ライフサイエンスコーパス: dysfunction

1 in the progression of cardiac remodeling and dysfunction.

2 oxic to epithelial cells and lead to barrier dysfunction.

3 t its phosphorylation by PKB display cardiac dysfunction.

4 of study and even therapies for hippocampal dysfunction.

5 matory disease, is closely related to immune dysfunction.

6 w therapeutic strategies to target nucleolar dysfunction.

7 litating fibroses, and obesity-related liver dysfunction.

8 enesis of obesity-associated cerebrovascular dysfunction.

9 hose without TG despite other forms of renal dysfunction.

10 al mechanisms play a key role in gut barrier dysfunction.

11 ets, hypercoagulable status, and endothelial dysfunction.

12 ctive snoRNP pseudouridylation and ribosomal dysfunction.

13 manifestations such as cytopenias and immune dysfunction.

14 respiratory distress syndrome and multiorgan dysfunction.

15 ht loss, behavioral sickness, and myocardial dysfunction.

16 er DWF is a consequence of chronic allograft dysfunction.

17 644 abrogates ketamine-induced smooth muscle dysfunction.

18 oth muscle contractility, leading to voiding dysfunction.

19 vation and preventing diet-induced metabolic dysfunction.

20 ry and inhibitory agents to treat complement dysfunction.

21 y allergic inflammation and gastrointestinal dysfunction.

22 ed ICP can contribute to meningeal lymphatic dysfunction.

23 level might be associated with mitochondrial dysfunction.

24 sclerosis-related retinal damage and visual dysfunction.

25 understand the factors contributing to motor dysfunction.

26 ER lipid metabolism and protects the ER from dysfunction.

27 res 4 to 6, and patients with moderate renal dysfunction.

28 ch as heart, is associated with their severe dysfunction.

29 roves diseases associated with mitochondrial dysfunction.

30 preventable developmental cause of cognitive dysfunction.

31 e kidney injury and "acute on chronic" renal dysfunction.

32 y dire consequences of generalized placental dysfunction.

33 beta-cells lacking Furin, causing beta-cell dysfunction.

34 ATP]) as opposed to an intrinsic endothelial dysfunction.

35 e cold sensitive and exhibited mitochondrial dysfunction.

36 hR) cluster fragmentation, and neuromuscular dysfunction.

37 he valve at least partially culpable for its dysfunction.

38 omote inflammatory responses and endothelial dysfunction.

39 , which are often accompanied by respiratory dysfunction.

40 th largely nonprogressive peripheral retinal dysfunction.

41 testinal somatic symptoms, and psychological dysfunction.

42 cted infection and sepsis treatment or organ dysfunction.

43 in metformin prescription in moderate kidney dysfunction.

44 plications in cardiac fibrosis and diastolic dysfunction.

45 thomechanisms in diseases with mitochondrial dysfunction.

46 xcretion, low autophagy, and premature organ dysfunction.

47 diseases associated with endothelial barrier dysfunction.

48 autoantibodies and diarrheal-type intestinal dysfunction.

49 erant phenotypes that promoted CD8(+) T cell dysfunction.

50 europsychiatric disease-associated cognitive dysfunction.

51 h as cardiovascular, metabolic, or cognitive dysfunctions.

52 tion, atrioventricular block, and sinoatrial dysfunction: 0.94% (95% CI: 0.75% to 1.16%) for sarcoido

53 ute to cognitive, metabolic, and physiologic dysfunction [1, 2].

54 3.3% vs 24.1%, P = 0.57) and transient nerve dysfunction (13.3% vs 10.3%, P = 1.00) were not signific

55 g multidimensional impairments; (2) physical dysfunction; (3) psychological disorder; (4) cognitive i

56 rcise prevented age- and WD-related vascular dysfunction across the lifespan, and this protection app

57 entricular remodeling (hypertrophy/diastolic dysfunction), age, injury (high-sensitivity troponin T),

58 including neuroinflammation, brain vascular dysfunction, altered brain metabolism, neurotransmitter

59 is frequently associated with mitochondrial dysfunction and altered neurotransmission.

60 include thrombotic complications, myocardial dysfunction and arrhythmia, acute coronary syndromes, ac

61 a therapeutic strategy for preventing heart dysfunction and arrhythmias in DMD patients.

