ライフサイエンスコーパス: disease type

1 rity of functional connectivity loss in each disease type.

2 ere prospectively enrolled and stratified by disease type.

3 SC GM and SC WM areas with MS disability and disease type.

4 ility status scale (EDSS) score, centre, and disease type.

5 ins that correlate with host specificity and disease type.

6 of granuloma types are seen and differ with disease type.

7 nticipated and when relevant to the specific disease type.

8 d using standard radiotherapy doses for each disease type.

9 nty, sex, and particular chronic respiratory disease type.

10 at more fully encompass the heterogeneity of disease types.

11 term that obfuscates more specific allergic disease types.

12 e identification of biomarkers that classify disease types.

13 erence in prevalence of the triggers between disease types.

14 and has a negative impact on outcome of all disease types.

15 h context-dependent roles across systems and disease types.

16 ignment of uniform radiotherapy doses within disease types.

17 n, mono-/heterocellular cultures and several disease types.

18 poor outcome in autoimmune and inflammatory disease (type 1 diabetes, anti-neutrophil cytoplasmic an

19 We enrolled 31 patients with Gaucher disease type 1 (GD), 29 GBA1 heterozygous carriers (Het

20 e mendelian disorder medullary cystic kidney disease type 1 (MCKD1), mapped more than a decade ago to

21 measures for treatment trials for Stargardt disease type 1 (STGD1) and other macular diseases are ne

22 an volume stability in adults with Gaucher's disease type 1 already controlled by intravenous ERT and

23 encing on a patient with Charcot-Marie-Tooth disease type 1 and identified a de novo mutation in PMP2

24 ir role in the progression of the autoimmune disease type 1 diabetes (T1D) is poorly understood.

25 Diagnosis of the autoimmune disease type 1 diabetes (T1D) is preceded by the appeara

26 requisites for development of the autoimmune disease type 1 diabetes (T1D).

27 The autoimmune disease type 1 diabetes is characterized by effector T-c

28 ther IKZF1 is associated with the autoimmune disease type 1 diabetes.

29 fficacy of emerging treatments for Stargardt disease type 1 in clinical trials.

30 The mainstay of treatment for Gaucher's disease type 1 is alternate-week infusion of enzyme repl

31 Gaucher disease type 1 is characterized by hepatosplenomegaly, a

32 Stargardt disease type 1 patients (carrying at least 1 mutation in

33 fied another family with Charcot-Marie-Tooth disease type 1 that has a mutation affecting an adjacent

34 asures was maintained in adults with Gaucher disease type 1 treated with eliglustat who remained in t

35 ylthioesterase-1, which is mutated in Batten disease type 1, acid sphingomyelinase, which is mutated

36 In Stargardt disease type 1, macular sensitivity declines significant

37 ong previously untreated adults with Gaucher disease type 1, treatment with eliglustat compared with

38 ant PMP2 mutations cause Charcot-Marie-Tooth disease type 1.

39 second leading cause of Charcot-Marie-Tooth disease type 1.

40 ith select nonpsychiatric disorders (Crohn's disease, type 1 and type 2 diabetes mellitus, multiple s

41 flammatory bowel disease, autoimmune thyroid disease, type 1 diabetes mellitus (T1D), and autoimmune

42 as hepatitis C vasculitis, graft-versus-host disease, type 1 diabetes, and systemic lupus erythematos

43 as rheumatoid arthritis, inflammatory bowel disease, type 1 diabetes, atopy, and obesity.

44 , obesity at age 5 years, inflammatory bowel disease, type 1 diabetes, cancer, and death.

45 Conditions such as coeliac disease, type 1 diabetes, Crohn's disease and ulcerative

46 , coronary artery disease, psoriasis, celiac disease, type 1 diabetes, inflammatory bowel disease, an

47 sease in murine models of inflammatory bowel disease, type 1 diabetes, multiple sclerosis, and other

48 f obesity at age 5 years, inflammatory bowel disease, type 1 diabetes, or cancer.

