ライフサイエンスコーパス: liver

1 C(12) accumulation, was increased in Sirt5KO liver.

2 RL) of the studied coccidiostats for chicken liver.

3 l clusters (IAC) before colonizing the fetal liver.

4 ion from islet cells and their action in the liver.

5 controlling complement activation within the liver.

6 -target radiotoxicity, mainly in kidneys and liver.

7 pansion of hepatocytes in normal and injured liver.

8 r bacterial burdens in the lung, spleen, and liver.

9 to acute and chronic toxicity, mainly in the liver.

10 ced fibrogenic genes and inflammation in the liver.

11 rated nuclear ESR activity in the developing liver.

12 is an important innate immune process in the liver.

13 ns that favor formation of metastases in the liver.

14 expression of acyl-CoA dehydrogenases in the liver.

15 CR4 antagonists AMD3100 and AMD3465 from the liver.

16 second most common malignancy arising in the liver.

17 ethylase for lipogenic gene transcription in liver.

18 6.3 could generally produce more protein in livers.

19 ncourage programs to opt into splitting more livers.

20 he lacrimal glands (49% +/- 13%, P < 0.001), liver (15% +/- 6%, P < 0.001), spleen (28% +/- 13%, P =

21 Bq for red marrow, 0.80 +/- 0.24 cGy/MBq for liver, 3.0 +/- 1.4 cGy/MBq for spleen, 0.055 +/- 0.014 c

22 ar decreases: lung (-70%), heart (-43%), and liver (-37%).

23 e intake triggers de novo lipogenesis in the liver(4-6), in which carbon precursors of acetyl-CoA are

24 taxin in mouse heart (77%), brain (86%), and liver (47%) is predominantly a 129-amino acid truncated

25 We identified 110 kidney, 67 liver, 85 pancreas, 68 heart, and 43 lung TRRs.

26 e, our understanding of tissue injury in the liver, adrenal glands, and lymphoid tissues remains limi

27 re grouped as having received a living donor liver allograft from either an offspring or a nonoffspri

28 racellular matrix deposition in the diseased liver and as such are important in the progression of li

29 linemic clamps, being highly up-regulated in liver and down-regulated in muscle and fat.

30 ated the local inflammatory responses in the liver and improved glycemic control immediately after al

31 Five-year liver and kidney allograft survivals were 67% and 64% in

32 r sEVs might induce cross-dressing following liver and kidney transplantation.

33 sic circadian rhythms, especially within the liver and kidney.

34 -dried weight (fdw) and 1390 ngg(-1) fdw for liver and muscle, respectively.

35 extrinsic insulin resistance was observed in liver and muscle.

36 isceral and subcutaneous adipose tissue, and liver and pancreatic fat at MRI.

37 othelial quiescence after secretion from the liver and right atrium, whereas a direct role in the reg

38 icant reduction (P < 0.05) in viral titer in liver and spleen at day 5 postinfection (d p.i.), althou

39 n to blood pool, at least 0.55 for lesion to liver, and at least 4.4 for lesion to bone.

40 for controlling complement activation in the liver, and in its absence, AP activation leads to chroni

41 rus was only isolated from some lung, brain, liver, and kidney samples that were ZsG and/or PCR posit

42 kaline phosphatase, creatinine, and improved liver, and renal antioxidative status.

43 ammation and steatosis of adipose tissue and liver are associated with a variety of serious health ri

44 tional activation in both adipose tissue and liver as well as serum levels were strongly associated w

45 Metabolic dysfunction of the liver, as an intermediate organ for VD metabolism, contr

46 sually accompanied by dyslipidemia and fatty liver, as seen in lipodystrophies.

47 tion (n = 12), ex vivo Whipple procedure and liver autotransplantation (n = 8) and multivisceral ex v

48 and altered intestinal barrier function (gut-liver axis) and by episodes of sepsis to cause cholestas

49 Although the total liver BA levels were similar between KO/KD and KO, there

50 FL and BM FDG uptake lower than the liver background after therapy was an independent predic

51 ate, data are limited regarding the trend of liver biochemistries over the course of illness.

52 ystems exist to characterize NAFLD and NASH, liver biopsy is the only accepted method for diagnosis o

53 nfected hepatocytes and chronic HCV-infected liver biopsy specimens.

54 eventually on histological examination from liver biopsy.