62 Age-related mitochondrial dysfunction and associated oxidative stress might induce

63 TRPV4(R269C)) causes dose-dependent neuronal dysfunction and axonal degeneration, which are rescued b

64 hromatin dysregulation to cerebellar circuit dysfunction and behavioral abnormalities in ASD.

65 ut the processes underlying renal transplant dysfunction and can be used for the development of molec

66 n sphingolipid metabolism contribute to cell dysfunction and death.

67 formation and their contribution to neuronal dysfunction and degeneration.

68 C4KO mice developed modest cardiac dysfunction and dilation in response to exercise.

69 , together with BIN1, to ameliorate synaptic dysfunction and disease progression.

70 -irradiation-induced colonic mucosal barrier dysfunction and endotoxemia.

71 ed strong associations with cytotoxic T-cell dysfunction and exclusion, respectively.

72 al of targeting Sirt3 expression in vascular dysfunction and hypertension.

73 ances have been made in understanding immune dysfunction and immunosuppression in multiple myeloma (M

74 ntribution to systolic and diastolic cardiac dysfunction and impaired clinical outcomes in patients w

75 mediated disease characterized by esophageal dysfunction and intraepithelial eosinophil accumulation.

76 , diabetes, and prediabetes) causes vascular dysfunction and is a risk factor for vascular contributi

77 alent disorder also involving elastic tissue dysfunction and is associated with glaucoma.

78 cleavage at aspartate 314 mediates synaptic dysfunction and memory impairment in mouse and cellular

79 ion of autophagy is associated with neuronal dysfunction and neurodegeneration.

80 ints to an association between mitochondrial dysfunction and Parkinson's disease (PD).

81 sfunction grade II or III, right ventricular dysfunction and pericardial effusions.

82 NT In persons with Parkinson's disease, gait dysfunction and the associated risk for falls do not ben

83 m cells (HSCs), leading to HSC depletion and dysfunction and the risk of malignant transformation ove

84 o treat diseases associated with endothelial dysfunction and vascular hyperpermeability.

85 atening disease characterized by endothelial dysfunction and vascular leakage.

86 trophy 1 (Opa1), retinal ganglion cell (RGC) dysfunction and visual loss occur by unknown mechanisms.

87 es to brain networks contribute to cognitive dysfunction, and grey matter atrophy is an early sign of

88 n people with diabetes, reflects endothelial dysfunction, and increases the risk of end-organ damage.

89 d tau pathology, neurodegeneration, synaptic dysfunction, and inflammation, highlight the need for fu

90 ever, uric acid is not responsible for brain dysfunction, and it has been suggested that purine nucle

91 nduced currents, implantable pulse generator dysfunction, and mechanical forces.

92 smodium parasite growth, blood-brain barrier dysfunction, and mortality in a mouse model of malaria.

93 a, anasarca, fever, reticulin fibrosis/renal dysfunction, and organomegaly.

94 wer comorbidities, had less left ventricular dysfunction, and received more inappropriate shocks (IAS

95 traditional notion that subclinical thyroid dysfunction, and subclinical hypothyroidism in particula

96 s a strong genetic predisposition, epidermal dysfunction, and T-cell driven inflammation.

97 nrichment in oxidative stress, mitochondrial dysfunction, and transcription initiation pathways with

98 ain cells, mechanisms of virus-induced brain dysfunction, and treatment strategies.

99 including petechial rash, blood coagulation dysfunction, and various biochemistry and blood cell cou

100 iratory distress syndrome, or multiple organ dysfunction; and direct tissue injury (n = 64, 21.9%) in

101 hese models (e.g., placental hypoxia, immune dysfunction, angiogenesis, oxidative stress) causes vari

102 D-Dimer cutoff levels adjusted for renal dysfunction appear feasible and safe assessing thromboem

103 ch inflammatory mediators contribute to this dysfunction are not clearly defined.

104 e and prognostic implications of hepatorenal dysfunction are unknown in this population.

105 Astrocyte dysfunctions are also linked to synapse pathologies asso

106 arison groups, thus suggesting that thalamic dysfunctions are present even before illness onset.

107 Despite this, the role of mitochondrial dysfunction as an initiator, propagator, or bystander re

108 n, pathological remodeling, and mitochondria dysfunction, as well.

109 d with oxidative stress and left ventricular dysfunction assessed by electron spin resonance spectros

110 mortality, hospital admissions, and symptoms/dysfunction associated with exposure to Asian dust.