49 ases including generalized vitiligo, Addison disease, type 1 diabetes, rheumatoid arthritis, and othe

50 res based on susceptibility loci for Crohn's disease, type 1 diabetes, systemic lupus erythematosus,

51 chronic disorders, including the autoimmune diseases type 1 diabetes and multiple sclerosis.

52 st cancer, neurodegenerative disorders, bone diseases, Type 1 and Type 2 diabetes).

53 In a wide array of kidney diseases, type 1 angiotensin (AT1) receptors are present

54 eviously been associated with two autoimmune diseases, type 1 diabetes (T1D) and multiple sclerosis.

55 context of risk assessment for seven complex diseases, type 1 diabetes (T1D), type 2 diabetes (T2D),

56 The most common endocrine diseases, type 1 diabetes, hyperthyroidism, and hypothyr

57 Our analysis of four autoimmune diseases--type 1 diabetes (T1D), rheumatoid arthritis, c

58 ationship between epilepsy and 12 autoimmune diseases: type 1 diabetes mellitus, psoriasis, rheumatoi

59 ugh classically viewed as a type 2-regulated disease, type 17 helper T (Th17) cells are known to be i

60 Ten patients with Charcot-Marie-Tooth disease type 1A (CMT1A) and nine patients with chronic i

61 Charcot-Marie-Tooth disease type 1A (CMT1A) is associated with increased gen

62 Charcot-Marie-Tooth disease type 1A (CMT1A) is caused by a 1.4 Mb duplicatio

63 Charcot-Marie-Tooth disease type 1A (CMT1A) is caused by duplication of peri

64 ting neuropathy known as Charcot-Marie-Tooth disease type 1A (CMT1A) is linked with duplication of th

65 Charcot-Marie-Tooth disease type 1A (CMT1A) is the most common heritable per

66 Charcot-Marie-Tooth disease type 1A (CMT1A) is the most common inherited neu

67 ted the genomic disorder Charcot-Marie-Tooth disease type 1A (CMT1A), a dominant peripheral neuropath

68 athy: duplications cause Charcot-Marie-Tooth disease type 1A (CMT1A), whereas deletions lead to hered

69 lication associated with Charcot-Marie-Tooth disease type 1A (CMT1A).

70 ropathy in subjects with Charcot-Marie-Tooth disease type 1A (CMT1A).

71 tically in patients with Charcot-Marie-Tooth disease type 1A (n = 32), chronic inflammatory demyelina

72 that might be useful in Charcot-Marie-Tooth disease type 1A and other neuropathies that involve axon

73 ities and axonal loss in Charcot-Marie-Tooth disease type 1A are poorly understood, in part because o

74 nation was absent in the Charcot-Marie-Tooth disease type 1A group, but identifiable in all patients

75 A key feature of Charcot-Marie-Tooth disease type 1A is secondary death of axons.

76 Charcot-Marie-Tooth disease type 1A is the most common inherited neuropathy

77 Charcot-Marie-Tooth disease type 1A is the most frequent inherited periphera

78 ned internodal length in Charcot-Marie-Tooth disease type 1A suggests a potential developmental defec

79 l hypercholesterolemia, and glycogen storage disease type 1a) were found to recapitulate key patholog

80 ortened in patients with Charcot-Marie-Tooth disease type 1A, compared with those in normal controls

81 findings in humans with Charcot-Marie-Tooth disease type 1A, we found that Schwann cell c-Jun was el

82 the most common form of Charcot-Marie-Tooth disease type 1A, whereas the reciprocal deletion of this

83 ng the C3 mouse model of Charcot-Marie-Tooth disease type 1A.

84 f axonal degeneration in Charcot-Marie-Tooth disease type 1A.

85 contrasting functions in Charcot-Marie-Tooth disease type 1A: on the one hand they are the genetic so

86 e for demyelination in a Charcot-Marie-Tooth disease type 1B (CMT1B) mouse model.

