ライフサイエンスコーパス: microangiopathy

1 herapy; and they had a greater prevalence of microangiopathy.

2 e of a membranoproliferative-like glomerular microangiopathy.

3 ic disease of complement-mediated thrombotic microangiopathy.

4 hese changes vary according to the degree of microangiopathy.

5 ies, dependent on the presence or absence of microangiopathy.

6 purpura (TTP), a life-threatening thrombotic microangiopathy.

7 in the development of glomerular thrombotic microangiopathy.

8 thereby interconnecting macroangiopathy and microangiopathy.

9 OF syndrome can have VWF-mediated thrombotic microangiopathy.

10 enal tissues, two target tissues of diabetic microangiopathy.

11 iagnosed with posttransplantation thrombotic microangiopathy.

12 inantly from the development of a thrombotic microangiopathy.

13 peripheral arterial disease, as well as with microangiopathy.

14 rated interest as a marker of bleeding-prone microangiopathy.

15 ckening, a histological hallmark of diabetic microangiopathy.

16 There were no episodes of thrombotic microangiopathy.

17 breakdown of homeostatic balance in diabetic microangiopathy.

18 osits, which are classic signs of thrombotic microangiopathy.

19 ink in the pathogenesis of POAG and diabetic microangiopathy.

20 ost other manifestations of diabetic retinal microangiopathy.

21 tients with transplant-associated thrombotic microangiopathy.

22 enia, hemolytic anemia, and renal thrombotic microangiopathy.

23 diagnostic challenge presented by thrombotic microangiopathy.

24 ith 9 +/- 5 years of diabetes and documented microangiopathy.

25 , but there was no evidence of haemolysis or microangiopathy.

26 othelins to vascular dysfunction in diabetic microangiopathy.

27 lved in the pathogenesis of diabetic retinal microangiopathy.

28 lement, endothelial barrier dysfunction, and microangiopathy.

29 , proteinuria, renal failure, and thrombotic microangiopathy.

30 at plasminogen activation takes place during microangiopathy.

31 MTS13 deficiency does not lead to continuous microangiopathy.

32 estive of hypertensive or arteriolosclerotic microangiopathy.

33 c anemia, and AKI with glomerular thrombotic microangiopathy.

34 ch may contribute to formation of thrombotic microangiopathy.

35 c syndrome (DHUS), a severe renal thrombotic microangiopathy.

36 nical endothelial dysfunction precedes overt microangiopathy.

37 is and treatment of TTP and other thrombotic microangiopathies.

38 cifications or all the diabetic-like retinal microangiopathies.

39 ring pathogenesis of Stx-mediated thrombotic microangiopathies.

40 C score-to stratify patients with thrombotic microangiopathy according to their risk of having severe

41 ggest that mechanisms other than generalized microangiopathy account for the altered CMRglu observed

42 ated tau; and cerebral amyloid angiopathy, a microangiopathy affecting both cerebral cortical capilla

43 2 (n = 10), grafts also developed thrombotic microangiopathy affecting mainly the glomeruli by day 30

44 Dermatomyositis is a microangiopathy affecting skin and muscle; activation an

45 Thrombotic microangiopathy after allogeneic HSCT shares similaritie

46 als developed severe C5-dependent thrombotic microangiopathy after induction of complement activation

47 ead to insulin resistance, hypertension, and microangiopathy, all of which are associated with type 2

48 Diabetes mellitus accelerates cardiovascular microangiopathies and atherosclerosis, which are a conse

49 y have therapeutic value in the treatment of microangiopathies and may be useful to bypass inhibitory

50 Renal microangiopathies and membranoproliferative GN (MPGN) ca

51 ars of diabetes and histological evidence of microangiopathy and 18 age-matched nondiabetic donors we

52 centres in Boston, MA, USA, with thrombotic microangiopathy and a possible diagnosis of thrombotic t

53 3 mg/d; P < 0.01); and abrogated thrombotic microangiopathy and decreased plasma aldosterone (<16 ve

54 attenuated histone-induced renal thrombotic microangiopathy and glomerular necrosis in mice.