111 tic benefit in the prevention of endothelial dysfunction associated with preeclampsia.

112 IL (interleukin)-6 levels and mitochondrial dysfunction, associated with increased mitophagy and the

113 rial respiratory culture predicted pulmonary dysfunction at discharge (odds ratio, 4.38; 95% CI, 1.66

114 Pulmonary dysfunction at discharge a priori defined as one of: mec

115 efined as greater than or equal to two organ dysfunctions at day 7 or death by day 28.

116 ities have been reported, including erectile dysfunction, atrial fibrillation, obstructive sleep apno

117 fERG in evaluating the expected neuroretinal dysfunction before the clinical development of diabetic

118 ncentrations of inflammatory and endothelial dysfunction biomarkers were determined at clinical prese

119 Viral infection can cause organ dysfunction, but its role in placentally related disorde

120 meliorates the Lm-induced intestinal barrier dysfunction by blocking the nuclear factor-kappaB and my

121 ditions of inherent or induced mitochondrial dysfunction, cancer cells manifest overlapping metabolic

122 Neutropenia and neutrophil dysfunction cause serious infections and inflammatory bo

123 t the site of injury, and widespread network dysfunction caused by structural, functional, and metabo

124 cally relevant entity, defined as any atrial dysfunction causing impaired heart performance, symptoms

125 iven advanced age, comorbidities, and immune dysfunction, chronic lymphocytic leukemia (CLL) patients

126 ta4 spectrin show exacerbated nervous system dysfunction compared to mice lacking beta1 or beta4 spec

127 ber of an organ's demand and long-term graft dysfunction constitute some of the major problems.

128 n HIV infection where gut-intestinal barrier dysfunction could facilitate T cell exposure to commensa

129 to assess the association between diastolic dysfunction (DD) and outcomes in patients with aortic st

130 nucleinopathy that is characterized by motor dysfunction, death of midbrain dopaminergic neurons and

131 ng downstream effects that contribute to RPE dysfunction/death.

132 utrient surplus ensues, leading to beta-cell dysfunction, dedifferentiation, and apoptosis.

133 brain helped protect against cerebrovascular dysfunction despite prolonged obesity.

134 doscopy and biopsy without evidence of graft dysfunction does not appear to confer survival advantage

135 he association of Sdc-1 with early allograft dysfunction (EAD), 1-year graft survival, and 1-year pat

136 factors, 90-day graft loss, early allograft dysfunction (EAD), L-GrAFT score, acute kidney injury, a

137 induced concentric hypertrophy and diastolic dysfunction (early diastolic transmitral flow velocity t

138 Environmental enteric dysfunction (EED) is an enigmatic disorder of the small

139 echanism contributes to peripheral metabolic dysfunction, effects on the brain remain unexplored.

140 te excitotoxicity and contribute to neuronal dysfunction, enhanced neuronal death, and neurodegenerat

141 of cellular activity associated with visual dysfunction, especially delayed RMDA, an AMD risk indica

142 Epithelial barrier dysfunction facilitates transepithelial allergen passage

143 nflammation, macrovascular and microvascular dysfunction, fibrosis, and tissue remodeling are needed

144 and B-type natriuretic peptide) and cardiac dysfunction for 24-48 h after events, but what is the re

145 lymphatic valves displaying a wide range of dysfunction, from fully competent to completely incompet

146 ) mice display elevated biomarkers of kidney dysfunction, glomerulosclerosis, C3/C5b-9 deposition, an

147 lic function was found in 23 (11%) patients, dysfunction grade I in 107 (51%), grade II in 31 (14.8%)

148 ular dysfunction, left ventricular diastolic dysfunction grade II or III, right ventricular dysfuncti

149 cted left atrial pressure (grade I diastolic dysfunction) had a measured pulmonary artery occlusion p

150 Cerebellar dysfunction has been demonstrated in autism spectrum dis

151 Myocardial dysfunction has been demonstrated in MFS patients and mo

152 Mitochondrial dysfunction has long been implicated in the neurodegener

153 ervous activity and hypoxia-induced vascular dysfunction has not been determined.