87 Glycogen storage disease type 1b (GSD-1b) is an autosomal-recessive disea

88 Charcot-Marie-Tooth disease type 1B is caused by mutations in myelin protein

89 tic model of early onset Charcot-Marie-Tooth disease type 1B, develop neuropathy in part because the

90 ing interface and causes Charcot-Marie-Tooth disease type 1B, severely inhibits dimerization, suggest

91 indicating diagnosis of Charcot-Marie-Tooth disease type 1B.

92 protein zero (MPZ) cause Charcot-Marie-Tooth disease type 1B.

93 Charcot-Marie-Tooth disease type 1C (CMT1C) is a dominantly inherited motor

94 yelinating neuropathy or Charcot-Marie-Tooth disease type 1D.

95 have been shown to cause Charcot Marie Tooth Disease type 2 (CMT-2) or distal hereditary motor neurop

96 ditary axonal neuropathy Charcot-Marie-Tooth disease type 2 (CMT2).

97 their 40s with recessive Charcot-Marie Tooth disease type 2 (CMT2).

98 The metabolic disease type 2 diabetes (T2D) is a risk factor for TB an

99 in an autosomal dominant Charcot-Marie-Tooth disease type 2 family.

100 Refractory coeliac disease type 2 is a rare subtype of coeliac disease with

101 ial disorders related to Charcot-Marie-Tooth disease type 2 were also excluded by sequencing POLG and

102 In patients with refractory coeliac disease type 2 who were treated with AMG 714 or placebo

103 or genetically undefined Charcot-Marie-Tooth disease type 2.

104 a confirmed diagnosis of refractory coeliac disease type 2.

105 arranted in patients with refractory coeliac disease type 2.

106 activity and symptoms of refractory coeliac disease type 2.

107 ndition that increases risk of chronic liver disease, type 2 diabetes and cardiovascular disease.

108 in the risk of chronic liver disease, heart disease, type 2 diabetes and liver cancer.

109 cardiovascular calcification (chronic kidney disease, type 2 diabetes mellitus, and atherosclerosis),

110 nflammatory disorders-such as chronic kidney disease, type 2 diabetes mellitus, and atherosclerosis-t

111 hat consists of dyslipidemia, cardiovascular disease, type 2 diabetes mellitus, and obesity.

112 mation-related traits such as cardiovascular disease, type 2 diabetes mellitus, and obesity.

113 human diseases (e.g. obesity, cardiovascular disease, type 2 diabetes mellitus, cancer) remains an un

114 factors may influence cancer, cardiovascular disease, type 2 diabetes mellitus, obesity, and nonalcoh

115 pathophysiologies, including cardiovascular disease, type 2 diabetes, Alzheimer's disease, and neuro

116 communicable diseases such as coronary heart disease, type 2 diabetes, and breast and colon cancers,

117 e association between ALA and cardiovascular disease, type 2 diabetes, and fracture risk.

118 dities were hypertension, cataracts, thyroid disease, type 2 diabetes, and glaucoma.

119 lished risk factors like age, cardiovascular disease, type 2 diabetes, and graft function, posttransp

120 olactin secretion and treatment of Parkinson disease, type 2 diabetes, and several other pathological

121 MI, systolic blood pressure, coronary artery disease, type 2 diabetes, and taller stature.

122 linked to increased risk for cardiovascular disease, type 2 diabetes, atherosclerosis,non-alcoholic

123 to test genome-wide PRSs for coronary heart disease, type 2 diabetes, atrial fibrillation, breast ca

124 bulinemia, chronic kidney or end-stage renal disease, type 2 diabetes, B-cell lymphoma, lichen planus

125 metabolic traits, including coronary artery disease, type 2 diabetes, blood pressure, waist-hip rati

126 rcoagulable state that drives cardiovascular disease, type 2 diabetes, fatty liver disease, and sever

127 ociated with obesity, lipids, cardiovascular disease, type 2 diabetes, inflammation, various cancers,

128 cially sitting, on mortality, cardiovascular disease, type 2 diabetes, metabolic syndrome risk factor

129 homeostasis to diseases, such as Alzheimer's disease, type 2 diabetes, obesity, and cancer.

