ライフサイエンスコーパス: GH

1 GH declines prior to the onset of weight gain in respons

2 GH excess leads to decreased colon cell phosphatase and

3 GH granules showed an excellent adsorption capacity (235

4 GH induced STAT3 phosphorylation and nuclear translocati

5 GH protein was upregulated in the amygdala following chr

6 GH receptor (GHR) antagonist therapy is more effective b

7 GH remains unchanged.

8 GH replacement can resolve the fatty liver condition in

9 GH resistance dramatically exacerbates liver fibrosis in

10 GH-deficient prophet of pituitary-specific positive tran

11 growth hormone/insulin-like growth factor 1 (GH/IGF1) axis.

12 growth hormone-insulin-like growth factor-1 (GH-IGF-1) axis.

13 Growth Hormone/Insulin-like Growth Factor-1 (GH/IGF-1) pathway as well as pathways related to synapse

14 h hormone/insulin-like growth factor type 1 (GH/IGF1) axis, whose alterations in gene expression appe

15 transducer and activator of transcription 5 (GH-Stat5) signaling compared to wild-type mice.

16 A GH carrier containing OP3-4 with BMP-2 was subperiosteal

17 Promoter and expression analysis in a GH-secreting rat cell line (GH3) revealed that STAT3 spe

18 Administration of a GH receptor (GHR) blocker in acromegaly patients induced

19 Finally, virus-mediated overexpression of a GH receptor antagonist was sufficient to block the fear-

20 ression of dominant-negative STAT3 abrogated GH expression.

21 ogether, these results indicate that adenoma GH hypersecretion is the result of STAT3-dependent GH in

22 elopment of fatty liver depends on adipocyte GH signaling.

23 clampsia) and 1.81 (95% CI, 1.44-2.27) after GH vs no HDP.

24 54 years and 5.08 (95% CI, 1.80-14.34) after GH vs no GH.

25 mortality was 1.57 (95% CI, 1.04-2.39) after GH vs no GH.

26 or eclampsia, 1.51 (95% CI, 1.27-1.80) after GH vs no HDP, 1.62 (95% CI, 1.46-1.79) after preterm del

27 lin-like growth factor 1 (IGF-1) that allows GH release from the pituitary.

28 To test the hypothesis that an altered GH/IGF1 axis relates to the longevity of African mole-ra

29 ent of idraparinux and its C5'-epi analogue (GH unit) has been developed.

30 signaling has been connected to cancer, and GH insensitivity has been reported in cachexia patients.

31 in 14 steps into the fully protected EF and GH disaccharide fragments.

32 with stronger associations when both GDM and GH were present.

33 -201 attenuated somatotroph tumor growth and GH secretion in a rat xenograft model.

34 Acute ethanol elevated DA in SI and GH rats and nor-BNI pretreatment augmented this effect i

35 Na2CO3 SRC and GH were strongly correlated.

36 Moreover, STAT3 and GH expression were concordant in a somatotroph adenoma t

37 g a positive feedback loop between STAT3 and GH in somatotroph tumor cells.

38 ons of the microbial community structure and GH potential for carbohydrate utilization were correlate

39 acid (RGD) motif in the exposed, antigenic, GH loop of capsid protein VP1.

40 th the specific inhibitor S3I-201 attenuated GH transcription and reduced GH secretion in the majorit

41 d worker bees from four genetic backgrounds (GH) and reared them in normal (within hives) or stressed

42 al analysis of a carbocyclic mechanism-based GH inactivator, the results of which show that the two M

43 Due to the intricate relationship between GH and IGF-1, the relative contribution of each hormone

44 to persistent GH stimulation are dictated by GH/STAT5-regulated transcription factors arranged in a h

45 an the customary testosterone, but likely by GH.

46 Microbiomes were generally more variable by GH in stressed bees, which also showed opposing and comp

47 TAT3 directly induces somatotroph tumor cell GH.

48 Increased circulatory GH culminated in a switch in whole body fuel metabolism

49 rms their predicted classification into clan GH-F together with GH43 alpha-L-arabinofuranosidases.