55 t required for the development of thrombotic microangiopathy and HUS induced by EHEC Shiga toxins in

56 , proteinuria (17 +/- 9 mg/d) and thrombotic microangiopathy and plasma aldosterone (18 +/- 18 pg/ml)

57 ity between the diabetic macroangiopathy and microangiopathy and suggests a molecular explanation beh

58 Microangiopathy and vascular disease also contribute to

59 mab inhibited complement-mediated thrombotic microangiopathy and was associated with significant time

60 ociated antigens was an early feature of the microangiopathy and was associated with thickening of th

61 lantation/chemotherapy-associated thrombotic microangiopathy, and in the hemolytic-uremic syndrome, i

62 tubular swelling, vacuolization, thrombotic microangiopathy, and increased expression of TGF-beta, c

63 eased in adults with VWF-mediated thrombotic microangiopathy, and intensive plasma exchange (PEx) bot

64 matrix and platelet aggregation, thrombotic microangiopathy, and neutrophilic infiltration.Sublytic

65 manifested with acute and chronic thrombotic microangiopathy; and (c) EC proinflammatory changes: inc

66 like, classically associated with thrombotic microangiopathy are the hemolytic-uremic syndrome (HUS)

67 to establish posttransplantation thrombotic microangiopathy as a discrete clinical or pathologic ent

68 e dropout may avoid or attenuate the retinal microangiopathy associated with diabetes.

69 might be effective in repairing the coronary microangiopathy associated with hypertension-induced LVH

70 - and endotheliumum-based selectin-dependent microangiopathy associated with mucin-producing carcinom

71 requently called upon to diagnose thrombotic microangiopathy, be aware of its association with ticlop

72 ical hemolytic uremic syndrome as thrombotic microangiopathy), biopsy appearance (dense deposit disea

73 nly identify a genetic cause of a glomerular microangiopathy but also suggest that the phosphatidylin

74 ll cells are potential informers of diabetic microangiopathy but may be preempted from carrying out r

75 1%), associated mainly with late thrombotic microangiopathy (C: 78%; C3: 11% of cases).

76 Thrombotic microangiopathies can be associated with defective regul

77 c syndrome (aHUS), a rare form of thrombotic microangiopathy caused by complement pathogenic variants

78 lytic uremic syndrome (aHUS) is a thrombotic microangiopathy caused by uncontrolled activation of the

79 olytic uremic syndrome (HUS) is a thrombotic microangiopathy characterized by intravascular hemolysis

80 P) is a rare and life-threatening thrombotic microangiopathy characterized by microangiopathic hemoly

81 family with patients affected by thrombotic microangiopathy characterized by significant serum compl

82 remic syndrome (aHUS) is a severe thrombotic microangiopathy characterized by uncontrolled complement

83 4 women with aHUS from the Vienna Thrombotic Microangiopathy Cohort.

84 c syndrome (aHUS) is a rare renal thrombotic microangiopathy commonly associated with rare genetic va

85 owed no significant improvements in diabetic microangiopathy, confirming the unique role of the pancr

86 rpura, in which life-threatening episodes of microangiopathy damage kidneys, heart, and brain.

87 f these cells in the pathogenesis of retinal microangiopathy deserves to be investigated.

88 months, the patient had relapsing thrombotic microangiopathy despite plasma exchange; splenectomy; an

89 toantibodies is associated with a thrombotic microangiopathy disease, atypical hemolytic uremic syndr

90 d diabetic subjects with very early diabetic microangiopathy (DMA+) (n = 16).

91 also more consistently diagnosed thrombotic microangiopathy due to severe ADAMTS13 deficiency than d

92 e platelet count (in trial 1) and thrombotic microangiopathy event-free status (no decrease in the pl

93 trial 2, 80% of the patients had thrombotic microangiopathy event-free status.

94 emolytic-uremic syndrome (HUS), a thrombotic microangiopathy, following infections by Shiga toxin-pro

95 ng pregnancy, and implications of thrombotic microangiopathies for subsequent pregnancies are evolvin

96 f the French Reference Center for Thrombotic Microangiopathies from 2000-2010 to identify all women w

97 pathway that are associated with thrombotic microangiopathies, glomerulonephritides, and chronic con

98 in diabetic patients with absent or minimal microangiopathy have pointed to possible dysfunction of

99 In a mouse model of thrombotic microangiopathy, HDL also largely prevented the thromboc

100 lication, including preeclampsia, thrombotic microangiopathy, heart failure, sepsis, or postpartum he

