ライフサイエンスコーパス: type 2

1 ously underrepresented the prevalence of EBV type 2.

2 lopathy (5 eyes); and macular telangiectasia type 2 (2 eyes).

3 In control tissues, type 2/3 and proinflammatory mediators showed an inverse

4 signatures, representing growth factors (A), type-2/3 cytokines (B), mixed type-1/2/3 cytokines (C),

5 contraction kinetics in knockout versus wild-type; (2) Aberrant activation of the glucose/lipid metab

6 rentiation in response to T cell-independent type 2 Ags (TI-2 Ags) has been understudied.

7 vide a mechanistic analysis of TSLP-mediated type 2 airway inflammation METHODS: To dissect the mecha

8 ferent treatment targets, such as control of type-2 airway inflammation, that can be achieved with cu

9 e absence of IL-25R signaling diminished the type 2 and enhanced the type 1 immune response that dire

10 Notch4 subverted T(reg) cells into the type 2 and type 17 helper (T(H)2 and T(H)17) effector T

11 the cardiac RyR2 (ryanodine-receptor channel type-2), and RyR2 single-channel open-probability were s

12 els of 7 cytokines representative of type 1, type 2, and type 3 inflammation, and 21 lipid mediators

13 9 was accompanied by an increase in multiple type 2 (anti-helminths) effectors, including interleukin

14 ial cells from participants with and without type 2 asthma obtained by bronchoscopy.

15 Alveolar type 2 (AT2) cells represent a metabolically active lung

16 Type 1 (B1(V)) and type 2 (B2(V)) virions package genomic RNA1 and RNA2, re

17 y also to select patients for treatment with type 2 biologics.

18 Genetic correlations revealed that type 2 bipolar disorder correlates strongly with recurre

19 C-C chemokine receptor type 2 (CCR2) is expressed on monocytes and facilitates

20 like humans, Dock8(-/-) mice have a profound type 2 CD4(+) helper T (T(H)2) cell bias upon pulmonary

21 r activation of conventional dendritic cells type 2 (cDC2) due to reduced type 1 interferon signallin

22 increased lung endothelial cell and alveolar type 2 cell proliferation.Conclusions: Postnatal rhIGF-1

23 Cytokines produced by T-helper type 2 cells and transforming growth factor beta 1 (TGFb

24 gates were catalytically active, whereas all Type 2 conjugates cleaved RNA target in a sequence-speci

25 dichotomy between IRF8(+) type 1 and IRF4(+) type 2 conventional dendritic cells (cDC1s and cDC2s, re

26 oordinated by four residues; conversely, the type 2 coordination is present in OvPrP with V136, R154,

27 death in the tissue of patients with severe type 2 CRSwNP.

28 characterized by RV species, microbiome, and type 2 cytokine (T2) response: endotype A, virus(RV-C)mi

29 Increases in airway type 2 cytokine activity, including interleukin-4 (IL-4)

30 report a role for the type 2 cytokine interleukin-13 in orchestrating metaboli

31 s, innate and adaptive immune responses, and type 2 cytokine production in a model of airway sensitiz

32 Type 2 cytokine responses promote parasitic immunity and

33 Interleukin (IL)-13 is a type 2 cytokine with important roles in allergic disease

34 In conclusion, type-2 cytokine-mediated gene repression and blockade of

35 We found that type-2 cytokine-mediated inhibition of the expression of

36 While eosinophilic inflammation caused by type 2 cytokines is responsive to corticosteroid and bio

37 Effects of type 2 cytokines were analyzed, alone or in combination,

38 rrier function caused by increased levels of type-2 cytokines (IL-4 and IL-13) that repress keratinoc

39 994, and July 31, 2018, 45 072 patients with type 2 diabetes (21 936 [48.7%] female; mean age 56.7 ye

