There are now also enhanced endoscopic techniques, such as narrow

There are now also enhanced endoscopic techniques, such as narrow band imaging and i-scan, which make the assessment of this finding much easier. In the present study, we found that the moderate-to-severe EGA had a high sensitivity and negative predictive value for the diagnosis of high-stage gastritis. More than half of the patients in the present study would have been effectively excluded from taking systemic map biopsies if this criterion had HSP inhibitor review been applied. As the prevalence of high-stage gastritis is very low, even in high-risk populations,7 the positive predictive value of this endoscopic finding was also low. The specificity of this finding was just

57.7%, which means that many patients with moderate-to-severe EGA might have OLGA gastritis stages 0–II, and the assessment of EGA cannot replace pathological gastritis staging as the gold standard of atrophy. Because previous studies have shown that moderate-to-severe EGA is related to a high risk of developing gastric cancer,2,4 adding OLGA gastritis staging could further stratify these patients into subgroups with different risk levels of developing gastric cancer. Regarding dysplastic lesions,

Kokkola et al. reported that 68% (57/84) of mild dysplastic lesions in the stomach had no visible endoscopic findings and were only detected by random biopsy specimens.24 Low-grade dysplastic lesions in the present study, not surprisingly, also shared the same characteristics.

The detection and surveillance of these Selleckchem Crizotinib lesions are crucial, as a recent study, which is based on data from the Dutch nation-wide histopathology registry, reported that the annual incidence of medchemexpress gastric cancer was 0.6% in the first 5 years.25 Interestingly, the present study showed that 85.7% (6/7) of the dysplastic lesions, like high-stage gastritis, also clustered in patients with moderate-to-severe EGA (P = 0.028). Although moderate-to-severe EGA has been shown to be a risk factor of gastric cancer in several studies,2,4,5 the pathological results of the present study showed that patients with this endoscopic finding could be further stratified into subgroups with different risk levels of gastric cancer. In our opinion, a detailed baseline pathological examination should be carried out in all of these patients, so that individualized follow-up frequencies can be defined for each subgroup. To conclude, moderate-to-severe EGA has a high sensitivity and negative predictive value for high-stage OLGA gastritis. As gastric neoplastic lesions cluster in patients with high-stage gastritis, this endoscopic finding could select the subgroup of patients who will benefit from taking systemic map biopsies and the appropriate candidates for a potentially cost-effective surveillance program in regions with low-to-moderate incidence of gastric cancer.

In addition, LSLs that had interacted with tumor-activated LSECs

In addition, LSLs that had interacted with tumor-activated LSECs in vivo decreased their antitumor cytotoxicity and interferon (IFN)-gamma secretion while they increased IL-10 release ex vivo. IFN-gamma/IL-10 ratio also decreased in the hepatic blood from tumor-injected mice. Immunosuppressant effects of tumor-activated LSECs on LSLs were abrogated in both LSECs from ManR−/− mice and tumor-activated LSECs

given anti-mouse ManR antibodies. Conclusion: ICAM-1–induced tumor COX-2 decreased antitumor activity during hepatic metastasis through Proteasome assay IL-1–induced ManR. ManR constituted a common mediator for prometastatic effects of IL-1, COX-2, and ICAM-1. A rise in hepatic IFN-gamma/IL-10 ratio and antitumor cytotoxicity by way of ManR blockade is consistent with the antimetastatic effects of IL-1, COX-2, and ICAM-1 inhibitors. These data support ManR and ManR-stimulating factors as targets for hepatic colorectal metastasis

therapy. Hepatology 2010;51:2172–2182 The specific blockade of major proinflammatory cytokines inhibits experimental hepatic metastasis, suggesting that inflammation-dependent mechanisms have prometastatic effects.1, 2 However, because inflammatory mediators also play an important role in the regulation of antitumor activity, the connection between inflammation and cancer progression3 deserves further attention. In 上海皓元医药股份有限公司 the liver, interleukin (IL)-1 up-regulates the endocytic activity of the RAD001 in vivo mannose receptor (ManR) expressed by liver sinusoidal endothelial

