ライフサイエンスコーパス: disease type

1 ere prospectively enrolled and stratified by disease type.

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

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

4 ins that correlate with host specificity and disease type.

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

6 d using standard radiotherapy doses for each disease type.

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

8 nticipated and when relevant to the specific disease type.

9 rity of functional connectivity loss in each disease type.

10 ignment of uniform radiotherapy doses within disease types.

11 term that obfuscates more specific allergic disease types.

12 e identification of biomarkers that classify disease types.

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

14 glycosaminoglycan types were affected in the disease types.

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

16 at more fully encompass the heterogeneity of disease types.

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

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

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

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

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

22 Clinical investigations of von Willebrand disease type 1 are defining the relationship between pla

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

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

25 ses, including the multifactorial autoimmune disease type 1 diabetes (T1D), shows associations at P <

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

27 The autoimmune disease type 1 diabetes in humans and NOD mice is determ

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

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

30 Gaucher disease type 1 is characterized by hepatosplenomegaly, a

31 Thus, dominant von Willebrand disease type 1 may be caused by heterodimerization of mu

32 ffected autosomal dominant polycystic kidney disease type 1 pedigrees.

33 Some families affected by von Willebrand disease type 1 show high penetrance with exceptionally l

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

35 everity from adult-onset Charcot-Marie-Tooth disease type 1 to childhood-onset Dejerine-Sottas neurop

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

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 er organ-specific illnesses, such as thyroid disease, type 1 diabetes, and mysasthenia gravis, or sys

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

59 peripheral neuropathies, Charcot-Marie-Tooth disease type 1A (CMT1A) and hereditary neuropathy with l

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

61 Seven of these had genetically proven CMT disease type 1A (CMT1A) due to chromosome 17p11.2-12 dup

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

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

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

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

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

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

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

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

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

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

72 Glycogen storage disease type 1a (GSD-1a), characterized by hypoglycemia,

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

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

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

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

77 Glycogen storage disease type 1a is caused by a deficiency in glucose-6-p

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

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

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

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

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

83 Charcot-Marie-Tooth disease type 1A, a hereditary demyelinating neuropathy,

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

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

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

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

88 y treat rodent models of Charcot-Marie-Tooth disease type 1A.

89 ransgenic mouse model of Charcot-Marie-Tooth disease type 1A.

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

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

92 ause a 'classical' Charcot-Marie-Tooth (CMT) disease Type 1B (CMT1B) phenotype with normal early mile

93 rotein zero (MPZ), cause Charcot-Marie-Tooth Disease type 1B (CMT1B), typically thought of as a demye

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

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

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

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

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

99 demyelinating neuropathy Charcot-Marie-Tooth disease type 1B.

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

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

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

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

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

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

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

107 ene product of autosomal dominant polycystic disease type 2, at the basal bodies of primary cilia.

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

109 emic nephropathy and medullary cystic kidney disease type 2.

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

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

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

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

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

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

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

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

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

119 rtality and increased risk of coronary heart disease, type 2 diabetes, and disability.

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

121 main adverse consequences are cardiovascular disease, type 2 diabetes, and several cancers.

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

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

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

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

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

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

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

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

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

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

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

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

134 pates in the pathogenesis of diabetic kidney disease, type 2 diabetic db/db and control db/m mice wer

135 55 incident cases of obesity-related chronic diseases (type 2 diabetes mellitus, cardiovascular disea

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

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

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

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

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

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

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

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

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

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

146 Charcot-Marie-Tooth disease type 2D (CMT2D) and distal spinal muscular atrop

147 Charcot-Marie-Tooth disease type 2D (CMT2D) and distal spinal muscular atrop

148 MA-V) in three families, Charcot-Marie-Tooth disease type 2D (CMT2D) in a single family, and as eithe

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

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

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

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

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

156 pathy type II and axonal Charcot-Marie-Tooth disease type 2L.

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

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

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

160 ause autosomal recessive Charcot-Marie-Tooth disease type 4A.

161 myotubular myopathy and Charcot-Marie-Tooth disease (type 4B), respectively, although the mechanisms

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

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

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

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

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

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

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

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

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

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

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

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

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

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

176 Disease type also correlated with PPR core total HRQoL s

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

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

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

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

181 Disease type and severity were rated by health care prov

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

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

184 The disease type and various disease features were abstracte

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

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

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

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

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

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

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

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

193 d to accurately classify tissue samples into disease types, based on their expression profiles.

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

195 have been proposed for psoriasin in various disease types, but none of these can fully explain its i

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

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

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

199 Niemann-Pick disease type C (NPC) is a fatal, autosomal recessive lip

200 Niemann-Pick disease type C (NPC) is a genetic disorder in which pati

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

202 Niemann-Pick disease type C (NPC) is a neurodegenerative disorder wit

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

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

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

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

207 Niemann-Pick disease type C (NPC) is characterized by lysosomal stora

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

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

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

211 orders such as Tangier disease, Niemann-Pick disease type C and atherosclerosis.

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

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

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

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

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

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

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

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

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

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

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

223 Niemann-Pick disease type C2 (NP-C2) is a fatal hereditary disease ch

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

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

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

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

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

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

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

231 across age, sex, PS, treatment context, and disease type (except possibly non-Hodgkin's lymphoma).

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

233 Body mass index, age, and disease type had no significant effect on this correlati

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

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

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

237 ts by patients suffering from the hereditary disease type I tyrosinaemia and its potent inhibition of

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

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

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

241 glucose homeostasis, causes glycogen storage disease type Ia (GSD-Ia), an autosomal recessive disorde

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

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

244 or P46 have been linked to glycogen storage diseases type Ia and type Ib, respectively.

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

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

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

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

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

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

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

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

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

254 d neutrophil dysfunction in glycogen storage disease type Ib.

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

256 Patients with glycogen storage disease type II (GSD II) typically excrete increased amo

257 Glycogen storage disease type II (GSDII), caused by a deficiency in acid

258 e-onset autosomal recessive glycogen storage disease type II (GSDII).

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

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

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

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

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

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

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

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

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

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

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

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

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

272 these cases had characteristic motor neuron disease-type inclusions in the dentate gyrus and cerebra

273 Disease type, initial severity, and time since diagnosis

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

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

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

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

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

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

280 and was not related to the duration of renal disease, type of renal disease, or growth hormone therap

281 A final diagnosis of Crohn's disease, type of reservoir (J,S), female gender, postope

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

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

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

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

286 gnitive deficits associated with Alzheimer's-disease-type pathologies.

287 sms involved in the development of Alzheimer disease-type pathology in patients with Down's syndrome

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

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

292 SP but involve the deposition of Alzheimer's disease-type tau often without involvement of the tau su

293 d carcinomas are fairly uncommon and include disease types that range from indolent localised papilla

294 ned loci could not unequivocally distinguish disease type, the existence of CIMP and the relative pre

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

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

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

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