40 Young adults with type 2 diabetes (aged 18-39 years) are at risk of early

41 We measured plasma sTNFR1 in people with type 2 diabetes (HbA(1c) >= 48 mmol/mol) at 2 hospital s

42 the Mineralocorticoid Receptor Antagonist in Type 2 Diabetes (MIRAD) trial, which randomized patients

43 udy baseline cohort with recent-onset type 1/type 2 diabetes (n = 206/381) and age-matched glucose-to

44 ion effects of these risk factors on odds of type 2 diabetes (n = 5,042 cases) and HbA(1c) levels (n

45 are lower in metformin-treated subjects with type 2 diabetes (T2D) and cardiovascular disease, yet ex

46 resistance (IR) precedes the development of type 2 diabetes (T2D) and increases cardiovascular disea

47 istance (IR) is an important risk factor for type 2 diabetes (T2D) and other cardiometabolic diseases

48 Patients with type 2 diabetes (T2D) fail to secrete insulin in respons

49 e methods to the schizophrenia GWAS data and type 2 diabetes (T2D) GWAS meta-analysis summary data.

50 Patients with type 2 diabetes (T2D) have a lower risk of Mycobacterium

51 signals from a recent GWAS meta-analysis of type 2 diabetes (T2D) in Europeans.

52 The interplay between obesity and type 2 diabetes (T2D) in poststroke recovery is unclear.

53 in Indians and misclassification of T1D and type 2 diabetes (T2D) is a particular problem in young a

54 The metabolic disease type 2 diabetes (T2D) is a risk factor for TB and the me

55 Type 2 diabetes (T2D) is associated with increased risk

56 new molecular targets are key priorities in type 2 diabetes (T2D) research.

57 ia-inducible factors (HIFs) in hypertension, type 2 diabetes (T2D), and cognitive decline in experime

58 re is emerging interest in multimorbidity in type 2 diabetes (T2D), which can be either concordant (T

59 tified 13 taxa with disrupted rhythmicity in type 2 diabetes (T2D).

60 a-cell degeneration, and the pathogenesis of type 2 diabetes (T2D).

61 00 signals robustly associated with risk for type 2 diabetes (T2D).

62 s (SCs) and skin biopsies from patients with type 2 diabetes (T2DM), we revealed the implication of L

63 scopies, 282 were performed on patients with type 2 diabetes (T2DM).

64 should also be considered for patients with type 2 diabetes and a body mass index of 30 to 35 if hyp

65 me (MetS) as a preceding metabolic state for type 2 diabetes and cardiovascular disease is widely rec

66 l glucose- and lipid-related biomarkers with type 2 diabetes and coronary artery disease.

67 axia (FRDA) include ataxia, muscle weakness, type 2 diabetes and heart failure, which are caused by i

68 ve glycemia and body weight in patients with type 2 diabetes and obesity but have limited weight-lowe

69 rol and cardiovascular disease (CVD) risk in type 2 diabetes and to assess if the presence of cardio-

70 cebo-controlled trial included patients with type 2 diabetes and urine albumin-to-creatinine ratio 30

71 e pathogenesis of several diseases including Type 2 diabetes and various cancers.

72 prevention and more intensive management of type 2 diabetes are urgently needed.

73 as assessed by PET/CT in 13 individuals with type 2 diabetes as part of a clinical study assessing th

74 Thus the microbiota may contribute to type 2 diabetes by generating imidazole propionate that

75 ), and 32% (95% CI: 24, 39) lower hazards of type 2 diabetes compared with abstaining, respectively.

76 frequency domain BRS indices were reduced in type 2 diabetes compared with control 2 and were positiv

77 Thirty participants who have type 2 diabetes consume beverages that have identical in

78 The insidious onset of type 2 diabetes delays diagnosis and increases morbidity

79 Mean age was 74 years, with a median type 2 diabetes duration of 16 years.

80 Type 2 diabetes had a higher risk for all cancer, HR 1.1

81 randomly assigned 5734 patients with CKD and type 2 diabetes in a 1:1 ratio to receive finerenone or

82 ventions to improve outcomes for adults with type 2 diabetes in LMICs.

