ライフサイエンスコーパス: type 3

1 2%), followed by bla NDM (5%) and bla OXA-48-type (3%).

2 spread btb-ER in the case of random pacing (type 3).

3 1), 94.6% (n=193, type 2), and 99.5% (n=203, type 3).

4 h either rapid (Type 2) or slow progression (Type 3).

5 arrhythmias associated with long QT syndrome type 3.

6 maturity-onset diabetes of the young (MODY) type 3.

7 ssion or localization of glucose transporter type 3.

8 do-Joseph disease and spinocerebellar ataxia type 3.

9 iedreich's ataxia and spinocerebellar ataxia type 3.

10 rogressive familial intrahepatic cholestasis type 3.

11 us type 2, and 390 days for Sabin-like virus type 3.

12 iedreich's ataxia and spinocerebellar ataxia type 3.

13 stimulus-transducing enzyme adenylyl cyclase type 3.

14 propose to categorize as type 1, type 2, and type 3.

15 0.78-0.83; type 2: 0.72; 95% CI, 0.69-0.74; type 3: 0.78; 95% CI, 0.75-0.82).

16 MacDonald-type "3 + 1" condensations of an N-methyltripyrrane with

17 MacDonald-type "3 + 1" condensations with a tripyrrane, followed b

18 1), 97.6% (n=200; type 2), and 99.5% (n=204, type 3); 1/5 IPV-Al: 99.5% (n=204, type 1), 96.1% (n=197

19 Ts Type 1: 42 (32 NET G1, 10 NET G2), a GNET Type 3: 1 well-differentiated NET G3, neuroendocrine car

20 bitor of 17beta-hydroxysteroid dehydrogenase type 3 (17beta-HSD3) is a strategy to treat prostate can

21 cord-like pleural tag) and prioritized into types 3, 2, and 1 when more than one type was present.

22 ), rhinovirus (34%), and parainfluenza virus type 3 (28%); respiratory syncytial virus was highly con

23 Patients with congenital type 3, 2A, and 2B are those most frequently affected by

24 e; and Bleeding Academic Research Consortium type 3, 4, and 5 bleeding through day 30, did not differ

25 ; 51% LQTS type 1; 33% LQTS type 2; 11% LQTS type 3; 5% multiple mutations) and 50 healthy controls.

26 ceptible to P. aeruginosa adhesion than wild-type (3.8-fold, 3.6-fold respectively).

27 tuned regulation of glycogen synthase kinase type 3, a prime target for lithium, seems to be key.

28 onspastic achalasia and 90% of patients with type 3 achalasia/spastic esophageal motility disorders,

29 tion study in humans has recently implicated type 3 adenylyl cyclase (AC3; ADCY3) in MDD.

30 rom androstenedione through aldoketoredutase type 3 (AKR1C3) in women with insulin resistance.

31 e protein involved in spinocerebellar ataxia type 3, also known as Machado-Joseph disease, causes den

32 cular dystrophy type 2L and Miyoshi myopathy type 3, although the pathogenic mechanism has remained e

33 ighest gold concentrations were found in the type 3 and 4 fluid inclusions with an average concentrat

34 a-melanocyte-stimulating hormone (alpha-MSH) type 3 and 4 receptors, decreased LSNA in leptin-treated

35 ilt from classical dopaminergic head groups (type 3 and 4) typically elicit more balanced signaling p

36 otein trimers from human parainfluenza virus-type 3 and spike-glycoprotein trimers from SARS-CoV-2 co

37 rogressive familial intrahepatic cholestasis type 3 and, with further refinement, the potential for h

38 1), Small (Type 2), Protruding or Pendulous (Type 3) and Creased or Ridged (Type 4).

39 us to human SRD5A3 (steroid 5alpha reductase type 3) and encode polyprenol reductases responsible for

40 y regulated by RSK3 (p90 ribosomal S6 kinase type 3) and PP2A (protein phosphatase 2A) at signalosome

41 1), 96.1% (n=197, type 2), and 98.5% (n=202, type 3); and 1/10 IPV-Al: 98.5% (n=201, type 1), 94.6% (

42 or 2 lymphatic abnormalities, 17 (20%) with type 3, and 12 (16%) with type 4.