130 stasis in disease states such as Alzheimer's disease, type 2 diabetes, obesity, and cancer.

131 stigated for the treatment of cardiovascular disease, type 2 diabetes, osteopenia, osteoporosis, and

132 ing number of diseases including Alzheimer's disease, type 2 diabetes, rheumatoid arthritis, and myel

133 55 incident cases of obesity-related chronic diseases (type 2 diabetes mellitus, cardiovascular disea

134 c heart disease, ischemic stroke), metabolic diseases (type 2 diabetes), certain types of cancer, and

135 ve diseases including cancer, cardiovascular diseases, type 2 diabetes mellitus, obesity, amnesia amo

136 kidney, liver, lung diseases, cardiovascular diseases, type 2 diabetes, obesity and cancer.

137 in 8,000 samples from a control group and 3 diseases: type 2 diabetes (T2D), coronary artery disease

138 y debilitating human diseases, such as heart disease, type-2 diabetes, and metabolic syndrome.

139 Charcot-Marie-Tooth disease type 2A (CMT2A) is caused by mutations in the ge

140 ons in MFN2, which cause Charcot-Marie-Tooth disease type 2A (CMT2A), primarily affect the nervous sy

141 utosomal dominant) cause Charcot-Marie-Tooth disease type 2A (CMT2A), the commonest axonal form of CM

142 rodegenerative condition Charcot-Marie-Tooth disease type 2A (CMT2A).

143 Charcot-Marie-Tooth disease type 2A associated with MFN2 mutations is clinic

144 Charcot-Marie-Tooth (CMT) disease type 2A is a progressive, neurodegenerative diso

145 Patients with von Willebrand disease type 2A present with increased bleeding due to m

146 von Willebrand disease type 2B (vWD-type 2B) is characterized by gain-o

147 Charcot-Marie-Tooth disease type 2C (CMT2C) is an autosomal dominant neuropa

148 also known as HMSN2C or Charcot-Marie-Tooth disease type 2C (CMT2C)) are phenotypically heterogeneou

149 Charcot-Marie-Tooth disease type 2D (CMT2D) is a peripheral nerve disorder c

150 ve toxicity resulting in Charcot-Marie-Tooth disease type 2D (CMT2D) is still largely unresolved.

151 a potential therapy for Charcot-Marie-Tooth disease type 2D (CMT2D), caused by dominant mutations in

152 Charcot-Marie-Tooth disease type 2D, a hereditary axonal neuropathy, is caus

153 eripheral nerve degeneration and lead to CMT disease type 2D.

154 utosomal-dominant axonal Charcot-Marie-Tooth disease type 2E (CMT2E) and type 2F (CMT2F).

155 F-L) have been linked to Charcot-Marie-Tooth disease type 2E (CMT2E) in humans.

156 for autosomal recessive Charcot-Marie-Tooth disease type 2H on chromosome 8q13-21.1 was excluded by

157 rm of axonal neuropathy, Charcot-Marie-Tooth disease type 2N (CMT2N).

158 with autosomal-dominant Charcot-Marie-Tooth disease type 2Z and spinal muscular atrophy, and the ons

159 hed platelets isolated from a von Willebrand disease type 3 patient with no detectable VWF, implying

160 The autosomal dominant form of the disease, type 4, is due to mutations in the SLC40A1 gene

161 Charcot-Marie-Tooth disease type 4B (CMT4B) is a severe, demyelinating perip

162 protein 2 (MTMR2) cause Charcot-Marie-Tooth disease type 4B1 (CMT4B1), a severe demyelinating periph

163 y peripheral neuropathy, Charcot-Marie-Tooth disease type 4C (CMT4C).