50 We show that locally expressed colon GH is abundant in conditions predisposing to colon cance

51 By manipulating the highly conserved -GH- residues in the CGHC active site of PDI, we created

52 n 15 min after resistance exercise contained GH concentrations that were approximately 7-fold greater

53 and epigenetic changes induced by continuous GH infusion (cGH) in male mice, which rapidly feminizes

54 Conversely, adiponectin decreased GH-release, and inhibited GHRH-, but not ghrelin-stimula

55 hyperphagic obesity, hypogonadism, decreased GH, and hypoinsulinemic diabetes due to impaired prohorm

56 ersecretion is the result of STAT3-dependent GH induction, which in turn promotes STAT3 expression, a

57 tion sequence leading to l-ido disaccharide (GH unit) with a total yield of 24% (36% for the EF fragm

58 into the architecture and role of SLH domain GHs and demonstrate that hemicellulose degradation can b

59 an be enhanced through non-native SLH domain GHs engineered into the genomes of Caldicellulosiruptors

60 Calkro_0402, another of the SLH domain GHs inC. kronotskyensis, when produced inE. coli, was ac

61 s in post-translational modifications during GH-induced signaling events and show that relatively sim

62 n GH3 cells induced expression of endogenous GH, and expression of a constitutively active STAT3 furt

63 constitutively active STAT3 further enhanced GH production.

64 thesized that keystone genes from the entire GH complement of Salmonella are required to degrade glyc

65 s renaturalization of the masculine episodic GH profile restored normal male-like levels of CYP2C11,

66 ignal transduction pathway by which episodic GH solely regulates the isoform's expression.

67 ate GH signaling leads to disease: excessive GH signaling has been connected to cancer, and GH insens

68 at high resolution, attaches to an extended GH loop via interactions with the RGD motif plus downstr

69 ng treatment with BA, and to a lesser extent GH (p < 0.001, treatment x time interaction).

70 The provision of extracellular GHs as public goods may influence microbial community dy

71 Deletion of NPY did not impact fed GH release; however, it reversed the fasting-induced sup

72 the GH receptor gene (Ghr(-/-), a model for GH resistance) by crossing them with Mdr2 knockout mice

73 ion, we found associations of a combined GDM/GH indicator with cardiometabolic disease in mothers and

74 We evaluated a combined GDM/GH risk indicator in both mothers and fathers because of

75 64,232 couples were categorized based on GDM/GH status (neither, either, or both).

76 These host-parasite genotype-by-genotype (GH x GP) interactions influence evolutionary and ecologi

77 own in three growing conditions: greenhouse (GH), plastic tunnel (PT) and open-field (OF) for two gro

78 response to specifically recognize Globo H (GH) and the GH-related epitopes, stage-specific embryoni

79 sed transgenic mice containing the human (h) GH gene (hGH1) locus to investigate the rhythmicity of h

80 r (SF) and negatively to the grain hardness (GH) and Na2CO3 SRC.

81 vGHRkd) mouse was developed to model hepatic GH resistance in humans that may occur after sexual matu

82 KSR2) causes selective inhibition of hepatic GH signaling in neonatal mice with impaired expression o

83 rowth hormone (GH) production and/or hepatic GH resistance.

84 These results demonstrate that hepatic GH actions normally serve to inhibit DNL, where loss of

85 s to dissect the mechanisms by which hepatic GH resistance leads to steatosis and overall insulin res

86 tes liver tumourigenesis in presence of high GH levels.

87 ctin-levels, while CORT-KOs displayed higher GH- and lower prolactin-levels than controls under both

88 -diet conditions as SST-KOs presented higher GH/prolactin-levels, while CORT-KOs displayed higher GH-

89 Cultivars with higher GH produced higher amount of coarse particles in flours

90 Life-long lack of growth hormone (GH) action can produce remarkable extension of longevity

91 Plasma growth hormone (GH) and hepatic autophagy each have been reported to pro

92 domains of the receptors of growth hormone (GH) and insulin-like growth factor 1 (IGF1).

93 puberty, the serum levels of growth hormone (GH) and its downstream effector IGF-1 increase and play

94 In humans, low levels of growth hormone (GH) and its mediator, IGF-1, associate with hepatic lipi

95 cal excess and deficiency of growth hormone (GH) are associated with cardiovascular mortality.

96 Levels of growth hormone (GH) are elevated in T1D, which aggravates both hyperglyc

97 ium glutamate (MSG), a total growth hormone (GH) blocker, and, using cultured hepatocytes, examined e

98 luteinizing hormone (LH) and growth hormone (GH) cells.