cells (LSECs).4, 5 ManR mediates uptake of glycoconjugates carrying mannose in an end position.6 Interestingly, this receptor uses a different binding domain to take up blood-borne collagen alpha chains,7, 8 and contributes to the adhesion of cancer cells to LSECs.9-11 Furthermore, ManR is involved in antigen uptake, processing, and presentation to T cells by LSECs,12 and it has been suggested that this process diminishes local immune response of the liver.13 However, it is not known how ManR is regulated during the hepatic microvascular infiltration of cancer cells. Furthermore, the contribution of ManR to antitumor defense mechanisms during hepatic metastasis is also unknown. Based on the inflammatory status of tumor-infiltrated hepatic sinusoids and the inflammatory regulation of hepatic ManR-mediated endocytosis, we hypothesized that IL-1–induced ManR-mediated endocytosis might contribute to prometastatic effects of tumor-activated LSECs via antitumor activity inhibition. This would be consistent with our previous observations demonstrating that experimental hepatic metastasis is promoted by IL-1,1, 9 that ManR-mediated endocytosis is up-regulated by this cytokine,4, 5 and that ManR-mediated LSEC activation increases metastasis through IL-1.

However, not all recipients are able to maintain sobriety Alcoho

However, not all recipients are able to maintain sobriety. Alcohol relapse can have a number of negative impacts, including: (i) liver dysfunction secondary to alcohol toxicity; (ii) non-compliance with medications or clinic visits; (iii) rejection secondary to non-compliance; (iv) graft failure secondary to rejection or alcohol toxicity; and (v) malignancies and cardiovascular diseases possibly related to smoking, which is highly associated with alcohol relapse.[2] The perception that recipients will relapse may also decrease the willingness of others to donate organs. Reports have differed in both the definitions

Selleck Tyrosine Kinase Inhibitor Library used for harmful drinking and its effects after LT. Shmeding et al. and Cuadrado et al. defined problem drinking by amount of alcohol[5, 6] and showed significantly lower survival in patients with problem drinking. On the other hand, Pageaux et al. reported no significant difference in

actual survival among heavy drinkers, occasional drinkers and abstinent patients.[7] De ABT-263 order Gottardi et al. defined harmful drinking as existence of alcohol-related damages like our definition and found no significant difference in patient survival.[3] In this study, we tried to minimize the effects of differences in follow-up periods and alcohol consumption periods, and defined problem drinking by the existence of final damages related to alcohol consumption. Although there are still limitations, the impact on survival and risk factors of harmful drinking were revealed in this study.

Pretransplant abstinence shorter than 18 months and smoking after transplantation were significant indicators for harmful relapse. Webb et al. noted that resumption of problem drinking can lead to non-compliance with the transplant medchemexpress follow-up program,[8] which can in turn lead to rejection. In our study, the incidence of non-compliance with immunosuppressant was significantly greater in patients with harmful relapse in univariate analysis but the incidence was not significant in multivariate analysis. Our previous report showed similar incidence of rejection between patients with abstinence and recidivism.[2] However, this finding is important to construct the best follow-up program after LT for ALC. Cuadrado et al. reported significantly lower patient survival in patients with alcohol relapse and suggested that alcohol consumption and tobacco use might have contributed to the cancer and cardiovascular events that were frequent causes of death.[6] In our study, one patient with harmful relapse died due to myocardial infarction, one patient with abstinence died due to subarachnoid hemorrhage, and four patients with abstinence and one patient with non-harmful relapse died due to malignancies. Post-transplant smoking was significantly often associated with harmful relapse. Careful follow up focusing on malignancy and cardiovascular complications is recommended after LT for ALC.

However, not all recipients are able to maintain sobriety Alcoho

However, not all recipients are able to maintain sobriety. Alcohol relapse can have a number of negative impacts, including: (i) liver dysfunction secondary to alcohol toxicity; (ii) non-compliance with medications or clinic visits; (iii) rejection secondary to non-compliance; (iv) graft failure secondary to rejection or alcohol toxicity; and (v) malignancies and cardiovascular diseases possibly related to smoking, which is highly associated with alcohol relapse.[2] The perception that recipients will relapse may also decrease the willingness of others to donate organs. Reports have differed in both the definitions

see more used for harmful drinking and its effects after LT. Shmeding et al. and Cuadrado et al. defined problem drinking by amount of alcohol[5, 6] and showed significantly lower survival in patients with problem drinking. On the other hand, Pageaux et al. reported no significant difference in

actual survival among heavy drinkers, occasional drinkers and abstinent patients.[7] De BYL719 manufacturer Gottardi et al. defined harmful drinking as existence of alcohol-related damages like our definition and found no significant difference in patient survival.[3] In this study, we tried to minimize the effects of differences in follow-up periods and alcohol consumption periods, and defined problem drinking by the existence of final damages related to alcohol consumption. Although there are still limitations, the impact on survival and risk factors of harmful drinking were revealed in this study.