83 abetic drug, is also effective in preventing type 2 diabetes in people at high risk(1,2).

84 Both type 1 and type 2 diabetes increase the risk of atherosclerotic car

85 management, beyond current programs in which type 2 diabetes is managed through diet, exercise, and m

86 e found that health system interventions for type 2 diabetes may be effective in improving glycemic c

87 hat post-disease-onset administration of the type 2 diabetes medication metformin reduces mitochondri

88 detection of muscle abnormalities related to type 2 diabetes mellitus (DM2) and DPN.PurposeTo assess

89 Type 1 and type 2 diabetes mellitus (T1DM and T2DM) increase the ri

90 Heart failure is a prominent complication of type 2 diabetes mellitus (T2D).

91 Currently, type 2 diabetes mellitus (T2DM) and obesity are major gl

92 Type 2 Diabetes mellitus (T2DM) is a disorder characteri

93 (AD) is a central nervous system disease and type 2 diabetes MELLITUS (T2DM) is a metabolic disorder,

94 Type 2 diabetes mellitus (T2DM) is associated with a hig

95 Patients with Type 2 diabetes mellitus (T2DM) show cognitive and mood

96 ) the 78 pure spectra, presumably related to type 2 diabetes mellitus (T2DM), from their synthetic li

97 elopment of obesity-related diseases such as type 2 diabetes mellitus (T2DM), hypertension, and dysli

98 hat increase the risk for the development of type 2 diabetes mellitus (T2DM).

99 d define eligibility criteria for those with type 2 diabetes mellitus (T2DM).

100 welve NGT subjects without family history of type 2 diabetes mellitus (T2DM; FH-) and 8 NGT with fami

101 Twenty patients with type 2 diabetes mellitus and chronic, stable heart failu

102 lozin versus placebo in 17 160 patients with type 2 diabetes mellitus and either multiple risk factor

103 Obesity and type 2 diabetes mellitus are global emergencies and long

104 vents in primary prevention populations with type 2 diabetes mellitus is highly heterogeneous.

105 se (CVD), pharmacologic agents used to treat type 2 diabetes mellitus must show cardiovascular safety

106 -of small HDL was lower in the subjects with type 2 diabetes mellitus than the control subjects.

107 r, double-blind trial in which patients with type 2 diabetes mellitus who were recently hospitalized

108 score as a decision aid in individuals with type 2 diabetes mellitus without clinical atheroscleroti

109 thelium isolated from donors with obesity or type 2 diabetes mellitus, AGO1 and THBS1 are expressed a

110 y diseases, particularly insulin resistance, type 2 diabetes mellitus, and cardiovascular disease.

111 iew addresses the interplay between obesity, type 2 diabetes mellitus, and cardiovascular diseases.

112 ommon disease states including hypertension, type 2 diabetes mellitus, and chronic kidney disease.

113 The association of NASH with obesity, type 2 diabetes mellitus, and dyslipidemia has led to an

114 wering therapies as first-line management of type 2 diabetes mellitus, considering heart failure or k

115 s including cancer, cardiovascular diseases, type 2 diabetes mellitus, obesity, amnesia among other d

116 ding premature coronary heart disease, early type 2 diabetes mellitus, ubiquitous abdominal obesity,

117 enatide 2 mg versus placebo in patients with type 2 diabetes mellitus, while aiming for glycemic equi

118 sing target for the treatment of obesity and type 2 diabetes mellitus.

119 FL adverse events in high-risk patients with type 2 diabetes mellitus.

120 that alcohol consumption is associated with type 2 diabetes mellitus.

121 markedly changed the treatment landscape of type 2 diabetes mellitus.