55 HAMP is also expressed in the fetal liver but its role in controlling fetal iron stores is n

56 ing the adipose tissue, skeletal muscle, and liver by 9 weeks post-infection.

57 y of perturbing protein synthesis in a mouse liver by targeting translation elongation factor 2 (eEF2

58 We previously showed that rat livers can be viably preserved three times longer by sup

59 f hepatitis B, the stage of Barcelona Clinic Liver Cancer (BCLC) B and C, and the presence of cirrhos

60 for FBP1 as a metabolic tumour suppressor in liver cancer and establish a critical crosstalk between

61 e, CRISPR-mediated knockout of FN3K in human liver cancer cells altered the abundance of redox metabo

62 arrying miR122 and PTX were delivered to the liver cancer cells efficiently due to their rubber-like

63 ine-approved image-guided therapy option for liver cancer using the radiopaque drug-carrier and micro

64 roach to examine the personalized biology of liver cancers and the influence of host tissues is with

65 the overall survival time in the breast and liver cancers group.

66 fairness balance, and have demonstrated that liver candidates awaiting transplant would benefit from

67 the tumor suppressor function of TGFbeta in liver carcinogenesis.

68 dmissions, malignancies, and death regarding liver, cardiovascular, and malignant disease, as well as

69 roliferation, lobular cholestasis, and acute liver cell necrosis, together with central vein thrombos

70 c conjugation for efficient uptake by target liver cells and indicate that GalNAc-conjugated PNAs hav

71 udy was to evaluate the relationship between liver chemistries and liver histology using data from th

72 o examine hemostasis in patients with stable liver cirrhosis (Non-ACLF) and in acute-on-chronic liver

73 pective observational study in patients with liver cirrhosis and an indication for fluoroquinolone-ba

74 Liver function of 113 patients with liver cirrhosis was prospectively investigated.

75 ed severe liver disease outcomes (defined as liver cirrhosis, complications of cirrhosis, or liver-re

76 isk factor for several common cancers (e.g., liver, colorectal, breast, pancreas).

77 onfirmed that the dark reddish-brown livers, liver colours 5 and 6, formed a distinct group.

78 ound the intensity of mRNA expression in the liver correlated with the pKa of DLNPs, indicating that

79 In NAFLD, Escherichia coli LPS may increase liver damage by inducing macrophage and platelet activat

80 loride (CCl(4)) to induce mutations, chronic liver damage, and carcinogenesis.

81 entifying key factors and pathways governing liver development will help elucidate the physiological

82 Among HIV-infected, model of end-stage liver disease (aHR, 1.04; P < 0.001), body mass index <2

83 End-stage liver disease (ESLD) is a major burden on public health,

84 Patients with end-stage liver disease (ESLD) suffer from a high symptom burden a

85 R) was estimated using the GFR assessment in liver disease (GRAIL) developed among patients with cirr

86 on Category 83), 2.55 (2.35-2.77); end-stage liver disease (Hierarchical Condition Category 27), 2.53

87 ious model consisting of Model for End-Stage Liver Disease (MELD) and LA at admission may predict inp

88 Our primary outcome was Model for End-Stage Liver Disease (MELD) score at waitlist removal for "too

89 nce), and the presence of nonalcoholic fatty liver disease (NAFLD) and nonalcoholic steatohepatitis (

90 Nonalcoholic fatty liver disease (NAFLD) encompasses a range of conditions,

91 Non-alcoholic fatty liver disease (NAFLD) is a frequent condition in obese p

92 HIV-uninfected patients, nonalcoholic fatty liver disease (NAFLD) is associated with incident metabo

93 Nonalcoholic fatty liver disease (NAFLD) is the most common pediatric chron

94 with reduced severity of nonalcoholic fatty liver disease (NAFLD), based on histologic analysis, com

95 ainst the development of non-alcoholic fatty liver disease (NAFLD).

96 As controls, 9 individuals without liver disease and 13 patients with mild primary biliary

97 Chronic HBV infection is a major cause of liver disease and cancer worldwide.

98 -matched nontransplant patients with chronic liver disease and COVID-19 (n = 375), incidence of acute

99 s of alanine transaminase (ALT) and clinical liver disease and mortality in 111,612 individuals from

100 ion of the risk score with plasma markers of liver disease and with cirrhosis and HCC in 110,761 indi

101 d to estimate hazard ratios (HRs) for severe liver disease at 5, 10, and a maximum follow-up time of

102 covariance, adjusted for model for end-stage liver disease at time of hospital admission, serum level

103 hy that progresses to fibrosis and end-stage liver disease by 2 years of age.

