ライフサイエンスコーパス: SAH

1 SAH catabolism is linked to S-adenosylmethionine metabol

2 SAH did not alter preadipocyte factor 1 (Dlk1) or peroxi

3 SAH increased Rxralpha methylation on a CpG unit (chr2:2

4 SAH is a potent feedback inhibitor of S-adenosylmethioni

5 SAH is the only Hcy metabolite significantly correlated

6 SAH-albumin showed the highest albumin oxidative state (

7 SAH-SOS1 peptides bound in a sequence-specific manner to

8 bilized alpha helices of son of sevenless 1 (SAH-SOS1) as prototype therapeutics that directly inhibi

9 Among 479 SAH patients, 53 (11%) had in-hospital NCSz.

10 ion of the recombinant mouse myosin VIIa-5IQ-SAH R502P (myoVIIa-sh1) construct.

11 e versa) in the naturally-occurring myosin-6 SAH similarly increased (or decreased) its stability.

12 sible mechanism of methazolamide in C57BL/6J SAH animal model in vivo and in blood-induced primary co

13 oism and mass spectrometry as expected for a SAH domain.

14 +) stores using cyclopiazonic acid abolished SAH-induced eHACSs and restored arteriolar dilation in S

15 alyzed hydrolysis of S-adenosylhomocysteine (SAH) and for sensing adenosine based on the inhibition o

16 rapid production of S-adenosylhomocysteine (SAH) and the mCys residue, while treatment of apo RlmN w

17 ociation of ADK with S-adenosylhomocysteine (SAH) hydrolase (SAHH).

18 lmethionine (SAM) or S-adenosylhomocysteine (SAH) in the catalytic site.

19 S-adenosylhomocysteine (SAH) is a negative regulator of most methyltransferases

20 l and progeny plasma S-adenosylhomocysteine (SAH) levels are both elevated after vitamin deficiency i

21 -362) complexed with S-adenosylhomocysteine (SAH) or 5'-deoxyadenosine (5'-dAdo) and l-methionine (l-

22 e the deamination of S-adenosylhomocysteine (SAH) to S-inosylhomocysteine (SIH).

23 ethionine (SAM), and S-adenosylhomocysteine (SAH) were measured in liver homogenates.

24 e-based metabolites: S-adenosylhomocysteine (SAH), 5'-methylthioadenosine (MTA), 5'-deoxyadenosine (5

25 zyme that hydrolyzes S-adenosylhomocysteine (SAH), a product and inhibitor of methyltransferases.

26 ene expression, Hcy, S-adenosylhomocysteine (SAH), and S-adenosylmethionine (SAM) levels, and SAM/SAH

27 creatinine, betaine, S-adenosylhomocysteine (SAH), and S-adenosylmethionine (SAM), and higher percent

28 cocrystallized with S-adenosylhomocysteine (SAH), Formycin A (FMA), and (3R,4S)-4-(4-Chlorophenylthi

29 of these nutrients, S-adenosylhomocysteine (SAH), S-adenosylmethionine (SAM), homocysteine, cysteine

30 pable of hydrolysing S-adenosylhomocysteine (SAH).

31 that responds to the S-adenosylhomocysteine (SAH).

32 uent accumulation of S-adenosylhomocysteine (SAH).

33 alyzed hydrolysis of S-adenosylhomocysteine (SAH).

34 AM) and inhibited by S-adenosylhomocysteine (SAH).

35 demethylated product S-adenosylhomocysteine (SAH).

36 oadenosine (MTA) and S-adenosylhomocysteine (SAH).

37 this assay, S-adenosyl-l-homocystine (AdoHcy/SAH), the by-product of PMT-involved methylation, is seq

38 ed the role of mitophagy following 48h after SAH injury in rats.

39 ion, eNOS activity and NO availability after SAH.

40 y and cardiac complications are common after SAH, and are associated with an increased risk of mortal

41 ediates acute microvessel constriction after SAH possibly by hemoglobin suppressing NO/cGMP signaling

42 s occurred between the 5th and 7th day after SAH, and 96 (80%) arose within temporal clusters of recu

43 high-amplitude Ca(2+) signals (eHACSs) after SAH that were not observed in endfeet from unoperated an

44 cyte trafficking at both 24 h and 48 h after SAH, along with an improvement in neurologic outcome.

45 yte trafficking, during the first 48 h after SAH.