99 Growth hormone (GH) excess in acromegaly is associated with increased pr

100 megaly is a human disease of growth hormone (GH) excess with considerable morbidity and increased mor

101 nomas result in dysregulated growth hormone (GH) hypersecretion and acromegaly; however, regulatory m

102 Growth hormone (GH) is a major metabolic homeostatic factor that is secr

103 LD) are reported to have low growth hormone (GH) production and/or hepatic GH resistance.

104 Growth hormone (GH) resistance has been associated with liver cirrhosis

105 ship between food intake and growth hormone (GH) secretion; however, the mechanism through which endo

106 Sex-dependent pituitary growth hormone (GH) secretory profiles-pulsatile in males and persistent

107 ed the importance of hepatic growth hormone (GH) signaling in the development of NAFLD.

108 Growth hormone (GH) signaling is required for promoting longitudinal bod

109 Disruption of hepatocyte growth hormone (GH) signaling through disruption of Jak2 (JAK2L) leads t

110 g 2 (SOCS2), an inhibitor of growth hormone (GH) signaling, was strongly induced after partial hepate

111 actor STAT5 in liver impairs growth hormone (GH) signalling and thereby promotes fatty liver disease.

112 anscriptionally regulated by growth hormone (GH) through growth hormone response elements (GHREs).

113 ed links between ghrelin and growth hormone (GH), a major downstream effector of the ghrelin receptor

114 Levels of pituitary growth hormone (GH), a metabolic homeostatic factor with strong lipolyti

115 nes such as prolactin (PRL), growth hormone (GH), adrenocorticotropic hormone (ACTH), and thyroid sti

116 rtisol and high aldosterone, growth hormone (GH), and prolactin levels, thereby presumably fostering

117 irculating hormones, such as growth hormone (GH), but the biological functions of this response are u

118 releasing hormone (GHRH) and Growth hormone (GH), underappreciated findings in ARID1B patients.

119 of MC4R function may enhance growth hormone (GH)-mediated growth, although this remains untested.

120 entral hypogonadism, and low growth hormone (GH).

121 ed) or Reporcin (recombinant growth hormone; GH; 10 mg/48 hours injected) and compared to a control c

122 y-like behaviors compared with group housed (GH) rats.

123 e measured with a high-sensitivity assay (hs-GH) predict cardiovascular morbidity and mortality at th

124 ls, we related baseline levels of fasting hs-GH to incidence of coronary artery disease, stroke, cong

125 increment of natural logarithm of fasting hs-GH) was independently associated with increased risk of

126 The addition of hs-GH to a model with conventional cardiovascular risk fact

127 Higher values of hs-GH were associated with an increased risk of cardiovascu

128 During a median follow-up of 16.2 years, hs-GH (hazard ratio [HR]/SD increment of natural logarithm

129 that STAT3 expression was enhanced in human GH-secreting adenomas compared with that in nonsecreting

130 We used transgenic mice expressing the human GH (hGH) gene, GH1, to assess the effect of high caloric

131 axilla using an injectable gelatin hydrogel (GH) carrier.

132 e-dimensional (3D) porous graphene hydrogel (GH) adsorbents.

133 eta-glucosidases of the glycoside hydrolase (GH) 1 family are tolerant to or even stimulated by gluco

134 e genes encode a unique glycoside hydrolase (GH) family 10 endoxylanase (BiXyn10A or BACINT_04215 and

135 he founding member of a glycoside hydrolase (GH) family, GH145.

136 served when we compared glycoside hydrolase (GH) profile of buffalo rumen metagenome with cow rumen,

137 Glycoside hydrolases (GH) are enzymes that mainly hydrolyze the glycosidic bon

138 active enzymes such as glycoside hydrolases (GHs) and glycosyltransferases (GTs) are of growing impor

139 proteins include five glycoside hydrolases (GHs) and one polysaccharide lyase, the genes for which w

140 Glycoside hydrolases (GHs) cleave glycosidic linkages in carbohydrates, typica

141 Glycoside hydrolases (GHs) distort carbohydrate ring geometry along particular

142 Glycoside hydrolases (GHs) have attracted considerable attention as targets fo

143 The conversion of glycoside hydrolases (GHs) into transglycosylases (TGs), i.e., from enzymes th

144 Processive glycoside hydrolases (GHs), like cellobiohydrolase Cel7A of Trichoderma reesei

145 nixE to nixL) encoding glycoside hydrolases (GHs).

146 containing multidomain glycoside hydrolases (GHs).

147 Salmonella contains 47 glycosyl hydrolases (GHs) that may degrade the glycan.

148 and layered structure of graphene hydroxide (GH) was investigated.