164 o Schwann cells to treat Charcot-Marie-Tooth disease type 4C and potentially other similar demyelinat

165 Charcot-Marie-Tooth disease type 4C is the most common recessively inherited

166 ent therapy for treating Charcot-Marie-Tooth disease type 4C to rescue the phenotype of the Sh3tc2-/-

167 essively inherited Charcot-Marie-Tooth (CMT) disease type 4E, which is predicted to alter the ability

168 In contrast, in Charcot-Marie-Tooth disease type 4J (also caused by FIG4 mutations), one of

169 the inherited disorders Charcot-Marie-Tooth disease type 4J, Yunis-Varon syndrome, and polymicrogyri

170 Recessive Charcot-Marie-Tooth disease type-4J (CMT4J) and its animal model, the pale t

171 erlying microglia activation in Niemann-Pick disease type A (NPA).

172 Mucopolysaccharidosis IIIA or Sanfilippo disease type A is a progressive neurodegenerative disord

173 ase) deficiency results in the lipid storage disease type A Niemann-Pick disease (NPD-A), mimicked in

174 omyelinase, which is mutated in Niemann Pick disease type A, and beta galactosidase-1, which is mutat

175 These include cathepsins and Niemann-Pick disease type A, B, and C genes.

176 uronal 2, CLN2), Fabry, Farber, Niemann-Pick disease type A, Sanfilippo type B (mucopolysaccharidosis

177 (ASMD) and have been linked to Niemann-Pick disease types A and B.

178 nd podocyturia varied markedly by glomerular disease type: a high correlation in minimal-change disea

179 Disease type also correlated with PPR core total HRQoL s

180 etinal thickness seems to be associated with disease type and duration of disease in non-highly myopi

181 asis; how they can be used as biomarkers for disease type and grade; and how miRNA-based treatments c

182 prospective study demonstrates the effect of disease type and intensity of treatment on HRQoL.

183 tion analyses of patient genomes reveal that disease type and severity may be explained by the occurr

184 Disease type and severity were rated by health care prov

185 degree of donor-recipient HLA matching, and disease type and status at transplantation.

186 ntation (HCT) is predominantly influenced by disease type and status, it is essential to be able to s

187 The disease type and various disease features were abstracte

188 fic cohorts covering 524 distinct ophthalmic disease types and 1800 disease sub-types across 35 diffe

189 We have also discussed the disease types and different classification systems inclu

190 rature, allowing very precise definitions of disease types and patient details.

191 utlook for targeting the iCP in a variety of disease types and with mechanisms besides inhibition.

192 DNA methylation profiles differ among disease types and, therefore, can be used in disease dia

193 r, most of these studies focused on only one disease type, and failed to address whether the identifi

194 ps in studies were compared by journal type, disease type, and funding source.

195 ies are concordant for autoantibody profile, disease type, and HLA class II haplotypes and whether cl

196 ons arise with regard to patient population, disease type, and therapy.

197 c classifiers that can distinguish different disease types as well as normal controls, and highlight

198 nly seven (10%) of 70 patients with the same disease types but with wild-type PIK3CA treated on the s

199 tissue, a mutation that causes Niemann-Pick disease type C (a neurodegenerative ataxia), slowing dow

200 g as well as siRNA knockdown of Niemann-Pick disease type C (NPC) 1 and NPC2 also cause inhibition of

201 Niemann-Pick disease type C (NPC) and Wolman disease are two members

202 ing cholesterol accumulation in Niemann-Pick disease type C (NPC) cells.

203 Niemann-Pick disease type C (NPC) is a lysosomal storage disorder cha

204 Niemann-Pick disease type C (NPC) is a severe neurovisceral lysosomal

205 Niemann-Pick disease type C (NPC) is associated with mutations in NPC

206 Niemann-Pick disease type C (NPC) is caused by defects in either the

207 Niemann-Pick disease type C (NPC) is caused by mutations in NPC1 or N

208 lysosomes of cells derived from Niemann-Pick disease type C (NPC) patients and demonstrate a greatly

209 Moreover, we propose that Niemann-Pick disease type C (NPC), a lysosomal storage disorder, may

210 ipid storage diseases, includes Niemann-Pick disease type C (NPC), caused predominantly (95%) by muta

211 encoding these proteins lead to Niemann-Pick disease type C (NPC).

