• Journal of Genetic Medicine
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• v.5 no.2
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• pp.119-124
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• 2008

Purpose: Aneuploidy is the cause of diseases such as Down syndrome or Edward syndrome and, more generally, is a major cause of mental retardation and fetal loss. The purpose of this study was to evaluate the association between MTHFR (C677T) or MTRR (A66G) polymorphisms and fetal aneuploidy. Materials and Methods: Data was collected from 37 women who had a fetus with aneuploidy (cases) and 78 women who had previously delivered at least two healthy children without aneuploidy and did not have a history of miscarriage or abnormal pregnancy (controls). The MTHFR (C677T) or MTRR (A66G) polymorphisms were analyzed by PCR-restriction fragment length polymorphism assay. Results: The frequencies of the MTHFR 677 CC, CT, and TT genotypes were 30.7%, 48.7%, and 20.6% in the control group and 37.8%, 48.6%, and 13.5% in the case group, respectively. There were no significant differences in genotype frequencies between the two groups. For the MTRR A66G polymorphism, the frequencies of the AA, AG and GG genotypes were 50%, 46.1%, and 3.9% in the control group and 13.5%, 81.1%, and 5.4% in case group, respectively. The frequency of the MTRR AG mutant was significantly increased in the case group, with an odds ratio of 6.5 (95% CI: 2.3-18.6, P<0.05). Conclusion: The results of this study suggest that mother carriers with the MTRR G allele have an increased risk of fetal aneuploidy, while the MTHFR T allele is not associated with increased risk of fetal aneuploidy. The MTRR A66G polymorphism may be a risk factor for producing a child with chromosomal aneuploidy.

• Journal of the Korean Society of Food Science and Nutrition
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• v.31 no.2
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• pp.263-270
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• 2002

In the recent studies, many researchers are interested in foods as functional components rather than nutrient sources. Cow's milk is considered as an excellent food sources because of its many nutrients. Casein is a major milk protein and has been reported to have hyperlipidemic and hypercholesterolemic effects. But several reporters have suggested that peptide fractions and hydrolysate of casein have hypolipidemic effects differing from intact protein, casein. Therefore, the objective of the study was to investigate how the casein peptide fractions affect lipid metabolism in rats fed normal or high fat diets. The peptide fractions and hydrolysate of casein were obtained by casein hydrolysis with trypsin. The male rats (Sprague-Dawley), weighing approximately 150 g, were fed each experimental diet containing casein (CAS), casein hydrolysate (CH), casein hydrolysate precipitate (Cpt) and two kinds of peptide fractions (CL & CB) for three weeks, respectively. In the exit I, the male rats were fed normal fat diets (7% soybean oil & cholesterol-free; Expt. I), and in the expt II, fed high fat diets (18% beef tallow & 1% cholesterol; Expt. II). Crude protein contents were calculated from nitrogen contents. Amino acid composition of each fraction was also analyzed. The concentration of total lipid, total cholesterol and triglyceride in serum, liver and feces were measured. As the results of study, tole rats fed peptide fractions with normal fat diets (Expt. I) had no effects on total lipid, total cholesterol and triglyceride concentration in serum and liver and fecal excretion. However, in the rats fed hydrophobic casein peptide fractions (CB) with high fat diet, fecal lipids excretion were significantly increased and the lipids concentration of serum and those of liver tended to decrease, numerically.

• Korean Journal of Food Science and Technology
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• v.37 no.4
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• pp.636-641
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• 2005

Mulberry leaves, high in dietary fiber and some nutritional materials, are thought to have hypocholesterolemic effect. Therefore, effect of mulberry leaf powder on serum lipid profiles were studied using rats with diet-induced hypercholesterolemia. Male Sprague-Dawley rats were fed AIN-93 diet (control group), and diets containing high-cholesterol and 0% mulberry leaves powder, high-cholesterol and 5% mulberry leaves powder, and high-cholesterol and 10% mulberry leaves powder for 4 weeks. Hypercholesterolemia was induced by adding 1% cholesterol and 0.5% cholic acid to all diets except in control group. Although no differences were observed in food intake and initial body weight among groups, mulberry leaf treatment resulted in significant decreases in food efficiency ratio and body weight gain. Mulberry leaf treatment decreased serum lipid profiles, atherogenic index, cardiac risk factor, low density lipoprotein cholesterol ratio, serum aspartate transaminase, and liver lipid levels. High density lipoprotein cholesterol, total cholesterol, serum HDL-cholesterol, and fecal lipid levels increased, suggesting mulberry leaves could improve hyperlipidemia and liver action, thereby proventing cardiovascular disease.

• Journal of the Korean Society of Food Science and Nutrition
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• v.35 no.8
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• pp.979-984
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• 2006

Although iron is essential for many physiological processes, excess iron can lead to tissue damage by promoting the generation of reactive oxygen species (ROS). There is increasing evidence that ROS might play an important role in the pathogenesis of cardiovascular disease. However, the effects of iron excess on platelet function and the thrombotic response to vascular injury are not well understood. We examined the effects of iron excess-induced oxidative stress and the antioxidants on platelet aggregation. Oxidative stress was accessed by either free iron $(Fe^{+2})$ or hydrogen peroxide $(H_2O_2)$, as well as their combination on washed rabbit platelets (WPs) in vitro. When WPs were stimulated with either $Fe^{+2}$ alone or a subthreshold concentration of collagen, which gave an aggregatory curve with a little effect, and a dose dependent increase in platelet aggregation was observed by increasing concentrations of $Fe^{+2}$ with $H_2O_2$. This aggregation was associated with the iron-catalyzed formation of hydroxyl radicals from $H_2O_2$, and were inhibited by NAD/NADP (proton acceptor), catalase $(H_2O_2\;scavenger)$, tiron (iron chelator), mannitol (hydroxyl radical scavenger), and indomethacin (cyclooxygenase inhibitor), but not by NADH/NADPH (proton donor), superoxide mutase, and aspirin. However, NADH/NADPH, an essential cofactor for the antioxidant capacity by the supply of reducing potentials, showed the effect of an enhanced radical formation, suggesting a role for NADH/NADPH-dependent oxidase. These results suggest that iron $(Fe^{+2})$ can directly interact with washed rabbit platelets and this aggregation be mediated by OH formation as in the Fenton reaction, inhibited by radical scavengers.