149 ies complicated by gestational hypertension (GH) and preeclampsia.

150 ation, but data on gestational hypertension (GH) are limited.

151 mellitus (GDM) and gestational hypertension (GH) with cardiometabolic disease has not been well studi

152 n pregnancy (HDP) (gestational hypertension [GH], preeclampsia, or eclampsia) and 1.81 (95% CI, 1.44-

153 furthermore, rhFGF21 did not prevent (125)I-GH binding.

154 If GH and receptors are made in the same cell (autocrine mo

155 ndition in diet-induced obese rodents and in GH-deficient patients.

156 ar mass were the most consistent findings in GH and preeclampsia.

157 Goat(-/-) mice showed a blunted increase in GH and a marked decrease in hepatic autophagy.

158 ted from ksr2(-/-) mice show no reduction in GH-stimulated STAT5 phosphorylation.

159 o effect on ethanol-stimulated DA release in GH rats.

160 elop intestinal and colon tumors resulted in GH-deficient double mutants with markedly decreased tumo

161 ort-stature humans harboring an inactivating GH receptor mutation do not develop cancer.

162 al air toxics before conception may increase GH risk.

163 lated peptides at 100 nM; 24-72 h) increased GH and ACTH secretion, Ca(2+) and ERK1/2 signaling and c

164 Taurine increased GH-dependent IGF1 synthesis in the liver, which subseque

165 For an interquartile-range increment, GH risk was significantly increased by 18% for sulfur di

166 Our results shed light on the intricate GH/IGF pathway, suggesting p73 as a good biomarker of th

167 t of POU1F1 in dominantly inherited isolated GH deficiency and demonstrates a significant impact of t

168 of the catalytic domain of Hypocrea jecorina GH Family 7 cellobiohydrolase Cel7A, namely a Michaelis

169 rmined that Salmonella required two keystone GHs for internalization, and left remodeled host glycans

170 The largest GH identified so far in this genus, Calkro_0111 (2,435 a

171 c screened 6 MOS sensors (LY2/G, LY2/AA, LY2/GH, LY2/gCT1, T30/1, and P30/1) to deconvolute the ranci

172 promoter of the signal transducers mediating GH regulation of CYP2C11 expression, which dramatically

173 JAK2 (JAK2(Deltahep)) to GH transgenic mice (GH(tg)) and compared them to GH(tg)STAT5(Deltahep) mice.

174 Relative to wild-type mice, GH injections reveal a significant reduction in JAK2 and

175 These data indicate that microbial GHs are undiscovered virulence factors.

176 anism through which endogenous NPY modulates GH release remains unknown.

177 an integrated neural circuit that modulates GH release relative to food intake, and provide essentia

178 Moreover, GH exposure of hepatocytes from hypox rats resulted in n

179 Reconcilibacillus cellulovorans' multidomain GHs assembled into cellulase complexes through glycosyla

180 ifference in endogenous production of murine GH.

181 st through translational fusion of a mutated GH linked to GH binding protein and tested three candida

182 and 5.08 (95% CI, 1.80-14.34) after GH vs no GH.

183 was 1.57 (95% CI, 1.04-2.39) after GH vs no GH.

184 Compared with having neither GDM nor GH, having either was associated with incident diabetes

185 the presynaptic Y2 receptor maintains normal GH output under long-term ad libitum-fed conditions.

186 Treatment with BA, but not GH, caused a 2-fold increase in phosphoglycerate dehydro

187 neered ligaments, recombinant IGF-1, but not GH, enhanced collagen content and mechanics.

188 determined whether this inhibitory action of GH is due to direct regulation of hepatic lipid metaboli

189 GH resistance results from direct actions of GH on lipid uptake and de novo lipogenesis, whereas its

190 Pharmacological blockade of GH signaling prevented the development of the phenotype.

191 wed that the SST/CORT role in the control of GH/prolactin secretions is maintained under LF- and HF-d

192 n POU1F1 present with combined deficiency of GH, PRL and TSH.

193 es, also associated with hypermethylation of GH-response elements in the CYP2C11 promoter.

194 al and temporal synchrony with initiation of GH expression in the embryonic pituitary.

195 Acute injections of GH after 7 d of calorie restriction also restored hepati

196 In contrast to the vast majority of GH, the catalytic apparatus of BT3686 does not comprise

197 Virus-mediated overexpression of GH in the amygdala was also sufficient to increase fear.

198 ng in the preclinical and clinical phases of GH and preeclampsia.