122 HF and cardiovascular death in patients with type 2 diabetes mellitus.

123 ed type 1 diabetes and high fat diet-induced type 2 diabetes mouse models and liver-specific Prmt1 de

124 Remission of type 2 diabetes occurred in 66.7% (4/6) after SG and in

125 educed LV volumes in patients with HFrEF and type 2 diabetes or prediabetes.

126 leotide polymorphisms (SNPs) associated with type 2 diabetes overlap with putative endocrine pancreat

127 The increasing prevalence of type 2 diabetes poses a major challenge to societies wor

128 Thirty-eight patients with type 2 diabetes received an 8-h measurement of EGP ([3-(

129 Association analysis of prevalent type 2 diabetes revealed 24 replicated proteins, of whic

130 and by the ablation of genes associated with type 2 diabetes risk in genome-wide association studies.

131 eby genetic determinants of smoking increase type 2 diabetes risk indirectly through their relationsh

132 s have linked tobacco smoking with increased type 2 diabetes risk.

133 It maps to the PRC1 locus, a type 2 diabetes susceptibility locus, but its specific r

134 cell growth and survival, but in people with type 2 diabetes the destructive effects of metabolic str

135 g response could inform selection of optimal type 2 diabetes treatment in the near future.

136 ceived long-term insulin treatment and whose type 2 diabetes was inadequately controlled (glycated he

137 ingness preference and rs10830963 on risk of type 2 diabetes was seen, this interaction did not persi

138 ys were determined, and those in common with type 2 diabetes were identified.

139 Thirteen individuals with type 2 diabetes were studied after 4 weeks' treatment wi

140 h a history of GDM are at risk of developing type 2 diabetes which is a risk factor for periodontitis

141 sets of consecutive participants with type 1/type 2 diabetes who reached the 5-year follow-up (n = 84

142 the data of 16,624 Han Chinese patients with type 2 diabetes who were enrolled in 2007-2015.

143 that could be used to identify patients with type 2 diabetes who would derive benefit from fenofibrat

144 e quality of life for people with type 1 and type 2 diabetes with reduced beta-cell function.

145 id polypeptide (IAPP) forms islet amyloid in type 2 diabetes, a process which contributes to pancreat

146 increasing number of patients suffering from type 2 diabetes, Alzheimer's disease, and diabetes-induc

147 ial target to decrease the risks of obesity, type 2 diabetes, and cardiovascular disease, and recent

148 recognized as a key risk factor for obesity, type 2 diabetes, and cardiovascular diseases.

149 ter adjusting for age, sex, body mass index, type 2 diabetes, and country.

150 es evaluating the risk of AKI in people with type 2 diabetes, and even fewer simultaneously investiga

151 imetics are effective drugs for treatment of type 2 diabetes, and there is consequently extensive int

152 atic cancer include family history, obesity, type 2 diabetes, and tobacco use.

153 morbidities that are influenced by NAFLD are type 2 diabetes, cardiovascular disease, and impaired ne

154 3) and 20% (95% CI: 3, 40) higher hazards of type 2 diabetes, compared with AAI 18.1-29.0 years and d

155 Progression of CKD in type 2 diabetes, despite dual inhibition of sodium-gluco

156 These results indicate that, in type 2 diabetes, DKD is associated with reduced renal an

157 lic diseases (hypertriglyceridemia, obesity, type 2 diabetes, hypertension, metabolic syndrome), but

158 obiome have been associated with obesity and type 2 diabetes, in epidemiological studies and studies

159 In patients with type 2 diabetes, increased dairy consumption to >=3 serv

160 on of groups at high risk for breast cancer, type 2 diabetes, inflammatory bowel disease, and coronar

161 idence of metabolic abnormalities, including type 2 diabetes, low HDL, high triglycerides, and female

162 as severe (lipodystrophy, n = 14), moderate (type 2 diabetes, n = 9), or mild (obesity, n = 8).