Pretransplant abstinence shorter than 18 months and smoking after transplantation were significant indicators for harmful relapse. Webb et al. noted that resumption of problem drinking can lead to non-compliance with the transplant MCE follow-up program,[8] which can in turn lead to rejection. In our study, the incidence of non-compliance with immunosuppressant was significantly greater in patients with harmful relapse in univariate analysis but the incidence was not significant in multivariate analysis. Our previous report showed similar incidence of rejection between patients with abstinence and recidivism.[2] However, this finding is important to construct the best follow-up program after LT for ALC. Cuadrado et al. reported significantly lower patient survival in patients with alcohol relapse and suggested that alcohol consumption and tobacco use might have contributed to the cancer and cardiovascular events that were frequent causes of death.[6] In our study, one patient with harmful relapse died due to myocardial infarction, one patient with abstinence died due to subarachnoid hemorrhage, and four patients with abstinence and one patient with non-harmful relapse died due to malignancies. Post-transplant smoking was significantly often associated with harmful relapse. Careful follow up focusing on malignancy and cardiovascular complications is recommended after LT for ALC.

However, not all recipients are able to maintain sobriety Alcoho

However, not all recipients are able to maintain sobriety. Alcohol relapse can have a number of negative impacts, including: (i) liver dysfunction secondary to alcohol toxicity; (ii) non-compliance with medications or clinic visits; (iii) rejection secondary to non-compliance; (iv) graft failure secondary to rejection or alcohol toxicity; and (v) malignancies and cardiovascular diseases possibly related to smoking, which is highly associated with alcohol relapse.[2] The perception that recipients will relapse may also decrease the willingness of others to donate organs. Reports have differed in both the definitions

DAPT in vivo used for harmful drinking and its effects after LT. Shmeding et al. and Cuadrado et al. defined problem drinking by amount of alcohol[5, 6] and showed significantly lower survival in patients with problem drinking. On the other hand, Pageaux et al. reported no significant difference in

actual survival among heavy drinkers, occasional drinkers and abstinent patients.[7] De Opaganib mw Gottardi et al. defined harmful drinking as existence of alcohol-related damages like our definition and found no significant difference in patient survival.[3] In this study, we tried to minimize the effects of differences in follow-up periods and alcohol consumption periods, and defined problem drinking by the existence of final damages related to alcohol consumption. Although there are still limitations, the impact on survival and risk factors of harmful drinking were revealed in this study.

Pretransplant abstinence shorter than 18 months and smoking after transplantation were significant indicators for harmful relapse. Webb et al. noted that resumption of problem drinking can lead to non-compliance with the transplant 上海皓元医药股份有限公司 follow-up program,[8] which can in turn lead to rejection. In our study, the incidence of non-compliance with immunosuppressant was significantly greater in patients with harmful relapse in univariate analysis but the incidence was not significant in multivariate analysis. Our previous report showed similar incidence of rejection between patients with abstinence and recidivism.[2] However, this finding is important to construct the best follow-up program after LT for ALC. Cuadrado et al. reported significantly lower patient survival in patients with alcohol relapse and suggested that alcohol consumption and tobacco use might have contributed to the cancer and cardiovascular events that were frequent causes of death.[6] In our study, one patient with harmful relapse died due to myocardial infarction, one patient with abstinence died due to subarachnoid hemorrhage, and four patients with abstinence and one patient with non-harmful relapse died due to malignancies. Post-transplant smoking was significantly often associated with harmful relapse. Careful follow up focusing on malignancy and cardiovascular complications is recommended after LT for ALC.


