ライフサイエンスコーパス: zinc deficiency

1 r activation of transcription in response to zinc deficiency.

2 in 50% were consistent with the presence of zinc deficiency.

3 f zinc homeostasis and adaptive responses to zinc deficiency.

4 mpaired regeneration, as well as significant zinc deficiency.

5 ome Mexican American children are at risk of zinc deficiency.

6 ated that these genes respond differently to zinc deficiency.

7 oped and developing countries pose a risk of zinc deficiency.

8 than were their wild-type littermates during zinc deficiency.

9 is that are commonly associated with dietary zinc deficiency.

10 p target whose expression is increased under zinc deficiency.

11 a central player in the response of yeast to zinc deficiency.

12 nduces target gene expression in response to zinc deficiency.

13 ith the increased oxidative stress caused by zinc deficiency.

14 opogenic CO2 emissions on the global risk of zinc deficiency.

15 ace of enterocytes and endoderm cells during zinc deficiency.

16 Ys1 mRNA expression patterns in response to zinc deficiency.

17 ell surfaces and internalized during dietary zinc deficiency.

18 purposes in the prevention and treatment of zinc deficiency.

19 zinc importers are upregulated during severe zinc deficiency.

20 a result showing gene-modulating effects of zinc deficiency.

21 d promoter element (ZRE) under conditions of zinc deficiency.

22 l disease (SCD) may be due, in part, to mild zinc deficiency.

23 ion that occur in the early stages of rodent zinc deficiency.

24 berrant Th1/Th2 cytokine balance observed in zinc deficiency.

25 xpression of its target genes in response to zinc deficiency.

26 0 (products of Th2) were not affected during zinc deficiency.

27 Apoptosis is potentiated by zinc deficiency.

28 health effects of mild-to-moderate maternal zinc deficiency.

29 (NIDDM) may cause vulnerability to moderate zinc deficiency.

30 her they are primary or secondary effects of zinc deficiency.

31 components required for GAS survival during zinc deficiency.

32 al regulation of target genes in response to zinc deficiency.

33 increase in the human population at risk of zinc deficiency.

34 hat ZnT mutations play in transient neonatal zinc deficiency.

35 ndernutrition, suboptimum breastfeeding, and zinc deficiency.

36 lows for the expression of genes required in zinc deficiency.

37 ecreases the oxidative stress that occurs in zinc deficiency.

38 the Tsa1 chaperone function in tolerance to zinc deficiency.

39 ting/refeeding, and increased with beta cell zinc deficiency.

40 ca burdened with high prevalence of iron and zinc deficiency.

41 ommunity-based sample of children at risk of zinc deficiency.

42 .24, 6.90) children had an increased risk of zinc deficiency.

43 sponse is induced under conditions of severe zinc deficiency.

44 regarding how cells respond to the stress of zinc deficiency.

45 ew all of the disease states associated with zinc deficiency.

46 lights a few of the diseases associated with zinc deficiency.

47 es of Arabidopsis to micronutrient (iron and zinc) deficiencies.

48 To discover molecular signatures of human zinc deficiency, a combination of transcriptome, cytokin

49 l trait A46, also known as bovine hereditary zinc deficiency, Adema disease, and hereditary parakerat

50 rease in cells in the proliferative phase as zinc deficiency advanced.

51 ly both in proportion and absolute number as zinc deficiency advanced.

52 Neither did zinc deficiency affect the intracellular distribution of

53 Zinc deficiency affects many organ systems, including th

54 Zinc deficiency alone induced unrestrained cellular prol

55 Zinc deficiency also affects development of acquired imm

56 d the populations who are at highest risk of zinc deficiency also receive most of their dietary zinc

57 Zinc deficiency alters autonomic nervous system regulati

58 Whether zinc deficiency alters the rate of production of myeloid

59 n patients owing to the less recognized mild zinc deficiency among the 'at-risk population' as in the

60 of this review is to present the evidence of zinc deficiencies and toxicities as well as treatment in

61 Some genes are induced under mild zinc deficiency and act as a first line of defense again

62 objective was to determine the prevalence of zinc deficiency and anemia and their interrelation among

63 The prevalence of zinc deficiency and anemia was high in this population o

64 nment and suggests that the relation between zinc deficiency and cognitive development may vary by ag

65 Zinc deficiency and contaminated water are major contrib

66 In many diseases, zinc deficiency and elevated level of Hh ligand co-exist

67 ncentrations among young children at risk of zinc deficiency and examined the relations between these

68 Because zinc deficiency and excess result in toxicity, animals h

69 sion, differential responsiveness to dietary zinc deficiency and excess, and differential responsiven

70 alcohol abuse is associated with significant zinc deficiency and immune dysfunction within the alveol

