ライフサイエンスコーパス: HIT

1 HIT in humans is directly mirrored in a murine genetic m

2 HIT is propagated by activated platelets, monocytes, end

3 HIT pathophysiology is dynamic and complex.

4 HIT pathophysiology is initiated by four essential compo

5 HIT requires treatment with alternative anticoagulants.

6 HIT was defined as a 4Ts score >/= 4 and positive (14)C-

7 HIT'nDRIVE aims to solve the "random walk facility locat

8 HIT, compared with moderate-intensity continuous trainin

9 HIT-positive plasma demonstrated greater mean inhibition

10 ransfusions were reported in 10.1% TTP, 7.1% HIT, and 25.8% ITP admissions.

11 aged 7-13 years were randomly assigned to a HIT or an active control group matched for enjoyment and

12 derived algorithm (n = 687), HemosIL-AcuStar-HIT-IgG was used as unique testing in 566 (82.4%) of 687

13 ositive HIPA were >3.0 U/mL (HemosIL-AcuStar-HIT-IgG) and titer >=16 (ID-H/PF4-PaGIA); cutoffs with 1

14 nalyzed by Zymutest-HIA-IgG, HemosIL-AcuStar-HIT-IgG, and ID-H/PF4-PaGIA in retrospective (n = 221) a

15 tients treated with rivaroxaban during acute HIT (group A, n = 25; group B, n = 21); major hemorrhage

16 patients who received DOAC therapy for acute HIT as either primary therapy (group A) or secondary the

17 rting efficacy and safety of DOACs for acute HIT is increasing, with the most experience reported for

18 ted thrombosis during DOAC therapy for acute HIT.

19 nux is effective and safe in suspected acute HIT; no HIT-specific complications occurred in the fonda

20 urred in all 10 Hamilton patients with acute HIT treated with rivaroxaban.

21 per 10 000 admissions (P< .001), adjudicated HIT decreased 79% from 10.7 to 2.2 per 10 000 admissions

22 Rates of suspected HIT, adjudicated HIT, and HITT, along with HIT-related expenditures were

23 rast, consuming CHO before, during and after HIT running attenuates bone resorption, effects that are

24 The findings suggest that although all HIT antibodies recognize PF4 in a complex with heparin,

25 ence of HIT, HIT with thrombosis (HITT), and HIT-related costs.

26 The HIT-like monoclonal antibody KKO and HIT patient antibodies recognize PF4-VWF complexes, prom

27 Beyond PF4 and HIT, the methods applied in the current study may be rel

28 erial thrombosis and mortality among TTP and HIT patients.

29 frequency of management failures defined as HIT-positive participants with a low 4Ts score (irrespec

30 rombocytopenia (HIT) syndrome (or autoimmune HIT), defined as a transient prothrombotic thrombocytope

31 strated by a case of persisting (autoimmune) HIT (>2-month platelet recovery with inversely parallel

32 ability of current laboratory- and gym-based HIT protocols for obese individuals with low fitness and

33 ervised home-based MICT and laboratory-based HIT, while reducing many of the major barriers to exerci

34 lic dysfunction, which was prevented by both HIT and MIT.

35 e-bound platelet factor 4 (PF4) activated by HIT antibodies contribute to the prothrombotic state in

36 e assay that measures cellular activation by HIT antibodies via FcgammaRIIA using DT40 cells.

37 le blood of 131RR donors after activation by HIT antibodies, with increased phospholipid procoagulant

38 combination of direct platelet activation by HIT immune complexes through FcgammaRIIA and transactiva

39 maRIIA-dependent activation of DT40 cells by HIT antibodies as well as platelet activation, as measur

40 rin-dependent cellular activation induced by HIT antibodies.

41 hypersensitivity (DTH) reactions and not by HIT or other rare conditions.

