me/ir2eb) “
“Contrary to widely held opinion, the headache

disorder we term “migraine” is not clinically stereotyped. The symptoms of a migraine attack may vary dramatically between afflicted individuals, and even in a given individual symptoms http://www.selleckchem.com/autophagy.html may be quite different from attack to attack. While on Monday you may experience the severe, one-sided, and throbbing headache (with associated nausea and vomiting) typical of “classical” migraine, Saturday’s migraine attack instead may involve a dull, generalized, and low-intensity headache absent any nausea but accompanied by the visual symptoms known as “aura.” The attacks’ symptoms are quite different – the headaches themselves are quite different – but both attacks are SP600125 “migraine. Not only do the symptoms

of migraine tend to vary from attack to attack, but even within a single attack there may occur a progression of symptoms. Acute migraine is dynamic, both in terms of symptomatology and the biologic process that produces those symptoms; if that process is allowed to progress unchecked for too long, the symptoms it generates can become quite difficult to treat. The concept of stratified care acknowledges the dynamic nature of an evolving migraine attack, and use of a stratified care approach to treatment of acute migraine implies that one selects his/her therapy based upon the headache’s intensity and the presences vs absence of associated symptoms (eg, nausea and vomiting). Very few migraineurs find that a single medication or alternative therapy is effective

for all their migraine headaches. For example, “three aspirin and a cup of coffee” may represent perfectly appropriate (and effective) therapy for early/mild migraine, but this treatment makes little sense if the headache is severe and accompanied by vomiting. For the migraineur’s therapeutic Vasopressin Receptor arsenal, it is often ideal to have two or three different therapies available for acute migraine treatment: (1) something for early/mild headache; (2) something for headaches that have escalated despite treatment with #1 or that have escalated rapidly to become moderate to severe (eg, “full-blown” migraine already present upon awakening); and (3) a “rescue” therapy if #2 fails. With this “stratified” approach, you hopefully will find yourself far more capable of controlling your acute migraine attacks. “
“Broad discrepancies in the number of migraine triggers have been reported in several studies. Migraineurs do not seem to recognize easily headache triggers in clinical practice. To evaluate how aware migraineurs are about their headache triggers. We recruited 120 consecutive migraineurs. Each patient was first asked to report spontaneously any migraine trigger. Subsequently, the patient selected from a list of commonly known triggers. Ninety-seven patients (72.

me/ir2eb) “
“Contrary to widely held opinion, the headache

disorder we term “migraine” is not clinically stereotyped. The symptoms of a migraine attack may vary dramatically between afflicted individuals, and even in a given individual symptoms Fostamatinib may be quite different from attack to attack. While on Monday you may experience the severe, one-sided, and throbbing headache (with associated nausea and vomiting) typical of “classical” migraine, Saturday’s migraine attack instead may involve a dull, generalized, and low-intensity headache absent any nausea but accompanied by the visual symptoms known as “aura.” The attacks’ symptoms are quite different – the headaches themselves are quite different – but both attacks are Compound Library order “migraine. Not only do the symptoms

of migraine tend to vary from attack to attack, but even within a single attack there may occur a progression of symptoms. Acute migraine is dynamic, both in terms of symptomatology and the biologic process that produces those symptoms; if that process is allowed to progress unchecked for too long, the symptoms it generates can become quite difficult to treat. The concept of stratified care acknowledges the dynamic nature of an evolving migraine attack, and use of a stratified care approach to treatment of acute migraine implies that one selects his/her therapy based upon the headache’s intensity and the presences vs absence of associated symptoms (eg, nausea and vomiting). Very few migraineurs find that a single medication or alternative therapy is effective