154 Mitochondrial mutations and dysfunction have been demonstrated in several age-relate

155 Both mucosal inflammation and psychologic dysfunction have been implicated in irritable bowel synd

156 Kidney dysfunction (hazard ratio, 2.28 [95% credible interval,

157 MMS-induced mitochondrial dysfunction, however, is AAG-independent.

158 BBB dysfunction, however, is evident in many neurological di

159 The incidence of erectile dysfunction (IIEF-5 <= 11) at 12 months after surgery wa

160 by telomere shortening, progressive telomere dysfunction impaired hepatic endoderm formation.

161 u hyperphosphorylation, and improve synaptic dysfunction in 3xTg mouse brain.

162 d cell lines probably underestimates mitotic dysfunction in advanced human cancers.

163 tered mtDNA copy number that result in organ dysfunction in aging and disease have often not been cla

164 a-Syn and the cardinal features of autonomic dysfunction in alpha-synucleinopathy.

165 vessels, is a major contributor of vascular dysfunction in Alzheimer's disease (AD) patients.

166 es modestly associated with gastrointestinal dysfunction in ASD is provided, and a pilot study of met

167 lying mechanisms of hyperacusis and auditory dysfunction in ASD.

168 athogenic for NLGN4 and can lead to synaptic dysfunction in autism.

169 As involved in tissue function in health and dysfunction in disease.

170 may be attributable to specific D1R and D2R dysfunction in distinct striatal sub-regions.

171 r investigating human astrocyte function and dysfunction in health and disease.

172 at least in part, offset left ventricle (LV) dysfunction in hearts from diabetic mice, improving cont

173 ced Sirt3 expression contributes to vascular dysfunction in hypertension, but increased Sirt3 protect

174 der-specific proteasome and immunoproteasome dysfunction in liver.

175 nals is associated with nigrostriatal axonal dysfunction in mild to moderate PD.

176 nterleukin-10) deficient-EPC-derived exosome dysfunction in myocardial repair and to investigate if m

177 ne the nature of hiatal and crural diaphragm dysfunction in patients with achalasia of the esophagus.

178 Cirrhotic cardiomyopathy (CCM) is cardiac dysfunction in patients with end-stage liver disease in

179 role for ER stress and resulting epithelial dysfunction in PF and suggest ER stress as a potential m

180 se and human model systems to show that CFTR dysfunction in platelets increased calcium entry though

181 l translation to rescue fetal cardiovascular dysfunction in risky pregnancy.

182 d with both onset and advancement of cardiac dysfunction in T1D.

183 dy strongly supports a role for HOPS complex dysfunction in the pathogenesis of dystonia, although va

184 etic mutations drive telomere shortening and dysfunction in these patients.

185 functional recovery from brain diseases and dysfunctions in later life.

186 management of common symptoms (eg, autonomic dysfunction) in patients with Lewy body dementia.

187 Adipose tissue metabolic dysfunction, including fibrosis, plays a central role in

188 -3 PUFA intake worsens MIA-induced early gut dysfunction, including modification of gut microbiota co

189 opathy (SAE) is an acutely progressing brain dysfunction induced by systemic inflammation.

190 maH2AX foci and of 53BP1-containing telomere dysfunction-induced foci (TIFs), indicating defects in D

191 ged metabolic stress leads to adipose tissue dysfunction, inflammation, and adipokine release that re

192 the oxidative stress, DNA damage, lysosomal dysfunction, inflammatory cascade, apoptosis, genotoxici

193 Sensory dysfunction is a common consequence of many forms of neu

194 beta-Cell dysfunction is a common contributor to the pathogenesis

195 Endothelial dysfunction is a hallmark of preeclampsia, a life-threat

196 l deficits is not fully known, mitochondrial dysfunction is a key component in methamphetamine neurop

197 Reward system dysfunction is a well-known correlate and predictor of d

198 separation, and spatial navigation, and its dysfunction is associated with neuropsychiatric disorder

199 Adipose tissue mitochondrial dysfunction is emerging as a key component in the etiolo

200 Synapse dysfunction is emerging as an early pathological event i

201 ulating neural function, and importantly its dysfunction is implicated in cognitive impairment in hum

202 gests that alcohol-induced PC alpha-defensin dysfunction is mediated by zinc deficiency and involved

203 ently, the main therapeutic option for these dysfunctions is neobladder reconstruction with gastroint

204 podocytes to induce apoptosis and glomerular dysfunction kidney disease.

