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- 주제어 : Chylomicron (검색결과 5 건)
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Chylomicron Retention Disease: a Description of a New Mutation in a Very Rare Disease
Helena Ferreira,Raquel Nuñez Ramos,Cinthia Flores Quan,Susana Redecillas Ferreiro,Vanessa Cabello Ruiz,Javi Juampérez Goñi,Jesus Quintero Bernabeu,Oscar Segarra Cantón,Marina Álvarez Beltran 대한소아소화기영양학회 2018 Pediatric gastroenterology, hepatology & nutrition Vol.21 No.2
Chylomicron retention disease, also known as Anderson’s disease, is a rare hereditary hypocholesterolemic dis-order, recessive inherited, characterized by nonspecific symptoms as abdominal distension, steatorrhea, and vomit-ing associated with failure to thrive. We describe a patient with failure to thrive, chronic diarrhea and steatorrhea who the diagnosis of chylomicron retention disease was established after several months of disease progression. The genetic study confirmed a homozygosity mutation in SAR1B gene, identifying a mutation never previous de-scribed [c.83_84delTG(p.Leu28Argfs*7)]. With this case report the authors aim to highlight for this very rare cause of failure to thrive and for the importance of an attempting diagnosis, in order to start adequate management with low fat diet supplemented with fat-soluble vitamins, reverting the state of malnutrition and avoiding possible irrever-sible and desvantating complications.
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Chylomicron Retention Disease: a Description of a New Mutation in a Very Rare Disease
Ferreira, Helena,Ramos, Raquel Nunez,Quan, Cinthia Flores,Ferreiro, Susana Redecillas,Ruiz, Vanessa Cabello,Goni, Javi Juamperez,Bernabeu, Jesus Quintero,Canton, Oscar Segarra,Beltran, Marina Alvarez The Korean Society of Pediatric Gastroenterology 2018 Pediatric gastroenterology, hepatology & nutrition Vol.21 No.2
Chylomicron retention disease, also known as Anderson's disease, is a rare hereditary hypocholesterolemic disorder, recessive inherited, characterized by nonspecific symptoms as abdominal distension, steatorrhea, and vomiting associated with failure to thrive. We describe a patient with failure to thrive, chronic diarrhea and steatorrhea who the diagnosis of chylomicron retention disease was established after several months of disease progression. The genetic study confirmed a homozygosity mutation in SAR1B gene, identifying a mutation never previous described [c.83_84delTG(p.Leu28Argfs*7)]. With this case report the authors aim to highlight for this very rare cause of failure to thrive and for the importance of an attempting diagnosis, in order to start adequate management with low fat diet supplemented with fat-soluble vitamins, reverting the state of malnutrition and avoiding possible irreversible and desvantating complications.
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Liposomal delivery systems for intestinal lymphatic drug transport
안혜지,박지호 한국생체재료학회 2016 생체재료학회지 Vol.20 No.4
Intestinal lymphatic drug delivery has been widely studied because drugs can bypass the first-pass metabolism in the liver via the lymphatic route, which increases oral bioavailability. Various lipid-based nanoparticles have been used to deliver hydrophobic drugs to the lymphatic pathway. This review focuses on the liposomal delivery systems used for intestinal lymphatic drug transport. Liposomal formulations have attracted particular attention because they can stimulate the production of chylomicrons and the incorporated drugs readily associate with enterocytederived chylomicrons, enhancing lymphatic drug transport. We believe that a full understanding of their contribution to intestinal drug translocation will lead to effective oral delivery with liposomal formulations.
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Lee, Sungmin,Son, Beomseok,Jeon, Jaewan,Park, Gaeul,Kim, Hyunwoo,Kang, Hyunkoo,Youn, HyeSook,Jo, Sunmi,Song, Jie-Young,Youn, BuHyun S. Karger AG 2018 Cellular physiology and biochemistry Vol.47 No.6
<P><B><I>Background/Aims:</I></B> Non-alcoholic fatty liver disease (NAFLD) is an emerging metabolic disease. Although it leads to severe hepatic diseases including steatohepatitis, cirrhosis, and hepatic cancer, little is known about therapy to prevent and cure hepatic steatosis, the first step of NAFLD. We conducted this investigation to unveil the mechanism of hepatic steatosis. <B><I>Methods:</I></B> We established a novel chronic NAFLD mouse model through whole body irradiation and verified the model through histological and biochemical analysis. To find molecular mechanism for hepatic steatosis, we analyzed hepatic transcriptomic profiles in this model and selected target molecule. To induce the expression of lactotransferrin (Ltf) and regulate the NAFLD, growth hormone (GH) and coumestrol was introduced to hepatocyte and mice. The universal effect of coumestrol was confirmed by administration of coumestrol to NAFLD mouse model induced by high-fructose, high-fat, and MCD diet. <B><I>Results:</I></B> It was observed that decreased hepatic Ltf expression led to excessive hepatic lipid accumulation in NAFLD mouse. Furthermore, we found that GH was decreased in irradiated mice and functioned as an upstream regulator of Ltf expression. It was observed that GH could stimulate Ltf expression and prevent uptake of dietary lipids in hepatocytes, leading to rescue of NAFLD. Finally, we suggested that coumestrol, a kind of isoflavonoid, could be used as an inducer of hepatic Ltf expression through cooperation with the GH signaling pathway both <I>in vitro</I> and <I>in vivo</I>. <B><I>Conclusions</I></B><I>:</I> Hepatic Ltf prevents hepatic steatosis through inhibition of dietary lipid uptake in radiation-induced NAFLD mouse model. We also suggest coumestrol as a drug candidate for prevention of NAFLD.</P>
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鄭漢鐘 진주산업대학교 1997 論文集 Vol.36 No.-
To study the effects of cardio-respiratory development on serum lipids in control, activity and obesity us, 36 men who aged 40-60yrs were checked by medical process and exercise stress testing. Subjects were divided into three groups that were control, activity and obesity group. Results of this study are as following. 1. %Body fat is 19.7% in control groups, 17.4% in activity group. Control and activity group are significantly leaner than obesity group(p<0.05). 2. It is not significantly different in amounts of WBC and RBC between groups. 3. Cholesterol is 245㎎/dℓ in obesity which is the significantly most plentiful among groups(p<0.05). But in Calcium and Pi, it is not significantly different between groups. 4. In serum cholesterol, total cholesterol is 179.0㎎/dℓ in activity group, which is the significantly least amount among groups(p<0.05). LDL-C(101.3㎎/dℓ) and triglycerides(135.5㎎/dℓ) of activity group are the significantly least amount among groups, too(p<0.05). Amount of HDL-C of activity group is greater than obesity group, but not significant. 5. Resting HR is 60.6beats/min in control group and 57.1beats/min in activity group, that are significantly lower than that of obesity(p<0.05). 6. Resting rate pressure product(RPP : myocardial oxygen consumption) is 6.60×103mmHg·bpm in activity group, which is less than those in obesity group(p<0.05). 7. Maximal oxygen consumption(VO2max) of activity group is 37.3mℓ/㎏/min, that is significantly greater than that of obesity group(p<0.05). 8. Correlation coefficients with VO2max have significance(p<0.001). : TCH(r=-0.853), HDL-C(r=0.633), LDL-C(r=-0.813),Triglycerides(r=-0.844),TCH/HDL-C(r=-0.834).
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