28%, P = .006). Our study

demonstrates that administering IV t-PA to patients based on PXD101 the stroke team’s interpretation of the CT scan versus review of the radiology interpretation does not lead to significant differences in clinical outcome, aICH, or sICH. “
“Idiopathic intracranial hypertension (IIH), is characterized by elevated intracranial pressure (ICP) without a clear cause. Recently it was shown that in more than 90% of the IIH patients there is stenosis of the transverse dural sinuses. In this study we assessed the changes in diameter of cerebral veins after lumbar puncture, in order to have some more insight regarding the volume and pressure influence on cerebral veins. We prospectively included 13 patients suspected with IIH, admitted for investigation in the Soroka medical center. All the patients had a lumbar puncture (LP) with opening pressure measurement and CSF analysis, and two MRI–MRV studies: one before the LP and one after it. Measurements of the cerebral venous sinuses diameter were performed. Significant stenosis of both transverse sinuses was found before LP in IIH patients with an average diameter of 1.77 mm of the right TS, and 1.57 mm of the left TS. After the LP, there was a

significant increase in all venous sinuses diameters (P < .05). There was no correlation between the changes in diameter of the venous sinuses after LP and opening pressure measured or BMI. Our results support other studies and demonstrated narrowing of the transverse sinuses in IIH patients. The main finding of this study is the increase BGJ398 nmr in cerebral sinuses diameter after LP. This observation should be considered when evaluating cerebral venous sinuses after LP. A larger scale study is warranted to validate our findings. “
“Aquaporin 4 (AQP-4) is the most MCE abundant aquaporin isoform in the brain. Alterations in its expression and

distribution have been correlated with the progression of several clinical disorders; however, the specific roles of AQP-4 in those disorders are not well understood. Visualizing AQP-4 in vivo is expected to provide fresh insights into its roles in disease pathology, as well as aiding the clinical assessment of those disorders. We developed a 11C-labeled analogue of the AQP-4 ligand TGN-020 (2-nicotinamido-1,3,4-thiadiazole) suitable for in vivo positron emission tomography (PET) imaging. In the present study, we report the first PET images of AQP-4 in the human brain. The results unequivocally demonstrated a specific distribution pattern for AQP-4 within the brain, namely, the subpial and perivascular endfeet of astrocytes. The choroid plexus, where both AQP-4 and AQP-1 are expressed, also showed substantial uptake of the ligand. Based on these initial results, we believe [11C]TGN-020 PET will be valuable in determining the role of AQP-4 in disease progression, and for the clinical assessment of water homeostasis under various settings.

3, 4 On the other hand, inflammatory cells, such as circulating monocytes, were often shown to contribute to the progression of liver fibrosis. Monocyte-derived macrophages purified from carbon tetrachloride-treated OTX015 in vivo animals, or CD14+CD16+ monocytes from patients with chronic liver disease

can directly activate stellate cells.5, 6 Therefore, further studies are needed to delineate the relationship between hepatocytes, inflammatory cells, and HSCs during liver fibrogenesis. A potential key factor of hepatocyte-driven liver fibrosis could be the activation of the proinflammatory nuclear factor-κB (NF-κB) pathway in hepatocytes. The family of NF-κB transcription factors belongs to the key regulators of inflammatory processes.7 Dysregulation of NF-κB can lead to constitutive overproduction of proinflammatory cytokines, which is associated with a number of chronic inflammatory disorders.8 Constitutive activation of NF-κB is also observed in patients with liver diseases such as hepatitis B, hepatitis C, or hepatocellular carcinoma.9 However, although previous work has found that active NF-κB is associated with fibrosis,10 the exact contribution to disease development and progression remained enigmatic. In addition, the question whether

activation of NF-κB is protective or disease aggravating is unresolved. Panobinostat research buy In resting cells, NF-κB is localized in the cytoplasm associated with inhibitory proteins (IκB).