101 e inability to reproduce HUS with thrombotic microangiopathy, hemolytic anemia, and acute kidney inju

102 olytic uremic syndrome, including thrombotic microangiopathy, hemolytic anemia, thrombocytopenia, and

103 newly established mouse model of thrombotic microangiopathy highly predictive for investigating the

104 In diabetic microangiopathy, hyperglycemia induces biochemical and m

105 ase series of posttransplantation thrombotic microangiopathy illustrates uncertainties regarding inci

106 R was associated with subclinical thrombotic microangiopathy in 2 patients.

107 lls (HUVECs), and Stx2B can cause thrombotic microangiopathy in Adamts13(-/-) mice.

108 he isolated Stx2B subunits induce thrombotic microangiopathy in Adamts13(-/-) mice.

109 more sensitive than FA in detecting macular microangiopathy in asymptomatic patients.

110 triggers may be required to cause thrombotic microangiopathy in many patients.

111 ignant nephrosclerotic lesions of thrombotic microangiopathy in salt-loaded, stroke-prone, spontaneou

112 noninvasively and objectively study diabetic microangiopathy in the conjunctival microcirculation of

113 prominent, such as development of thrombotic microangiopathy in the graft or systemic consumptive coa

114 omplicated by a potentially fatal thrombotic microangiopathy in the recipient baboons.

115 arked interstitial hemorrhage and thrombotic microangiopathy in the renal vasculature.

116 een demonstrated to predispose to thrombotic microangiopathies including atypical hemolytic uremic sy

117 ly stages, the pathology is characterized by microangiopathies, including microaneurysms, microhemorr

118 re examined by light microscopy for possible microangiopathy, including changes in endothelial cell-t

119 aldosterone in the development of thrombotic microangiopathy, independent of hypertension.

120 hese data are consistent with a mechanism of microangiopathy involving endothelial cell injury (assoc

121 The hallmark of all thrombotic microangiopathies is vascular endothelial cell injury of

122 Thrombotic microangiopathy is a significant complication of HIV inf

123 Thrombotic microangiopathy is a significant complication with this

124 Diabetic retinal microangiopathy is characterized by increased permeabili

125 Thrombotic microangiopathy is characterized by microvascular thromb

126 such pregnancies for episodes of thrombotic microangiopathy is essential but, the best strategy to p

127 A complement-induced microangiopathy is important in dermatomyositis and in t

128 ment of T3SS-dependent intestinal thrombotic microangiopathy (iTMA) and ischemic enteritis in approxi

129 , as are present in patients with thrombotic microangiopathy, lack an inhibitory effect on complement

130 cular integrity in the degenerative cerebral microangiopathies leading to stroke and dementias.

131 (78 +/- 7 mg/d) were greater and thrombotic microangiopathy lesions were comparable to SHAM.

132 ng the box C/D snoRNA U8, cause the cerebral microangiopathy leukoencephalopathy with calcifications

133 nephritis (n = 3), HIV-associated thrombotic microangiopathy (n = 1), and HIV-negative patients with

134 flammation to AKI is discussed in thrombotic microangiopathies, necrotizing and crescentic GN, acute

135 process likely contributes to the thrombotic microangiopathy observed after PBPC transplantation in t

136 TGF-beta as an important contributor to the microangiopathy of diabetic retinopathy and nephropathy.

137 rombocytopenic purpura (TTP) is a thrombotic microangiopathy of obscure etiology.

138 phalopathy syndrome (PRES) is a small vessel microangiopathy of the cerebral vasculature that occurs

139 Microangiopathy of the pre-diabetic and diabetic type ch

140 BMBs might only be a biomarker for microangiopathy, or alternatively BMBs might provide use

141 WF in SCD pathology and connect SCD to other microangiopathies, particularly thrombotic thrombocytope

142 rove useful in the future care of thrombotic microangiopathy patients and might be a rational basis f

143 lates with clinical parameters in thrombotic microangiopathy patients.