163 ciated with increased risk of development of type 2 diabetes, nonalcoholic fatty liver disease (NAFLD

164 Despite being the frontline therapy for type 2 diabetes, the mechanisms of action of the biguani

165 In patients with CKD and type 2 diabetes, treatment with finerenone resulted in l

166 In patients with type 2 diabetes, we also observed that intravenous infus

167 Among individuals with type 2 diabetes, ~30% exhibit hypomagnesemia.

168 However, other type 2 diabetes-associated SNPs that truncate SLC30A8 co

169 actors, including obesity, hypertension, and type 2 diabetes.

170 strong predictability for family history of type 2 diabetes.

171 for the treatment of insulin resistance and type 2 diabetes.

172 nide class that was previously used to treat type 2 diabetes.

173 lzheimer's disease, Parkinson's disease, and type 2 diabetes.

174 ing, particularly age at menarche (AAM), and type 2 diabetes.

175 macologic agents used to treat patients with type 2 diabetes.

176 c steatohepatitis and cardiovascular risk in type 2 diabetes.

177 to the development of insulin resistance and type 2 diabetes.

178 ions in an independent case-control study of type 2 diabetes.

179 the liver, leading to insulin resistance and type 2 diabetes.

180 opment of a new proposal aimed at preventing type 2 diabetes.

181 associated with both prevalent and incident type 2 diabetes.

182 rolled despite optimal medical treatment for type 2 diabetes.

183 r the treatment of chronic kidney disease in type 2 diabetes.

184 BCAAs) associate with insulin resistance and type 2 diabetes.

185 of metabolic stress and prevent the onset of type 2 diabetes.

186 ssion of CKD beyond MRE therapy in mice with type 2 diabetes.

187 to reveal new therapeutic opportunities for type 2 diabetes.

188 skeletal muscle is beneficial in obesity and Type 2 diabetes.

189 igative areas into insulin insensitivity and type 2 diabetes.

190 olygenic risk for coronary heart disease and type 2 diabetes.

191 treatment of periodontitis in patients with type 2 diabetes.

192 eral metabolic diseases including obesity or type 2 diabetes.

193 ssociation of AAI and drinking duration with type 2 diabetes.

194 red energy metabolism metabolic syndrome and type 2 diabetes.

195 r risk factor for metabolic diseases such as type 2 diabetes.

196 hyperinsulinemia precedes the development of type 2 diabetes.

197 sk of diabetic ketoacidosis in patients with type 2 diabetes: a systematic review and meta-analysis o

198 rter-2 inhibitors as combination therapy for type 2 diabetes: a systematic review and meta-analysis.

199 Type-2 diabetes (T2D) is a global disease caused by the

200 yloid deposits is a pathological hallmark of type-2 diabetes (T2D).

201 adjusted for age, sex, body mass index, and type-2 diabetes in the phase 2 validation cohort, the mi

202 act surgery in patients with well-controlled type-2 diabetes.

203 pensation but downregulated in dysfunctional type 2 diabetic (T2D) human beta cells.

204 sis in non-diabetic human islets, but not in type 2 diabetic (T2D) islets, indicating dysregulation o

205 cing cells in HPS from both non-diabetic and type 2 diabetic donors.

206 the islets of rodent diabetes models and of type 2 diabetic patients, possibly explaining their impa

207 plitude and the delay in P1-implicit time in type 2 diabetic subjects were statistically significant

208 In type 2 diabetics with micro- or macro-albuminuria UPPod:

209 Only well-controlled type-2 diabetics, free of pre-proliferative retinopathy,

210 Group-1: Patients with type-2 DM and CP; group-2: Non-diabetic individuals with

211 intronic CCTG microsatellite expansion in DM type 2 (DM2), is coordinately expressed with MBNL1 in th

212 We have recently shown that the EBV type 2 (EBV-2) strain has the unique ability to infect m

213 occurred in 63 patients (type 1 EI in 35 and type 2 EI in 28), and no type 3 EI was observed during f

214 sis of population structure reveals that EBV type 2 exists as two genomic subgroups and was more comm

215 mice carrying a familial hemiplegic migraine type 2 (FHM2) mutation have slower clearance during sens

216 Similar findings are observed in Type 2 Hi asthma, where high levels of both 15LO1-PEBP1

217 This study investigated herpes simplex virus type 2 (HSV-2) seroprevalence utility as a predictor of

218 Type 2 immune cells and eosinophils are transiently pres

219 (CRSwNP) is generally associated with severe type 2 immune reactions in the white population.