46 ffective elimination of blood and heme after SAH that otherwise leads to neuronal injury and cognitiv

47 ytic Ca(2+) oscillations was increased after SAH, with peak Ca(2+) reaching approximately 490 nM.

48 Initiation of CO inhalation after SAH rescued the absence of microglial HO-1 and reduced i

49 nt manifestation of early brain injury after SAH and a predictor of death or poor functional outcome

50 pathophysiology of early brain injury after SAH is still unclear.

51 in the regulation of microcirculation after SAH.

52 are compromised in function by 10 min after SAH and identify focal microvascular constriction and lo

53 modified Rankin Scale 4-6 at 3 months after SAH.

54 A common complication observed after SAH is the development of delayed cerebral ischemia at s

55 effectively analyze cognitive outcomes after SAH.

56 suggest that exposure to excess oxygen after SAH may represent a modifiable factor for morbidity and

57 obins penetrated into brain parenchyma after SAH.

58 The postoperative ICU period after SAH is associated with a significant morbidity and morta

59 ctivated in neurons in the acute phase after SAH.

60 The study of brain nerve protection after SAH is of great significance.

61 ng and the risk of aneurysm rebleeding after SAH.

62 ated to poor acute neurological status after SAH and predicts future ischaemia and worse functional o

63 arly goal-directed hemodynamic therapy after SAH has recently been shown to improve clinical outcomes

64 Thus, after SAH, signaling events that normally lead to vasodilation

65 ients at risk for developing vasospasm after SAH.

66 grin receptors and prevented vasospasm after SAH.

67 Early worsening after SAH occurs in 35% of patients, is predicted by clot burd

68 The addition of adenosine to an SAH solution resulted in the inhibition of SAHH activity

69 ermore, by achieving this flexibility via an SAH domain, the CPC avoids a need for dimerization (requ

70 es positively correlated with tissue Hcy and SAH levels.

71 tant form of H. pylori MTAN bound to MTA and SAH to 1.63 and 1.20 A, respectively.

72 -MB-T8 . Hg(2+) probe combining the SAHH and SAH systems was used for sensitive and selective detecti

73 methods to discover and characterize SAM and SAH binding proteins using fluorescent CCs.

74 nto 4 groups: Sham, SAH, SAH+VDAC1siRNA, and SAH+RAPA.

75 ion in 609 consecutively admitted aneurysmal SAH patients.

76 tially ominous conditions such as aneurysmal SAH (aSAH) or cryptogenic "angiogram-negative" SAH (cSAH

77 on criteria were age >/=18 years, aneurysmal SAH, endotracheal intubation with mechanical ventilation

78 The mean interval between SAH and PPV was 4.4 months (range, 3-5 months).

79 These data indicate a causal link between SAH-induced eHACSs and inversion of NVC.

80 ent methylases that are able to tightly bind SAH.

81 -ammonium of K9 positioned adjacent to bound SAH.

82 tive site architecture of viperin with bound SAH (a SAM analog) or 5'-dAdo and l-Met (SAM cleavage pr

83 Hypomethylation stress, caused by SAH accumulation, inhibits the formation of the methylat

84 ated DNA, substrate H3 peptide, and cofactor SAH, thereby defining the spatial positioning of the SRA

85 In conclusion, SAH did not affect adipogenesis per se but altered adipo

86 is the occurrence of nontraumatic convexity SAH unaccounted for by aneurysmal rupture.

87 benefit of broad application of the current SAH treatment mainstays, and re-examines agents previous

88 After demonstrating SAH-dependent photo-crosslinking of the CC to these prot

89 young flies and suppression of age-dependent SAH accumulation lead to increased life span.

90 Sinus thrombosis presenting as diffuse SAH is extremely rare, as is showcased in this report.

91 solated stable single alpha-helical domains (SAH).

92 The elevated SAH level in the cell dissociates SahR from its DNA oper

93 brovascular pathology following experimental SAH.

94 isorder, lower Hunt-Hess grade, lower Fisher SAH group, and the presence of bilateral arterial narrow

95 disease, lower Hunt-Hess grade, lower Fisher SAH group, higher number of affected arteries, and the p

96 orality, fluctuation of cerebral blood flow, SAH grade, and cerebral vasospasm of SAH mice.

97 f neurological deficits that commonly follow SAH.

98 findings suggest that inflammation following SAH is associated with poor outcome and that this effect

99 AC1siRNA worsened the brain injury following SAH.

100 neurons were reduced by Rapamycin following SAH injury.