A variety of stimuli can activate the NF-κB signaling pathway. This leads to phosphorylation, polyubiquitination, and proteasome-dependent degradation of IκB proteins. Liberated NF-κB dimers can translocate into the nucleus and regulate NF-κB-dependent gene expression.11 The IκB kinase (IKK) complex is the master regulator for activation of the NF-κB signaling pathway.12 The kinase complex comprises the two catalytic subunits, IKK1 (IKKα) and IKK2 (IKKβ), and the regulatory subunit 上海皓元 NEMO (IKKγ), which mediates NF-κB activation in response to a number of different stimuli by phosphorylating IκB proteins.12 Genetic studies revealed that NF-κB p65 (RelA), IKK2, or NEMO have a critical role in protecting hepatocytes during an embryonic phase.13 However, in the adult liver NF-κB inhibition in hepatocytes by conditional knockout of Rela or Ikbkb (encoding IKK2), or overexpression of IκBα super-repressor has no spontaneous liver phenotype.14-16 In this study we show that hepatic activation of NF-κB signaling is sufficient to induce liver fibrosis. Activation of the NF-κB pathway leads to development of chronic inflammation, which precedes the development of liver fibrosis. Continuous NF-κB activation is necessary for the maintenance of chronic inflammation, because turning off the IKK2 overexpression leads to a rapid decrease in multiple inflammatory cytokines and later on in a decrease in activated HSCs.

3, 4 On the other hand, inflammatory cells, such as circulating monocytes, were often shown to contribute to the progression of liver fibrosis. Monocyte-derived macrophages purified from carbon tetrachloride-treated EX 527 in vitro animals, or CD14+CD16+ monocytes from patients with chronic liver disease

can directly activate stellate cells.5, 6 Therefore, further studies are needed to delineate the relationship between hepatocytes, inflammatory cells, and HSCs during liver fibrogenesis. A potential key factor of hepatocyte-driven liver fibrosis could be the activation of the proinflammatory nuclear factor-κB (NF-κB) pathway in hepatocytes. The family of NF-κB transcription factors belongs to the key regulators of inflammatory processes.7 Dysregulation of NF-κB can lead to constitutive overproduction of proinflammatory cytokines, which is associated with a number of chronic inflammatory disorders.8 Constitutive activation of NF-κB is also observed in patients with liver diseases such as hepatitis B, hepatitis C, or hepatocellular carcinoma.9 However, although previous work has found that active NF-κB is associated with fibrosis,10 the exact contribution to disease development and progression remained enigmatic. In addition, the question whether

activation of NF-κB is protective or disease aggravating is unresolved. Pexidartinib order In resting cells, NF-κB is localized in the cytoplasm associated with inhibitory proteins (IκB).

A variety of stimuli can activate the NF-κB signaling pathway. This leads to phosphorylation, polyubiquitination, and proteasome-dependent degradation of IκB proteins. Liberated NF-κB dimers can translocate into the nucleus and regulate NF-κB-dependent gene expression.11 The IκB kinase (IKK) complex is the master regulator for activation of the NF-κB signaling pathway.12 The kinase complex comprises the two catalytic subunits, IKK1 (IKKα) and IKK2 (IKKβ), and the regulatory subunit medchemexpress NEMO (IKKγ), which mediates NF-κB activation in response to a number of different stimuli by phosphorylating IκB proteins.12 Genetic studies revealed that NF-κB p65 (RelA), IKK2, or NEMO have a critical role in protecting hepatocytes during an embryonic phase.13 However, in the adult liver NF-κB inhibition in hepatocytes by conditional knockout of Rela or Ikbkb (encoding IKK2), or overexpression of IκBα super-repressor has no spontaneous liver phenotype.14-16 In this study we show that hepatic activation of NF-κB signaling is sufficient to induce liver fibrosis. Activation of the NF-κB pathway leads to development of chronic inflammation, which precedes the development of liver fibrosis. Continuous NF-κB activation is necessary for the maintenance of chronic inflammation, because turning off the IKK2 overexpression leads to a rapid decrease in multiple inflammatory cytokines and later on in a decrease in activated HSCs.