“Background and Aim:  The objective of this 11-year cohort


“Background and Aim:  The objective of this 11-year cohort retrospective study conducted in adult patients with chronic hepatitis C virus (HCV) who underwent liver transplantation (LT) was to identify whether human leukocyte antigen (HLA) mismatching is associated with the recurrence of HCV and with the time to recurrence of HCV. Methods:  Among the 181 patients (74% men; mean age: 54 years, range 25–71) who underwent a LT between 1995 and 2006 in the study center, 163 had relevant data in their medical

chart documenting HCV recurrence, and 107 (65.64%) reported a histological evidence of HCV recurrence. Results:  Survival was 78% at 5 years. There was no significant relationship between the total score of HLA-mismatches and the recurrence of HCV. Similarly, there was no significant relationship HM781-36B manufacturer between the total score of HLA mismatches and the time to recurrence of HCV. For the analyses at each individual locus, a significant relationship selleck compound between the individual scores of HLA-mismatches and the recurrence of HCV were observed. Out of the 40 patients who experienced a rejection, the rate of recurrence was not different according to the severity of the rejection (75% mild, 64% moderate and 64% for severe rejection). Conclusions:  In conclusion, this

large study did not demonstrate any relationship between the total score of HLA mismatches and HCV-recurrence. Contrarily a significant relationship between the individual MCE公司 scores of HLA mismatches (HLA-A3, HLA-B35, HLA-DR3, HLA-DR7, HLA-DQ2, HLA-DQ2-0) and the recurrence of HCV were observed. “
“The anti-inflammatory and antiapoptotic heme degrading enzyme heme oxygenase-1 (HO-1) has been shown recently to interfere with replication of hepatitis C virus (HCV). We investigated the effect of HO-1 products carbon monoxide (CO), iron and biliverdin on HCV replication using the replicon cell lines Huh-5-15 and LucUbiNeo-ET, stably expressing HCV proteins NS3 through NS5B. Incubation of these cell lines in the presence of the CO donor methylene chloride transiently reduced HCV

replication, whereas an increase of iron in cell culture by administration of FeCl3 or iron-saturated lactoferrin did not interfere with HCV replication. Likewise, depletion of iron by deferoxamine during induction of HO-1 by cobalt-protoporphyrin IX did not restore HCV replication. The most prominent effect was observed after incubation of replicon cell lines in the presence of biliverdin. Biliverdin seems to interfere with HCV replication–mediated oxidative stress by inducing expression of antiviral interferons, such as interferon alpha2 and alpha17. Conclusion: The antioxidant biliverdin reduces HCV replication in vitro by triggering the antiviral interferon response and might improve HCV therapy in the future. (HEPATOLOGY 2009.) Hepatitis C virus (HCV) infection represents one of the leading causes of chronic hepatitis worldwide, resulting in cirrhosis, steatosis, and hepatocellular carcinoma.

The general literature was reviewed for articles in English descr

The general literature was reviewed for articles in English describing temperatures achievable in the skin and IA space using clinically relevant ice protocols, and the effect of cooling on haemostasis and coagulation. The literature demonstrates that typical methods of ice application can cool both the Selleckchem Dinaciclib skin and IA space. Published, general literature studies have also consistently demonstrated that experimental cooling of blood and/or tissue, both in vitro and in vivo in humans and in animal models, can significantly impair coagulation and prolong bleeding. In PWH with acute haemarthrosis, ice application has potential to increase haemorrhage morbidity by further

impairing coagulation and haemostasis. Ice has not been shown to improve overall outcome, stop bleeding nor swelling from haemarthrosis. Although ice can help manage acute, haemarthrosis-related pain, there are other available interventions that will not impair coagulation and haemostasis. “
“Summary.  Joint bleeding, or haemarthrosis, is the most common type of bleeding episode experienced

by individuals LY294002 cost with haemophilia A and B. This leads to changes within the joints, including synovial proliferation, which results in further bleeding and chronic synovitis. Blood in the joint can also directly damage the cartilage, and with repeated bleeding, there is progressive destruction of both cartilage and bone. The end result is known as haemophilic arthropathy which is characterized by pain, stiffness and deformity. The

joint most commonly affected is the knee. Haemophilic arthropathy can be prevented through regular prophylaxis and physiotherapy. However, when necessary, there are multiple surgical and non-surgical options available. These procedures are indicated to improve the joint function and quality of life for haemophilic patients worldwide. In this review, the role of surgical and non-surgical treatment of advanced knee arthropathy and its complications will be described. Haemophilia A and B are X-linked coagulation disorders caused by the deficiency of factor VIII (FVIII) MCE公司 and factor IX (FIX) respectively. The degree of clotting factor deficiency influences the phenotype and in the severe form of the disease (FVIII/FIX < 1 IU dL−1) spontaneous bleedings occurring into joints and muscles represent the more common manifestations of these diseases [1]. This presence of blood within the joint has also been shown to damage articular cartilage directly [2]. Recurrent bleeding into joints causes synovial proliferation and neoangiogenesis, increasing the joint’s susceptibility to further bleeding and leading to the development of so called ‘target joints’ [3,4]. Iron from repeated haemarthroses accumulates in the synovium and promotes a cytokine-mediated inflammatory response leading to the progressive destruction of both cartilage and bone [5,6].