199 The physicochemical properties of GH granules were systematically characterized by transmi

200 The recovery of GH secretion was associated with a reduction in hypothal

201 ance, and a defect in feedback regulation of GH.

202 sing hormone (GHRH) regulates the release of GH by the pituitary but also exerts separate actions on

203 gulating the endogenous pulsatile release of GH does not exist.

204 nd Y2 receptors in regulating the release of GH under fed and fasting states.

205 Restoration of GH by infusion during the week of calorie restriction ma

206 cantly associated with 8%-20% higher risk of GH.

207 e gene expression as an additional source of GH x GP interactions.

208 de that the impaired metabolism in states of GH resistance results from direct actions of GH on lipid

209 The progressive suppression of GH release in MC4RKO mice occurred alongside increased a

210 We conclude that the suppression of GH release in MC4RKO mice occurs independently of increa

211 We demonstrate early-onset suppression of GH release in rapidly growing MC4R deficient (MC4RKO) mi

212 ux (hyperinsulinaemia and the suppression of GH release) override conventional mechanisms of pubertal

213 understanding of the catalytic mechanisms of GHs and GTs, not only the molecular details of chemical

214 In contrast, the ghrelin function on GH secretion was entirely mediated by G protein signalin

215 Compared with other GH-18 members, YKL-39 has the least extended chitin-bind

216 ral, sex-biased gene responses to persistent GH stimulation are dictated by GH/STAT5-regulated transc

217 Pharmacological GH administration stimulates collagen synthesis; however

218 IA-602, at a dose that did not affect plasma GH levels, significantly reduced TRL, as well as markers

219 T mice developed massive increases in plasma GH and a concomitant increase in hepatic autophagy, allo

220 in prohormone processing of proinsulin, pro-GH-releasing hormone, and proghrelin in association with

221 a complex multistep mechanism of processive GHs.

222 us polyposis coli (APC), reversing progrowth GH signals.

223 however, regulatory mechanisms that promote GH hypersecretion remain elusive.

224 nstrated that Magmas overexpression protects GH-secreting rat pitutitary adenoma cell lines from apop

225 receptor knock-out mice) to assess pulsatile GH secretion under both fed and fasting conditions.

226 line loss of the MC4R, we assessed pulsatile GH release and insulin-like growth factor-1 (IGF-1) prod

227 the fasting-induced suppression of pulsatile GH secretion.

228 r its quasi-3-fold exit, binds to rearranged GH loops of VP3 and VP1, and attaches to the top surface

229 ed by these vaccines were shown to recognize GH expressing tumor cells (MCF-7) and mediate the comple

230 cise biochemical milieu, but not recombinant GH, enhances collagen content and tensile strength of en

231 but attenuated hyperinsulinaemia, recovered GH release, and normalized linear growth rate to that se

232 -201 attenuated GH transcription and reduced GH secretion in the majority of derivative cultures.

233 The reduced GH maintained its layered structure and developed a lot

234 Failure to adequately regulate GH signaling leads to disease: excessive GH signaling ha

235 in a cell non-autonomous fashion to regulate GH-stimulated IGF-1 expression in the liver of neonatal

236 Thus, ghrelin requires GH in the amygdala to exert fear-enhancing effects.

237 n the transglycosylation activity of several GHs.

238 ion of several pituitary hormones (specially GH/PRL), which was accompanied by increased sst2/sst5/D2

239 refore, an adult-onset, hepatocyte-specific, GH receptor (GHR) knockdown (aLivGHRkd) mouse was develo

240 inhibited GHRH-, but not ghrelin-stimulated GH-secretion.

241 Leptin and resistin stimulated GH-release, a response that was blocked by somatostatin.

242 population-based retrospective cohort study, GH was identified in matched pairs of mothers with GDM o

243 rein the postsynaptic Y1 receptor suppresses GH secretion in fasting.

244 ceptor (GHR) via ubiquitination, suppressing GH pathway activity.

245 These findings demonstrate that GH granules are promising adsorbents for the removal of

246 We also demonstrate that GH suppresses p53 and reduces apoptosis in human colon c

247 These data indicate that GH stimulation of autophagy is necessary over the long t

248 We propose that GH is a molecular component of the "field change" milieu

249 Here we report that GH treatment limited to a few weeks during development i

250 atory cholestasis, therefore suggesting that GH resistance plays a causal role in the disease and pro

251 testinal organoids, and confirm in vivo that GH suppresses colon mucosal p53/p21.