23-27 This evidence has led the providers of the updated AASLD guidelines for the diagnosis and management of HCC to drop alpha-fetoprotein from the surveillance armamentarium for HCC in patients with cirrhosis, although this decision was debated.10, 28, 29 However, alpha-fetoprotein may have a prognostic meaning in patients with HCC, and is included in prognostic classifications see more such as the Cancer of the Liver Italian Program score, although also in this setting the results of various studies have provided inconsistent findings.11-14, 30, 31 Recently,

Tandon and Garcia-Tsao11 performed a comprehensive, systematic review of prognostic indicators in HCC and identified alpha-fetoprotein as one of the most robust prognostic indexes, although they observed that the appropriate cutoff level and group of patients in which this serum marker may be helpful remain to be established. Thus, we deemed it of interest to evaluate whether alpha-fetoprotein might be a prognostic indicator in patients who might benefit most from the application of curative treatment, and therefore where prognostication should be of utmost

importance. In this study we demonstrated that alpha-fetoprotein has no prognostic relevance in patients with well-compensated cirrhosis, optimal performance status, and a single, small HCC (i.e., ≤3 cm) identified during surveillance and treated with curative intent. The poor prognostic performance of alpha-fetoprotein we observed this website in this particular setting may be due to several reasons. First, alpha-fetoprotein levels were within the normal 上海皓元医药股份有限公司 range in more than half of the population, and reached markedly elevated levels

(i.e., >200 ng/mL) in less than 10% of the patients. These findings are strikingly in keeping with previous features (i.e., 11.1%) observed in a population of 153 patients with small (<2 cm) HCC seen in our geographical area.32 Even when patients were more broadly subdivided according to normal or elevated alpha-fetoprotein levels (i.e., above or below 20 ng/mL) no survival difference surfaced between the two groups. Furthermore, in order to avoid limitations related to the use of pretest fixed cutoffs of a continuous variable, we also performed an analysis using an ad hoc alpha-fetoprotein cutoff identified by ROC curve. However, even this analysis showed that alpha-fetoprotein had negligible prognostic accuracy (area under the ROC curve = 0.536, 95% CI = 0.465-0.606), and the ROC curve-identified alpha-fetoprotein cutoff (i.e., 100 ng/mL) had largely inadequate sensitivity (23%, 95% CI = 15%-33%). Second, as previously reported by others,33, 34 we too observed that increased alpha-fetoprotein levels were associated with female gender and greater hepatic cytolytic activity, although they had no association with clinical and tumoral characteristics, and were not influenced by current and past antiviral therapy.

Using a mouse model of diethylnitrosamine (DEN)-induced HCC, we found that TLR4 mutant (TLR4mut) mice shows an increase in the initiation and progression of HCC and a decrease in the animal survival compared to wild-type (WT) littermates. Our studies indicate that TLR4-controlled immunity supporting the senescent induction and the expression of DNA repair proteins plays an integrated defense role against genotoxic carcinogenesis and tumor progression in the liver. Ectopic expression of DNA damage repairing protein Ku70 attenuates the DEN-induced