42 hat peri-thrombus endothelium is targeted by HIT antibodies, but the binding site(s) has not been ide

43 bivalrudin has the advantage of not causing HIT, a major concern is lack of an antidote for this dru

44 CD-HIT is a widely used program for clustering biological s

45 The enhanced CD-HIT is capable of handling very large datasets in much s

46 ing technologies, we have developed a new CD-HIT program accelerated with a novel parallelization str

47 utilizes the powerful clustering program CD-HIT to cluster similar MITEs into MITE families.

48 ients, even among those with a high clinical HIT probability.

49 with HIT, an at least intermediate clinical HIT-risk (4Ts score >/=4 points), and received treatment

50 isk of subsequent "breakthrough" of clinical HIT with manifestation of thrombocytopenia.

51 Aggregation tests performed with collagen, HIT plasma, and monoclonal antibodies cross-linking Fcga

52 f thromboembolic and bleeding complications, HIT, and pregnancy outcome).

53 argatroban = 47) for suspected or confirmed HIT.

54 sing rivaroxaban for serologically confirmed HIT (4Ts score >/=4 points; positive platelet factor 4 [

55 having this property could explain "delayed HIT" seen in some individuals after discontinuation of h

56 " platelets are more sensitive for detecting HIT antibodies than platelet-rich plasma (PRP)-based ass

57 nts with anti-PF4-heparin antibodies develop HIT, implying that only a subset of these antibodies is

58 d antibody production in patients developing HIT.

59 ry, as well as for 15 other serially-diluted HIT sera.

60 We observed that post-TPE/diluted HIT sera-when first testing SRA-negative-continue to tes

61 ticoagulant with transition to a DOAC during HIT-associated thrombocytopenia).

62 ts were randomized 1:1 to 9 months of either HIT (4x4-minute intervals at 85%-95% of peak effort) or

63 Ts score plus negative PaGIA result excluded HIT, whereas any other combination of results justified

64 re appears to be a robust means of excluding HIT.

65 Bcd1, an essential zinc finger HIT protein functionally conserved in eukaryotes, has be

66 Zinc finger HIT-type containing 1 (Znhit1) is an evolutionarily cons

67 n MPPs, Pcid2 interacts with the Zinc finger HIT-type containing 1 (ZNHIT1) to block Snf2-related CRE

68 Approved for HIT are 2 direct thrombin inhibitors (DTI; lepirudin, ar

69 ivity of washed platelet (vs PRP) assays for HIT.

70 on assay and a PF4-dependent immunoassay for HIT antibodies indicates that patients with subacute HIT

71 ay have the potential to reduce the risk for HIT during treatment with heparin.

72 ted our prospective study of rivaroxaban for HIT), using rivaroxaban for serologically confirmed HIT

73 stics and non-anticoagulant therapeutics for HIT.

74 clinical practice, its predictive value for HIT in diverse settings and patient populations is unkno

75 bound to peri-injury endothelium and formed HIT antigenic complexes that were dissociated by heparin

76 xposure serologically indistinguishable from HIT, is controversial.

77 ersists for weeks in patients recovered from HIT.

78 Furthermore, HIT'nDRIVE, when applied to a large panel of pan-cancer

79 or avoiding heparin on the incidence of HIT, HIT with thrombosis (HITT), and HIT-related costs.

80 be performed at home without equipment (Home-HIT).

81 high-intensity interval training (HIT) (Home-HIT) intervention in obese individuals with elevated car

82 e of three 12-week training programmes: Home-HIT (n = 9), laboratory-based supervised HIT (Lab-HIT; n

83 w that 12 weeks of virtually supervised Home-HIT in obese individuals with elevated cardiovascular di

84 n during exercise, virtually supervised Home-HIT resulted in comparable structural and endothelial en

85 We provide strong evidence that Home-HIT is an effective novel strategy to remove barriers to

86 Hospital HIT-related expenditures decreased by $266 938 per year

87 4 tetramerization and inhibits KKO and human HIT IgG-induced platelet activation and platelet aggrega

88 d heparin is specifically inhibited by human HIT antibodies that activate platelets, whereas inhibiti

89 pite being a critically important element in HIT etiology, relatively little is known about the speci

90 48 276P or 326Q alleles was less frequent in HIT patients, suggesting a protective effect of these po

91 breadth of molecular and cellular players in HIT.