212 tribute to neurodegeneration in Niemann-Pick disease type C (NPC).

213 ose defects are responsible for Niemann-Pick disease type C (NPC).

214 tic effects in animal models of Niemann-Pick disease type C and several other neurodegenerative state

215 t deficiency in patient-derived Niemann-Pick disease type C fibroblasts by fluorescence as well as co

216 microglia phenotypes occur in a Niemann-Pick disease type C mouse model and patient.

217 late endosomal membrane protein Niemann-Pick disease type C protein 1 (NPC1) arising during early sta

218 analyzed the involvement of the Niemann-Pick disease type C-1a (NPC1a) protein, a cholesterol transpo

219 enylketonuria and miglustat for Niemann-Pick disease type C.

220 izes mutations in patients with Niemann-Pick disease type C.

221 nes isolated from wild-type and Niemann-Pick disease type C1 (NPC1) deficient cells.

222 uno and the cholesterol-binding Niemann-Pick disease type C1 protein (NPC1) suggests how the modified

223 coimmunoprecipitated with NPC1 (Niemann-Pick disease type C1), an endocytic regulator of LDL traffick

224 ly reduced in cells depleted of Niemann-Pick disease type C1, a lysosomal protein required for choles

225 Niemann-Pick disease, type C1 (NPC1) is a heritable lysosomal storage

226 Niemann-Pick disease, type C1 (NPC1) is a lysosomal storage disorder

227 Niemann-Pick disease, type C1 (NPC1), which arises from a mutation in

228 etase, beta-subunit), and NPC2 (Niemann-Pick disease type C2); and secondary to myeloid leukemia.

229 his therapy, matched by sex, immune-mediated disease type, cancer type, and time from initial cancer

230 ANCA serotype as opposed to the traditional disease type classification.

231 cell types, and cell lines, and showed that disease types could be stratified in a data-driven manne

232 Their 3-year progression rate to Alzheimer's disease-type dementia was 50% compared to 21% for subjec

233 The 3-year progression rate to Alzheimer's disease-type dementia was 59% in the high Alzheimer's di

234 Their 3-year progression rate to Alzheimer's disease-type dementia was 61% compared to 22% for subjec

235 airment stage and progression to Alzheimer's disease-type dementia.

236 C may be more closely related to Alzheimer's Disease-type disease rather than to cerebral small vesse

237 contexts (e.g. different cells, tissues and disease types, etc.).

238 .006), independently of antibiotic exposure, disease type, feeding mode, and week of chemotherapy.

239 NA and miRNA expression profiles, tissue and disease type from this vector.

240 Randomisation was stratified by disease type, geographical region, and number of previou

241 ation is feasible in all models examined but disease type has a major impact on outcome, as assessed

242 with OI, particularly those with less severe disease (type I), displayed a teriparatide-induced anabo

243 t long-term complication of glycogen storage disease type I (GSD I) and malignant transformation to h

244 eumatoid arthritis, Sjogren syndrome, celiac disease, type I diabetes mellitus, and systemic lupus er

245 Unlike disseminated disease, type I IFN signaling in the brain was required

246 Glycogen storage disease type Ia (GSD Ia) is caused by autosomal mutation

247 as von Gierke's Disease or Glycogen storage disease type Ia (GSD Ia), is characterized by decreased

248 Glycogen storage disease type Ia (GSD-Ia) is characterized by impaired gl

249 Glycogen storage disease type Ia (GSD-Ia), which is characterized by impa

250 Glycogen storage disease type Ia (GSDIa, von Gierke disease) is the most

251 Glycogen storage disease type-Ia (GSD-Ia) is caused by a lack of glucose-

252 lpha or G6PC) deficiency in glycogen storage disease type-Ia (GSD-Ia) leads to impaired hepatic autop

253 Glycogen storage disease type Ib (GSD-Ib) is an autosomal-recessive syndr

254 Glycogen storage disease type Ib (GSD-Ib) is caused by a deficiency in th

255 Glycogen storage disease type Ib (GSD-Ib) is caused by deficiencies in th

256 flammatory bowel disease in glycogen storage disease type Ib (GSD-Ib).

