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1 iron deficiency anemia, thrombocytosis, and hyperhomocysteinemia.
2 e the most common cause of severe hereditary hyperhomocysteinemia.
3 LF) diet for 6 to 8 months to produce graded hyperhomocysteinemia.
4 eta-synthase (Cbs)-heterozygous mice develop hyperhomocysteinemia.
5 uced the prevalence of folate deficiency and hyperhomocysteinemia.
6 ue to vegetarianism is increasing and causes hyperhomocysteinemia.
7 hepatic necroinflammation and apoptosis, and hyperhomocysteinemia.
8 uced activity, increased thermolability, and hyperhomocysteinemia.
9 hionine intake with B vitamin deficiency and hyperhomocysteinemia.
10 s of excess dietary methionine from those of hyperhomocysteinemia.
11 al macrophages was higher in the presence of hyperhomocysteinemia.
12 tion of placebo and after methionine-induced hyperhomocysteinemia.
13 associated with poor cognition, anemia, and hyperhomocysteinemia.
14 n peritoneal macrophages were not changed by hyperhomocysteinemia.
15 ncreased incidence of stroke associated with hyperhomocysteinemia.
16 ized by a plethora of vascular disorders and hyperhomocysteinemia.
17 s in young patients with iron deficiency and hyperhomocysteinemia.
18 on may contribute to vascular dysfunction in hyperhomocysteinemia.
19 ontribute to endothelial dysfunction in mild hyperhomocysteinemia.
20 o inactivating nitric oxide in chronic, mild hyperhomocysteinemia.
21 ively low blood folate levels and consequent hyperhomocysteinemia.
22 iciency in the elderly and its role in their hyperhomocysteinemia.
23 th elevated levels of homocysteine, known as hyperhomocysteinemia.
24 thogenesis of both homocystinuria and modest hyperhomocysteinemia.
25 ence of this mutation is not associated with hyperhomocysteinemia.
26 H2S in the thrombotic events associated with hyperhomocysteinemia.
27 mmation, and activation of fibrogenesis) and hyperhomocysteinemia.
28 -induced hearing loss associated with plasma hyperhomocysteinemia.
29 -beta-synthase (cbs) were used as a model of hyperhomocysteinemia.
30 steatosis or UPR activation despite inducing hyperhomocysteinemia.
31 macrovascular occlusion in individuals with hyperhomocysteinemia.
32 ocysteine; hence, their malfunction leads to hyperhomocysteinemia.
33 functional changes in cerebral arterioles in hyperhomocysteinemia.
34 sion of cochlear methionine cycle genes, and hyperhomocysteinemia.
35 regulation and has possible implications for hyperhomocysteinemia.
36 ugmentation was significantly blunted during hyperhomocysteinemia (1.06 +/- 1.00 ml/min/g vs. 0.58 +/
37 hial artery vasodilation was impaired during hyperhomocysteinemia (4.4 +/- 2.6% vs. 2.6 +/- 2.3%, pla
38 been observed in renal disease patients with hyperhomocysteinemia, a cardiovascular disease risk fact
42 instead, these inadequacies could result in hyperhomocysteinemia, a recently identified risk factor
44 lymorphism is a genetic determinant for mild hyperhomocysteinemia, a risk factor for cardiovascular d
45 m is the most frequent genetic cause of mild hyperhomocysteinemia, a risk factor for cardiovascular d
47 tomography (PET) to test the hypothesis that hyperhomocysteinemia adversely effects coronary microvas
48 o diet-induced hyperhomocysteinemia and that hyperhomocysteinemia alters tissue methylation capacity
52 al failure, a condition associated with both hyperhomocysteinemia and atherosclerosis, treatment with
54 ulating methylation; the MCD+B diet worsened hyperhomocysteinemia and depressed liver methylation pot
57 on to the fatty liver and no contribution to hyperhomocysteinemia and ER stress in intragastric alcoh
58 s containing ethanol or homocysteine induced hyperhomocysteinemia and glucose intolerance in control,
60 Using an atherogenic diet that produces both hyperhomocysteinemia and hypercholesterolemia, we tested