92 cell tolerance may play an important role in HIT pathogenesis.

93 es contributes to the prothrombotic state in HIT and showed that HIT antibodies bind to monocyte Fcga

94 ategies, directed at the initiating steps in HIT pathophysiology and with potential combinations stag

95 48 (Q276P, R326Q, and D872E) were studied in HIT patients and 2 control groups, with or without antib

96 NF split into iSHH-I and iSHH-II subtypes in HIT-2000-BIS4 and the validation cohort, without prognos

97 erived thrombin contributes to thrombosis in HIT and identifies potential new targets for lessening t

98 found to increase the risk of thrombosis in HIT patients (odds ratio: 5.9; 95% confidence interval:

99 The mechanism of thrombosis in HIT remains poorly understood.

100 at might propagate the risk of thrombosis in HIT.

101 Platelet transfusions in HIT were associated with higher odds of arterial thrombo

102 A-mediated platelet reactivity and influence HIT susceptibility.

103 and afternoon (PM) high-intensity interval (HIT) (8 x 5 min at 85% VO2peak ) running protocol (inter

104 Here we introduce HIT'nDRIVE, a computational method that integrates genom

105 after HTx, but studies have not investigated HIT effects in the de novo HTx state.

106 entary lifestyle or 8-10 weeks of isocaloric HIT or MIT.

107 n = 9), laboratory-based supervised HIT (Lab-HIT; n = 10) or virtually supervised home-based moderate

108 ashed platelets and PRP, standard laboratory HIT tests, and physicochemical methods to identify a pla

109 mation of delayed-onset (or autoimmune-like) HIT antibodies that activate platelets even in the absen

110 After a few minutes, HIT antigen was detected within the thrombus itself at t

111 liver-specific IGF-1 transgenic mouse model (HIT) to increase their circulating IGF-1 levels to inves

112 onmetastatic ND and MBEN based on a modified HIT SKK 2000 regimen excluding intraventricular methotre

113 etramer/KKO-Fab complex (a murine monoclonal HIT-like antibody) and (3) PF4 monomer/RTO-Fab complex (

114 The Hi-Myc/HIT mice had increased incidence and invasiveness of pro

115 ffective and safe in suspected acute HIT; no HIT-specific complications occurred in the fondaparinux-

116 ) and (3) PF4 monomer/RTO-Fab complex (a non-HIT anti-PF4 monoclonal antibody).

117 ether, these studies demonstrate assembly of HIT immune complexes along VWF strings released by injur

118 e by characterizing PF4-dependent binding of HIT antibodies to intact platelets and found that most a

119 PF4/heparin immunization and breakthrough of HIT, we also tested 89 plasmas from 2 serosurveillance t

120 in immunization and clinical breakthrough of HIT.

121 unity to prevent thrombotic complications of HIT, while sparing systemic hemostatic pathways.

122 e diagnostic rubric for the determination of HIT by leveraging machine-learning-based classification

123 izing heparin exposure to the development of HIT is 5 days irrespective of the patient's previous hep

124 -based SERS analytical tool for diagnosis of HIT in the clinical laboratory, without perturbing the e

125 lifestyle, we report a very modest effect of HIT and no effect of resistance training on AHN in adult

126 The primary outcome was the effect of HIT versus moderate-intensity continuous training on the

127 The composite endpoint of HIT-specific complications (thromboembolic events, amput

128 40 to 100 days (median) after an episode of HIT, depending on the assay performed.

129 rin-dependent immunization and expression of HIT.

130 improving the specificity and feasibility of HIT laboratory testing.