43 gressive reduction in type 1 (antiviral) and type 3 (antifungal) responses.

44 low) expression gradient of adenylyl cyclase type 3 appears, which coincides with altered OR frequenc

45 ly denoted as autosomal-recessive cutis laxa type 3 (ARCL3).

46 in patients with Pontocerebellar Hypoplasia Type 3 are also exhibited by these Piccolo deficient ani

47 ed nitro derivative to a new scaffold of the type 3-aryl-1H-pyrrolo-imidazo[1,2-a]pyridine.

48 , myeloproliferative, and mental retardation-type 3) as a chromatin-interacting protein that promotes

49 ional analyses reveal that the percentage of type 3 B cells is reduced and the frequency of CD27(+) t

50 viously suggested, but also distinct anergic type 3 B cells, as well as IL-10-producing CD27(+) trans

51 e genomic RNA1 and RNA2, respectively, while type 3 (B3+4(V)) virions copackage genomic RNA3 (B3) and

52 counterparts from bovine parainfluenza virus type 3 (BPIV3) F protein to direct incorporation into th

53 tential duration maps were available; (3) 17 type-3 BrS pattern patients not showing type-1 BrS patte

54 tion in infected mice, absence of type 1 and type 3, but not type 2, ILCs affects the survival of inf

55 n in vitro and that the absence of type 1 or type 3, but not type 2, ILCs affects the survival of ocu

56 tivate Type 2 cells but never to stimuli for Type 3 cells.

57 ed as type 1 ("dust"), type 2 ("sphere"), or type 3 ("cloud").

58 e/phenotype correlation for Bartter syndrome type 3: complete loss-of-function mutations associated w

59 Steroid 5alpha-reductase type 3 congenital disorder of glycosylation (SRD5A3-CDG)

60 Polyphenoloxidases (PPO) of the type-3 copper protein family are considered to be catech

61 as binding motifs are designed to coordinate type-3 Cu sites.

62 in the clinic, but not in 2D or single-cell-type 3D cultures.

63 Type 3 CXLRS was a risk factor for the development of a

64 intestinal homeostasis through secretion of type 3 cytokines such as interleukin (IL)-17 and IL-22.

65 ENP showed an age-related increase in type 3 cytokines with type 2 mediators sustained at high

66 ncrease in type 2 cytokines and a decline in type 3 cytokines.

67 pe 2 cytokines and high levels of type 1 and type 3 cytokines.

68 rated release of pro-inflammatory type 1 and type 3 cytokines.

69 n TNBC to epistatic interactions between the type 3 Dearing M2 gene segment and type 1 Lang genes.

70 genome of one mammalian orthoreovirus (MRV) type 3, denoted TO-151/BR, detected in a female child in

71 7% showed type 2 disease (n = 9), 66% showed type 3 disease (n = 35), and 9.5% showed type 4 disease

72 s with high affinity to the NCAM fibronectin type-3 domain.

73 nd the second module of the NCAM fibronectin type-3 domain.

74 pported RORgammat activity and expression of type 3 effector genes.

75 type 1 EI in 35 and type 2 EI in 28), and no type 3 EI was observed during follow up.

76 a classification one type 1, six type 2, two type 3, eight type 4, and two type 5 lesions were identi

77 nd Epac2 decreases sodium-hydrogen exchanger type 3 expression in the proximal tubule, leading to pol

78 ult in familial hypocalciuric hypercalcaemia type 3 (FHH3), a disorder of extracellular calcium (Ca(2

79 esangial curved, comma-like, banded collagen type 3 fibers of 40-65 nm periodicity.

80 metrical complex comprising the trimeric HAd type 3 fibre knob (HAd3K) and human desmoglein 2 (DSG2).

81 characterized by the deposition of collagen type 3 fibrils in the glomeruli.

82 Nicotinic acetylcholine, serotonin type 3, gamma-amminobutyric acid type A, and glycine rec

83 ead of replication-competent, oncolytic HAdV type 3 (HAdV3).