HCC in TLR4mut mice, MG-132 order suggesting that Ku70 may act as a tumor suppressor by restoring immunity, senescent response, and autophagy flux in TLR4mut liver. All animals received care according to the Guide for the Care and Use of Laboratory Animals. TLR4mut mice (C3H/He background) were originally obtained from The Jackson Laboratory (Bar Harbor, ME). Fifteen-day-old WT and TLR4mut mice were injected intraperitoneally with or without DEN (25 mg/kg) (Sigma-Aldrich, St. Louis, MO).18 The mice were fed normal chow and

sacrificed on months 1, 3, 6, and 18 after DEN injection to observe tumor development and animal survival. For adenovirus infection experiments, the mice were infected intramuscularly with 1 × 105 viral particles (V.P.) of Ku70 adenovirus or green fluorescent protein (GFP) adenovirus per mouse on day 1, 7, and 14 after DEN injection, and were sacrificed at day 30 and month CAL-101 price 6 after DEN injection. For assessing HCC, external visible tumors (>0.5 mm) were counted and measured by stereomicroscopy.19 The largest liver lobes were fixed in 4% formalin, paraffin-embedded, and sliced into sections. Sections were stained with hematoxylin and eosin and the tumor areas were measured as described.20

Liver function was monitored by measuring serum alanine aminotransferase 上海皓元 activities. Western blot assays of liver tissue were performed with commercial antibodies as described,21 using β-actin as loading controls. Detergent-soluble and insoluble fractions of livers were performed as described.22 Immunohistochemistry and immunofluorescence assays were performed as described.23 To detect total contents of reactive oxygen species (ROS), frozen liver sections or single cell suspensions were prepared as described21 and incubated with 2′,7′-dichlorofluorescein diacetate (Sigma-Aldrich, St. Louis, MO) as described.23 Terminal deoxynucleotidyl transferase–mediated deoxyuridine triphosphate nick-end labeling (TUNEL) staining was performed with detection kit (Roche, Basel, Switzerland) following the manufacturer’s instructions. Data are expressed as the mean ± SE. Groups were compared via one-way analysis of variance followed by a Tukey-Kramer or Dunnett multiple comparisons test. Comparisons between two groups were performed via an unpaired Student t test. The survival rates were analyzed using the Kaplan-Meier method. P < 0.05 was considered significant.

However FVIII can be activated and/or inactivated by a number of coagulation-related serine proteases, including FXa,

APC and FIXa. The physiological relevance of these reactions remains unclear, however FVIII-binding to VWF protects against cleavage by these proteases with the exception of thrombin [74–77]. This protection is mediated by two mechanisms First, VWF-bound FVIII is unable to bind to phospholipid or platelets [78,79], second, direct protease-binding sites within the FVIII light chain are hidden whilst FVIII is in complex with VWF [80,81]. This protection from proteolysis serves to increase FVIII circulatory life-span. The VWF-bound or -unbound state of FVIII modulates FVIII cellular LEE011 ic50 interactions and removal from the circulation. Several cellular receptors implicated in FVIII Doxorubicin molecular weight clearance have been described and extensively reviewed elsewhere (see [82]). In particular, the role of the low-density lipoprotein receptor-related

protein (LRP), a member of the LDLR family and its effects on FVIII clearance, have been studied in vitro and in vivo in murine model studies. LRP is a multifunctional scavenger receptor abundant in the liver that can bind to at least 30 ligands with high affinity [83]. FVIII can bind to LRP via the A3 1811–1818 region within light chain, and 484–509 region of the A2 domain within the heavy chain [84,85]. The latter site is cryptic and exposed only on activation of FVIII, whereas the LRP-binding site within the FVIII light chain is only exposed when FVIII is not bound to VWF [86]. VWF does not bind to LRP, and because of the higher affinity of FVIII for VWF, prevents binding of bound FVIII to the receptor, suggesting that LRP-mediated clearance is of minimal importance in the FVIII life-cycle. However an LRP-knockout mouse model