131 ions that involve patients with a history of HIT (eg, treatment of venous thromboembolism or acute co

132 at among patients with a previous history of HIT who are reexposed to intraoperative (but not postope

133 evious heparin exposure status or history of HIT.

134 nticoagulation in patients with a history of HIT.

135 egy for avoiding heparin on the incidence of HIT, HIT with thrombosis (HITT), and HIT-related costs.

136 Main outcome measures were the incidences of HIT-specific complications (thromboembolic venous/arteri

137 cessful outpatient rivaroxaban management of HIT-associated thrombosis.

138 ility to individual and combined measures of HIT.

139 er microvascular injury in a murine model of HIT in which human FcgammaRIIa was expressed as a transg

140 These data provide a model of HIT wherein a combination of direct FcgammaRIIA-mediated

141 uses thrombocytopenia in an in vivo model of HIT, whereas RTO does not.

142 uate thrombus formation in a murine model of HIT.

143 used to analyze the murine genetic model of HIT.

144 ivation via FcgammaRIIa, the sine qua non of HIT, has become much better appreciated.

145 However, the B-cell origin of HIT antibody production is not known.

146 dic system that simulate the pathogenesis of HIT.

147 ntibodies are central to the pathogenesis of HIT.

148 f epitope specificity in the pathogenesis of HIT.

149 by IdeS could suppress the pathogenicity of HIT antibodies.

150 de new tools to probe the pathophysiology of HIT.

151 y responsible for scoring, the prevalence of HIT, or the composition of the study population.

152 IA result reduced the pretest probability of HIT from 1.9% to 0% (95% CI, 0-1.3%), 6.7% to 0% (95% CI

153 /H-PaGIA result increased the probability of HIT in the low score group to 15.4% (95% CI, 5.9-30.5).

154 hed data on drug efficacy and probability of HIT-related thromboembolism and major bleeding.

155 by 4Ts score as having a low probability of HIT.

156 date the intrinsic PF4-binding properties of HIT-like monoclonal antibody (KKO) versus non-pathogenic

157 We also performed a literature review of HIT treatment using DOACs (rivaroxaban, apixaban, dabiga

158 bly exert a protective effect on the risk of HIT in patients with antibodies to PF4/Hs.

159 ombus endothelium is the predominant site of HIT antigen assembly.

160 will summarize our current understanding of HIT by reviewing pathogenesis, essential clinical and la

161 d aerobic capacity and reduced obesity, only HIT improved glucose tolerance.

162 ogic feature characteristic of delayed-onset HIT (ie, where heparin use precedes HIT but is not requi

163 ie, no sooner than observed in typical-onset HIT.

164 bating IdeS in whole blood containing 5B9 or HIT plasma samples led to cleavage of anti-PF4/H antibod

165 antibodies is accurate for ruling in or out HIT in >=95% of cases within 60 minutes.

166 Overall, HIT'nDRIVE may help clinicians contextualize massive mul

167 kg(-1) dw in all trials immediately post PM HIT (P < 0.01) and remained lower at 17 h (171, 194 and

168 osphorylation (P < 0.05) immediately post PM HIT and similar mRNA expression (all P < 0.05) of PGC-1a

169 h (171, 194 and 316 mmol kg(-1) dw) post PM HIT in LCHF and LCAL (P < 0.001) compared to HCHO.

170 The annual rate of patients with a positive HIT assay decreased 63% from 16.5 to 6.1 per 10 000 admi

171 T reexposed to heparin 4.4 years (mean) post-HIT; 17 patients were given heparin intraoperatively (wi

172 OS was superior compared with the precedent HIT '91 trial.

173 ed-onset HIT (ie, where heparin use precedes HIT but is not required for subsequent development or wo

174 The algorithm accurately predicted HIT in 51 (7.4%) of 687 patients and excluded it in 604

175 [73%]) suggests that patients with previous HIT may be especially predisposed to forming recurrent a

176 f recurrent HIT in 20 patients with previous HIT reexposed to heparin 4.4 years (mean) post-HIT; 17 p

177 confirmed by HIPA: 10 patients with probable HIT despite negative HIPA and 2 possible false-positive

178 atment of patients with suspected and proven HIT.