144 this was later correlated with disseminated microangiopathy (platelet-rich clots in small blood vess

145 tanding the pathogenesis of other thrombotic microangiopathies, post-HSCT TMA remains poorly understo

146 or reactivity, which might indicate cerebral microangiopathy, predicted depressive disorders only, in

147 Posttransplantation thrombotic microangiopathy (PTMA) is a complication of allogeneic h

148 o be an important risk factor for thrombotic microangiopathy rather than a specific diagnostic marker

149 Posttransplantation thrombotic microangiopathy remains a diagnostic and therapeutic cha

150 Thrombotic microangiopathy resolved with discontinuation of the dru

151 We hypothesized that microangiopathy, resulting from long-standing systemic h

152 in DGKE-associated aHUS patients, thrombotic microangiopathy results from impaired EC proliferation a

153 with biopsy-proven de novo renal thrombotic microangiopathy (RTMA), occurring 5 to 120 d (median, 14

154 reduced (>20%) in other forms of thrombotic microangiopathy secondary to hematopoietic progenitor ce

155 tive roles in the pathogenesis of thrombotic microangiopathy, SHRSP were adrenalectomized and infused

156 y of the changes described relate to retinal microangiopathy, since ultrastructural, structural, and

157 Transplantation-associated thrombotic microangiopathy (TA-TMA) is a challenging diagnosis afte

158 Transplant-associated thrombotic microangiopathy (TA-TMA) is a common and poorly recogniz

159 transplantation (HSCT)-associated thrombotic microangiopathy (TA-TMA) is not completely understood.

160 Transplant-associated thrombotic microangiopathy (TA-TMA) occurs frequently after hematop

161 molytic-uremic syndrome (HUS) are thrombotic microangiopathies that occur in the absence of an inflam

162 represents a specific variant of thrombotic microangiopathy that is characterized by glomerular endo

163 olytic-uremic syndrome (HUS) is a thrombotic microangiopathy that is characterized by microangiopathi

164 the evaluation and management of thrombotic microangiopathy that occurs following allogeneic hematop

165 re was no evidence of spontaneous thrombotic microangiopathy, the hepatocyte-specific FH-deficient an

166 patients with posttransplantation thrombotic microangiopathy; these criteria may result in a clearer

167 ng the syndromes characterised by thrombotic microangiopathy, thrombotic thrombocytopenic purpura is

168 We show that cerebral microangiopathy thus partly explains stroke severity in

169 mune system in the development of thrombotic microangiopathy (TM) after alpha1,3-galactosyltransferas

170 transplantation (BMT)-associated thrombotic microangiopathy (TM) contributes to transplant-related m

171 Thrombotic microangiopathy (TM) is associated with abnormalities of

172 ism, however, results in a severe thrombotic microangiopathy (TM) that includes pronounced thrombocyt

173 ism, however, results in a severe thrombotic microangiopathy (TM) that includes pronounced thrombocyt

174 ism, however, results in a severe thrombotic microangiopathy (TM) that includes vascular injury, micr

175 All failing grafts exhibited thrombotic microangiopathy (TM) with platelet-rich fibrin thrombi i

176 All grafts developed thrombotic microangiopathy (TM).

177 contributes to the development of thrombotic microangiopathy (TMA) after hematopoietic stem cell tran

178 n of impaired C regulation in the thrombotic microangiopathy (TMA) atypical hemolytic uremic syndrome

179 lytic uremic syndrome (aHUS) is a thrombotic microangiopathy (TMA) characterized by excessive activat

180 Thrombotic microangiopathy (TMA) commonly involves injury of kidney

181 have described the occurrence of thrombotic microangiopathy (TMA) following IV abuse of extended-rel

182 Calcineurin inhibitor-induced thrombotic microangiopathy (TMA) has been described in up to 14% of

183 Thrombotic microangiopathy (TMA) has been increasingly reported in

184 Thrombotic microangiopathy (TMA) in renal transplants (rTx-TMA) is

185 cell transplant (HSCT)-associated thrombotic microangiopathy (TMA) is a complication that occurs in 2

186 Thrombotic microangiopathy (TMA) is a life-threatening condition th

187 Thrombotic microangiopathy (TMA) is a well-known complication after

188 Thrombotic microangiopathy (TMA) is a well-recognized complication

189 Transplant-associated thrombotic microangiopathy (TMA) leads to generalized endothelial d

190 Thrombotic microangiopathy (TMA) occurring after allogeneic hematop

191 Thrombotic microangiopathy (TMA) occurs in IgA nephropathy, but its

192 Thrombotic microangiopathy (TMA) significantly predicted graft fail

193 us adverse side effects of FK506, thrombotic microangiopathy (TMA) stands out as an infrequent but se

194 olytic uremic syndrome, a type of thrombotic microangiopathy (TMA) that causes renal failure.