has a twofold increase in FVIII levels as compared with control mice, and an increased FVIII half-life, suggesting a significant role for LRP-related clearance mechanisms of FVIII [87]. A recent hypothesis to resolve this apparent contradiction has been suggested by Lenting et al. [88]. Because of high affinity of both molecules and the molar excess of VWF as compared with FVIII, almost all circulating FVIII is bound in complex with VWF. However a small (approximately 2%), but significant proportion circulates unbound, and it is this pool of free FVIII 上海皓元医药股份有限公司 that is cleared by LRP-mediated mechanisms. Moreover, clearance of the free FVIII results in a shift in the balance of bound and free FVIII, and a further release of FVIII from VWF [88]. The close association of FVIII and VWF levels and half-life suggests that the remaining FVIII is cleared as part of the VWF complex. Clearance of the VWF complex from the circulation remains an enigma, however very recent data has thrown some light on possible mechanisms. Studies of cell types within the liver and spleen demonstrate that isolated FVIII, VWF and FVIII–VWF complex can be endocytosed by macrophages within these organs [89].

26, 27 Liver is a sinusoid-enriched organ and thus may contain niche cells capable of sustaining HSCs. Still, in this study, the formal possibility cannot be excluded that these cells were blood HSPCs adherent to ABT-888 datasheet the endovascular compartment of the liver, which could not be perfused out. Moreover, after LT, either donor HSPCs generate mature HSCs inside grafted liver or circulate to recipient BM for hematopoiesis. These possibilities remain to be determined in future studies. The authors thank the Liver Transplantation Center at Queen Mary hospital of the University of Hong

Kong for outstanding clinical liver transplantation care. The authors also thank Ms. Kammy Yik, Banny Lam, and Waiyee Ho for data organization of LT donors and recipients. The authors also thank Dr. Mo Yang at the Department of Pediatrics and Adolescent Medicine of the University of Hong Kong for his useful help on the experiment. The authors also thank Ms Amy Lam Ixazomib and Mr. Jimmy Chen of Applied Biosystems for their technical support. “
“Surgery in the patient

with cirrhosis is problematic, as encephalopathy, ascites, sepsis and bleeding are common in the postoperative period. Accurate preoperative assessment and planning, and careful postoperative management have the potential to reduce the frequency and severity of such complications, and reduce the length of hospital stay, but there is little literature evidence to prove this. Operative mortality and other risks correlate

with the severity of the liver disease, co-morbidities and the type of surgery. The Child-Turcott-Pugh 上海皓元 (CTP) score or model for end-stage liver disease (MELD) score may be used to determine the severity of the liver disease, but must also take into account recent changes in the patient’s condition. Surgery that does not involve opening the peritoneum may have slightly better outcomes, as the risk of ascitic leak, sepsis and difficult fluid management are reduced. Mortality rates range from 10% in CTP-A patients to 82% in CTP-C patients. The presence of portal hypertension is an important negative predictor, especially in abdominal surgery, as refractory ascites may occur. Careful monitoring in the postoperative period and early intervention of complications are essential. Hepatic resections in cirrhosis are associated with other considerations such as leaving sufficient liver tissue to prevent liver failure, and are beyond the scope of this review. Surgical procedures in patients with liver cirrhosis carry a significant risk of complications and have a high mortality. Accurate preoperative risk stratification can be difficult, and occasionally the patient is only found to have cirrhosis at the time of surgery. Even when the patient has previously diagnosed liver disease, the severity may easily be miscalculated as many of the tools we use are imprecise. The literature in this field is sparse, and outdated with respect to contemporary surgical technology.

Liver disease, varices, and non-UGIH were excluded. Co-morbidities, medications, mortality, ASA Score, Glasgow Blatchford Score (GBS) and details Barasertib chemical structure of endoscopy (if performed) were examined. Results: There were 49 episodes over the period. The median age was 88.10 years. The main presentation of UGIH was malaena (44.90%). There were 30 episodes managed conservatively and 19 episodes which were managed through use of endoscopy. There was only 1 therapeutic endoscopy performed, with only 2 (10.53%, CI: ± 13.8%) being associated with a change in medical management of a patient. ASA score was similar between the 2 groups. An increasing ASA score was associated with an increased 30-day

mortality. A higher GBS did not correlate with an increase in 30-day mortality. Conclusion: Although the risks of endoscopy is low, its usefulness in elderly patients is limited and costly. Further studies are needed to HIF activation decide when it useful. ASA could be useful in determining those more at risk of dying within the next 30-days and potentially those with which it seems futile to perform endoscopy. Table 1: Endoscopic Benefits Endoscopy resulted in a change in management

