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1 uced the prevalence of folate deficiency and hyperhomocysteinemia.
2 ue to vegetarianism is increasing and causes hyperhomocysteinemia.
3 hepatic necroinflammation and apoptosis, and hyperhomocysteinemia.
4 uced activity, increased thermolability, and hyperhomocysteinemia.
5 hionine intake with B vitamin deficiency and hyperhomocysteinemia.
6 th elevated levels of homocysteine, known as hyperhomocysteinemia.
7 s of excess dietary methionine from those of hyperhomocysteinemia.
8 al macrophages was higher in the presence of hyperhomocysteinemia.
9 tion of placebo and after methionine-induced hyperhomocysteinemia.
10 associated with poor cognition, anemia, and hyperhomocysteinemia.
11 n peritoneal macrophages were not changed by hyperhomocysteinemia.
12 ncreased incidence of stroke associated with hyperhomocysteinemia.
13 on may contribute to vascular dysfunction in hyperhomocysteinemia.
14 ontribute to endothelial dysfunction in mild hyperhomocysteinemia.
15 o inactivating nitric oxide in chronic, mild hyperhomocysteinemia.
16 ively low blood folate levels and consequent hyperhomocysteinemia.
17 iciency in the elderly and its role in their hyperhomocysteinemia.
18 thogenesis of both homocystinuria and modest hyperhomocysteinemia.
19 ence of this mutation is not associated with hyperhomocysteinemia.
20 H2S in the thrombotic events associated with hyperhomocysteinemia.
21 mmation, and activation of fibrogenesis) and hyperhomocysteinemia.
22 -beta-synthase (cbs) were used as a model of hyperhomocysteinemia.
23 ized by a plethora of vascular disorders and hyperhomocysteinemia.
24 steatosis or UPR activation despite inducing hyperhomocysteinemia.
25 macrovascular occlusion in individuals with hyperhomocysteinemia.
26 functional changes in cerebral arterioles in hyperhomocysteinemia.
27 regulation and has possible implications for hyperhomocysteinemia.
28 e the most common cause of severe hereditary hyperhomocysteinemia.
29 LF) diet for 6 to 8 months to produce graded hyperhomocysteinemia.
30 eta-synthase (Cbs)-heterozygous mice develop hyperhomocysteinemia.
31 ugmentation was significantly blunted during hyperhomocysteinemia (1.06 +/- 1.00 ml/min/g vs. 0.58 +/
32 hial artery vasodilation was impaired during hyperhomocysteinemia (4.4 +/- 2.6% vs. 2.6 +/- 2.3%, pla
33 been observed in renal disease patients with hyperhomocysteinemia, a cardiovascular disease risk fact
37 instead, these inadequacies could result in hyperhomocysteinemia, a recently identified risk factor
39 lymorphism is a genetic determinant for mild hyperhomocysteinemia, a risk factor for cardiovascular d
40 m is the most frequent genetic cause of mild hyperhomocysteinemia, a risk factor for cardiovascular d
42 tomography (PET) to test the hypothesis that hyperhomocysteinemia adversely effects coronary microvas
43 o diet-induced hyperhomocysteinemia and that hyperhomocysteinemia alters tissue methylation capacity
47 al failure, a condition associated with both hyperhomocysteinemia and atherosclerosis, treatment with
51 on to the fatty liver and no contribution to hyperhomocysteinemia and ER stress in intragastric alcoh
52 s containing ethanol or homocysteine induced hyperhomocysteinemia and glucose intolerance in control,
53 Using an atherogenic diet that produces both hyperhomocysteinemia and hypercholesterolemia, we tested
56 that expression of Tg-CBS rescued the severe hyperhomocysteinemia and neonatal lethality of Cbs delet
57 ociated with the degree of liver injury were hyperhomocysteinemia and strain-dependent differences in
59 /-) genotype sensitizes mice to diet-induced hyperhomocysteinemia and that hyperhomocysteinemia alter
62 objective was to determine the prevalence of hyperhomocysteinemia and vitamin B-12 deficiency in elde
63 generative diseases that are associated with hyperhomocysteinemia and, more recently, have implicated
64 Hypothyroidism may be a treatable cause of hyperhomocysteinemia, and elevated plasma homocysteine l
65 In vivo studies using CBS+/-, a model for hyperhomocysteinemia, and sibling CBS+/+ control mice re
66 steatosis, endoplasmic reticulum stress, and hyperhomocysteinemia, and this correlates with induction
67 )S increases progressively with the grade of hyperhomocysteinemia, and under conditions of severely e
68 hionine intake with B vitamin deficiency and hyperhomocysteinemia; and (iii) normal methionine intake
71 e cellular hypomethylation in the setting of hyperhomocysteinemia because of cystathionine beta-synth
72 hat supplementation with B vitamins prevents hyperhomocysteinemia but is not sufficient to prevent th
74 alcoholic mouse liver and that correction of hyperhomocysteinemia by betaine or other approaches may
75 to tPA can be inhibited by homocysteine and hyperhomocysteinemia can be induced by L-methionine supp
79 abolism, combined methylmalonic acidemia and hyperhomocysteinemia, cblC type, is caused by mutations
87 of mouse to up-regulate BHMT which prevents hyperhomocysteinemia, endoplasmic reticulum stress, and
89 ), as was the prevalence of mild-to-moderate hyperhomocysteinemia (>12 microM; NHD, 57%; SHD, 94%; P
90 13.0 vs. 11.0+/-3.0 micromol/L, P<0.01), and hyperhomocysteinemia (>90th percentile for controls, 14.