220 ion of protective immunity and amplifies the type 2 immune response that may favor the development of

221 ss to chronic disease, based on a persistent type 2 immune response to respiratory infection with a n

222 sthma treatment in high altitude reduced the type 2 immune response, corrected the increased CRTH2 ex

223 ulmonary immune cell composition and reduced type 2 immune responses and reduced similar responses af

224 e mechanisms underlying the heterogeneity of type 2 immune responses between individuals and between

225 This report shows that blocking of type 2 immune responses can treat infection.

226 Type 2 immune responses operate under varying conditions

227 However, the early events that initiate type 2 immune responses remain poorly defined.

228 ating that IgE production was not limited to type 2 immune responses yet was generally constrained in

229 associated with exaggerated allergen-induced type 2 immune responses, these responses are strongly in

230 o the lung (especially ILC2s), and decreased type 2 immune responses.

231 -33-ST2 pathway is an important initiator of type 2 immune responses.

232 ranscriptionally characterized by markers of type-2 immune activation, inflammation, cellular infiltr

233 genetic processes associated with heightened Type 2 immunity are not merely a tissue "background" but

234 in promoting inflammatory ILC2 responses and type 2 immunity at mucosal barriers.

235 Thus, type 2 immunity can be mobilized as an effective tissue-

236 ll be crucial for treating diseases in which type 2 immunity is an important component.

237 Increasing evidence indicates that type 2 immunity is associated with disease progression b

238 OPV + IPV immunization schedule and gains in type 2 immunity with addition of second dose of IPV.

239 ecent studies suggest that BHLHE40 regulates type 2 immunity, but this has not been demonstrated in v

240 different layers of heterogeneity influence type 2 immunity.

241 clinical improvement of AD and biomarkers of type 2 immunity.

242 ues forms the basis for how tissues instruct type 2 immunity.

243 h inactivated polio vaccine (IPV), to ensure type 2 immunity.

244 vailable agents target different aspects of "Type 2" immunity, and their indications often include ov

245 o express chemokines that recruit a combined type 2/immunoregulatory immune response, which produces

246 nd IL-10, was observed in mice after S. suis type 2 infection.

247 class of biologic agents that target airway type 2 inflammation has provided a new model for treatin

248 We have shown the presence of increased type 2 inflammation in patients with severe asthma and t

249 Upregulation of IL33 instigated type 2 inflammation in the metastatic microenvironment a

250 st cell and eosinophil numbers and attenuate type 2 inflammation in these subjects.

251 s were examined, including markers of atopy, type 2 inflammation, immune cell populations, and cytoki

252 Although frequently associated with type 2 inflammation, literature characterizing the milie

253 signature showed progressive enrichment for type 2 inflammation, T(H)17 signaling, and natural kille

254 ophilia is recognized as a common feature of type 2 inflammation, the roles basophils play in regulat

255 IL-4 and IL-13 is required to broadly block type 2 inflammation, which translates to protection from

256 icated in promoting ILC2 accumulation during type 2 inflammation.

257 ls and identify NMB as a potent inhibitor of type 2 inflammation.

258 in a large part because they decrease airway type 2 inflammation.