257 d neutrophil dysfunction in glycogen storage disease type Ib is poorly understood.

258 Glycogen storage disease type Ib, characterized by disturbed glucose home

259 d neutrophil dysfunction in glycogen storage disease type Ib.

260 Glycogen storage disease type-Ib (GSD-Ib), deficient in the glucose-6-pho

261 aepithelial lymphocytes in refractory celiac disease type II (RCD II).

262 Refractory celiac disease type II (RCDII) is a severe complication of celi

263 et acid maltase deficiency (glycogen storage disease type II [GSD II]), glycogen accumulates inside m

264 e (acid maltase deficiency, glycogen storage disease type II) in children and adults can be challengi

265 ysfunction occur in tandem in cardiovascular disease, type II diabetes and ageing.

266 n many fatal diseases, including Alzheimer's disease, type II diabetes mellitus, transmissible spongi

267 teins with cell membranes, as in Alzheimer's disease, type II diabetes, and a host of others.

268 treat osteoporosis, hypercalcaemia, Paget's disease, type II diabetes, and obesity and are being act

269 , including Alzheimer's disease, Parkinson's disease, type II diabetes, and secondary amyloidosis.

270 disorders, including Alzheimer and Parkinson diseases, type II diabetes, and a number of systemic amy

271 orders, including Alzheimer's disease, prion diseases, type II diabetes, and others.

272 al incurable diseases, including Alzheimer's disease, type-II diabetes, Jacob-Creutzfeld disease, and

273 Glycogen storage disease type III (GSDIII) is a metabolic disorder charac

274 ential pharmacological agents for a range of disease types including neurodegenerative conditions and

275 Disease type, initial severity, and time since diagnosis

276 Glycogen storage disease type IV (GSD IV) is a rare autosomal recessive d

277 Glycogen storage disease type IV (GSD IV) is a rare autosomal recessive d

278 In deriving ECV, coronary artery disease type LGE, but not non-coronary artery disease ty

279 isease type LGE, but not non-coronary artery disease type LGE, has been consistently excluded.

280 sk stratification of patients, regardless of disease type (limited or diffuse) or duration of disease

281 tive HSCT study that enrolls patients across disease types must account for this heterogeneity; yet,

282 tunities for the amelioration of Alzheimer's-disease-type neuropathology through inhibition of amyloi

283 as univariate analysis identified underlying disease, type of operation, and high levels of serum amy

284 across subgroups (gender, age, preadmission diseases, type of admission) and sensitivity analyses (d

285 P antibodies, but not with disease duration, disease type, or other autoantibodies.

286 t between the treatment groups stratified by disease type (P = .42).

287 ts with at least 1 skeletal-related event by disease type, pain as assessed by the Brief Pain Invento

288 le of Willis atherosclerosis and Alzheimer's disease-type pathology was more robust for female subjec

289 H. pylori isolates from patients of distinct disease types, ranging from gastritis to gastric cancer,

290 Although responses vary by land-use and disease types, results suggest that agricultural land-us

291 ssess its value as a potential biomarker for disease type, severity, progress or therapeutic success.

292 adjustment for demographic characteristics, disease type, smoking, and ACA, anti-beta2GPI positivity

293 oding, this analysis of symptom codes across disease types suggests that fungal diseases may be diffi

294 selected on the basis of previous evidence: disease type (three-vessel disease or left main coronary

295 s in the patient demographics, geography, or disease types treated with an MIS approach between HSAs

296 ibiting PFK1 activity cause glycogen storage disease type VII, also known as Tarui disease, and mice

297 ROC curve of the algorithm for each corneal disease type was over 0.910 and in general it had sensit

298 Disease type was significantly associated with the degre

299 Rules for early termination within each disease type were based on a Bayesian hierarchical proba

300 There was a racial disparity with respect to disease type, with 38% of HRVO patients being black comp