195 uremic syndrome (aHUS) develop a thrombotic microangiopathy (TMA) that in most cases is attributable

196 proliferative lesions, glomerular thrombotic microangiopathy (TMA) was found as a common genetic back

197 veno-occlusive disease (VOD) and thrombotic microangiopathy (TMA) were lower in the nonsirolimus arm

198 nt activation has a major role in thrombotic microangiopathy (TMA), a disorder that can occur in a va

199 d complement activation, systemic thrombotic microangiopathy (TMA), and vital organ damage.

200 nt activity, the development of a thrombotic microangiopathy (TMA), and widespread end organ injury.

201 Many patients with syndromes of thrombotic microangiopathy (TMA), including thrombotic thrombocytop

202 re associated with a rare form of thrombotic microangiopathy (TMA), known as atypical hemolytic uremi

203 hemolytic uremic syndrome (HUS), thrombotic microangiopathy (TMA), or HUS-like events, exceeding the

204 us-2 (HIV-2) strain develop renal thrombotic microangiopathy (TMA), which morphologically resembles a

205 drugs have been reported to cause thrombotic microangiopathy (TMA), yet evidence supporting a direct

206 ry that shares many features with thrombotic microangiopathy (TMA).

207 picture consistent with an acute thrombotic microangiopathy (TMA).

208 considered to be caused by severe thrombotic microangiopathy (TMA).

209 aris degeneration, and glomerular thrombotic microangiopathy (TMA).

210 transplant, along with widespread thrombotic microangiopathy (TMA).

211 ate immunity, as characterized by thrombotic microangiopathy (TMA).

212 s TTP from HUS and other types of thrombotic microangiopathy (TMA); therefore, the term TTP/HUS shoul

213 The thrombotic microangiopathies (TMAs) and C3 glomerulopathies (C3Gs)

214 Thrombotic microangiopathies (TMAs) are a group of life-threatening

215 the second hit for development of thrombotic microangiopathies (TMAs), a group of life-threatening di

216 explore the relationships of early diabetic microangiopathy to alterations of cardiac sympathetic to

217 Endothelial dysfunction links thrombotic microangiopathy to steroid-refractory graft-versus-host

218 nstrated biological recurrence of thrombotic microangiopathy under treatment.

219 d intravascular coagulopathy associated with microangiopathy, verrucous endocarditis, and arterial em

220 The overall incidence of thrombotic microangiopathy was 19%, and it was significantly higher

221 Thrombotic microangiopathy was an adverse event unique to the TBI a

222 Significant improvement in microangiopathy was observed in all post-SPK diabetics (

223 l growth factor (VEGF) results in thrombotic microangiopathy, we addressed the possibility that Gsalp

224 Although the microangiopathies were ameliorated by AL-3152 treatment

225 (MA(+): n = 49) and without (MA(-): n = 52) microangiopathy were compared with 48 healthy control su

226 214 patients with thrombotic microangiopathy were included in the derivation cohort.

227 ignificant improvements (P<0.05) in diabetic microangiopathy were observed in all 12 diabetics 18 mon

228 a group of conditions termed the thrombotic microangiopathies, which are characterized by prominent

229 hic hemolytic anemia characterize thrombotic microangiopathy, which includes two major disorders: thr

230 ng data on the risk of developing thrombotic microangiopathy while on Ticlopidine and the possible me

231 A patient who developed thrombotic microangiopathy while on ticlopidine therapy is reported

232 cts of the pathophysiology of the thrombotic microangiopathies will be discussed.

233 Amelioration of galactose-induced retinal microangiopathies with AL-3152 in the prevention group s

234 DM is an undeniably a complement-mediated microangiopathy with destruction of capillaries, hypoper

235 he first reported pontine autosomal dominant microangiopathy with leukoencephalopathy (PADMAL) family

236 lytic uremic syndrome (aHUS) is a thrombotic microangiopathy with severe renal injury secondary to an

237 ury and in particular developed a thrombotic microangiopathy, with mesangiolysis, endothelial swellin

238 sociated with graft failure was a thrombotic microangiopathy, with resulting ischemic injury.