• 제목/요약/키워드: Brain metabolism

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Effects of Sunghyangchungisan(SHCS) on Cellular Ion Contents and Metabolism in Cat Brain Cortical Slices under Hypoxic Insult (성향정기산(星香正氣散)이 저산소(低酸素) 발작상태(發作狀態)의 고양이 대뇌(大腦) 피질(皮質) 절편(切片)의 이온 함량(含量)과 대사(代謝)에 미치는 효과(效果))

  • Kim, Young-Kyun;Kwon, Jeong-Nam;Cho, Su-In;Kim, Na-Ri
    • The Journal of Internal Korean Medicine
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    • v.22 no.4
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    • pp.537-546
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    • 2001
  • 목적: 고양이 대뇌피질 절편을 사용하여 저산소 발작을 유발한 뒤, 성향정기산이 세포의 이온 환경과 대사의 변화와 관련하여 어떤 영향을 미치는지 연구하였다. 방법: 고양이의 대뇌 피질 절편에 저산소 발작을 유발한 뒤 flame photometry scintillation, Spectrophotometry, method of Jorgensen and Skou, method of Fiske and Subbarow, oxygen monitor, luciferin-luciferase assay 등을 이용하여 세포내 이온함량과 세포대사를 측정하였다. 결과: 성향정기산은 저산소증으로 유발된 세포내의 $K^+$$Na^+$의 함량의 변화를 현저하게 지연시켰다. 성향정기산은 Na-K-ATPase의 억제제인 와바인 또는 대사억제제인 2.4-DNP로 유발된 세포내 $K^+$함량의 변화에 어떤 효과도 보이지 않았다. 또한, 정상 상태의 절편뿐만 아니라 저산소 상태의 절편에서 분리된 과립체의 분설에 있어서 Na-K-ATPase의 활동도에 영향을 미치지 않았다. 성향정기산은 저산소 발작하에서 산소 소비량과 세포의 ATP함량이 떨어지는 것을 현저하게 막았다. 또한 ATP를 생산하는 기능을 보호하는 저산소 조직의 사립체를 돕는데 효과적이었다. 결론: 성향정기산은 대뇌 조직의 저산소 발작하에서 세포의 이온 환경과 대사를 보호하는 유익한 효과가 있음을 알 수 있다.

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Effect of Heavy Metals on the Secretion of Amylase in Rat Pancreatic Fragments (중금속류가 취절편의 Amylase 분비에 미치는 영향)

  • Kim, Hea-Young;Kim, Won-Joon
    • The Korean Journal of Pharmacology
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    • v.17 no.2
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    • pp.31-36
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    • 1981
  • Heavy metals which are present as trace elements in human body have been known to modify various enzymatic reaction. These metals can be essential or non-essential. Zinc, copper and calcium are essential in maintaining some biological processes, whereas non-essential metals such as cadmium, lead and mercury produce accumulatve toxic effect. Cadmium accumulated in pancreas can cause toxicity and damage of pancreatic cells, thereby influencing CHO metabolism. Lead compounds are known to produce toxic effects on the kidney, digestive system and brain fellowed by inhibition of activity of ${\rho}-aminolevulinic$ acid and biosynthesis of hemoproteins and cytochrome. Evidence has been accumulated that zinc not only acts as a cofactor in enzyme reaction but also prevents toxic effect induced by heavy metal such as copper and cadmium. To demonstrate the effect of heavy metals on pancreatic secretion, part of uncinate pancreas was taken and incubated in Krebs-Ringer bicarbonate buffer with heavy metals used. Additional treatment with CCK-OP was performed when needed. After incubation during different period of time, medium was analyzed for amylase activity using Bernfeld's method. The present study was attempted in order to elucidate the effect of several kinds of heavy metal on exocrine pancreatic secretion in vitro. The results obtained are as follows: 1) CCK-OP stimulated significantly amylase release from pancreatic fragments in vitro. 2) CCK-OP response of amylase release from pancreatic fragments was inhibited by treatmant with cadmium, especially high doses of cadmium. 3) CCK-OP response of amylase release from pancreatic fragments was inhibited when pretreated with $10^{-4}M$ copper chloride. 4) Lead chloride at the concentration of $10^{-3}M\;and\;10^{4}M$ stimulated the basal amylase release in vitro but CCK-OP response did not augment by lead chloride. 5) Zine chloride did not affect amylase release from pancreatic fragment in vitro. From the results mentioned above, it is suggested that CCK-OP response was inhibited it the amylase release from pancreatic fragments pretreated with cadmium and copper chloride.

