ライフサイエンスコーパス: primary disease

1 ins and visualizing unanticipated regions of primary disease.

2 6 (72.3%) were attributable to the patient's primary disease.

3 reviewed to identify patients with recurrent primary disease.

4 ntly lower in metastatic PCs compared to the primary disease.

5 There was no difference in survival based on primary disease.

6 ong 27 patients who presented with localized primary disease.

7 l studies have been done with specimens from primary disease.

8 eated for recurrent disease and 14 (61%) for primary disease.

9 o help identify clinicoradiologically occult primary disease.

10 tinel lymph node metastasis in patients with primary disease.

11 f severely injured patients independently of primary disease.

12 xpressed differentially in metastatic versus primary disease.

13 B, or HER2-E signatures in metastatic versus primary disease.

14 imaging for both biochemical recurrence and primary disease.

15 compared with normal controls and those with primary disease.

16 exhibit all the pathological features of the primary disease.

17 oportionately worse prognosis than localized primary disease.

18 detected in approximately 13% of adults with primary disease.

19 ricted to surveillance for recurrence of the primary disease.

20 and predicts a poor outcome in patients with primary disease.

21 ide guidance for follow-up of the survivor's primary disease.

22 tential insights into disease mechanisms for primary diseases.

23 on, hepatic artery thrombosis, and recurrent primary disease, 180 required dialysis, and 45 underwent

24 ian survival was 72 months for patients with primary disease, 28 months for those with local recurren

25 Relapse of primary disease (29%) and chronic graft-versus-host dise

26 Relapse of primary disease (56%) and subsequent malignancies (25%)

27 atients aged 7-18 years (27 with mediastinal primary disease) after primary treatment.

28 The correlation between MVI occurrence and primary disease, age, gender, tumor size, tumor stage, a

29 Two hundred seventy-eight patients (56%) had primary disease and 222 (44%) recurrent disease.

30 This was out of a total of 115 patients with primary disease and 91 patients with recurrent disease.

31 radiotherapy and chemotherapy (aRCeBCSs) for primary disease and a population-based reference group.

32 e specific niche adaptations that facilitate primary disease and Acute Lymphoblastic Leukaemia (ALL)

33 s (VZV) establishes lifelong infection after primary disease and can reactivate.

34 provided by their application to SV, in both primary disease and connective tissue diseases (CTD), is

35 y achieving margin-negative resection of the primary disease and delivering effective adjuvant and/or

36 sis was performed for patients with T1 or T2 primary disease and one to three involved nodes (n = 404

37 CMV primary disease and reactivation greatly increase the ri

38 late cytopenias is important to evaluate for primary disease and secondary marrow neoplasm in both pe

39 l (OS) between patient subcohorts divided by primary disease and stratified by targeted therapy recei

40 the biology of uveal melanoma, management of primary disease and surveillance strategies to detect re

41 ts) could not be attributed to the patient's primary disease and thus were suspicious for an adverse

42 amples, RB loss was infrequently observed in primary disease and was predominantly associated with tr

43 year, cardiopulmonary events, recurrence of primary disease, and malignancy were the main causes of

44 Age-related complications, recurrence of primary disease, and malignancy were the major causes of

45 ons during the development from precursor to primary disease, and primary testicular GCTs (TGCTs) are

46 thrombocytopenic purpura focused entirely on primary disease, and secondary forms were not addressed.

47 nctional PCC enzyme in liver and thus reduce primary disease-associated toxins in a dose-dependent ma

48 sly received platinum-containing therapy for primary disease but <=1 prior non-platinum-containing re

49 omography/CT is limited in the assessment of primary disease but is gaining acceptance in prostate ca

50 state cancer that responds to antagonists in primary disease, but inevitably becomes reactivated, sig

51 Many of these factors have been defined for primary disease, but relatively few have been investigat

52 resence of chromosomal rearrangements as the primary disease cause.

53 The challenge remains to separate primary disease-causing factors from secondary disease-m

54 Collectively, these data identify a primary disease-causing molecular defect in cone cells a

55 Variable expression, independently from the primary disease-causing mutation, can partly be explaine

56 Factors such as primary disease, chronic graft-vs-host disease, prolonge

57 signature was better at predicting OSmet in primary disease compared with metastatic tissue.