104 liver injury (DILI) is a necro-inflammatory liver disease caused by several drugs commonly used in c

105 Nonalcoholic fatty liver disease is the most prevalent liver disease worldw

106 rs protection from specific risk factors for liver disease is unclear.

107 Studies were included that reported severe liver disease outcomes (defined as liver cirrhosis, comp

108 iabetic CHCpatients and might have a role in liver disease progression.

109 RI identified patients with advanced chronic liver disease who are at increased risk for a first hepa

110 These mice spontaneously developed liver disease with hepatic steatosis, inflammation, and

111 ic fatty liver disease is the most prevalent liver disease worldwide, affecting 20%-25% of the adult

112 y bowel disease and cirrhosis, whereas other liver disease, including biliary stone disease (OR, 4.06

113 dren aged younger than 12 years with chronic liver disease, listed for deceased donor livers January

114 ndings may also apply to non-alcoholic fatty liver disease, which shares similar pathological and met

115 pulation with increasing prevalence of fatty liver disease.

116 (NAFLD) is the most common pediatric chronic liver disease.

117 abolic syndrome, such as non-alcoholic fatty liver disease.

118 f cancer or predisposing factors for chronic liver disease.

119 serious AEs can occur in those with advanced liver disease.

120 LD, but the majority do not develop advanced liver disease: cirrhosis, hepatic decompensation, or hep

121 r alcohol abuse; 2.37 (95% CI 1.53-3.68) for liver disease; 2.04 (95% CI 1.30-3.20) for kidney diseas

122 er mechanistic studies in the progression of liver diseases and in the discovery of drugs for the tre

123 idate to liver transplantation for alcoholic liver diseases and severe acute alcoholic hepatitis.

124 In cholestatic liver diseases, ductular reactive (DR) cells extend into

125 Embryonic deletion of integrin beta1 in the liver disrupts the normal development of hepatocyte pola

126 e symptoms and organ damage (eg, cytopenias, liver dysfunction, portal hypertension, malabsorption, a

127 , debilitating fibroses, and obesity-related liver dysfunction.

128 crose, Rebaudioside A significantly improved liver enzymes, hepatic steatosis and hepatic fibrosis.

129 tasis, the accumulation of bile acids in the liver, fails to promote liver injury in the absence of t

130 cirrhosis (Non-ACLF) and in acute-on-chronic liver failure (ACLF) by CCT and ROTEM including agreemen

131 ors to predict survival and acute-on-chronic liver failure (ACLF) in patients awaiting LT, as well as

132 he progression of acute and acute-on-chronic liver failure (ACLF).

133 cted with azoxymethane (AOM) to induce acute liver failure and HE.

134 on the management acute or acute on chronic liver failure in the ICU, related to five groups (cardio

135 with reduced ammonia concentrations in acute liver failure patients.

136 been shown to contribute to HE during acute liver failure; however, TGFbeta1 must be activated to bi

137 We found marked advance of liver fibrosis (chronic damage), as well as necrosis of

138 oint to it being a key chemokine controlling liver fibrosis and inflammation in the context of YAP/TA

139 The link between liver fibrosis and the natural history of COVID-19 shoul

140 or 3 mg, 25% and 42%, respectively, improved liver fibrosis by one stage or more without worsening of

141 echanistic pathways that lead to accelerated liver fibrosis have not been well defined.

142 Liver fibrosis interferes with normal liver function and

143 VD deficiency is associated with liver fibrosis progression.

144 f mice with bile duct ligation (BDL)-induced liver fibrosis, by monitoring echocardiography and intra

145 cal conditions such as rheumatoid arthritis, liver fibrosis, or obesity.

146 ith advanced compared with earlier stages of liver fibrosis.

147 , and a measure (L(f) ) was used to quantify liver fibrosis.

148 as such are important in the progression of liver fibrosis.