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A Case of Citrullinemia Diagnosed at the Neonatal Period (신생아기에 진단된 Citrullinemia 1례)

  • Song, Seung Kyu;Oh, Kyung Chang;Hong, Mi Ae;Kim, Hee Taeg;Shin, Hye Jung;Kim, Soon Young;Chang, Jin Keun;Jo, Heui Seung;Kim, Beyong Il;Yang, Sei Won;Choi, Jung-Hwan
    • Clinical and Experimental Pediatrics
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    • v.45 no.4
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    • pp.524-528
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    • 2002
  • Citrullinemia is a rare inborn error of metabolism of the urea cycle, and was first reported by McMurray, et al. in 1962. It is inherited as an autosomal recessive trait. The normal synthesis of argininosuccinic acid is blocked in this disease due to a deficiency of argininosuccinic acid synthetase(AS), which has been demonstrated in liver cells and fibroblasts. The clinical symptoms are vomiting, lethargy or irritability, convulsion and mental retardation. The diagnosis is made by the finding of an increased plasma citrulline level. Every effort should be made to reduce the blood ammonia level as rapidly as possible before irreversible brain damage occurs. This report describes a case of citrullinemia that was diagnosed through organic acid analysis and amino acid analysis, and reviews the related literatures.

Effect of Atrial Natriuretic Peptide on the Proliferation and Activity of Osteoblastic Cells

  • Lee, Jong-Ryeul;Ko, Seon-Yle;Kim, Jung-Keun;Kim, Se-Won
    • The Korean Journal of Physiology and Pharmacology
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    • v.4 no.4
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    • pp.283-289
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    • 2000
  • Natriuretic peptides comprise a family of three structurally related peptides; atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), and C-type natriuretic peptide (CNP). The present study was performed to investigate the effect of ANP on the proliferation and activity of ROS17/2.8 and HOS cells which are well-characterized osteoblastic cell lines. ANP dose-dependently decreased the number of ROS17/2.8 and HOS cells after 48-hour treatment. ANP generally increased the alkaline phosphatase activity of ROS17/2.8 and HOS cells after 48 hr treatment, regardless of the fact that basal activity of alkaline phosphatase was much lower in HOS cells compared to that of ROS17/1.8 cells. ANP increased the NBT reduction by ROS17/2.8 and HOS cells. ANP showed the variable but no significant effect on the nitric oxide production by ROS17/2.8 and HOS cells. ROS17/2.8 and HOS cells produced and secreted gelatinase into culture medium, and this enzyme was thought to be the gelatinase A type with the molecular weight determination. The gelatinase activity produced by ROS17/2.8 cells was increased by the treatment of ANP. However, the enzyme activity was not affected by ANP treatment in the HOS cell culture. In summary, ANP decreased the proliferation and increased the alkaline phosphatase activity and NBT reduction of osteoblasts. These results indicate that ANP is one of the important regulators of bone metabolism.

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Momordica charantia extract supplementation tend to affect improvements in body composition and metabolic parameters on tennis players: A pilot study

  • Kwak, Jae-Jun;Yook, Jang Soo;Ha, Min-Seong
    • Journal of the Korean Applied Science and Technology
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    • v.36 no.4
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    • pp.1164-1171
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    • 2019
  • Dietary supplements derived from natural sources are an essential factor in optimizing athletic performance. It has been proposed that the extract of Momordica charantia (M. charantia) that is known as a bitter melon can be potentially used as a novel supplement for health promotion. This pilot study aimed to examine the effects of the M. charantia extract when administered in the form of a sports drink, and we evaluated changes in body composition and metabolic factors in tennis players after 4-week consumption of the extract. Eight male college tennis players were instructed to consume an M. charantia extract 6 times per day (3 in the morning and 3 in the afternoon, and the total daily intake was 600 ml). Collected data were analyzed using paired t-tests to examine the changes over time after consumption of the M. charantia extract. The results revealed a significant increase in the trunk muscle mass, basal metabolic rate, and daily calorie intake (p < 0.05). Levels of protein, minerals, and total body water showed an increased tendency (not statistically significant), whereas intracellular water and extracellular water showed a decreased trend. Furthermore, fat-free mass, skeletal muscle mass, and muscle mass showed an increased tendency. In conclusion, consumption of the M. charantia extract caused an increase in parameters related to protein, muscle mass, and metabolism. It seems that follow-up studies related to fatigue, inflammation, and stress hormones related to the M. charantia extract consumption would be needed.