84 infections, 85 caused by human parechovirus type 3 (HPeV-3) and 48 by human parechovirus other than

85 e vectors based on human parainfluenza virus type 3 (HPIV-3) and Newcastle disease virus (NDV) have b

86 al virus (RSV) and human parainfluenza virus type 3 (HPIV3) are major pediatric respiratory pathogens

87 al virus (RSV) and human parainfluenza virus type 3 (HPIV3) are major viral agents of acute pediatric

88 al virus (RSV) and human parainfluenza virus type 3 (HPIV3) are two major causes of pediatric pneumon

89 Human parainfluenza virus type 3 (HPIV3), a paramyxovirus, is a major viral cause

90 yxoviruses such as human parainfluenza virus type-3 (HPIV3) and measles virus (MeV) are a substantial

91 ster-randomized controlled trial utilizing a Type-3 Hybrid implementation-effectiveness design conduc

92 and BCL6 as regulators affecting type 1 and type 3 ILC lineages.

93 y reduced survival of the infected type 1 or type 3 ILC-deficient mice compared with type 2 ILC-defic

94 Type 1, type 2, and type 3 ILC-deficient mice were used to gain insights int

95 a cytokine produced by innate lymphoid cells type 3 (ILC3) during Enterobacteriaceae infections.

96 r 4,000 genes was seen in the HSV-1-infected type 3 ILCs, whereas 414 were upregulated in the infecte

97 pesvirus genes were detected in the infected type 3 ILCs, whereas only 11 herpesvirus genes were dete

98 CL10, CCL3, and CCL4 than infected type 1 or type 3 ILCs.

99 ) are innate lymphocytes that participate in type 3 immune responses during infection and inflammatio

100 ether, these findings suggest dual roles for type 3 immune responses during infection.

101 ing C. difficile infection (CDI) has been on type 3 immunity because of the established role for this

102 Here, we review the complex role of type 3 immunity during CDI and delineate what is known a

103 Therapeutically, knowledge of type 3 immunity has translated into the development of I

104 Type 3 immunity is mediated by retinoic acid-related orp

105 a previously unappreciated pathway by which type 3 immunity is modulated and immune-mediated pathoge

106 TYK2 is a mediator of type 3 immunity through intracellular signaling of IL-23

107 such as Epidermal Growth Factor, Fibronectin Type 3, Immunoglobulin, and Thrombospondin type 1 domain

108 okines representative of type 1, type 2, and type 3 inflammation, and 21 lipid mediators were measure

109 r numbers of eosinophils and both type 2 and type 3 innate lymphoid cells (ILC2 and ILC3), specifical

110 had a significant and persistent decrease in type 3 innate lymphoid cells (ILC3) in the lamina propri

111 Type 3 innate lymphoid cells (ILC3s) and enteric glia, a

112 Type 3 innate lymphoid cells (ILC3s) are critical for lu

113 Type 3 innate lymphoid cells (ILC3s) are involved in mai

114 trating gamma-delta (gammadelta) T cells and Type 3 innate lymphoid cells (ILC3s) as important produc

115 Type 2 innate lymphoid cells (ILC2s) and type 3 innate lymphoid cells (ILC3s) have been implicate

116 ate that PGE2-EP4 signaling acts directly on type 3 innate lymphoid cells (ILCs), promoting their hom

117 lial cells resulted in loss of AHR-dependent type 3 innate lymphoid cells and T helper 17 cells and i

118 Type 3 innate lymphoid cells producing predominantly GM-

119 N-gamma, IL-17A, and IL-22, all hallmarks of type 3 innate lymphoid cells, were expanded in the blood

120 ere tdTomato-C3aR(-), except some LP-derived type 3 innate lymphoid cells.

121 HLA-DR+CD56+ granulocytes; and reductions in type 3 innate lymphoid cells.

122 d metabolic responses that are controlled by type-3 innate lymphoid cells (ILC3)(1-3).