149 nvestigated the signal from the inflammatory liver for this pathogenic process in the hepatic conditi

150 utpatient physical frailty testing using the Liver Frailty Index and resilience testing using the Con

151 We measured 36 emerging and legacy PFAS in livers from 31 juvenile seabirds from Massachusetts Bay,

152 Liver fibrosis interferes with normal liver function and facilitates hepatocellular carcinoma

153 combines serum creatinine levels and maximum liver function capacity (LiMAx(R)), namely the CreLiMAx

154 Liver function of 113 patients with liver cirrhosis was

155 , serious adverse events related to abnormal liver function tests (OR 11.19, 95% CI: 2.09-60.02) or p

156 d to quantify glycocalyx damage within human liver grafts after organ preservation and correlate the

157 Thus, fetal liver HAMP operates cell-autonomously to increase fetal

158 e cellular complexity and scale of the early liver have constrained analyses examining its emergence

159 ctose in glucose and lipid metabolism in the liver, heart, skeletal muscle, and adipose tissue.

160 ral- and non-viral-mediated gene transfer to liver, heart, skeletal muscle, and the central nervous s

161 e relationship between liver chemistries and liver histology using data from the CyNCh (Cysteamine Bi

162 ated with greater dysbiosis but no change in liver histology.

163 ellular-derived particles were infectious in liver-humanized mice with high RNA copy numbers detectab

164 The liver imaging features generated by CNN may have the pot

165 Conclusion The functional liver imaging score derived from gadoxetic acid-enhanced

166 ith the development of risk factors of fatty liver in adulthood.

167 gramming of circadian gene expression in the liver in analogy to what is observed in other experiment

168 ave the greatest instability in the CNS, and liver in the periphery.

169 Other changes in the liver included hepatic steatosis, portal fibrosis, lymph

170 The fatty liver index (FLI), a noninvasive steatosis biomarker, ha

171 In this context, adipose tissue and liver inflammation have been particularly well studied;

172 portant role of YAP in KCs for regulation of liver inflammation in NASH.

173 ct of fecal microbiota independent of active liver inflammation or injury.

174 verteporfin inhibited KC activation, reduced liver inflammation, and decreased serum ALT/AST levels.

175 NASH progression in HFD-fed mice by inducing liver inflammation, injury, and p38 activation.

176 Drug induced liver injury (DILI) is a necro-inflammatory liver diseas

177 Prevalence of liver injury and associated clinical characteristics are

178 cued FXR signaling and partially ameliorated liver injury and sinusoidal ischemia in SCD mice.

179 toxicity with limited evidence of benefit in liver injury due to other causes.

180 comes, maternal TB, all-cause mortality, and liver injury during pregnancy through 12 months postpart

181 2)O(2) and glycerol transport, and prevented liver injury in experimental animal models.

182 of bile acids in the liver, fails to promote liver injury in the absence of the microbiome in vivo.

183 c role of PDGFR-alpha in HSCs during chronic liver injury in vivo via regulation of HSC survival and

184 ogical interactions pathway in patients with liver injury is indicative of an immune-based mechanism

185 ere damage such as cardiovascular, renal and liver injury or/and multiple organ failure, suggesting a

186 rentiation; however, its function in chronic liver injury sequelae, such as fibrosis, is unknown.

187 e and COVID-19 (n = 375), incidence of acute liver injury was lower in LT recipients (47.5% vs. 34.6%

188 licate the involvement of macrophage AQP3 in liver injury, and provide evidence for mAb inhibition of

189 caused stellate cell activation, leading to liver injury, by a mechanism involving AQP3-mediated H(2

190 difference was observed after other types of liver injury, PDGFR-alpha loss in HSCs led to a signific

191 critical for tissue protection during acute liver injury.

192 ransport as therapy for macrophage-dependent liver injury.

193 operates cell-autonomously to increase fetal liver iron stores.

194 anifests when triglyceride (TG) input in the liver is greater than TG output, resulting in the excess

195 asting-induced downregulation of GRK2 in the liver is key for allowing complete glucagon-mediated res

196 Although the liver is the primary site for clinical islet transplanta

197 lthough AnxA6 is abundantly expressed in the liver, its function in hepatic physiology remains unknow

198 nic liver disease, listed for deceased donor livers January 1, 2005-December 31, 2017.

199 n in, central and peripheral nervous system, liver, kidney and skeletal muscle.

200 ity of different organs including the heart, liver, kidney, lungs, immune system, gastro-intestinal s

201 id-organ transplant recipients (heart, lung, liver, kidney, multiorgan) at The Hospital for Sick Chil

202 induction immunosuppression for simultaneous liver/kidney transplantation (SLKT).