101 between the inflammatory response following SAH and in-hospital NCSz studying clinical (systemic inf

102 iated with a proinflammatory state following SAH as reflected in clinical symptoms and serum biomarke

103 f heightened leukocyte trafficking following SAH, induced via endovascular perforation of the anterio

104 lusion, mitophagy induced by VDAC1 following SAH injury may in fact play a significant role in neurop

105 s exceeded that of commercial antibodies for SAH and proved critical to cellular applications, as we

106 strategy, but retained full selectivity for SAH over its close structural analogue, the highly abund

107 it provides potential as a novel therapy for SAH.

108 after stimulation with purified albumin from SAH patient plasma.

109 d a modest constriction in brain slices from SAH model rats; this latter effect was reversed by BK ch

110 Furthermore, SAH-induced oxidative stress creates a proinflammatory a

111 a risk factor for subarachnoid haemorrhage (SAH).

112 s frequently after subarachnoid haemorrhage (SAH).

113 c attack (TIA) and subarachnoid haemorrhage (SAH).

114 disordered except for a single alpha-helix (SAH) at the N terminus and a short nascent helix, LH, fl

115 rvivin and Borealin, the single alpha-helix (SAH) domain of INCENP supports CPC localization to chrom

116 approximately 32-nm-long single alpha-helix (SAH) domain.

117 Single alpha-helix (SAH) domains are rich in charged residues (Arg, Lys, and

118 Subarachnoid hemorrhage (SAH) carries a 50% mortality rate.

119 ollowing aneurysmal subarachnoid hemorrhage (SAH) have remained elusive.

120 ral vasospasm after subarachnoid hemorrhage (SAH) in rats.

121 Aneurysmal subarachnoid hemorrhage (SAH) is a potentially devastating clinical problem.

122 ry after aneurysmal subarachnoid hemorrhage (SAH) is not understood.

123 lices obtained from subarachnoid hemorrhage (SAH) model rats.

124 study of aneurysmal subarachnoid hemorrhage (SAH) patients, we explored the link between the inflamma

125 to poor outcome in subarachnoid hemorrhage (SAH) patients.

126 Aneurysmal subarachnoid hemorrhage (SAH) remains a devastating condition with high mortality

127 Subarachnoid hemorrhage (SAH) results in significant nerve dysfunction, such as h

128 esenting symptom of subarachnoid hemorrhage (SAH) that is presumed to result from transient intracran

129 Subarachnoid hemorrhage (SAH) usually results from ruptured aneurysm, but how lea

130 t of patients after subarachnoid hemorrhage (SAH), especially with regards to hemodynamic management,

131 ith the presence of subarachnoid hemorrhage (SAH), SAH is not required for vasospasm in bTBI, which s

132 atement: Aneurysmal subarachnoid hemorrhage (SAH)--strokes involving cerebral aneurysm rupture and re

133 ity of nontraumatic subarachnoid hemorrhage (SAH).

134 processes including subarachnoid hemorrhage (SAH).

135 ly period following subarachnoid hemorrhage (SAH).

136 s with RCVS develop subarachnoid hemorrhage (SAH).

137 ences of aneurysmal subarachnoid hemorrhage (SAH).

138 ating albumin in severe alcoholic hepatitis (SAH) patients and their contribution to neutrophil activ

139 in patients with severe alcoholic hepatitis (SAH), but little information is available on how to pred

140 in patients with severe alcoholic hepatitis (SAH), but little information is available on how to pred

141 High SAH levels were significantly associated with low H19 me

142 R 2.0, 95% CI 1.2 to 3.5; p=0.01) and higher SAH and intraventricular haemorrhage sum scores (OR 1.05

143 metry (LC/MS)-based S-adenosyl homocysteine (SAH) detection assay for histone methyltransferases (HMT

144 describe a suite of S-adenosyl homocysteine (SAH) photoreactive probes and their application in chemi

145 ethyl donor product S-adenosyl-homocysteine (SAH) and its ortholog scTrm10 from Saccharomyces cerevis

146 d in high levels of S-adenosyl-homocysteine (SAH) and low levels of S-adenosyl-methionine (SAM).

147 via methylation to S-adenosyl-homocysteine (SAH), which accumulates during aging.