58 ng female patients with cancer survive their primary disease, concerns about reproductive health rela

59 Epidemiologic investigations require a primary disease definition, but whether to combine data

60 yte function at a molecular level may be the primary disease determinant, with noncompaction arising

61 ecurrent disease in their past experience of primary disease diagnosis and treatment.

62 ain disease, where tau is believed to be the primary disease driver, as well as secondary tauopathies

63 ms that govern disease phenotype to a single primary disease driver.

64 onal studies established CD8+ T cells as the primary disease-driving cell type in AA.

65 These comprise general effects of the primary disease, e.g., inflammatory state, more specific

66 int, invasive-disease-free survival, was the primary disease endpoint for the analysis in this report

67 All patients had a planned primary disease evaluation 4-6 weeks after the completio

68 001) patients had a complete response at the primary disease evaluation visit.

69 ficity values of 93% and 95% per patient for primary disease evaluation, 93% and 96% for locoregional

70 ge of patients are at risk for recurrence of primary disease following lung transplantation.

71 related diseases, even if they do not share primary disease genes.

72 In cases of unknown primary disease, genetic fingerprints can be used to def

73 mortality from 100% to 45% (P<0.0001) in the primary disease hamster model and from 78% to 32% (P<0.0

74 Results clearly indicate that unlike primary disease, IL-6 plays no role in recurrent HSK.

75 Relapse occurred at the site of primary disease in 10 patients, at a distant site in thr

76 s, these do not translate to improvements in primary disease indicators-observations which will likel

77 radial margin positivity (RMP) is defined as primary disease involvement at the cut edge of the mesen

78 attributable to recurrence or progression of primary disease is decreasing, with increases in rates o

79 gs indicate that epigenetic heterogeneity in primary disease is directly informative for risk of bioc

80 HLH is crucial, as definitive treatment for primary disease is hematopoietic stem cell transplant.

81 of synchronous lymph node (LN) metastases in primary disease is still unknown.

82 disease similar to that of human infection: primary disease, latent infection, and reactivation tube

83 ences resulting from permanent damage by the primary disease, LCH (eg, diabetes insipidus, fractures,

84 ertion in RPGRIP1 (RPGRIP1 (ins/ins)) as the primary disease locus while a homozygous deletion in MAP

85 ning candidate pathogenic lesions beyond the primary disease locus.

86 Excision of the primary disease, lymph node metastases, and in some inst

87 temporal trends in clinical presentation and primary disease management among patients with low-risk

88 n of therapy, which have negative effects on primary disease management.

89 Treatment of the primary disease may be curative in some patients.

90 raising the possibility that it represents a primary disease mechanism and not a secondary hypoxia-in

91 icrotubule cytoskeleton, is likely to be the primary disease mechanism in HSP caused by missense muta

92 f the neuromuscular junction is considered a primary disease mechanism in human myasthenia gravis and

93 due to defective N-linked glycosylation is a primary disease mechanism in this disorder.

94 tionable treatment options: 16 targeting the primary disease mechanism, 16 with specific prevention s

95 n, supporting haploinsufficiency as the main primary disease mechanism.

96 ains unclear whether immune dysfunction is a primary disease mediator or a secondary reactionary phen

97 ouths with SCA, despite establishment as the primary disease-modifying therapy for SCA, and that ther

98 ine the pathologic and molecular features of primary disease most likely to spread to the LNs.

99 stical significance, patients with recurrent primary disease (n = 11) had a greater percentage of sam

100 margin (n = 1) and unanticipated regions of primary disease (n = 2).

101 CHR) (n=44), IF/TA (n=42), recurrence of the primary disease (n=11), de novo glomerulonephritis (n=7)

102 icity, n=4; urinary leak, n=2; recurrence of primary disease, n=1; lymphocele, n=1; and unknown, n=1.

103 amilial hypertrophic cardiomyopathy (FHC), a primary disease of heart muscle.

104 Primary disease of the gland is never separated from the

105 Castleman's disease is a rare primary disease of the lymph node caused by infection wi

106 ARVC is a primary disease of the myocardium characterized by fibro

107 Arrhythmogenic cardiomyopathy (ACM) is a primary disease of the myocardium, predominantly caused

108 Muscular dystrophies are primary diseases of muscle due to mutations in more than

109 oles in the milieu of diseases including the primary diseases of myelin.