10.53% (CI95: ±13.8%) Therapeutic endoscopy performed for UGIH 5.26% (CI95: ±10.04) CJ KIELY,1 J BENHAMU,2 TN EADE,2 V PATTULLO,1 D STIEL1 1Department of Gastroenterology and Hepatology, Royal North Shore Hospital, St Leonards, NSW, Australia, 2Department of Radiation Oncology, Royal North Shore Hospital, St Leonards, NSW, Australia Introduction: Concurrent chemoradiotherapy (CCRT) is standard of care for locally advanced head and neck cancers. Treatment related toxicities (mucositis, dysphagia, nausea, xerostomia and dysgeusia) result in malnutrition and can limit CRRT dosing and scheduling1. Prophylactic gastrostomy tube (GT) insertion prior to

CCRT for head and neck cancers is an option to avoid treatment related malnutrition and 上海皓元 potential treatment breaks, as compared to reactive nasogastric tube (NGT) insertion2. Although GTs are generally well tolerated3, there are limited data on their safety and utility 4–5. Aims: To evaluate the safety, efficacy and tolerability of prophylactic GT insertion for patients undergoing CCRT for head and neck cancers in a large tertiary hospital setting. Methods: Data were available for 45 patients referred for GT insertion between 2007 and 2012. Clinical, biometric, biochemical and histological data were collected prospectively. Results: Mean age at commencement of therapy was 57 years ± standard deviation 10.5, and mean pre-treatment body mass index (BMI) was 26.7±4.9 kg/m2. Thirty-five patients (78%) underwent endoscopic GT insertion, nine (20%) surgical and one (2%) radiological insertion. Five patients were deemed unsuitable at endoscopy, requiring a second procedure.

Furthermore, under these conditions CAV1 accumulates in the lipid droplet fraction in BVD-523 cell line wildtype mouse hepatocytes. Conclusion: Our data demonstrate that lack of CAV1 alters hepatocyte energy metabolism homeostasis under physiological and pathological conditions. (HEPATOLOGY 2011) Liver regeneration is a remarkably rapid and efficient process by which remnant hepatocytes, normally a quiescent population

of cells, proliferate and restore the hepatic mass lost after chemical injury or partial hepatectomy.1-3 Studies examining the role of caveolin-1 (CAV1) during liver regeneration after partial hepatectomy in mice have produced contradictory results.4, 5 Using CAV1−/− mice developed in the Kurzchalia Laboratory (KCAV1−/− mice6) our research concluded that CAV1 plays an

important role in the modulation of cellular processes during the first hours of liver regeneration.4 KCAV1−/− mice failed to undergo liver regeneration and to accumulate hepatic lipid droplets and progression through the Palbociclib cell cycle was arrested before entering S-phase in KCAV1−/− hepatocytes. As blood glucose and hepatic glycogen levels decrease a few hours after partial hepatectomy, hepatic lipid metabolism becomes essential for hepatocytes to undergo proliferation.7 Therefore, we postulated that CAV1 plays an important role in the modulation of lipid metabolism during liver regeneration in mice. Consistent with this hypothesis, we demonstrated that the wildtype phenotype is rescued by supplementing the diet of KCAV1−/− mice with glucose 上海皓元 prior to surgery and during regeneration. In contrast, a separate study in CAV1−/− outbred mice from Jackson Laboratories (JAXCAV1−/− mice) described that JAXCAV1−/− mice showed a higher index of regeneration than wildtype mice after partial hepatectomy and with no significant