Functional PstI/RsaI Polymorphisms in the CYP2E1 Gene among South Indian Populations

  • Lakkakula, Saikrishna;Maram, Rajasekhar;Munirajan, Arasambattu Kannan;Pathapati, Ram Mohan;Visweswara, Subrahmanyam Bhattaram;Lakkakula, Bhaskar V.K.S.
    • Asian Pacific Journal of Cancer Prevention
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    • v.14 no.1
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    • pp.179-182
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    • 2013
  • Human cytochrome P4502E1 (CYP2E1) is a well-conserved xenobiotic-metabolizing enzyme expressed in liver, kidney, nasal mucosa, brain, lung, and other tissues. CYP2E1 is inducible by ethanol, acetone, and other low-molecular weight substrates and may mediate development of chemically-mediated cancers. CYP2E1 polymorphisms alter the transcriptional activity of the gene. This study was conducted in order to investigate the allele frequency variation in different populations of Andhra Pradesh. Two hundred and twelve subjects belonging to six populations were studied. Genotype and allele frequency were assessed through TaqMan allelic discrimination (rs6413419) and polymerase chain reaction-sequencing (-1295G>C and -1055C>T) after DNA isolation from peripheral leukocytes. The data were compared with other available world populations. The SNP rs6413419 is monomorphic in the present study, -1295G>C and -1055C>T are less polymorphic and followed Hardy-Weinberg equilibrium in all the populations studied. The -1295G>C and -1055C>T frequencies were similar and acted as surrogates in all the populations. Analysis of HapMap populations data revealed no significant LD between these markers in all the populations. Low frequency of $CYP2E1^*c2$ could be useful in the understanding of south Indian population gene composition, alcohol metabolism, and alcoholic liver disease development. However, screening of additional populations and further association studies are necessary. The heterogeneity of Indian population as evidenced by the different distribution of $CYP2E1^*c2$ may help in understanding the population genetic and evolutionary aspects of this gene.

A Case of Multiple Thromboembolisms in Hyperhomocysteinemia (과호모시스턴혈증에서 발생된 다발성 혈전증 1예)

  • Park, Jae-Sun;Bae, Won-Ki;Lee, Sang-Jun;Chung, Rae-In;Jin, Seong-Lim;Lee, Hyuk-Pyo;Kim, Joo-In;Choi, Soo-Jeon;Yum, Ho-Kee
    • Tuberculosis and Respiratory Diseases
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    • v.47 no.2
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    • pp.239-246
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    • 1999
  • Hyperhomocysteinemia is an independent risk factor for cardiovascular, cerebrovascular and peripheral vascular diseases complicated with atherosclerosis and thromboembolism. Increased plasma homocystein level develops from genetic defect of enzyme for homocystein metabolism or vitamine deficiency, has direct toxic effect for vascular endothelium and makes damages to antithrombotic action of vascular endothelial cell. Most of hyperhomocysteinemia is asymptomatic, but rarely develops cardiopulmonary or cerebrovascular accidents. In case of thromboembolism with unknown cause, the hyperhomocysteinemia should be considered as one of the many etiologies. The authors, first in korea, report a case of multiple thromboembolisms of deep vein of lower extremity, pulmonary vessels, superior sagittal and transverse sinus of brain in a patient with the hyperhomocysteinemia with a review of literature.