110 ng progression of neurological disability in primary diseases of myelin.

111 ysiology of cardiac ischemia and infarction, primary diseases of the myocardium, and the effects of v

112 Baseline characteristics, primary disease, operative time, complication rate, and

113 EBV, however, may result in severe primary disease or cancer.

114 me of Mtb infection, defining progression to primary disease or latent infection and reactivated tube

115 DSS at 10 years was 31.6% for 87 primary disease patients, 25.9% for 26 recurrent patient

116 The primary disease presentation was a pure lower limb predo

117 ulted in utilization of genetically targeted primary disease prevention at short-term follow-up.

118 A first step in primary disease prevention is identifying common, modifi

119 balance the benefits and harms of aspirin in primary disease prevention, the Task Force issued a guid

120 with unsaturated FAs as a potential tool for primary disease prevention.

121 ed for evidence-based dietary guidelines for primary disease prevention.

122 The primary disease process in myelofibrosis with myeloid me

123 These differences may reflect a primary disease process in this area or be secondary eff

124 not known whether this neuronal damage is a primary disease process, or occurs only secondary to dem

125 teractions among many factors, including the primary disease process, use of medications such as cort

126 Four primary disease progression clusters (slow, moderate and

127 ransplant-/infection-related (n = 3), due to primary disease progression in advanced adult cerebral a

128 Five patients died of primary disease progression within 6 months after stent

129 d death but appears to be a marker of severe primary disease rather than an independent predictor of

130 age, sex, self-reported race and ethnicity, primary disease, receipt of chemotherapy in the past 30

131 e effects of donor and recipient genetics in primary disease recurrence and transplant-related comorb

132 e acute GVHD while retaining protection from primary disease relapse and infectious complications.

133 There were no primary disease relapses.

134 e pretreatment with medroxyprogesterone, and primary disease resembles that observed in humans.

135 We developed a primary disease risk score (DRS) that combined all 32 id

136 e craniospinal axis (RR 1.6), and relapse of primary disease (RR 3.5) to be independently associated

137 egulatory consequences of non-coding SNPs in primary disease samples.

138 only due to chronic rejection, recurrence of primary disease, sepsis, lympho-proliferative disease, o

139 tors for poor socioprofessional outcome were primary disease severity (onset in infancy or hereditary

140 Synchronous primary disease should be considered when planning diagn

141 Three of 5 patients with primary disease showed positive tumor delineation in the

142 ication factors were WHO performance status, primary disease site, and stage.

143 Unfavorable primary disease site, nodal involvement at diagnosis, al

144 e stratification factors: extent of disease, primary disease site, previous treatment, ECOG performan

145 xpected stage distribution in 2020 varied by primary disease site.

146 t requires therapeutic strategies beyond the primary disease site.

147 etation of future trials should consider the primary disease states of patients and the balance of me

148 Linkage studies have clearly identified a primary disease susceptibility locus lying within the ma

149 After resolution of the primary disease, SVV and VZV establish latent infection

150 positive, 18-65 years old, without high-risk primary disease, T-cell depletion, previous vaccination

151 By standard histopathology, 7 patients had primary disease that was either benign or not colon canc

152 ne deficiency (CVID) is an assorted group of primary diseases that clinically manifest with antibody

153 Despite being effective in treating primary disease, their effectiveness in primary and seco

154 When stratified by primary disease, this association persisted only for rec

155 ith gene expression changes occurring in the primary disease tissue, facilitating a drug perturbation

156 dose, treatment indication, institution, and primary disease type.

157 Patients whose primary disease was arthritis were randomized to the ASM

158 icity, urological problems, or recurrence of primary disease were remarkable for the lack of expressi

159 verses portal hypertension and addresses the primary disease while achieving superior survival result

160 s disease-specific survival in patients with primary disease who undergo complete gross resection.

161 In patients with primary disease who underwent complete resection of gros

162 conveyed nearly complete protection against primary disease with either virus but did not prevent mu

163 atment of myelomatous SCID-hu mice, carrying primary disease, with recombinant Wnt3a stimulated bone

164 oma and control patients who were matched by primary disease without IMD.

165 Of the 200 patients, 46% had primary disease without metastasis, 47% had metastasis,