, 2000; Therrien, 2005; Wroe, McHenry & Thomason, 2005; Christian

, 2000; Therrien, 2005; Wroe, McHenry & Thomason, 2005; Christiansen, 2006; Slater & Van Valkenburgh, 2008; Meloro Selleck INCB024360 & Slater, 2012). However, it is difficult to evaluate these hypotheses without a living analogue. The clouded leopards, Neofelis spp., seem to show skull features considered to be characteristic of the primitive sabretooth condition (Christiansen, 2006, 2008). Unfortunately, little is known of their ecology and hunting behaviour (Nowak, 1991; Sunquist & Sunquist, 2002; Grassman et al., 2005; Christiansen, 2006, 2008). Moreover, other morphometric analyses failed to find much similarity between

extant Neofelis nebulosa and sabretoothed carnivores (Slater & Van Valkenburgh, 2008). In another study (Goswami, Milne & Wroe,

2010), N. nebulosa clustered with the nimravids Dinictis and Hoplophoenus, but not the other sabretooths. Therefore, the status of N. nebulosa is controversial, but still it is one of the very few living analogues of the primitive Doxorubicin cost sabretooth previously proposed. To speculate about the hunting behaviour of primitive sabretooth cats, Christiansen (2006) used N. nebulosa and considered available evidence of killing large prey (Rabinowitz, Andau & Chai, 1987; Grassman et al., 2005) and each other (Seager & Demorest, 1978) with a powerful nape bite and suggested the following: ‘It may be that its enlarged gape and hypertrophied MCE canines are an adaptation for nape killing of large prey, but this is, at present, speculation’. Christiansen (2011), based on a dynamic model,

speculated about mandibular adductor histochemistry and morphology in sabrecats. But all these ideas would remain speculations ‘… until a Pleistocene sabrecat is unearthed from the permafrost, as have been numerous proboscideans and other megaherbivores’ (Christiansen, 2011). Until a frozen Pleistocene sabrecat is found, a strategy to test ideas about killing behaviour, mandibular adductor histochemistry and morphology is to identify a living primitive sabretooth analogue that allows further study. The sabretooth ecomorphology originated not only in the order Carnivora, but also among predatory marsupials such as the borhyaenids (see, e.g. Blanco, Jones & Grinspan, 2011 and references therein). The living predatory marsupials are the didelphids and dasyurids; among them we found the southern short-tailed opossum Monodelphis dimidiata, a very small species. Monodelphis dimidiata is a grassland-dwelling opossum from Uruguay, Argentina and Brazil. The species presents sexual dimorphism, adult male body mass is between 100 and 150 g and adult female body mass is between 30 and 70 g (González, 2001). The diet in the wild includes plants, insects, arachnids and small rodents.

, 2000; Therrien, 2005; Wroe, McHenry & Thomason, 2005; Christian

, 2000; Therrien, 2005; Wroe, McHenry & Thomason, 2005; Christiansen, 2006; Slater & Van Valkenburgh, 2008; Meloro Napabucasin solubility dmso & Slater, 2012). However, it is difficult to evaluate these hypotheses without a living analogue. The clouded leopards, Neofelis spp., seem to show skull features considered to be characteristic of the primitive sabretooth condition (Christiansen, 2006, 2008). Unfortunately, little is known of their ecology and hunting behaviour (Nowak, 1991; Sunquist & Sunquist, 2002; Grassman et al., 2005; Christiansen, 2006, 2008). Moreover, other morphometric analyses failed to find much similarity between

extant Neofelis nebulosa and sabretoothed carnivores (Slater & Van Valkenburgh, 2008). In another study (Goswami, Milne & Wroe,