71 s suggest the need for prevention of chronic zinc deficiency and improvement of general nutritional s

72 This study was designed to determine if zinc deficiency and inappropriate urinary zinc losses ar

73 genes allow cells to adapt to conditions of zinc deficiency and include genes involved in maintainin

74 Prepubertal children with SCD-SS may have zinc deficiency and may benefit from zinc supplementatio

75 To identify targets of zinc deficiency and mechanisms of zinc acclimation, we u

76 hageal cell proliferation induced by dietary zinc deficiency and reduced the incidence of esophageal

77 protein, a transcription factor that senses zinc deficiency and responds by up-regulating genes invo

78 Zinc deficiency and retinitis pigmentosa are both import

79 ost resistance to infections observed during zinc deficiency and supplementation.

80 Further investigation of the incidence of zinc deficiency and the ability of anemia to screen for

81 r data suggest a causal relationship between zinc deficiency and the overproduction of Hh ligand.

82 he identification of populations at risk for zinc deficiency and to monitoring the effects of zinc in

83 improved water and sanitation, vitamin A and zinc deficiencies, and ambient particulate matter pollut

84 Thirty were increased in zinc deficiency, and 17 were decreased.

85 nds to copper limitation and is turned on in zinc deficiency, and Crr1 is required for growth in zinc

86 -regulation of zinc transporter genes during zinc deficiency, and the WAKL4 T-DNA insertion resulted

87 Iron and zinc deficiency are prevalent during infancy in low-inco

88 isiae, homeostatic and adaptive responses to zinc deficiency are regulated by the Zap1 transcription

89 iciency anemia, night blindness, and risk of zinc deficiency are summarized.

90 ifying population groups at elevated risk of zinc deficiency, are sparse and difficult to interpret b

91 ing the public health importance of maternal zinc deficiency as it relates to fetal growth and develo

92 , and infants are particularly vulnerable to zinc deficiency as they require large amounts of zinc fo

93 us DNA sequences was decreased markedly with zinc deficiency, as assayed by electrophoretic mobility-

94 hageal cell proliferation induced by dietary zinc deficiency, as measured by the labeling index, the

95 Specifically, we focus on a zinc deficiency B. distachyon basic leucine zipper trans

96 everity was associated with greater relative zinc deficiency (B = -1.503, t9 = -2.82, p = .026).

97 ed households may be predisposed to iron and zinc deficiency because of nondietary factors such as ch

98 using a periorificial and/or acrodermatitis: zinc deficiency, biotin deficiency, kwashiorkor, and ess

99 tion in foliar tissue under ozone stress and zinc deficiency, but did not affect the sensitivity to i

100 e (SGA) infants are susceptible to postnatal zinc deficiency, but whether this susceptibility is due

101 people estimated to be placed at new risk of zinc deficiency by 2050 was 138 million (95% CI 120-156)

102 Mild to moderate zinc deficiency can be best detected through a positive

103 ty to NMBA-induced carcinogenesis induced by zinc deficiency can be inhibited by alpha-difluoromethyl

104 f zinc ions in rhodopsin and examine whether zinc deficiency can lead to rhodopsin dysfunction.

105 These data support the concept that zinc deficiency can result in alterations in iron transp

106 Zinc deficiency caused no change in the cell cycle statu

107 Dietary zinc deficiency causes a marked increase in the accumula

108 Zinc deficiency causes exaggerated inflammatory response

109 t with this hypothesis, we demonstrated that zinc deficiency causes increased reactive oxygen species

110 It was recently shown that zinc deficiency causes sizable losses among the precurso

111 Zinc deficiency causes thymic atrophy and lymphopenia.

112 Zinc deficiency, cell-mediated immune dysfunction, susce

113 Zinc deficiency correlates only with severe chronic panc

114 The mechanisms through which zinc deficiency could influence health outcomes are well

115 he mechanisms responsible for the effects of zinc deficiency, cultured human Ntera-2 (NT2) neuronal p

116 In HuT-78, a Th0 cell line, zinc deficiency decreased gene expression of thymidine k

117 Zinc deficiency decreased natural killer cell lytic acti

118 nd behavior in animals; the relation between zinc deficiency, depression, and ADHD in patient and com

119 Secondary outcomes were prevalence of zinc deficiency, diarrhea prevalence, and growth.

120 his nutritional requirement in humans is the zinc deficiency disease, acrodermatitis enteropathica.