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Isolation and characterization of a cDNA encoding a mammalian cathepsin L-like cysteine proteinase from Acanthmoeba healui

  • Hong, Yeon-Chul;Hwang, Mi-Yul;Yun, Ho-Cheol;Yu, Hak-Sun;Kong, Hyun-Hee;Yong, Tai-Soon;Chung, Dong-Il
    • Parasites, Hosts and Diseases
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    • v.40 no.1
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    • pp.17-24
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    • 2002
  • We have cloned a cDNA encoding a cysteine proteinase of the Acanthamoeba healui OC-3A strain isolated from the brain of a granulomatous amoebic encephalitis patient. A DNA probe for an A. healui cDNA library screening was amplified by PCR using degenerate oligonucleotide primers designed on the basis of conserved amino acids franking the active sites of cysteine and asparagine residues that are conserved in the eukaryotic cysteine proteinases. Cysteine proteinase gene of A. healui (AhCPI) was composed of 330 amino acids with signal sequence, a proposed pro-domain and a predicted active site made up of the catalytic residues, $Cys^{25},{\;}His^{159},{\;}and{\;}Asn^{175}$. Deduced amino acid sequence analysis indicates that AhCPI belong to ERFNIN subfamily of C 1 peptidases. By Northern blot analysis. no direct correlation was observed between AhCPI mRNA expression and virulence of Acanthamoeba, but the gene was expressed at higher level in amoebae isolated from soil than amoeba from clinical samples. These findings raise the possibility that AhCPI protein may play a role in protein metabolism and digestion of phagocytosed bacteria or host tissue debris rather than in invasion of amoebae into host tissue.

Molecular Genetic Testing and Diagnosis of Wilson Disease (윌슨병의 진단과 분자유전학적 검사)

  • Seo, Jeong Kee
    • Pediatric Gastroenterology, Hepatology & Nutrition
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    • v.11 no.sup1
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    • pp.72-82
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    • 2008
  • Wilson disease (WD) is an autosomal recessive disorder of copper metabolism that results in accumulation of copper primarily in the liver, the brain and the cornea. Mutations in the WD gene, ATP7B cause failure of copper excretion from hepatocyte into bile and a defective synthesis of ceruloplasmin. More than 370 mutations are now recognized, scattering throughout the ATP7B gene. Since WD has protean clinical presentations, awareness of WD in clinical practice is important for the early diagnosis and prevention of accumulated copper toxicity. None of the laboratory parameters alone allows a definite diagnosis of WD. There are numerous pitfalls in the diagnosis of WD. Low serum ceruloplasmin concentrations, increased 24 hour urinary copper excretion, increased hepatic copper concentrations and the presence of Kayser-Fleischer rings in the cornea are major diagnostic points. A combination of any two of these 4 laboratory findings is strong support for a diagnosis of WD. Molecular methods are now being used to aid diagnosis. Molecular genetic testing has confirmed the diagnosis in individuals in whom the diagnosis is not clearly established biochemically and clinically. Siblings should be screened for WD once an index case has been diagnosed. Discrimination of heterozygotes from asymptomatic patients is essential to avoid inappropriate lifelong therapy for heterozygotes. Genetic testing, either by haplotype analysis or by mutation analysis, is the only reliable tool for differentiating heterozygote carriers from affected asymptomatic patients. Currently, genetic testing is of limited value in the primary diagnosis. However, genetic testing will soon play an essential role in diagnosing WD as rapid advancement of biomedical technology will allow more rapid, easier and less expensive mutation detection.

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Tetany in a 13-Year-Old Girl with Wilson's Disease (테타니가 발생한 윌슨병 1예)

  • Ra, Chae-Ik;Kim, Sang-Yong;Koh, Hong
    • Pediatric Gastroenterology, Hepatology & Nutrition
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    • v.14 no.1
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    • pp.86-90
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    • 2011
  • Wilson's disease is an autosomal recessive disorder of copper metabolism consequence of which leads to accumulation of copper in the liver, brain, cornea and other tissues. The manifestations are more likely to be hepatic in the early childhood and neurological in the adolescents. In addition, the abnormalities that develop during disease progression may result in other manifestations such as hematologic, endocrine, or renal findings. We report a thirteen year-old girl who manifested tetany shortly after the initial diagnosis of Wilson's disease. Despite aggressive calcium, magnesium and vitamin D replacement, the hypocalcemia and hypomagnesemia did not respond to the therapy promptly. It took more than three weeks for blood levels of the minerals to be normal. We concluded that tetany occurred in our patient because of hypoparathyroidism as a rare complication of Wilson disease, vitamin D deficiency resulting from various conditions, and inconclusive hypomagnesemia.