148 lex with cofactor S-adenosyl-L-homocysteine (SAH) and six substrate peptides, respectively, and revea

149 The affinity of S-adenosyl-l-homocysteine (SAH) for SAM binding proteins was used to design two SAH

150 nt biosensors for S-adenosyl-l-homocysteine (SAH) that provide a direct "mix and go" activity assay f

151 ble conversion of S-adenosyl-L-homocysteine (SAH) to adenosine (ADO) and L-homocysteine, promoting me

152 U4G5U6U7-3'), and S-adenosyl-l-homocysteine (SAH), the by-product of the methylation reaction.

153 ) is converted to S-adenosyl-l-homocysteine (SAH).

154 mouse model and a new severe acute hypoxia (SAH) mouse model of DWMI activates the initial step of t

155 In SAH patients, exposure to hyperoxia was associated with

156 and plasma oxidative stress were assessed in SAH patients (n = 90), alcoholic cirrhosis patients (n =

157 ere systemic medical complications common in SAH.

158 d eHACSs and restored arteriolar dilation in SAH brain slices to two mediators of NVC (a rise in endf

159 al edema, and improves cognitive function in SAH mice as well as offers neuroprotection in blood- or

160 crocirculation, and neurological function in SAH rats.

161 Expression of the above-mentioned genes in SAH-albumin-stimulated healthy neutrophils was comparabl

162 ced oxidative protein product) was higher in SAH versus alcoholic cirrhosis patients and healthy cont

163 and intracellular ROS levels were highest in SAH-albumin-treated neutrophils (P < 0.05).

164 a marked depletion of SAM and an increase in SAH in various brain regions with parallel downregulatio

165 risk factors for development of infection in SAH.

166 romotes oxidative stress and inflammation in SAH patients through activation of neutrophils.

167 factors with their association to outcome in SAH can help us to identify patients at risk.

168 erangements associated with poor outcomes in SAH can improve our understanding of the widespread phys

169 us toll-like receptors were overexpressed in SAH neutrophils compared to healthy neutrophils (P < 0.0

170 dings identify astrocytes as a key player in SAH-induced decreased cortical blood flow.

171 eased on Cebpalpha and Rxralpha promoters in SAH-treated adipocytes, consistent with the reduction in

172 Thus, the INCENP SAH could act as a flexible "dog leash," allowing Aurora

173 The INCENP SAH domain also mediates INCENP's microtubule binding, w

174 myosin 10, our data suggest that the INCENP SAH might stretch up to approximately 80 nm under physio

175 These include SAH hydrolase, methionyl-tRNA synthase, 5-methyltetrahyd

176 o deaminate analogues of adenosine including SAH, 5'-methylthioadenosine (MTA), adenosine (Ado), and

177 We propose that increased SAH levels and inflammation affect widespread epigenetic

178 Increasing SAH decreased 1) the SAM/SAH ratio, 2) protein-arginine

179 cute effect of endovascular puncture-induced SAH on parenchymal vessel function in rat, using intrava

180 pression was associated with increased liver SAH levels in the tx-j model of WD, with consequent glob

181 MTA, SAH and 5'-deoxyadenosine (5'dADO) are product inhibitor

182 hylthioadenosine/S-adenosylhomocysteine (MTA/SAH) nucleosidase in bacteria has started to be apprecia

183 Interestingly, the inhibitors of MTA/SAH nucleosidase are very effective against the Lyme dis

184 f these reactions, and are substrates of MTA/SAH nucleosidase, underscoring its importance in a wide

185 H (aSAH) or cryptogenic "angiogram-negative" SAH (cSAH) owing to overlapping clinical and imaging fea

186 c and therapeutic management of nontraumatic SAH.

187 in 73 consecutive patients with nontraumatic SAH diagnosed at nonenhanced CT.

188 ssions correlate with neither tissue Hcy nor SAH levels.

189 The mechanism of action of SAH-SOS1 peptides was demonstrated by sequence-specific

190 There are few reported cases of SAH secondary to dural sinus thrombosis; however most of

191 When SAHH catalyzed the cleavage of SAH, the generated HCys reacted with NDA to form highly

192 se (AHCY) known to increase concentration of SAH before analysis of G6PC, PCK1, and SEPP1 expression.

193 SahH enables a direct conversion of SAH to homocysteine and thereby restores the activated m

194 Gene expression of SAH neutrophils was analyzed and compared to gene expres

195 ere, we review the structure and function of SAH domains, as well as the tools to identify them in na

196 SAHH catalyzed the hydrolysis of SAH to produce homocysteine.

197 we were able to monitor in vivo increase of SAH levels upon chemical inhibition of MTAN using flow c

198 ced in tx-j mice with consequent increase of SAH levels.