99 ysfunction, and ERG defects; those with mild hyperhomocysteinemia have delayed retinal morphological/
100 that precipitate low blood folate levels and hyperhomocysteinemia have not been investigated previous
114 Using a Tg-I278T Cbs(-/-) mouse model of hyperhomocysteinemia (HHcy) which replicates the connect
116 Vitamin B deficiencies, which can lead to hyperhomocysteinemia (Hhcy), are commonly reported in pa
122 rs, including smoking, hypercholesterolemia, hyperhomocysteinemia, hypertension, and diabetes mellitu
123 therefore, support the hypothesis that acute hyperhomocysteinemia impairs microvascular dilation in t
126 rocess, has been shown to be associated with hyperhomocysteinemia in experimental and human studies.
127 his article is to evaluate the prevalence of hyperhomocysteinemia in heart transplant recipients but
130 generation of APC by thrombin is impaired in hyperhomocysteinemia in monkeys and that hyperhomocystei
131 ose folic acid lowers but fails to normalize hyperhomocysteinemia in patients with predialysis chroni
137 ients have a persistent excess prevalence of hyperhomocysteinemia in the era of fortification but rem
139 d fortification program on the prevalence of hyperhomocysteinemia in the older population with coexis
140 in metabolism seem to be the major causes of hyperhomocysteinemia in this particular population.
143 rol and low-density lipoprotein cholesterol, hyperhomocysteinemia, increased lesional oxidative stres
144 ysfunction, we investigated whether moderate hyperhomocysteinemia induced by an oral methionine load
145 he first time, that the relationship between hyperhomocysteinemia induced by folate deficiency and pr
154 ospective and case-control studies show that hyperhomocysteinemia is an independent risk factor for a
160 These prospective observations confirm that hyperhomocysteinemia is an independent risk factor for c
172 zed H2S-generating reactions to the grade of hyperhomocysteinemia is in stark contrast to the respons
176 from vascular complications whereas dietary hyperhomocysteinemia is often used to induce atheroscler
179 , mildly elevated plasma total homocysteine (hyperhomocysteinemia) is associated with increased risk
183 e acknowledged left ventricular hypertrophy, hyperhomocysteinemia, lipoprotein(a) excess, hypertrigly
185 These findings suggest that inflammation and hyperhomocysteinemia may be important mechanisms by whic
186 tor V and that the prothrombotic tendency in hyperhomocysteinemia may be related to impaired inactiva
187 y be increased in Alzheimer disease (AD) and hyperhomocysteinemia may contribute to disease pathophys
189 in vivo and suggest that methionine-induced hyperhomocysteinemia may reverse hyperfibrinolysis in AP
192 Relative to their RTR counterparts, the hyperhomocysteinemia of HD patients seems to be consider
193 th comparable baseline tHcy levels, the mild hyperhomocysteinemia of maintenance HD patients is much
196 rly in populations with folate deficiency or hyperhomocysteinemia or both, may lower blood arsenic co
198 Elevated blood levels of homocysteine (Hcy), hyperhomocysteinemia or homocystinuria, have been associ
199 16 microM) or in human volunteers with acute hyperhomocysteinemia (plasma tHcy, 45 +/- 6 microM).
202 in hyperhomocysteinemia in monkeys and that hyperhomocysteinemia produces resistance to APC in monke
206 dies with human beings and animals with mild hyperhomocysteinemia provided encouraging results in the
207 emodialysis patients (ie, >90%) exhibit mild hyperhomocysteinemia refractory to treatment with either
213 d 59-fold and 72-fold in human patients with hyperhomocysteinemia secondary to mutations in methylene
215 -vitamin-deficient diet for 10 weeks induced hyperhomocysteinemia, significantly impaired spatial lea
216 ine beta-synthase knockout mice, a model for hyperhomocysteinemia, suggesting that one-carbon metabol
217 e United Kingdom have a higher prevalence of hyperhomocysteinemia than do their European counterparts
221 as an inhibitory mechanism in patients with hyperhomocysteinemia, the sensitivity of DDAH-1 to inhib
224 tamin B(12), and vitamin B(6)) would prevent hyperhomocysteinemia, vascular dysfunction, and atherosc
225 hen methionine-rich diets are used to induce hyperhomocysteinemia, vascular pathology is often observ
234 rposes of this study were to explore whether hyperhomocysteinemia was related to MTX administration a
235 nd the difference between extreme and severe hyperhomocysteinemia, we have examined two mouse models
236 e, hypertension, diabetes, dyslipidemia, and hyperhomocysteinemia were established as aggravating fac
237 e, hypertension, diabetes, dyslipidemia, and hyperhomocysteinemia were found significantly different
240 morphisms may play a role in the etiology of hyperhomocysteinemia, which is correlated with cardiovas
241 Bangladeshi men have a high prevalence of hyperhomocysteinemia, which is more closely associated w
243 volunteers or patients newly diagnosed with hyperhomocysteinemia with a C677T polymorphism of the MT
244 s enzyme are the leading cause of hereditary hyperhomocysteinemia with attendant cardiovascular and o
245 cular changes may mediate the association of hyperhomocysteinemia with human age-related cognitive de
246 d B vitamin-deficient diets developed severe hyperhomocysteinemia without any increase in vascular pa
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