123 The type 3 inositol 1,4,5-trisphosphate receptor (ITPR3) is

124 endotoxin on expression and function of the type 3 inositol trisphosphate receptor (ITPR3), because

125 e, it binds, deubiquitylates, and stabilizes type 3 inositol-1,4,5-trisphosphate receptor (IP3R3), mo

126 ormone-inactivating (TH-inactivating) enzyme type 3 iodothyronine deiodinase (D3) is an oncofetal pro

127 , we report structural findings of the human type-3 IP(3)R (IP(3)R-3) obtained by cryo-EM (at an over

128 Bartter syndrome type 3 is a clinically heterogeneous hereditary salt-los

129 FICANCE STATEMENT Pontocerebellar Hypoplasia Type 3 is a devastating developmental disorder associate

130 ado-Joseph disease or spinocerebellar ataxia type 3 is an inherited neurodegenerative disease associa

131 rogressive familial intrahepatic cholestasis type 3 is caused by biallelic variations of ABCB4, most

132 iedreich's ataxia and spinocerebellar ataxia type 3 is not restricted to the cerebellar nuclei.

133 solated dilation of the ascending aorta; and type 3, isolated dilation of the sinus of Valsalva and/o

134 stricts for poliovirus type 1 and poliovirus type 3; it ranged between 90% and 93% for poliovirus typ

135 f104, inositol 1,4,5-trisphosphate receptor, type 3 (ITPR3), and discoidin domain receptor tyrosine k

136 ular pseudodrusen, increased injections, and type 3 lesion.

137 Instead, sodium-hydrogen exchanger type 3 levels in the proximal tubule were dramatically r

138 ed for patients with sodium channel-mediated type 3 long QT syndrome (LQT3).

139 Long QT syndrome type 3 (LQT3) is a lethal disease caused by gain-of-func

140 In LQTS type 2 (LQT2) and LQTS type 3 (LQT3), T-wave alternans was observed followed by

141 [NaV1.5]) cause congenital long-QT syndrome type 3 (LQT3).

142 r2Reovirus in TNBC to interactions between a type 3 M2 gene segment and type 1 genes.

143 d HCV, presence of anti- muscarinic receptor type 3 (M3R) antibodies in SS, the role that M3R plays i

144 ta2 integrin heterodimer complement receptor type 3/Mac-1.

145 In spinocerebellar ataxia type 3/Machado-Joseph disease (SCA3/MJD), the expanded c

146 ata may yield valuable information regarding type 3 macular neovascularization (MNV).

147 CRSsNP and NENP demonstrated a decline in type 3 mediators and increase in type 2 mediators, where

148 rs and increase in type 2 mediators, whereas type 3 mediators increased with age in ENP.

149 Interestingly, the age-related decrease in type 3 mediators was associated with those of CT scores

150 TMEM67) is mutated in Meckel Gruber Syndrome type 3 (MKS3) resulting in a pleiotropic phenotype with

151 m 15 eyes (13 patients) with treatment-naive type 3 MNV in their post-nascent stage and age-related m

152 otational three-dimensional visualization of type 3 MNV.

153 s and to be useful to offer new insight into type 3 MNV.

154 a 3D visualization of the region occupied by type 3 MNV.

155 BRAF mutation, negative for KRAS mutation); type 3 (MSS or MSI low, non-CIMP, negative for BRAF muta

156 We previously reported that type 3 muscarinic acetylcholine receptors (M3-Rs) physic

157 em: type 1 SBS (n = 9), type 2 (n = 13), and type 3 (n = 10).

158 years, seven female), spinocerebellar ataxia type 3 (n = 10, age range 34-67 years, three female), an

159 Two eyes were associated with a type 3 neovascularization eccentric to PEVAC.

160 The latter were compatible with type 3 neovascularization or retinal angiomatous prolife

161 nd serous) and vascularized PEDs (type 1 and type 3 neovascularization) associated with drusen and a

162 ceptor hypoxic response initiates and drives type 3 neovascularization, mainly in the outer retina.

163 nti-VEGF therapy, and may be associated with type 3 neovascularization.

164 es as inhibitors of the Na(+)/H(+) exchanger type 3 (NHE3) are described based on a hit from high-thr

165 We found protective type 3 NKp44(+) ILCs (ILC3s) to be significantly diminis

166 V-3) and 48 by human parechovirus other than type 3 (non-HPeV-3), were detected among 132 children.

167 pathogenic mutations in BRAF but not KRAS), type 3 (not MSI-high or CIMP, with pathogenic mutations

168 MEM231 mutations in orofaciodigital syndrome type 3 (OFD3) and MKS patients that compromise transitio

169 oft tissue component at the pleural end; and type 3, one or more soft tissue cord-like pleural tag) a

170 ants (aged 6-11 months) receiving monovalent type 3 OPV (CTRI/2014/05/004588).