179 In proven HIT, approved treatments reduce but do not eliminate thr

180 Suspected HIT is more frequent than proven HIT, because of the widespread use of Hep and the inadeq

181 One patient developed recurrent HIT beginning 7 days after cardiac surgery, with newly r

182 The risk of recurrent HIT 1 to 2 weeks after heparin reexposure is approximate

183 ostoperative) heparin, the risk of recurrent HIT appears to be low, but is possible if antibodies wit

184 assay [EIA]), and the frequency of recurrent HIT in 20 patients with previous HIT reexposed to hepari

185 fter cardiac surgery, with newly regenerated HIT antibodies exhibiting strong heparin-independent pla

186 potential treatment of patients with severe HIT.

187 se that a rigorous definition of spontaneous HIT syndrome should include otherwise unexplained thromb

188 ssay (ELISA)+/serotonin-release assay (SRA)+/HIT+ < ELISA+/SRA+/HIT- ~ ELISA+/SRA-/HIT- < ELISA-/SRA-

189 onin-release assay (SRA)+/HIT+ < ELISA+/SRA+/HIT- ~ ELISA+/SRA-/HIT- < ELISA-/SRA-/HIT-.

190 (SRA)+/HIT+ < ELISA+/SRA+/HIT- ~ ELISA+/SRA-/HIT- < ELISA-/SRA-/HIT-.

191 +/SRA+/HIT- ~ ELISA+/SRA-/HIT- < ELISA-/SRA-/HIT-.

192 ve serologically-confirmed acute or subacute HIT; for this situation, a negative platelet activation

193 bodies indicates that patients with subacute HIT undergoing repeated TPE before heparin reexposure sh

194 samples in a patient with recent (subacute) HIT who underwent serial TPE precardiac surgery, as well

195 ome-HIT (n = 9), laboratory-based supervised HIT (Lab-HIT; n = 10) or virtually supervised home-based

196 erefore, we developed a virtually supervised HIT protocol targeting this group that can be performed

197 Suspected HIT is more frequent than proven HIT, because of the wid

198 The annual rate of suspected HIT decreased 42%, from 85.5 per 10 000 admissions in th

199 fondaparinux for the treatment of suspected HIT from the institutional perspective.

200 Rates of suspected HIT, adjudicated HIT, and HITT, along with HIT-related e

201 f fondaparinux in the treatment of suspected HIT.

202 ) in samples from 58 patients with suspected HIT and circulating anti-PF4/heparin antibodies.

203 Consecutive cases with suspected HIT from 2003 through 2012 were reviewed.

204 an and danaparoid in patients with suspected HIT.

205 value of the 4Ts in patients with suspected HIT.

206 nitial management of patients with suspected HIT.

207 5-point improvement in Headache Impact Test (HIT)-6.

208 greater mean inhibition of KKO binding than HIT-negative plasma (78.9% vs 26.0%; P < .0001) and indu

209 These results demonstrate that HIT patients homozygous for the FcgammaRIIA 131R allele

210 We demonstrated that HIT was a safe, efficient exercise method in de novo HTx

211 We hypothesized that HIT could be introduced early after HTx and that it coul

212 e prothrombotic state in HIT and showed that HIT antibodies bind to monocyte FcgammaRIIA, which activ

213 The HIT immune response is remarkably transient, with hepari

214 The HIT-2000-BIS4 trial aimed to avoid highly detrimental cr

215 The HIT-like monoclonal antibody KKO and HIT patient antibod

216 rt and a validation cohort (n = 71) from the HIT group and Russia.