61 cal perturbations of methylmalonic acidemia, hyperhomocysteinemia and hypomethioninemia caused by the
64 that expression of Tg-CBS rescued the severe hyperhomocysteinemia and neonatal lethality of Cbs delet
65 ociated with the degree of liver injury were hyperhomocysteinemia and strain-dependent differences in
67 /-) genotype sensitizes mice to diet-induced hyperhomocysteinemia and that hyperhomocysteinemia alter
70 objective was to determine the prevalence of hyperhomocysteinemia and vitamin B-12 deficiency in elde
71 generative diseases that are associated with hyperhomocysteinemia and, more recently, have implicated
72 Hypothyroidism may be a treatable cause of hyperhomocysteinemia, and elevated plasma homocysteine l
73 In vivo studies using CBS+/-, a model for hyperhomocysteinemia, and sibling CBS+/+ control mice re
74 steatosis, endoplasmic reticulum stress, and hyperhomocysteinemia, and this correlates with induction
75 )S increases progressively with the grade of hyperhomocysteinemia, and under conditions of severely e
76 hionine intake with B vitamin deficiency and hyperhomocysteinemia; and (iii) normal methionine intake
79 e cellular hypomethylation in the setting of hyperhomocysteinemia because of cystathionine beta-synth
80 hat supplementation with B vitamins prevents hyperhomocysteinemia but is not sufficient to prevent th
82 alcoholic mouse liver and that correction of hyperhomocysteinemia by betaine or other approaches may
83 to tPA can be inhibited by homocysteine and hyperhomocysteinemia can be induced by L-methionine supp
87 abolism, combined methylmalonic acidemia and hyperhomocysteinemia, cblC type, is caused by mutations
95 of mouse to up-regulate BHMT which prevents hyperhomocysteinemia, endoplasmic reticulum stress, and
97 ), as was the prevalence of mild-to-moderate hyperhomocysteinemia (>12 microM; NHD, 57%; SHD, 94%; P
98 13.0 vs. 11.0+/-3.0 micromol/L, P<0.01), and hyperhomocysteinemia (>90th percentile for controls, 14.
107 ysfunction, and ERG defects; those with mild hyperhomocysteinemia have delayed retinal morphological/
108 that precipitate low blood folate levels and hyperhomocysteinemia have not been investigated previous
112 ies in homocysteine (Hcy) metabolism lead to hyperhomocysteinemia (HHcy) and cause endothelial dysfun
113 tritional and genetic deficiencies, leads to hyperhomocysteinemia (HHcy) and endothelial dysfunction,
116 ) were compared in patients with and without hyperhomocysteinemia (HHcy) and varying severity of HHcy
129 Using a Tg-I278T Cbs(-/-) mouse model of hyperhomocysteinemia (HHcy) which replicates the connect
131 Vitamin B deficiencies, which can lead to hyperhomocysteinemia (Hhcy), are commonly reported in pa
132 with a B-vitamin deficient diet that induces hyperhomocysteinemia (HHcy), cerebral vessel disease, an
133 roduction and altered caveolin expression in hyperhomocysteinemia (HHcy), leading to endothelial dysf
140 rs, including smoking, hypercholesterolemia, hyperhomocysteinemia, hypertension, and diabetes mellitu
141 therefore, support the hypothesis that acute hyperhomocysteinemia impairs microvascular dilation in t
144 rocess, has been shown to be associated with hyperhomocysteinemia in experimental and human studies.
145 his article is to evaluate the prevalence of hyperhomocysteinemia in heart transplant recipients but
148 generation of APC by thrombin is impaired in hyperhomocysteinemia in monkeys and that hyperhomocystei
149 ose folic acid lowers but fails to normalize hyperhomocysteinemia in patients with predialysis chroni
155 ients have a persistent excess prevalence of hyperhomocysteinemia in the era of fortification but rem
157 d fortification program on the prevalence of hyperhomocysteinemia in the older population with coexis
158 in metabolism seem to be the major causes of hyperhomocysteinemia in this particular population.