205 ) hypofunction and parvalbumin (PV) neuronal dysfunction leading to disinhibition of mesostriatal dop

206 otion abnormalities, global left ventricular dysfunction, left ventricular diastolic dysfunction grad

207 here is significant variability in cognitive dysfunction, likely reflecting biological heterogeneity.

208 yopathy (HCM) with left ventricular systolic dysfunction (LVSD), defined as occurring when left ventr

209 first time that integrin-associated proteins dysfunction may contribute to reduced phenylalanine flux

210 s indicates that participants with menstrual dysfunction might have decreased adaptive response to ex

211 ents with primary or secondary mitochondrial dysfunction, might be due to its function as cofactor fo

212 xtracellular matrix, which can lead to organ dysfunction, morbidity, and death.

213 ect of chronic PDE9a inhibition, 2 diastolic dysfunction mouse models were studied: (1) TAC-deoxycort

214 As part of the cirrhosis-associated immune dysfunction, mucosal-associated invariant T (MAIT) cells

215 sis factor-alpha levels and improved cardiac dysfunction, myocardial inflammation, and oxidative stre

216 notype was characterized by visceroautonomic dysfunction (neonatal bradycardia/apnea, feeding problem

217 in oxidative phosphorylation, mitochondrial dysfunction, nutrient metabolism, cardiac beta-adrenergi

218 eral contributions to K2KO-induced metabolic dysfunction observed.

219 ic stress predominate and beta cell death or dysfunction occurs.

220 s of lipoedema, such as adipose hypertrophy, dysfunction of blood and lymphatic vessels, the overall

221 bone volume and strength, partly due to the dysfunction of bone marrow mesenchymal stromal/stem cell

222 monstrate the mechanism of manganese-induced dysfunction of dopamine neurons, and reveal a potential

223 How a dysfunction of GABAergic cortical interneurons interacts

224 Dysfunction of neuronal circuits is an important determi

225 calization, and the pathological effects, as dysfunction of RPEs leads to AMD.

226 ed the role of ER Ca(2+) imbalance caused by dysfunction of sarco/ER Ca(2+) ATPase, ryanodine recepto

227 Dysfunction of SLG1 results in plants with thermosensiti

228 e upper quarter, which may contribute to the dysfunction of the cervicothoracic and glenohumeral join

229 oiesis and often include a dysregulation and dysfunction of the immune system.

230 Metabolic dysfunction of the liver, as an intermediate organ for V

231 ial genome, the typical downstream effect is dysfunction of the mitochondrial respiratory chain.

232 Thus, chronic dysfunction of the NAc may result in mPFC transcriptomal

233 tive and neurological diseases are rooted in dysfunction of the neuroimmune system; therefore, manipu

234 ral crest gives rise to numerous cell types, dysfunction of which contributes to many disorders.

235 ng a potential synergistic effect of cardiac dysfunction on fibrosis risk in NAFLD.

236 ently monitoring young children with adrenal dysfunction or severe asthma that are treated with high

237 ts and 89% of patients with active allograft dysfunction (P = 0.001).

238 synergistically induce macrophage metabolic dysfunction, particularly during cardiac remodeling, are

239 supporting an important role for peripheral dysfunction, particularly within skeletal muscle.

240 letion of ACC2 prevented HFD-induced cardiac dysfunction, pathological remodeling, and mitochondria d

241 Synaptic dysfunction plays a central role in Alzheimer's disease

242 Microvascular dysfunction plays an important role in the pathogenesis

243 toms and organ damage (eg, cytopenias, liver dysfunction, portal hypertension, malabsorption, and wei

244 45a mediates sepsis-associated microvascular dysfunction, potentially by means of Fli-1-mediated modu

245 e intracellular calcium causes mitochondrial dysfunction, premature zymogen activation, and necrosis,

246 omote metabolic reprogramming, mitochondrial dysfunction, reactive-oxygen species generation, and DNA

247 mplement proteins and their receptors in CNS dysfunction, recent data suggest that they exert neuropr

248 Complex motor dysfunction remains common in HIV and is associated with

249 otective effect on diabetes-driven cognitive dysfunction remains elusive.

250 way inflammation with associated mucociliary dysfunction remains largely unaddressed.

251 h ultimately leads to delirium and cognitive dysfunction, remains elusive.

252 ADHF was defined as systolic or diastolic dysfunction requiring continuous vasoactive or diuretic

253 ger neurodegeneration and neurodevelopmental dysfunction, respectively.