171 ucleotide 2493 with known polymorphism among type 3 OPV lots also produced low assay variability and

172 Eleven type 3 OPV samples were analyzed by 8 laboratories using

173 d a greater interfering effect on monovalent type 3 OPV seroresponse than did persistent infections,

174 nts who received a single dose of monovalent type 3 OPV.

175 nucleotide 472 in the 5' noncoding region of type 3 OPV.

176 e of a Bleeding Academic Research Consortium type 3 or 5 bleed).

177 The primary safety outcome was type 3 or 5 bleeding according to the Bleeding Academic

178 isk of Bleeding Academic Research Consortium type 3 or 5 bleeding was statistically similar between t

179 nt was Bleeding Academic Research Consortium type 3 or 5 bleeding.

180 eding (Bleeding Academic Research Consortium types 3 or 5) event rates among PARIS study participants

181 L) in type 2 , and 9 umol/L (6-14 umol/L) in type 3 ( P = 0.141).

182 0% (40-77%) for type 2, and 60% (40-77%) for type 3 ( P = 0.45).

183 pe 2 papilla (odd ratio 7.18, p = 0.045) and Type 3 papilla (odd ratio 7.44, p = 0.016) were associat

184 The failure rates of SBC with Type 3 papilla and Type 4 papilla were 11.11% and 6.25%,

185 A significant proportion of type 3 patients had detectable VWFpp (41%).

186 ese patients had a lower bleeding score than type 3 patients who had a complete absence of VWF:Ag and

187 mutations with rapid VWF clearance, whereas type 3 patients with no VWFpp were homozygous for null a

188 rogressive familial intrahepatic cholestasis type 3 patients.

189 orders as well as Pontocerebellar Hypoplasia type 3 (PCH3).

190 s (2a: superficial ulcers; 2b: deep ulcers); type 3: perforation (3a: perforation without communicati

191 rogressive familial intrahepatic cholestasis type 3 (PFIC3), a rare disease that can be lethal in the

192 rogressive familial intrahepatic cholestasis type 3 (PFIC3), an inherited juvenile-onset, cholestatic

193 Parainfluenza virus type 3 (PIV3) infections are a major cause of morbidity

194 Parainfluenza virus type 3 (PIV3) is major pathogen of children, and no reli

195 ibit the growth of human parainfluenza virus type 3 (PIV3), a nonsegmented negative-strand RNA virus

196 Type 3 pleural tags indicated minimal increase in the li

197 o express stabilized virus-like particles of type 3 poliovirus that can induce a protective immune re

198 Proportions to type 3 poliovirus were 166 (98.2%) of 169, 94.9-99.4; 18

199 pe 2 poliovirus, the absence of detection of type 3 poliovirus worldwide since November 2012, and cor

200 preferred a narrow "humidity-range" and HPIV type 3 preferred the season with lower humidity.

201 for use with fused deposition modeling (FDM) type 3D printers.

202 N-terminal propeptide of type 3 procollagen (PRO-C3) is a biomarker of liver fibr

203 roteasome (Prosome, Macropain) subunit alpha type 3 (PSMA3) binding to p21 and protects p21 from PSMA

204 say identified that proteasome subunit alpha type 3 (Psma3) interacts with ameloblastin.

205 newly described primate T-lymphotropic virus type 3 (PTLV-3).

206 recombinant bovine/human parainfluenza virus type 3 (rB/HPIV3) vector expressing the RSV fusion F pro

207 a chimeric bovine/human parainfluenza virus type 3 (rB/HPIV3) vector to express RSV wild-type (wt) G

208 ed chimeric bovine/human parainfluenza virus type 3 (rB/HPIV3) vector to express various modified for

209 ed chimeric bovine/human parainfluenza virus type 3 (rB/HPIV3) was developed previously as a vector e

210 The serotonin type 3 receptor (5-HT(3)) is a ligand-gated ion channel

211 The 5-hydroxytryptamine (5-HT) type 3 receptor is a member of the cysteine (Cys)-loop r

212 he concept that inositol-1,4,5-trisphosphate type 3 receptor signaling in HBCs, together with altered

213 s of alpha7 or the chimeric alpha7-serotonin-type 3 receptor, a feature important for preserving an a

214 or fosaprepitant, and a 5-hydroxytryptamine type 3-receptor antagonist, in patients with no previous

215 gand-gated ion channels, 5-hydroxytryptamine type 3 receptors (5-HT3Rs) are activated by the binding

216 receptors (D2R) and greater availability of type-3 receptors (D3R).