217 ided into iSHH-I and iSHH-II subtypes in the HIT-2000-BIS4 cohort and a validation cohort (n = 71) fr

218 We investigated the effects of the HIT Ab complex on tissue factor (TF) expression and rele

219 receptor IIA (FcgammaRIIA), infusion of the HIT-like monoclonal antibody KKO increased fibrin and pl

220 sures the effect of plasma on binding of the HIT-like monoclonal antibody KKO to platelet factor 4 (P

221 At the 1-year follow-up, the HIT group demonstrated greater improvements than the mod

222 ura (TTP), heparin-induced thrombocytopenia (HIT) and immune thrombocytopenic purpura (ITP).

223 siology of heparin-induced thrombocytopenia (HIT) and in applying this knowledge to the treatment of

224 sential in heparin-induced thrombocytopenia (HIT) and other immune-mediated thrombocytopenia and thro

225 orithm for heparin-induced thrombocytopenia (HIT) based on the 4Ts score and 2 rapid immunoassays (IA

226 f previous heparin-induced thrombocytopenia (HIT) can be appropriate if platelet-activating antibodie

227 results in heparin-induced thrombocytopenia (HIT) from cellular activation involving Fc receptors.

228 esting for heparin-induced thrombocytopenia (HIT) has important shortcomings.

229 to remove heparin-induced thrombocytopenia (HIT) IgG antibodies before cardiac/vascular surgery in p

230 Heparin-induced thrombocytopenia (HIT) is a potentially devastating form of drug-induced t

231 Heparin-induced thrombocytopenia (HIT) is a prothrombotic disorder initiated by antibodies

232 Heparin-induced thrombocytopenia (HIT) is a prothrombotic disorder mediated by complexes b

233 Heparin-induced thrombocytopenia (HIT) is a relatively common prothrombotic adverse drug r

234 Heparin-induced thrombocytopenia (HIT) is a thrombotic complication of heparin therapy med

235 Heparin-induced thrombocytopenia (HIT) is an adverse drug reaction occurring in up to 5% o

236 Heparin-induced thrombocytopenia (HIT) is an autoimmune thrombotic disorder caused by immu

237 Heparin-induced thrombocytopenia (HIT) is an immune complication of heparin therapy caused

238 Heparin-induced thrombocytopenia (HIT) is an immune-mediated disorder that can cause fatal

239 Heparin-induced thrombocytopenia (HIT) is caused by platelet-activating anti-platelet fact

240 Heparin-induced thrombocytopenia (HIT) is characterized by a high incidence of thrombosis,

241 suspected heparin-induced thrombocytopenia (HIT) is critical for guiding initial patient management.

242 Heparin-induced thrombocytopenia (HIT) is due primarily to IgG antibodies specific to plat

243 Heparin-induced thrombocytopenia (HIT) is due to immunoglobulin G (IgG) antibodies, which

244 clusion of heparin-induced thrombocytopenia (HIT) is needed to determine which patients can continue

245 hreatening heparin-induced thrombocytopenia (HIT) is treated with the alternative nonheparin anticoag

246 elines for heparin-induced thrombocytopenia (HIT) management recommend heparin cessation and switchin

247 ients with heparin-induced thrombocytopenia (HIT) remain at risk for recurrent thromboembolic complic

248 pontaneous heparin-induced thrombocytopenia (HIT) syndrome (or autoimmune HIT), defined as a transien

249 agnosis of heparin-induced thrombocytopenia (HIT), a difficult-to-diagnose immune-related complicatio

250 lopment of heparin-induced thrombocytopenia (HIT), a potentially fatal immune disorder affecting 1-5%

251 a (TTP) or heparin-induced thrombocytopenia (HIT), and Trousseau syndrome, but some patients present

252 nvolved in heparin-induced thrombocytopenia (HIT), beta-2-glycoprotein-1 implicated in antiphospholip

253 eatment of heparin-induced thrombocytopenia (HIT), few data are available comparing the cost-effectiv

254 atran) for heparin-induced thrombocytopenia (HIT),and also outline aHIT prevention strategy through d

255 ly cause a heparin-induced thrombocytopenia (HIT)-like prothrombotic disorder.