121 Zinc deficiency disrupts their folding, and the ubiquiti

122 Therefore, zinc deficiency due to loss-of-function ZnT8 mutations s

123 Dietary zinc deficiency during pregnancy down-regulated ZnT1 and

124 Maternal dietary zinc deficiency during pregnancy exacerbated these effec

125 Maternal zinc deficiency during pregnancy may be widespread among

126 ould be considered in populations at risk of zinc deficiency, especially where there are elevated rat

127 to down-regulate sulfate assimilation under zinc deficiency experience increased oxidative stress.

128 Before transplant, patients with zinc deficiency had higher urinary zinc to creatinine ra

129 Zinc deficiency has also been implicated in diarrheal di

130 x months of age; however, transient neonatal zinc deficiency has been documented in exclusively breas

131 Zinc deficiency has been shown to contribute to the prog

132 oblem reserved for underdeveloped countries, zinc deficiency has increasing pediatric prevalence in t

133 mutation, associated with transient neonatal zinc deficiency, has on ZnT1, ZnT3, and ZnT4 upon hetero

134 tation in SLC30A2 and can result in neonatal zinc deficiency if unrecognized.

135 Zinc deficiency impairs overall immune function and resi

136 lectrolytic iron in addressing both iron and zinc deficiencies in low socio-economic populations of s

137 Growth retardation has been associated with zinc deficiency in adolescent human populations, but ani

138 Zinc deficiency in an experimental human model caused an

139 ed transcriptional activation in response to zinc deficiency in cells, suggesting a conserved pathway

140 During the last decade, the significance of zinc deficiency in childhood growth, morbidity, and mort

141 Zinc deficiency in children is an important public healt

142 inding of NF-kappaB to DNA were decreased by zinc deficiency in HuT-78.

143 bution to progress toward the eradication of zinc deficiency in infants and young children in the dev

144 Although there is a greater risk of zinc deficiency in persons consuming lactoovovegetarian

145 Zinc deficiency in pregnant experimental animals limits

146 Zinc deficiency in rats enhances esophageal cell prolife

147 reased cell proliferation induced by dietary zinc deficiency in rats plays a critical role in esophag

148 an extensive discussion of the influence of zinc deficiency in selected diseases.

149 role in human immunity, and it is known that zinc deficiency in the host is linked to increased susce

150 ified the gene responsible for the inherited zinc deficiency in the lethal milk (lm) mouse.

151 ears focused attention on the possibility of zinc deficiency in the United States.

152 Zinc deficiency in this yeast induces the unfolded prote

153 Zinc deficiency increased mZIP4 protein levels at the pl

154 Zinc deficiency increased plasma membrane levels of mZip

155 Zinc deficiency increased the forestomach cell prolifera

156 nal TBARS in group 2 indicates that moderate zinc deficiency increases oxidative stress to the retina

157 umulation of IRP2 protein was independent of zinc deficiency-induced intracellular nitric oxide produ

158 ve element isoform mRNA was decreased during zinc deficiency-induced iron accumulation.

159 We conclude that zinc deficiency induces the production of a low-molecula

160 Zinc deficiency is a cause of immune dysfunction and inf

161 Zinc deficiency is a major cause of childhood morbidity

162 Zinc deficiency is a potential risk factor for disease i

163 Zinc deficiency is a relatively common problem in childr

164 Zinc deficiency is also associated with acute and chroni

165 One consequence of zinc deficiency is an elevation in cell and tissue iron

166 common nutritional deficiency in the world; zinc deficiency is associated with poor growth and devel

167 Zinc deficiency is closely associated with stunting, res

168 D2 may contribute more to Zap1 function when zinc deficiency is combined with other environmental str

169 Zinc deficiency is common among populations at high risk

170 Zinc deficiency is currently responsible for large burde

171 Zinc deficiency is discussed in another, and the arsenic

172 elopment of intervention programs to control zinc deficiency is hampered by the lack of sensitive, sp

173 Zinc deficiency is implicated in the pathogenesis of hum

174 Zinc deficiency is increasingly recognized as an importa

175 deficiency, but whether they can also reduce zinc deficiency is less certain.

176 e public health importance of this degree of zinc deficiency is not well defined.

177 Zinc deficiency is one of the most consistently observed

178 Maternal zinc deficiency is relatively common in developing count

179 ansplant is rapidly improved and biochemical zinc deficiency is reversed after liver transplantation.

180 morbidity and mortality in populations with zinc deficiency is unclear.