• Clinical and Experimental Pediatrics
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• v.48 no.12
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• pp.1370-1377
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• 2005

Purpose : Delineation of serum lipid and lipoprotein values in children after Kawasaki disease(KD) is important because of the predilection of this disease for the coronary arteries. Methods : The KD group was composed of 51 patients who were hospitalized from Jan. 2002 to Dec. 2003. Control was 25 patients with non-KD febrile illness. The levels of total lipid, phospholipid, triglyceride, HDL-cholesterol(HDL-C), LDL-cholesterol, total cholesterol, apolipoprotein A1(apo A1), apolipoprotein B, and Lipoprotein(a) were measured and compared with Echocardiographic findings. Measurements were obtained in four time periods: acute febrile, subacute, convalescent phase and 1 year after KD. Results : HDL-C($33.64{\pm}7.49mg/dL$ vs $50.43{\pm}14.41mg/dL$, P<0.01) and apo A1($99.75{\pm}6.39mg/dL$ vs $113.34{\pm}11.35mg/dL$, P<0.05) were decreased more in the acute febrile period of KD than in the control, but these changes were not correlated with cardiac complications. All lipid profiles were markedly elevated in the subacute stage and normalized in the convalescent stage; there were no changes until 1-year follow up. There were no significant differences in the changes of lipid profiles, including Lp(a) and coronary dilatation, in any time periods. Conclusion : KD is associated with important abnormalities in lipid metabolism, but these changes were transient and appear to be due to the disease itself. These data lead us to infer that KD dose not cause such permanent changes in lipid abnormalities as to be considered a risk factor for atherosclerosis, beyond that caused by the disease itself.

• Journal of Chest Surgery
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• v.39 no.12 s.269
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• pp.879-890
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• 2006

Background: The dysfunction of multiple organs is found to be caused by reactive oxygen species as a major modulator of microvascular injury after hemorrhagic shock. Hemorrhagic shock, one of many causes inducing acute lung injury, is associated with increase in alveolocapillary permeability and characterized by edema, neutrophil infiltration, and hemorrhage in the interstitial and alveolar space. Aggressive and rapid fluid resuscitation potentially might increased the risk of pulmonary dysfunction by the interstitial edema. Therefore, in order to improve the pulmonary dysfunction induced by hemorrhagic shock, the present study was attempted to investigate how to reduce the inflammatory responses and edema in lung. Material and Method: Male Sprague-Dawley rats, weight 300 to 350 gm were anesthetized with ketamine(7 mg/kg) intramuscular Hemorrhagic Shock(HS) was induced by withdrawal of 3 mL/100 g over 10 min. through right jugular vein. Mean arterial pressure was then maintained at $35{\sim}40$ mmHg by further blood withdrawal. At 60 min. after HS, the shed blood and Ringer's solution or 5% albumin was infused to restore mean carotid arterial pressure over 80 mmHg. Rats were divided into three groups according to rectal temperature level($37^{\circ}C$[normothermia] vs $33^{\circ}C$[mild hypothermia]) and resuscitation fluid(lactate Ringer's solution vs 5% albumin solution). Group I consisted of rats with the normothermia and lactate Ringer's solution infusion. Group II consisted of rats with the systemic hypothermia and lactate Ringer's solution infusion. Group III consisted of rats with the systemic hypothermia and 5% albumin solution infusion. Hemodynamic parameters(heart rate, mean carotid arterial pressure), metabolism, and pulmonary tissue damage were observed for 4 hours. Result: In all experimental groups including 6 rats in group I, totally 26 rats were alive in 3rd stage. However, bleeding volume of group I in first stage was $3.2{\pm}0.5$ mL/100 g less than those of group II($3.9{\pm}0.8$ mL/100 g) and group III($4.1{\pm}0.7$ mL/100 g). Fluid volume infused in 2nd stage was $28.6{\pm}6.0$ mL(group I), $20.6{\pm}4.0$ mL(group II) and $14.7{\pm}2.7$ mL(group III), retrospectively in which there was statistically a significance between all groups(p<0.05). Plasma potassium level was markedly elevated in comparison with other groups(II and III), whereas glucose level was obviously reduced in 2nd stage of group I. Level of interleukine-8 in group I was obviously higher than that of group II or III(p<0.05). They were $1.834{\pm}437$ pg/mL(group I), $1,006{\pm}532$ pg/mL(group II), and $764{\pm}302$ pg/mL(group III), retrospectively. In histologic score, the score of group III($1.6{\pm}0.6$) was significantly lower than that of group I($2.8{\pm}1.2$)(p<0.05). Conclusion: In pressure-controlled hemorrhagic shock model, it is suggested that hypothermia might inhibit the direct damage of ischemic tissue through reduction of basic metabolic rate in shock state compared to normothermia. It seems that hypothermia should be benefit to recovery pulmonary function by reducing replaced fluid volume, inhibiting anti-inflammatory agent(IL-8) and leukocyte infiltration in state of ischemia-reperfusion injury. However, if is considered that other changes in pulmonary damage and inflammatory responses might induce by not only kinds of fluid solutions but also hypothermia, and that the detailed evaluation should be study.