. The stimulatroy effects were not affected by the cervical vagotomy but completely abolished by propranolol. Meantime, it was also observed that both vagotomy and propranolol significantly reduced the pancreatic secretory function. These results indicate that the reticular formation in the mesencephalone may exert a stimulatory effect upon the Pancreatic secretory function not through the vagus nerve but through the sympathetic pathway in anesthetized rats.

• 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.

• Journal of Veterinary Clinics
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• v.10 no.1
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• pp.111-130
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• 1993

Lead toxicity was evaluated in forty-five cats on a balanced diet, Treated with 0(control), 10, 100(low), 1, 000, 2, 000, and 4, 000(high) ppm of lead acetate orally on a body weight basis. The objectives were to establish toxic dosage level of leaf in cats, to characterize changes in behavior and clinical pathology, and to demonstrate what blood lead concentrations correlate with the known dosages of lead. Some high dose cats showed projectile vomiting, hyperactivity, and seizures. The growth rates did not appear to be altered in any of the dosed groups. Normal blood lead concentration in cats were lower than that of humans, dogs, and cattle. Blood lead concentrations of 3 to 20$\mu\textrm{g}$/100$m\ell$ could be termed a 'subclinical' range in the cat. Clinical lead toxicity in cats may have blood lead concentrations ranging 20 to 120$\mu\textrm{g}$/100$m\ell$. Zinc protoporphyrin concentrations were proportional to lead dosages and a significant ZPP elevation, greater than 50$\mu\textrm{g}$/100$m\ell$, may be indicative of clinical lead toxicity. The enzyme aminolevulinic acid dehydratase showed an inverss dose response relationship for all lead dosages and a significant ZPP elevation, greater than 50$\mu\textrm{g}$/100$m\ell$, may be indicative of clinical lead toxicity. The enzyme aminolevulinic acid dehydratase showed an inverse dose response relationship for all lead dosages and appears to be a good indicator of lead exposure in cats. Urinary aminolevuliruc acid concentrations generally increased with lead dosage, but individual values varied. Hair lead concentrations rose proportionately to lead dosages. Lead at least in high doses appears to inhibit chemotactic activity of polymorphonuclear cells and monocytes. No consistent dose response relationships were observed in hemoglobin, RBC, WBC, neutrophil, lymphocyte, monocyte, and eosinophil counts. There were no consistent dose related changes in total protein, plasma protein, BUN, and ALT values. Reticulocyte counts did not increase significantly in most lead dosage levels, and are probably of little value in diagnosing lead toxicity in cats. The fact that no significant changes were found in nerve conduction velocities may support that there was no segmental demyelination resulting from lead ingestion. The lethal dose in cats appear to range from 60 to 150mg/kg body weight. A reliable diagnosis of lead poisoning can be made utilizing blood lead, ZPP, and ALAD, and hair lead.

• Food Science and Preservation
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• v.15 no.5
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• pp.743-748
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• 2008

Amyloid $\beta$ peptide ($A{\beta}$) is known to increase oxidative stress in nerve cells, leading to apoptosis that is characterized by free radical formation and lipid peroxidation. Neurodegenerative diseases such as Alzheimer's disease (AD) are characterized by large deposits of $A{\beta}$ in the brain. In our study, neuronal protective effects of green tea, along with water activity (0.813), and leaf storage periods (fresh leaf, or leaf stored for up to 4 weeks) were investigated. We measured protective effects against $A{\beta}$-induced cytotoxicity in neuron-like PC12 cells. Powdered green tea was extracted with distilled water at $70^{\circ}C$ for 5 min, and this extract was freeze-dried and stored at $-20^{\circ}C$ until use. In cell viability assays using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), the fresh extract, and that obtained after 1 week of leaf storage, showed the best protective effects against $A{\beta}$-induced neurotoxicity. As oxidative stress causes membrane breakdown, the protective effect of green tea extracts was investigated using lactate dehydrogenase (LDH) and trypan blue exclusion assays. LDH release into the medium was inhibited (by 20-25%) in all tests. In addition, all green tea extracts (fresh, or stored before extraction for up to 4 weeks) showed better cell protective effects ($93.3{\pm}1.8-96.2{\pm}2.4$) than did vitamin C ($91.0{\pm}1.6$), used as a positive control. The results suggest that effectiveness of green tea extracts falls with prolonged leaf storage.

• Journal of Life Science
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• v.29 no.4
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• pp.402-409
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• 2019

Korean red ginseng made from steaming and drying fresh ginseng has long been used as a traditional herbal medicine due to its effects on the immune, endocrine, and central nerve systems and its anti-inflammatory activity. In this study, we investigated the molecular mechanism responsible for the anti-inflammatory effects of a formulated Korean red ginseng extract (RGE) in response to lipoteichoic acid (LTA), a cell wall component of gram-positive bacteria. RGE inhibited LTA-induced nitric oxide (NO) secretion and inducible nitric oxide synthase (iNOS) expression in BV-2 microglial cells, without affecting cell viability. RGE also inhibited nuclear translocation of nuclear factor kappa B ($NF-{\kappa}B$) p65 and degradation of $I{\kappa}B-{\alpha}$. In addition, RGE increased the expression of heme oxygenase-1 (HO-1) in a dose-dependent manner, and the inhibitory effect of RGE on iNOS expression was abrogated by small interfering RNA-mediated knockdown of HO-1. Moreover, RGE induced nuclear translocation of nuclear factor E2-related factor 2 (Nrf2), a transcription factor that regulates HO-1 expression. Furthermore, the phosphoinositide-3-kinase (PI-3K) inhibitor and mitogen-activated protein kinase (MAPK) inhibitors suppressed RGE-mediated expression of HO-1, and RGE enhanced the phosphorylation of Akt, extracellular signal-regulated kinases (ERKs), p38, and c-JUN N-terminal kinases (JNKs). These results suggested that RGE suppressed the production of NO, a proinflammatory mediator, by inducing HO-1 expression via PI-3K/Akt- and MAPK-dependent signaling in LTA-stimulated microglia. The findings indicate that RGE could be used for the treatment of neuroinflammation induced by grampositive bacteria and that it may have therapeutic potential for various neuroinflammation-associated disorders.