203 In control human livers, LCN2 expressed exclusively in mononuclear cells,

204 hology confirmed that the dark reddish-brown livers, liver colours 5 and 6, formed a distinct group.

205 65% of the lesions were located in the right liver lobe.

206 ads (colony-forming units per milliliter) in liver, lung, and spleen were not different between group

207 s in blood, brain, heart, intestine, kidney, liver, lung, muscle and spleen were determined on day 21

208 tic castration-resistant prostate cancer and liver metastases assigned to (177)Lu-PSMA alone (n = 31)

209 excluded because of unequivocal evidence of liver metastases at baseline whole-body MRI, two partici

210 lowing 3 months of PTX therapy for recurrent liver metastases.

211 h a previous diagnosis of breast cancer with liver metastasis presented with a complaint of increasin

212 positive primary status, and size of largest liver metastasis.

213 ted by CNN may have the potential to predict liver metastasis.

214 e oxygen electrode, we measured isolated rat liver mitochondrial respiration in the presence and abse

215 ocytes to other nonadipose tissues including liver, muscle, and pancreas.

216 ecipient leukocytes, which recapitulated the liver myeloid and lymphoid composition, and underwent pa

217 le its expression was markedly induced in AH livers, not only in mononuclear cells but also notably i

218 activity and the AMPKbeta1 abundance in the liver of E4bp4-LKO mice.

219 Moreover, MCJ levels in the liver of NAFLD patients are elevated relative to healthy

220 lar pathology in the oral mucosa, lungs, and liver of the BMP9/10ib mice, as well as significantly re

221 In the liver of the mice treated with OCA, the levels of cytoch

222 transient changes in gene expression in the livers of both mouse strains.

223 reased CHOP levels were detected in diseased livers of children homozygous for the Z allele.

224 croarray data (n = 303 profiles) measured in livers of fathead minnows after exposure to 38 different

225 riptomic analysis reveals that preneoplastic livers of Ncoa5(+/-) mice are similar to the livers of n

226 Livers of Nod2(-/-) tumorigenic mice had increased expre

227 livers of Ncoa5(+/-) mice are similar to the livers of nonalcoholic steatohepatitis patients as well

228 DUBmut virus infections resulted in similar liver pathology.

229 as a dosage-sensitive modifier of Jag1(+/-) liver phenotypes with a permissive role in biliary devel

230 he potential for significant prolongation of liver preservation before transplantation.

231 elineating two temporally distinct phases of liver recovery.

232 -art systems biology approaches to models of liver regeneration, pharmacologically and genetically ac

233 However, liver-related complications are rare.

234 er cirrhosis, complications of cirrhosis, or liver-related death) or advanced fibrosis/non-alcoholic

235 containing transposons were quantified after liver repopulation via high-throughput sequencing.

236 livers with >=30% macrosteatosis (steatotic livers) represent a possible expansion to the donor pool

237 of index symptoms after receiving palliative liver RT with median response duration of 3 months.

238 s, mostly fragrance ingredients, using trout liver S9 fractions (RT-S9) and incorporated into in vitr

239 We obtained liver samples from 125 of 169 patients (76%) having reac

240 Together, these data reveal that liver sinusoidal endothelial cells sense the microbiome,

241 3 binding and targeted the mutated RSPO to a liver specific receptor, ASGR1.

242 In other studies, using adult liver-specific G6pc-deficient mice at both pre-tumor and

243 Our data further suggest that liver-specific increase in SOX9 levels is a potential th

244 or the in situ determination of the grade of liver steatosis at the operation room as a fast, quantit

245 CV cirrhosis (defined histologically or when liver stiffness >=12 kPa) treated with DAAs.

246 Liver stiffness (LS) was measured using Vibration Contro

247 There was no association between liver stiffness and any patient variable or MRI scanner

248 Curative treatment with DAA attenuated the liver stiffness and inflammation but did not improve VD

249 At follow-up, liver stiffness measured with TE was similar among all H

250 gitudinal association between an increase in liver stiffness on MRE and fibrosis progression in NAFLD

251 Purpose To determine normal liver stiffness, and associated normal ranges for childr

252 Lung-, spleen- and liver-targeted SORT lipid nanoparticles were designed to

253 verse events consisted primarily of elevated liver tests (6%), myelotoxicity (7%) and rash (5%).