199 lowing endovascular perforation induction of SAH in mice, a heavily-utilized model.

200 data may shed new light on the management of SAH patients.

201 ary cortical neuron (PCNs) cellular model of SAH in vitro.

202 Here, using a murine model of SAH, we demonstrated that expression of the inducible HO

203 eractions between the homocysteine moiety of SAH and the 5'-alkylthiol binding site of MTAN have neve

204 ty patients (40.4%) reported LOC at onset of SAH.

205 validation, we used a control population of SAH patients from the CONSCIOUS-1 study (n = 413).

206 rine 3T3-L1 preadipocytes in the presence of SAH impaired both basal and induced glucose uptake as we

207 TAN was also crystallized in the presence of SAH, allowing the determination of the structure of a te

208 ting methyltransferase activity by relief of SAH inhibition.

209 f rare but clinically significant sources of SAH.

210 A subset of SAH domains contain a characteristic ER/K motif, compose

211 Prednisolone is advocated for treatment of SAH, but can increase susceptibility to infection.

212 e advances in the diagnosis and treatment of SAH, outcome remains unfavorable.

213 rovide evidence for the potential utility of SAH-SOS1 peptides in neutralizing oncogenic KRAS in huma

214 d flow, SAH grade, and cerebral vasospasm of SAH mice.

215 appear to play a major role in either MCH or SAH-induced DWMI and is therefore not a likely target fo

216 cement of the ISR does not ameliorate MCH or SAH-induced DWMI.

217 SR has no detectable effect on either MCH or SAH-induced DWMI.

218 in complex with an H3K36M peptide and SAM or SAH.

219 neurologic examination findings, the Ottawa SAH Rule was highly sensitive for identifying subarachno

220 exion on examination" resulted in the Ottawa SAH Rule, with 100% (95% CI, 97.2%-100.0%) sensitivity a

221 Upon binding Nip100, only Pac11 SAH residues make direct protein-protein interactions, b

222 Endovascular perforation SAH rat model, brain slices and cultured pericytes were

223 Post-SAH r-OPN treatment also prevented vasospasm.

224 tment with LJP-1586 was initiated at 6h post-SAH.

225 Experiments focused on the initial 48 h post-SAH and sought to establish whether blockade of vascular

226 leukocyte trafficking at 24 h and 48 h post-SAH were examined.

227 neurological impairments at 24-72 hours post-SAH.

228 e spastic cerebral arteries at 24 hours post-SAH.

229 n slices but caused vasoconstriction in post-SAH brain slices.

230 Pre-SAH administration of r-OPN prevented vasospasm and neur

231 e accumulation of the homocysteine precursor SAH, suppresses GPx-1 expression and leads to inflammato

232 ties and unfolding behavior of the predicted SAH domain from myosin-10 were characterized.

233 The expressed and purified SAH domain was highly helical, melted non-cooperatively,

234 linical and imaging differences between RCVS-SAH, aSAH, and cSAH that may be useful for improving dia

235 identify predictors that differentiate RCVS-SAH from aSAH and cSAH.

236 Predictors differentiating RCVS-SAH from aSAH were younger age, chronic headache disorde

237 Predictors differentiating RCVS-SAH from cSAH were younger age, female sex, prior hypert

238 Patients with RCVS with SAH (RCVS-SAH) are often misdiagnosed as having potentially ominou

239 Consecutive patients with RCVS-SAH (n = 38), aSAH (n = 515), or cSAH (n = 93) whose con

240 e presence of subarachnoid hemorrhage (SAH), SAH is not required for vasospasm in bTBI, which suggest

241 e randomly divided into 4 groups: Sham, SAH, SAH+VDAC1siRNA, and SAH+RAPA.

242 nes related to liver injury, levels of SAHH, SAH, DNA methyltransferases genes (Dnmt1, Dnmt3a, Dnmt3b

243 nM) and was reusable for detecting the SAHH/SAH system.

244 d S-adenosylmethionine (SAM) levels, and SAM/SAH ratios in mouse tissues.

245 hylation enzymes on tissue SAH, SAM, and SAM/SAH ratios.

246 interesting positive association between SAM/SAH ratio and high H19 methylation levels was detected a

247 Modulation of the cellular SAM/SAH ratio can influence activity of methyltransferase en

248 ses were accompanied by elevated hepatic SAM/SAH ratios and augmented biliary tHcy secretion rates.

249 boflavin in these processes and a higher SAM/SAH ratio during the rainy season.