217 revealed treated retinoblastoma tumor with a Type 3 regression pattern, pre- and subretinal fibrovasc

218 Type 3 resistant starch (RS3) was developed from native

219 modified food starches with high contents of type 3 resistant starch (RS3).

220 rsus 249 (46% [42-51]) participants, and the type 3 response comprised 196 (73% [67-78]) versus 196 (

221 sava starch, typically, has resistant starch type 3 (RS3) content of 2.4%.

222 asma citrulline concentrations were lower in type 3 SBS but not significantly different: 15 umol/L (1

223 for 20 patients with spinocerebellar ataxia type 3 (SCA3) and 5 unaffected individuals, and correctl

224 Spinocerebellar ataxia type 3 (SCA3) belongs to the family of polyglutamine neu

225 Spinocerebellar ataxia type 3 (SCA3) is a dominantly inherited neurodegenerativ

226 Spinocerebellar ataxia type 3 (SCA3) is a neurodegenerative disorder caused by

227 e diseases, including spinocerebellar ataxia type 3 (SCA3), are caused by CAG repeat expansions that

228 neurodegeneration in Spinocerebellar Ataxia Type 3 (SCA3), one of nine inherited, incurable diseases

229 on's disease (HD) and spinocerebellar ataxia type 3 (SCA3), respectively.

230 sease and ataxin 3 in spinocerebellar ataxia type 3 (SCA3).

231 namics were accompanied by the corresponding type 3 secreted effector repertoires associated with the

232 to a second subversion mechanism, namely the type 3 secretion (T3S) injectisome.

233 Here, we show that Pla facilitates type 3 secretion into primary alveolar macrophages but n

234 sively in EHEC, thereby indirectly enhancing type 3 secretion pleiotropically.

235 The type 3 secretion protein PcrV and Psl exopolysaccharide

236 The type 3 secretion system (T3SS) and the bacterial flagell

237 -LcrV fusion protein and secreted it via the type 3 secretion system (T3SS) at 37 degrees C under cal

238 locus of enterocyte effacement (LEE)-encoded type 3 secretion system (T3SS) is the major virulence de

239 pB protein, a component within the bacterial type 3 secretion system (T3SS), which is mainly expresse

240 the injection of virulence factors through a type 3 secretion system (T3SS).

241 are directly injected into host cells via a type 3 secretion system (T3SS).

242 Experimental overproduction of a type 3 secretion system (T3SS1) in this pathogen leads t

243 ltative intracellular pathogen that uses its type 3 secretion system 2 (T3SS2) to invade and replicat

244 ression because T6SS-1 and some effectors of type 3 secretion system 3 (T3SS-3), which is also requir

245 ent to completely overcome the repression of type 3 secretion system activity normally associated wit

246 EHEC, YhaJ directly activates expression of type 3 secretion system components and effectors.

247 A type 3 secretion system is used by many bacterial pathog

248 strain of P. aeruginosa lacking a functional type 3 secretion system needle tip complex (DeltaPcrV) s

249 ciated with human disease and none encoded a type 3 secretion system synonymous with typical enteroha

250 erine (d-Ser) resulted in down-regulation of type 3 secretion system-dependent colonization, thereby

251 needle tip complex (DeltaPcrV) supernatant] type 3 secretion system.

252 higella was independent of the status of the type 3 secretion system.

253 ct Salmonella pathogenicity island 2 (SPI-2) type 3 secretion system.

254 e, and virulence due to hyperactivity of the type 3 secretion system.

255 Pathogen type 3 secretion systems (T3SS) manipulate host cell pat

256 Type 3 secretion systems (T3SSs) of bacterial pathogens

257 olidify the role of Pla in promoting optimal type 3 secretion using primary human tissue with relevan

258 are secreted into the vacuole lumen through type 3 secretion.