252 This study determined that GHs recognize the terminal monosaccharides (N-acetylneur

253 The GH carrier containing OP3-4 with BMP-2 enlarged the radi

254 The GH content in bacterial genera is best described by thei

255 The GH electrodes exhibited high gravimetric as well as high

256 specifically recognize Globo H (GH) and the GH-related epitopes, stage-specific embryonic antigen 3

257 ases (SCF(betaTrCP2) and CHIP) determine the GH responsiveness of cells by controlling its endocytosi

258 ne how bone cells integrate signals from the GH/IGF-1 to enhance skeletal mineralization and strength

259 hypothesis that an amino acid change in the GH binding domain (W104A) would increase biological acti

260 troducing the W104A amino acid change in the GH binding domain enhances antagonist activity.

261 poglycemia occurred in mice deficient in the GH secretagogue ghrelin as a result of knockout of the g

262 ficiency resulted in severe steatosis in the GH(tg) background.

263 ificantly extended in vivo activities in the GH-deficient rat model and leptin-deficient obese mouse

264 g that enhanced glycolysis drives DNL in the GH-resistant liver.

265 layers, creating a near-3D structure in the GH.

266 ence thereof, we challenged mice lacking the GH receptor gene (Ghr(-/-), a model for GH resistance) b

267 considered to be a primary oscillator of the GH axis, we examined its acute effects on GHRH neurons i

268 warf mice show that this short period of the GH exposure during early development produces persistent

269 ludes expansion of 4%, rearrangements of the GH loops of VP3 and VP1, and disordering of C-terminal e

270 e, congenital liver-specific ablation of the GH receptor (GHR) results in reductions in circulating I

271 ur in response to enhanced activation of the GH-IGF-1 axis.

272 novel mechanism involving activation of the GH-Stat5 signaling pathway.

273 (DMP-GHRKO) mice to address the role of the GH/IGF axis in osteocytes.

274 ansfected cells, rhFGF21 did not prevent the GH stimulatory effects on thymidine incorporation, colla

275 sphorylation and ubiquitylation regulate the GH receptor (GHR) at the cell surface: two ubiquitin lig

276 This long-range interaction sequesters the GH genes from the three hCS genes which co-assemble into

277 naemia promotes growth while suppressing the GH-IGF-1 axis.

278 ed conformations for the EF loop of VP2, the GH loop of VP3, and the N-terminal extensions of VP1 and

279 Therapeutically, GH supplementation was able to correct growth retardatio

280 racterized the enzymatic activities of these GHs and demonstrated their involvement in sequential deg

281 that PTH sensitized the response of bone to GH by increasing Janus kinase-2 and IGF-1R protein level

282 h diminished oxidative damage as compared to GH(tg)STAT5(Deltahep) mice, despite equally severe steat

283 pecific deletion of JAK2 (JAK2(Deltahep)) to GH transgenic mice (GH(tg)) and compared them to GH(tg)S

284 r reduced longevity of dwarf mice exposed to GH treatment early in life.

285 anslational fusion of a mutated GH linked to GH binding protein and tested three candidate molecules.

286 eption and in early gestation in relation to GH risk in the Consortium on Safe Labor/Air Quality and

287 Similar to GH(tg)STAT5(Deltahep) mice, JAK2 deficiency resulted in

288 ransgenic mice (GH(tg)) and compared them to GH(tg)STAT5(Deltahep) mice.

289 responsive genes included those encoding two GH/STAT5-regulated transcriptional repressors: male-bias

290 cific contacts with the promoters of the two GH genes in the cluster.

291 During infection, Salmonella used its two GHs sialidase nanH and amylase malS for internalization

292 active approximately 900-kDa complexes upon GH binding.

293 y the neighboring linear epitopes of the VP1 GH and VP2 EF loops.

294 In order to elucidate whether GH resistance plays a causal role in the establishment a

295 insulinemia; however, the mechanism by which GH is reduced is not clear.

296 hypox) male rats served as controls in which GH was eliminated after the critical imprinting period.

297 res for 6,074 singleton pregnancies in which GH was present and 199,980 normotensive pregnancies.

298 mics alone do not universally correlate with GH catalytic itineraries.

299 ntified 36 studies, including 745 women with GH and 815 women with preeclampsia.

300 ligible studies included pregnant women with GH or preeclampsia, evaluating left ventricular structur