256 eatment of heparin-induced thrombocytopenia (HIT).

257 assays for heparin-induced thrombocytopenia (HIT).

258 effect of heparin-induced thrombocytopenia (HIT).

259 genesis of heparin-induced thrombocytopenia (HIT).

260 ion called heparin-induced thrombocytopenia (HIT).

261 disorder, heparin-induced thrombocytopenia (HIT).

262 system for heparin-induced thrombocytopenia (HIT).

263 eding, and heparin-induced thrombocytopenia [HIT]).

264 rin-induced thrombocytopenia and thrombosis (HIT) patients homozygous for arginine (R) at position 13

265 rin-induced thrombocytopenia and thrombosis (HIT), but many antibody-positive patients have normal pl

266 on may provide a new therapeutic approach to HIT.

267 with the HR and HH genotypes in response to HIT plasma or 5B9, a recently developed humanized monocl

268 -brain barrier; it affects susceptibility to HIT by altering the brain concentration of haloperidol.

269 ABCB5 alleles alter susceptibility to HIT in mouse and humans.

270 enetic factors that affect susceptibility to HIT, but it is likely that additional pharmacogenetic su

271 ansporter (Abcb5) affected susceptibility to HIT.

272 se strains are differentially susceptible to HIT.

273 onded with a >/=5-point improvement in total HIT-6 during treatment cycles 1, 2 and 3, respectively.

274 toms caused by haloperidol-induced toxicity (HIT), which limits its clinical utility.

275 effect of a 6 week high-intensity training (HIT) regimen on measures of cognitive control and workin

276 home-based high-intensity interval training (HIT) (Home-HIT) intervention in obese individuals with e

277 Low-volume high-intensity interval training (HIT) is a time-efficient alternative to traditional mode

278 shown that high-intensity interval training (HIT) is safe, well tolerated, and efficacious in the mai

279 te whether high-intensity interval training (HIT) is superior to moderate-intensity training (MIT) in

280 effects of high-intensity interval training (HIT) or of purely anaerobic resistance training on AHN.

281 g (ET) and high intensity interval training (HIT), generally regarded as a time-efficient alternative

282 Whether high-intensity interval training (HIT), referring to alternating short bouts of very inten

283 of the different anticoagulants for treating HIT.

284 cently completed prospective clinical trial (HIT [for heparin-induced thrombocytopenia] 5801 study; n

285 cal and laboratory features confirmed "true" HIT in at least 74 of 195 (38.0%) patients; 35 of 74 (47

286 to 2200 tumors from four major cancer types, HIT'nDRIVE revealed many potentially clinically actionab

287 elucidating molecular mechanisms underlying HIT, as well as other physiological processes driven by

288 Insights into the unique HIT antibody response continue to emerge, but without co

289 the use of alternative anticoagulants until HIT could be excluded.

290 e prediction for tumor samples by only using HIT'nDRIVE-seeded driver gene modules from gene interact

291 Disruption of PF4-VWF-HIT antibody complexes by drugs that prevent or block VW

292 Platelet adhesion to the PF4-VWF-HIT antibody complexes is inhibited by antibodies that b

293 The 6-week HIT regimen resulted in improvements on measures of cogn

294 ran voluntarily on a running wheel, whereas HIT on the treadmill had a smaller, statistically non-si

295 e success and feasibility of a hospital-wide HIT prevention strategy.

296 10 624 hospitalizations with TTP; 6332 with HIT and 79 980 with ITP.

297 d HIT, adjudicated HIT, and HITT, along with HIT-related expenditures were compared in the pre-interv

298 ospitalized patients who were diagnosed with HIT, an at least intermediate clinical HIT-risk (4Ts sco

299 y, share a number of serologic features with HIT Abs, including platelet activation, and may pose hea

300 nd/or plasma exchange, whereas patients with HIT need an alternative anticoagulant to replace heparin