259 ory states in the sinonasal cavity, with non-type 2 inflammatory disease on one end, type 2 inflammat

260 non-type 2 inflammatory disease on one end, type 2 inflammatory, eosinophil-heavy disease on the oth

261 Increased permeability, IL-33 levels, type 2 innate lymphoid cell activation, and T(h)2 cell d

262 Human type 2 innate lymphoid cells (ILC2s) are identified by c

263 us metaplasia phenotype that is dependent on type 2 innate lymphoid cells (ILC2s).

264 these aligned with pathways associated with type 2 innate lymphoid cells, monocytes, neutrophil traf

265 Type-2 innate lymphoid cells (ILC2s) are a potent source

266 OCT characteristic of Macular telangiectasia type 2 (MacTel 2).

267 Macular telangiectasia type 2 (MacTel), a late-onset macular degeneration, has

268 ge-related increase in type 3 cytokines with type 2 mediators sustained at high levels.

269 decline in type 3 mediators and increase in type 2 mediators, whereas type 3 mediators increased wit

270 t for myocardial injury (45.6%), followed by type 2 MI (34.2%) and type 1 MI (12%) (p < 0.001).

271 In an adjusted model, type 2 MI was associated with higher all-cause (hazard r

272 ears; 30% women); 55% had type 1 MI, 32% had type 2 MI, and 13% had myocardial injury.

273 mortality among young adults with type 1 MI, type 2 MI, or myocardial injury.

274 We found that MOL type 2 (MOL2) is enriched in the spinal cord when compar

275 e 1 myocardial infarction by 11% (510/4471), type 2 myocardial infarction by 22% (205/916), and acute

276 nd acute myocardial infarction, particularly type 2 myocardial infarction, because of respiratory fai

277 Neurofibromatosis type 2 (NF2) is an autosomal dominant Mendelian tumor pr

278 Oculocutaneous Albinism type 2 (OCA2) is a gene of great interest because of gen

279 atus of 0 or 1, who were scheduled to have a type 2 or 3 radical hysterectomy.

280 Monovalent type 2 oral poliovirus vaccine (mOPV2) stockpile is low.

281 n and superoxide ion through both type 1 and type 2 pathways, alleviating the aerobic requirement for

282 The development of molecules targeting these type-2 pathways has transformed severe asthma treatment,

283 lung function, particularly in patients with type 2 phenotype.

284 s EADs and abolishes PVT in long QT syndrome type 2 rabbits by counterbalancing the reduced repolariz

285 te the broad implications of the cannabinoid type 2 receptor (CB2) in neuroinflammatory processes, a

286 gnaling of BMPR2 (bone morphogenetic protein type 2 receptor) via two downstream transcription factor

287 nal transduction pathways of the cannabinoid type-2 receptor (CB2R) can represent a helpful option in

288 : To dissect the mechanisms of TSLP-mediated type 2 responses, mice were treated with TSLP and antige

289 In cardiac myocytes, clusters of type-2 ryanodine receptors (RyR2s) release Ca(2+) from t

290 evere acute respiratory syndrome-coronavirus type 2 (SARS-CoV-2) has spread worldwide infecting nearl

291 aL) potentiates EADs in the long QT syndrome type 2 setting through (1) providing additional depolari

292 Classical DCs include type 1 and type 2 subsets, which can detect different pathogens, pr

293 an important mediator for the development of type 2 T-helper cell (Th2)-driven inflammatory disorders

294 ng each bladder infection, a highly T helper type 2 (T(H)2)-skewed immune response directed at bladde

295 and sputum samples of patients according to type 2 (T2)-asthma endotypes.

296 Although T-helper type 2 (Th2) cell pathology is implicated in severe dise

297 ype response than RV-A without T-helper cell type 2 (Th2) upregulation.

298 n essential requirement for NCSTN during the type 2 transitional-marginal zone precursor stage and pe

299 ansas City classification: type 1: erythema; type 2: ulcers (2a: superficial ulcers; 2b: deep ulcers)

300 misfolding as a result of some, but not all, type 2 VWD variants.