161 rol and low-density lipoprotein cholesterol, hyperhomocysteinemia, increased lesional oxidative stres
163 ysfunction, we investigated whether moderate hyperhomocysteinemia induced by an oral methionine load
164 he first time, that the relationship between hyperhomocysteinemia induced by folate deficiency and pr
173 ospective and case-control studies show that hyperhomocysteinemia is an independent risk factor for a
179 These prospective observations confirm that hyperhomocysteinemia is an independent risk factor for c
192 zed H2S-generating reactions to the grade of hyperhomocysteinemia is in stark contrast to the respons
196 from vascular complications whereas dietary hyperhomocysteinemia is often used to induce atheroscler
199 , mildly elevated plasma total homocysteine (hyperhomocysteinemia) is associated with increased risk
201 g level of homocysteine (Hcy), also known as hyperhomocysteinemia, is a risk factor for Alzheimer's d
204 e acknowledged left ventricular hypertrophy, hyperhomocysteinemia, lipoprotein(a) excess, hypertrigly
206 These findings suggest that inflammation and hyperhomocysteinemia may be important mechanisms by whic
207 tor V and that the prothrombotic tendency in hyperhomocysteinemia may be related to impaired inactiva
208 y be increased in Alzheimer disease (AD) and hyperhomocysteinemia may contribute to disease pathophys
210 in vivo and suggest that methionine-induced hyperhomocysteinemia may reverse hyperfibrinolysis in AP
213 Relative to their RTR counterparts, the hyperhomocysteinemia of HD patients seems to be consider
214 th comparable baseline tHcy levels, the mild hyperhomocysteinemia of maintenance HD patients is much
217 rly in populations with folate deficiency or hyperhomocysteinemia or both, may lower blood arsenic co
219 Elevated blood levels of homocysteine (Hcy), hyperhomocysteinemia or homocystinuria, have been associ
220 16 microM) or in human volunteers with acute hyperhomocysteinemia (plasma tHcy, 45 +/- 6 microM).
223 in hyperhomocysteinemia in monkeys and that hyperhomocysteinemia produces resistance to APC in monke
227 dies with human beings and animals with mild hyperhomocysteinemia provided encouraging results in the
228 emodialysis patients (ie, >90%) exhibit mild hyperhomocysteinemia refractory to treatment with either
234 d 59-fold and 72-fold in human patients with hyperhomocysteinemia secondary to mutations in methylene
236 -vitamin-deficient diet for 10 weeks induced hyperhomocysteinemia, significantly impaired spatial lea
237 ine beta-synthase knockout mice, a model for hyperhomocysteinemia, suggesting that one-carbon metabol
239 e United Kingdom have a higher prevalence of hyperhomocysteinemia than do their European counterparts
243 as an inhibitory mechanism in patients with hyperhomocysteinemia, the sensitivity of DDAH-1 to inhib
246 tamin B(12), and vitamin B(6)) would prevent hyperhomocysteinemia, vascular dysfunction, and atherosc
247 hen methionine-rich diets are used to induce hyperhomocysteinemia, vascular pathology is often observ
256 rposes of this study were to explore whether hyperhomocysteinemia was related to MTX administration a
257 nd the difference between extreme and severe hyperhomocysteinemia, we have examined two mouse models
258 e, hypertension, diabetes, dyslipidemia, and hyperhomocysteinemia were established as aggravating fac
259 e, hypertension, diabetes, dyslipidemia, and hyperhomocysteinemia were found significantly different
262 morphisms may play a role in the etiology of hyperhomocysteinemia, which is correlated with cardiovas
263 Bangladeshi men have a high prevalence of hyperhomocysteinemia, which is more closely associated w
265 volunteers or patients newly diagnosed with hyperhomocysteinemia with a C677T polymorphism of the MT
266 s enzyme are the leading cause of hereditary hyperhomocysteinemia with attendant cardiovascular and o
267 cular changes may mediate the association of hyperhomocysteinemia with human age-related cognitive de
268 d B vitamin-deficient diets developed severe hyperhomocysteinemia without any increase in vascular pa