259 response to high expression of the bacterial type-3 secretion system (T3SS).

260 ins SipD and IpaD of Gram-negative bacterial type-3 secretion systems that breach immune barriers and

261 a paradigmatic example, Salmonella uses two type-3 secretion systems to inject effector proteins tha

262 Type 3 seeds were composed of more than 90% necrotic mat

263 xene templated Diels-Alder cycloaddition and type-3 semipinacol rearrangement to generate the trans-p

264 Type 3 seroprevalence was below 75% for both age groups

265 /NK cell-related genes and downregulation of type 3 signature genes.

266 dy participants (N=913) underwent an in-home Type 3 sleep apnea study, clinic BP measurements, and an

267 in motor function in patients with type 2 or type 3 SMA over a period of 24 months.

268 netically confirmed type 2 or non-ambulatory type 3 SMA.

269 me in patients with type 2 or non-ambulatory type 3 SMA.

270 it to "correct" the gene proximity for cell type 3D specific arrangements.

271 causing severe outbreaks worldwide (sequence type 3 [ST3]), recurrent outbreaks in certain regions (e

272 Simian T-cell lymphotropic virus type 3 (STLV-3) is almost identical to HTLV-3.

273 In this study, we use glycoconjugates of type 3 Streptococcus pneumoniae CPS (Pn3P) to assess whe

274 eralocorticoid excess syndrome and Bartter's type 3 syndrome.

275 e 1 (T1) endotype, type 2 (T2) endotype, and type 3 (T3) endotype, respectively.

276 ) imaging via GCaMP3 expressed in Type 2 and Type 3 taste bud cells.

277 BARC (Bleeding Academic Research Consortium) type 3 to 5 bleeding at 1 year after randomization.

278 BARC type 3 to 5 bleeding occurred in 46 patients (6.1%) in t

279 group, Bleeding Academic Research Consortium type 3 to 5 bleeding occurred in 8.1% of patients assign

280 to 3 and 7.5% of eyes (n = 4) converted from type 3 to a combined retinoschisis-retinal detachment wi

281 endently of gene expression (noncanonical or type 3 TR signaling).

282 that transient receptor potential canonical type 3 (TRPC3) channels are involved in hypothalamic glu

283 onfiguration was most prevalent, followed by type 3, type 2, type 5 and type 4 in that order.

284 with reporter constructs containing the wild-type 3'-UTR or when a specific anti-miR-206* inhibitor w

285 novalent, recombinant, chimpanzee adenovirus type-3 vector-based Ebola Zaire vaccine (ChAd3-EBO-Z).

286 gimen with recombinant chimpanzee adenovirus type 3 vectored Ebola Zaire vaccine (ChAd3-EBO-Z) follow

287 bola vaccine candidate chimpanzee adenovirus type 3-vectored Ebola Zaire vaccine (ChAd3-EBO-Z) and bo

288 -defective recombinant chimpanzee adenovirus type 3-vectored ebolavirus vaccine (cAd3-EBO), encoding

289 of an aerosolized human parainfluenza virus type 3-vectored vaccine that expresses the glycoprotein

290 n of a cocktail of human parainfluenza virus type 3-vectored vaccines against individual ebolaviruses

291 Human parainfluenza virus type 3-vectored vaccines offer benefits, including needl

292 vascular endothelial growth factor receptor type 3 (VEGFR3).

293 The atypical vesicular glutamate transporter type 3 (VGLUT3) is expressed by subpopulations of neuron

294 tients who had previously been classified as type 3 VWD.

295 Seroconversion for type 3 was noted in 175 infants (94%, 90-97) on bOPV sho

296 ause maturity onset of diabetes in the young type 3, whereas murine HNF6 participates in fetal liver

297 ked to a disease, Pontocerebellar Hypoplasia type 3, which causes brain atrophy.

298 oteins (Cathepsin D, Galectin-4, Paraoxonase type 3) with a novel association with incident diabetes.

299 increased risk of diabetes, and Paraoxonase type 3, with a decreased risk of diabetes, remained sign

300 operties of type-1 (with calcium, ALA-1) and type-3 (without calcium, ALA-3) alpha-lactalbumin (ALA)