250 pe mice that l-dopa results in a reduced SAM/SAH ratio that is associated with hypomethylation of PP2

251 Increasing SAH decreased 1) the SAM/SAH ratio, 2) protein-arginine methylation, and 3) expre

252 ular SAMe and MTA levels, a drop in the SAMe/SAH ratio, and global DNA hypomethylation.

253 ns (COSBID) recruited 9 patients with severe SAH, who underwent open neurosurgery.

254 s were randomly divided into 4 groups: Sham, SAH, SAH+VDAC1siRNA, and SAH+RAPA.

255 osticate long-term outcome after spontaneous SAH in a multidimensional manner.

256 secutively treated patients with spontaneous SAH who were part of a prospective observational cohort

257 Our findings demonstrate that SAH accumulation in endothelial cells suppresses the exp

258 Here, we provide evidence that SAH-induced changes in astrocyte Ca(2+) signaling lead t

259 Taken together, these data suggest that SAH accumulation in endothelial cells can induce tRNA(Se

260 all enzymes required for the SAM cycle: the SAH hydrolase AhcY, the methionine biosynthesis enzymes

261 This enables the SAH domain to act as a constant force spring in the mech

262 ted phosphorylation of segments flanking the SAH domain.

263 r 1,619 consecutive patients enrolled in the SAH outcome project July 1996 to March 2014.

264 The microtubule-binding capacity of the SAH domain is important for mitotic arrest in conditions

265 two noncanonical Drosophila homologs of the SAH hydrolase Ahcy (S-adenosyl-L-homocysteine hydrolase

266 rce spectroscopy experiments showed that the SAH domain unfolded at very low forces (<30 pN) without

267 lecular dynamics simulations showed that the SAH domain unfolds progressively as the length is increa

268 We further demonstrate that the SAH probes can enrich MT-associated proteins and be used

269 These SAH domains provide unique structural features essential

270 ned effects of methylation enzymes on tissue SAH, SAM, and SAM/SAH ratios.

271 hyl sinks to enable the conversion of SAM to SAH.

272 of active caspase-3 in methazolamide-treated SAH mice comparing with vehicle-treated SAH animals.

273 iRNA) was also administered to r-OPN-treated SAH rats, and those effects were evaluated.

274 ated SAH mice comparing with vehicle-treated SAH animals.

275 SAM binding proteins was used to design two SAH-derived capture compounds (CCs).

276 stered intraventricularly to rats undergoing SAH by endovascular perforation, and its protective effe

277 r altered endfoot Ca(2+) signaling underlies SAH-induced inversion of NVC.

278 emic medical center (the Columbia University SAH Outcomes Project or SHOP).

279 vasodilation (control) and vasoconstriction (SAH).

280 n model that applied to the whole group were SAH, trimethylamine, choline, and female sex, whereas pl

281 Our data support a model in which SAH increases the amplitude of spontaneous astrocytic Ca

282 Animals in which SAH was induced exhibited reduced acute functional capac

283 e variant (HpMTAN-D198N) cocrystallized with SAH.

284 ated healthy neutrophils was comparable with SAH patient neutrophils, except for genes associated wit

285 rom Saccharomyces cerevisiae in complex with SAH.

286 functional binding activity correlated with SAH-SOS1 cytotoxicity in cancer cells expressing wild-ty

287 idespread physiologic changes occurring with SAH and with further research, may provide clinicians wi

288 Patients with SAH given prednisolone are at greater risk for developin

289 ative human data revealed that patients with SAH have markedly higher HO-1 activity in cerebrospinal

290 increased 90-day mortality in patients with SAH treated with prednisolone, independent of model for

291 ctive, hypothesis-driven study patients with SAH underwent MRI within 0-3 days of ictus (prior to vas

292 In 61 patients with SAH, 131 MRI were performed.

293 In patients with SAH, there is a significant increase in albumin oxidatio

294 e (400 mg 3 times each day) in patients with SAH.

295 e used to select therapies for patients with SAH.

296 We enrolled 1312 consecutive patients with SAH; 643 (49%) had premorbid HTN.

297 main bound to H3K36M or H3K36I peptides with SAH (S-adenosylhomocysteine).

298 Patients with RCVS with SAH (RCVS-SAH) are often misdiagnosed as having potentia

299 eractions of the proteins COMT and SAHH with SAH-CC with biotin used in conjunction with streptavidin

300 ortex parenchymal arterioles with or without SAH.