effects on mouse survival after the operation, suggesting that CAV1 is not involved in liver regeneration.5 Here, by using three different strains of CAV1 null mice, we reassessed and confirmed the requirement of the expression of CAV1 in mice for efficient liver regeneration and lipid storage. 2-DG, 2-deoxy-glucose; ADRP, adipophilin; CAV1, caveolin-1; JAXCAV1−/−, mice provided by Jackson laboratory: KCAV1−/− and KCAV1+/+, CAV1 knockout and wildtype generated in the laboratory of Temo Kurzchalia; Balb/CCAV1−/− and Balb/CCAV1+/+ mice, CAV1 knockout and wildtype mice with a Balb/C genetic background; FASN, fatty acid synthase; G6PD, glucose-6-phosphate dehydrogenase; GyK, glycerol kinase; LD, lipid droplets; NEFA, nonesterified fatty acids; TAG, triacylglycerol; TLC, thin layer chromatography. KCAV1−/− mice were backcrossed onto a Balb/C background by mating KCAV1+/− females to wildtype Balb/C males (Animal Resources Centre, WA).

Furthermore, under these conditions CAV1 accumulates in the lipid droplet fraction in Alvelestat supplier wildtype mouse hepatocytes. Conclusion: Our data demonstrate that lack of CAV1 alters hepatocyte energy metabolism homeostasis under physiological and pathological conditions. (HEPATOLOGY 2011) Liver regeneration is a remarkably rapid and efficient process by which remnant hepatocytes, normally a quiescent population

of cells, proliferate and restore the hepatic mass lost after chemical injury or partial hepatectomy.1-3 Studies examining the role of caveolin-1 (CAV1) during liver regeneration after partial hepatectomy in mice have produced contradictory results.4, 5 Using CAV1−/− mice developed in the Kurzchalia Laboratory (KCAV1−/− mice6) our research concluded that CAV1 plays an

important role in the modulation of cellular processes during the first hours of liver regeneration.4 KCAV1−/− mice failed to undergo liver regeneration and to accumulate hepatic lipid droplets and progression through the http://www.selleckchem.com/products/abt-199.html cell cycle was arrested before entering S-phase in KCAV1−/− hepatocytes. As blood glucose and hepatic glycogen levels decrease a few hours after partial hepatectomy, hepatic lipid metabolism becomes essential for hepatocytes to undergo proliferation.7 Therefore, we postulated that CAV1 plays an important role in the modulation of lipid metabolism during liver regeneration in mice. Consistent with this hypothesis, we demonstrated that the wildtype phenotype is rescued by supplementing the diet of KCAV1−/− mice with glucose MCE公司 prior to surgery and during regeneration. In contrast, a separate study in CAV1−/− outbred mice from Jackson Laboratories (JAXCAV1−/− mice) described that JAXCAV1−/− mice showed a higher index of regeneration than wildtype mice after partial hepatectomy and with no significant

effects on mouse survival after the operation, suggesting that CAV1 is not involved in liver regeneration.5 Here, by using three different strains of CAV1 null mice, we reassessed and confirmed the requirement of the expression of CAV1 in mice for efficient liver regeneration and lipid storage. 2-DG, 2-deoxy-glucose; ADRP, adipophilin; CAV1, caveolin-1; JAXCAV1−/−, mice provided by Jackson laboratory: KCAV1−/− and KCAV1+/+, CAV1 knockout and wildtype generated in the laboratory of Temo Kurzchalia; Balb/CCAV1−/− and Balb/CCAV1+/+ mice, CAV1 knockout and wildtype mice with a Balb/C genetic background; FASN, fatty acid synthase; G6PD, glucose-6-phosphate dehydrogenase; GyK, glycerol kinase; LD, lipid droplets; NEFA, nonesterified fatty acids; TAG, triacylglycerol; TLC, thin layer chromatography. KCAV1−/− mice were backcrossed onto a Balb/C background by mating KCAV1+/− females to wildtype Balb/C males (Animal Resources Centre, WA).