254 f genes in fatty acid oxidation in humanized livers through its interaction with RNA-binding protein

255 od and tissues of ART-suppressed bone-marrow-liver-thymus (BLT) humanized mice and rhesus macaques in

256 nts with AH or alcoholic cirrhosis or normal liver tissue from hepatic resection.

257 d metabolomic and transcriptomic analyses of liver tissue from patients with AH or alcoholic cirrhosi

258 clinical specimens, cell lysates, and mouse liver tissue samples, demonstrating its highly sensitive

259 atients as well as the adjacent noncancerous liver tissues of a subset of HCC patients with a relativ

260 a-AASA) and pipecolic acid both in brain and liver tissues, similar to the biochemical picture in ALD

261 r intravenous administration showed that the liver-to-plasma AUC ratios could be significantly improv

262 r infusion was safe and resulted in enhanced liver transduction, even in the setting of vector readmi

263 Liver transplant activity in 6 centers from these countr

264 was associated with a 25% lower risk of post-liver transplant HCC recurrence (95CI 0.57-0.99).

265 A cox-regression analysis for post-liver transplant HCC recurrence highlighted that even af

266 reports the experience of the Irish National Liver Transplant Programme with the Mayo Protocol.

267 outcomes of 7 renal transplant recipients, 1 liver transplant recipient, 1 heart transplant recipient

268 We included consecutive adult liver transplant recipients who had their surgery betwee

269 the leading cause of mortality in kidney and liver transplant recipients.

270 ogy of cirrhosis, alpha-fetoprotein (AFP) at liver transplant, tumor diameter, tumor pathology, and v

271 ns earlier can delay or prevent the need for liver transplant; however, treatment typically occurs la

272 ng data from the adult-to-adult living donor liver transplantation (A2ALL) study, which represents th

273 We studied outcomes following living donor liver transplantation (LDLT) post-PVTT downstaging (DS)

274 CC) is an increasingly common indication for liver transplantation (LT) in the United States and in m

275 m glycomic signature in the first week after liver transplantation (LT) that is associated with graft

276 PV samples from IRI+ orthotopic liver transplantation (OLT) patients (n = 35) decreased

277 t function in patients undergoing orthotopic liver transplantation (OLT).

278 Liver transplantation and PSC-related events accounted f

279 blation therapy for presumed HCC followed by liver transplantation between January 2011 and December

280 datory to properly evaluate the candidate to liver transplantation for alcoholic liver diseases and s

281 Liver transplantation has been increasingly reported ove

282 rmacological approaches are ineffective, and liver transplantation represents the only curative optio

283 clinical outcomes, particularly surrounding liver transplantation.

284 in an in situ and ex situ model of rat donor liver transplantation.

285 is at the forefront of innovation in modern liver transplantation.

286 e first-choice imaging technique to evaluate liver transplants.

287 Obesity/diabetes-associated liver tumors are specifically vulnerable to cyclin D1 de

288 r very large (>=8 cm) primary and metastatic liver tumors with curative treatment intent.

289 athy (HE), pulmonary hypertension (PaHT), or liver tumors, among other complications.

290 patocellular adenomas (HCAs) are rare benign liver tumors.

291 s hypothesized to be the result of undesired liver uptake caused by poor physicochemical properties.

292 ual lymphoma (18)F-FDG uptake to physiologic liver uptake, converting the ordinal Deauville scale int

293 ed for patients with a ratio of FLR to total liver volume (FLR/TLV) of <25% (RASPE group).

294 Her venous pressure was elevated, but the liver was not enlarged, and the lung fields were clear.

295 (-/-) and Tr(-/-)Mdr2(-/-) mice had elevated liver weights and serum alanine transferase values.

296 Thirty-one livers were enroled and assessed by viability criteria b

297 nction of YAP/TAZ during regeneration of the liver, where Hippo's role in growth control has been stu

298 Amiodarone accumulates in the liver, where it increases x-ray attenuation due to its i

299 ld not predict effects on development of the liver, which was the tissue most sensitive to AFFF.

300 Donor livers with >=30% macrosteatosis (steatotic livers) repr

301 Here, we show that liver X receptors (LXRs)-a class of nuclear receptors an