2010), N. nebulosa clustered with the nimravids Dinictis and Hoplophoenus, but not the other sabretooths. Therefore, the status of N. nebulosa is controversial, but still it is one of the very few living analogues of the primitive see more sabretooth previously proposed. To speculate about the hunting behaviour of primitive sabretooth cats, Christiansen (2006) used N. nebulosa and considered available evidence of killing large prey (Rabinowitz, Andau & Chai, 1987; Grassman et al., 2005) and each other (Seager & Demorest, 1978) with a powerful nape bite and suggested the following: ‘It may be that its enlarged gape and hypertrophied MCE canines are an adaptation for nape killing of large prey, but this is, at present, speculation’. Christiansen (2011), based on a dynamic model,

speculated about mandibular adductor histochemistry and morphology in sabrecats. But all these ideas would remain speculations ‘… until a Pleistocene sabrecat is unearthed from the permafrost, as have been numerous proboscideans and other megaherbivores’ (Christiansen, 2011). Until a frozen Pleistocene sabrecat is found, a strategy to test ideas about killing behaviour, mandibular adductor histochemistry and morphology is to identify a living primitive sabretooth analogue that allows further study. The sabretooth ecomorphology originated not only in the order Carnivora, but also among predatory marsupials such as the borhyaenids (see, e.g. Blanco, Jones & Grinspan, 2011 and references therein). The living predatory marsupials are the didelphids and dasyurids; among them we found the southern short-tailed opossum Monodelphis dimidiata, a very small species. Monodelphis dimidiata is a grassland-dwelling opossum from Uruguay, Argentina and Brazil. The species presents sexual dimorphism, adult male body mass is between 100 and 150 g and adult female body mass is between 30 and 70 g (González, 2001). The diet in the wild includes plants, insects, arachnids and small rodents.

Interestingly, mRNA levels of Fsp27 in ob/ob hepatocytes and AML1

Interestingly, mRNA levels of Fsp27 in ob/ob hepatocytes and AML12 cells were not affected by FA treatment, but were significantly enhanced by PPAR agonists (Fig. 5A,B). Cideb expression was not affected by treatment with FAs or PPAR agonists (Supporting Fig. 6A,B). In addition, the expression level of Cidea (but not Fsp27 and Cideb) was up-regulated in the primary hepatocytes that were isolated from mice treated with an HFD for 2 days and incubated with saturated FAs (Fig. 5C and Supporting Fig. 6C). Consistent with increased gene expression, Cidea protein levels were higher in ob/ob hepatocytes treated with saturated FAs relative to the control cells (Fig. 5D and Supporting Fig. 6D). Fsp27

protein levels were also increased in cells treated with PPAR agonists (Fig. RG7420 price 5D and Supporting Fig. 6E). Interestingly, despite no effects on inducing Cidea mRNA level, OAs, LAs, and LNAs were able to increase Cidea and Fsp27 protein levels (Fig. 5D and Supporting Fig. 6D,E), suggesting a post-transcriptional regulation of Cidea and Fsp27 by these FAs.

find more Overall, these data indicated that gene expression of the CIDE family members was differentially regulated by dietary FAs and PPAR agonists, and that Cidea expression was specifically induced by saturated FAs. To identify the transcription factor(s) responsible for saturated FA-induced Cidea expression in hepatocytes, we checked expression levels of several key transcriptional regulators in livers of HFD-fed mice. We observed that levels of hepatic SREBP1c mRNA and its downstream target genes (i.e., FAS and ACC1) were increased in animals fed with HFDs for 2 days and continued to increase with HFD treatment (Fig. 6A

and Supporting Fig. 7A), which correlated well with the increased Cidea expression. In addition, protein levels of the mature nuclear form of SREBP1c were significantly increased in livers 上海皓元医药股份有限公司 of HFD-fed mice (Fig. 6A and Supporting Fig. 7C). mRNA levels and its nuclear form of SREBP1c were also increased in ob/ob hepatocytes treated with PAs and SAs (Fig. 6B and Supporting Fig. 7D). Hepatic expression of other transcriptional regulators, including SREBP2, PPARα, and liver X receptor alpha, were not affected by HFD treatment (Supporting Fig. 7B). The strong correlation between expression levels of SREBP1c and Cidea suggests that SREBP1c may serve as a transcriptional activator for saturated FA-induced Cidea expression. To test this hypothesis, we first overexpressed SREBP1c in AML12 cells and observed that Cidea (but not Fsp27 and Cideb) expression was significantly increased (Supporting Fig. 8A). The addition of PAs further enhanced this expression (Supporting Fig. 8A). Next, we knocked down SREBP1c in ob/ob hepatocytes (an 80% reduction in mRNA levels; Supporting Fig. 8B) and observed that mRNA levels of FAS, one of its downstream targets, were also reduced (Supporting Fig. 8B).