181 ells relative to zinc-replete cells, whereas zinc deficiency is visually asymptomatic but distinguish

182 inc by enterocytes, and the ensuing systemic zinc deficiency leads to dermatological lesions and immu

183 In children in developing countries, zinc deficiency may be common and associated with immune

184 Decreased production of IL-2 in zinc deficiency may be due to decreased activation of NF

185 Mild-to-moderate zinc deficiency may be relatively common worldwide, but

186 ive development are unclear, it appears that zinc deficiency may lead to deficits in children's neuro

187 both animal and human studies suggests that zinc deficiency may lead to delays in cognitive developm

188 Zinc deficiency may result in abnormal dark adaptation o

189 These responses to dietary zinc deficiency mimic those found in the adult intestine

190 to diverse physiological stresses, including zinc deficiency, nitrogen starvation, and inhibition of

191 study supports the contention that moderate zinc deficiency occurs frequently in subjects with NIDDM

192 American race-ethnicity was associated with zinc deficiency (odds ratio: 0.26; P = 0.02).

193 We investigate the effect of zinc deficiency on DNA damage, expression of DNA-repair

194 ntestine and the effects of maternal dietary zinc deficiency on these patterns of expression were exa

195 ion of undernutrition (stunting, anemia, and zinc deficiency), overweight, and obesity in Ecuador to

196 y-treatment effect on PZn (P = 0.026) and on zinc deficiency (P = 0.032) was found; PZn in the Zn+fil

197 In the early phases zinc deficiency, p53 targets responsible for cell cycle

198 ed, makes it difficult to isolate effects of zinc deficiency per se from those of generalized protein

199 m1 and various CAH genes are up-regulated in zinc deficiency, probably due to reduced carbonic anhydr

200 the result of vesicular zinc trapping and ER zinc deficiency rather than overload.

201 decades, the estimated global prevalence of zinc deficiency remains high.

202 The biochemistry of human nutritional zinc deficiency remains poorly defined.

203 2-49 y have excess body weight and anemia or zinc deficiency, respectively.

204 Zinc deficiency results in dysfunction of both humoral a

205 In zinc deficiency, RNAPI is specifically degraded by prote

206 Subacute zinc deficiency significantly increases systemic inflamm

207 y exploring the transcriptional responses to zinc deficiency, studies of the yeast Saccharomyces cere

208 layed some classic manifestations of dietary zinc deficiency, such as reduced food intake and poor bo

209 Thymocyte apoptosis is potentiated by zinc deficiency, suggesting that these iron chelators ma

210 d ZIP3 are expressed in roots in response to zinc deficiency, suggesting that they transport zinc fro

211 udies using cultured HepG2 cells showed that zinc deficiency suppressed cell proliferation and cell p

212 two exclusively breast-fed infants developed zinc deficiency that was associated with low milk zinc c

213 metabolic consequences (much more than with zinc deficiency) that included altered energy, polyamine

214 ded phosphatidate phosphatase was induced by zinc deficiency through a mechanism that involved intera

215 rs with infants harboring transient neonatal zinc deficiency (TNZD).

216 e needed from other populations with endemic zinc deficiency to confirm the potential age-specific ef

217 Finally, zinc deficiency up-regulates the mammalian ER stress res

218 oexistence of OW/OB and stunting, anemia, or zinc deficiency was found in 2.8%, 0.7%, and 8.4% of sch

219 rely deficient in both copper and zinc ions, zinc deficiency was not a consistent feature shared by t

220 Zinc deficiency was present in all affected individuals

221 Greater zinc deficiency was required to alter mZip3 distribution

222 oncentrations (ie, population at new risk of zinc deficiency) was our measure of impact.

223 Using an in vivo model of acute dietary zinc deficiency, we show that feeding a zinc deficient d

224 ties of specific serum microRNAs for dietary zinc deficiency were identified by acute responses to zi

225 fects on the fecal microbiota of protein and zinc deficiency were probed independently in a murine mo

226 In contrast, during periods of dietary zinc deficiency when secretion of zinc by the pancreas a

227 and conservation are derepressed during mild zinc deficiency, whereas the energy-dependent zinc impor

228 unologic functions, is adversely affected by zinc deficiency, which can dysregulate intracellular kil

229 is proteolytically removed during prolonged zinc deficiency while the remaining eight-transmembrane

230 Although the mechanisms linking zinc deficiency with cognitive development are unclear,

231 ism by which L. monocytogenes can respond to zinc deficiency within a variety of environments and dur

232 ine the public health importance of maternal zinc deficiency worldwide.

233 We hypothesized that subacute zinc deficiency would amplify immune responses and oxida

234 In response to zinc deficiency, Zap1 activates transcription of many ge

235 Thus, during zinc deficiency, Zap1 mediates the repression of two of

236 duration are the immunological hallmarks of zinc deficiency (ZD) in humans and higher animals.

237 Dietary zinc deficiency (ZD) in mice enhances cellular prolifera

238 Zinc deficiency (ZD) in rats increases esophageal cell p

239 IP4 gene, which is induced during periods of zinc deficiency, ZIP5 gene expression is unaltered by di