254 BAT dysfunction resulting from p62 deficiency is manifest af

255 Radiation-induced cognitive dysfunction (RICD) is a progressive and debilitating hea

256 sk of Mortality and Pediatric Logistic Organ Dysfunction scores at PICU admission were 11.0 (6.0-17.0

257 ortant role of ECC remodeling in the cardiac dysfunction secondary to chronic sympathetic activity.

258 e for both Abeta and tau in driving neuronal dysfunction seen in AD.

259 Sinus node (SAN) dysfunction (SND) manifests as low heart rate (HR) and i

260 h may be relevant to disorders involving GAD dysfunction such as schizophrenia or vitamin B6 deficien

261 life-threatening multisystemic smooth muscle dysfunction syndrome (MSMDS) due to mutations in the gen

262 ians' accuracy at identifying multiple organ dysfunction syndrome and predicting new or progressive m

263 o the objective assessment of multiple organ dysfunction syndrome using Proulx criteria.

264 predicting new or progressive multiple organ dysfunction syndrome, compared to the objective assessme

265 associated with irreversible multiple organ dysfunction syndrome.

266 In mice with telomere dysfunction, telomerase reactivation in the intestinal e

267 Reactive oxygen species (ROS), mitochondrial dysfunction, telomere shortening, genomic instability, e

268 iptional alterations and severe neurological dysfunction than MeCP2 loss.

269 Our data reveal a distinct immune dysfunction that is associated with diminished recogniti

270 ition and may provide insight into metabolic dysfunction that occurs in SAM.

271 rus (LCMV) clone 13 (CL13), result in immune dysfunction that predisposes the host to severe infectio

272 pathies are rare eye diseases of optic nerve dysfunction that present in various genetic forms.

273 As an in vitro model of haematopoietic dysfunction, the BM chip may serve as a human-specific a

274 associated pathogenesis, including vascular dysfunction, thrombosis, dysregulated inflammation, and

275 e diseases, the contributions of transporter dysfunction to disease pathophysiology remain ambiguous

276 ell hyperplasia and associated mucosecretory dysfunction to the development of idiopathic pulmonary f

277 As LV diastolic dysfunction typically precede heart failure symptoms, we

278 Interestingly, as micro-vascular dysfunction typically precedes the onset of retinal vasc

279 lls will confer protection against beta-cell dysfunction under diabetogenic conditions.

280 d model recapitulates characteristics of BBB dysfunction under hypoxic physiological conditions and w

281 Mitochondrial dysfunction underlies many heritable diseases, acquired

282 vascular pathology associated with cognitive dysfunction using APPSwDI transgenic mice expressing hum

283 ggest that ZIKV NS1 contributes to placental dysfunction via modulation of glycosaminoglycans on trop

284 Barrier dysfunction was also observed in mice that lacked platel

285 2, this specific prefrontal-ventral striatal dysfunction was associated with fewer days of alcohol ab

286 Mitochondrial dysfunction was highlighted as a crucial vulnerability f

287 lance: no overt constitutional or neurologic dysfunction was noted for any study animals.

288 bosis, is more common, but acute LV systolic dysfunction was noted in ~20%.

289 exposure is associated with islet beta-cell dysfunction, we investigated LD accumulation in the inta

290 ranscriptional profile of this airway immune dysfunction, we performed the first single-cell transcri

291 th HLA DSA in patients with active allograft dysfunction were associated with rejection and allograft

292 ation (inflammatory response and endothelial dysfunction) were related to the severity of liver cirrh

293 red a cornerstone in I/R-related endothelial dysfunction, which further impairs local microcirculatio

294 opathy are cardiac hypertrophy and diastolic dysfunction, which lead to heart failure, especially hea

295 ical activities of adipose tissues and their dysfunctions, which lead to several metabolic diseases i

296 term benefit over SAR in patients with renal dysfunction who require CABG.

297 healthy brain, a mechanism of widespread BBB dysfunction with age and a strategy for enhanced drug de

298 mice, acceleration and exacerbation of that dysfunction with WD consumption, the remarkable protecti

299 linical deterioration at follow-up, acute RV dysfunction, with or without deep vein thrombosis, is mo

300 TS is associated with the following: dysfunction within cortical-striatal-thalamic-cortical (