for all their migraine headaches. For example, “three aspirin and a cup of coffee” may represent perfectly appropriate (and effective) therapy for early/mild migraine, but this treatment makes little sense if the headache is severe and accompanied by vomiting. For the migraineur’s therapeutic Idelalisib chemical structure arsenal, it is often ideal to have two or three different therapies available for acute migraine treatment: (1) something for early/mild headache; (2) something for headaches that have escalated despite treatment with #1 or that have escalated rapidly to become moderate to severe (eg, “full-blown” migraine already present upon awakening); and (3) a “rescue” therapy if #2 fails. With this “stratified” approach, you hopefully will find yourself far more capable of controlling your acute migraine attacks. “
“Broad discrepancies in the number of migraine triggers have been reported in several studies. Migraineurs do not seem to recognize easily headache triggers in clinical practice. To evaluate how aware migraineurs are about their headache triggers. We recruited 120 consecutive migraineurs. Each patient was first asked to report spontaneously any migraine trigger. Subsequently, the patient selected from a list of commonly known triggers. Ninety-seven patients (72.

13 Although these estimates are convenient in large-scale epidemiologic studies,14 they have significant limitations that affect their reliability; for example, HOMA-IR coefficient of variation can exceed 30%13 and can be affected by degrees of obesity and by ethnicity.14-17 In addition, the HOMA-IR

cutoff values used to define insulin resistance in the HCV literature vary significantly, ranging from 1.5 to >3.6, 18 These cutoff values are either arbitrarily defined9, 11, 19 or derived from non-HCV populations which are often heterogeneous without a comprehensive description of the population, have small sample size, include diabetics, and have limited criteria for excluding presence of liver disease.10, learn more 18, 20 Furthermore, even within the HCV population, there is a large variation in the reported mean HOMA-IR values ranging from 1 to >3.10, 21, 22 Reliability of surrogate estimates is essential in interpreting the reported conclusions in the literature such as prevalence of insulin resistance and its impact on the

natural history and treatment of HCV. Moreover, identification of a reliable surrogate estimate of insulin resistance is needed as direct measurements can be impractical and costly when evaluating large populations. The gold standards for direct physiologic measurement of insulin resistance are the validated hyperinsulinemic euglycemic clamp test and insulin suppression test.23 see more Despite the known limitations of the surrogate estimates in other populations,

no study has evaluated the reliability and accuracy of these markers in comparison to the direct measurement of insulin resistance in the HCV population. In this study, we evaluated the correlation between the directly measured resistance to insulin mediated glucose uptake during insulin suppression test and surrogate estimates of insulin resistance in a large, ethnically diverse, nondiabetic HCV population. In addition, we evaluated the impact of obesity and ethnicity on the relationship between the direct measurement and the surrogate estimates. As HOMA-IR is the most MRIP commonly used estimate of insulin resistance in the HCV population, we addressed misclassification rates using different HOMA-IR cutoff values as well as the within-person variation of HOMA-IR estimates from repeat measurements. G-AUC, glucose area under the curve during oral glucose tolerance test; HOMA-IR, homeostasis model assessment of insulin resistance; I-AUC, insulin area under the curve during oral glucose tolerance test; IMGU, insulin-mediated glucose uptake; OGTT, oral glucose tolerance test; QUICKI, quantitative insulin sensitivity check index; SFGH, San Francisco General Hospital; SSPG, steady-state plasma glucose concentration; SSPI, steady-state plasma insulin concentration; UCSF, University of California San Francisco.

20 reported that injection of 5 × 1010 particles of IL-22 adenovirus resulted

in serum levels of 35,000-95,000 pg/mL IL-22 and causes hematological changes, loss of body weight, STI571 and thymic atrophy, whereas we have previously shown that injection of 2 × 108 particles of IL-22 adenovirus resulted in serum levels of 5,000 pg/mL IL-22 (similar to those in liver-specific IL-22TG mice) and did not induce obvious adverse phenotypes.14 These findings suggest that only very high doses of IL-22 may cause severe adverse phenotypes. However, it is unlikely that therapeutic application of IL-22 will reach such high concentrations of IL-22 (35,000-95,000 pg/mL) in the serum reported in the study by Liang et al.20 Regardless, monitoring IL-22 levels will be important in any therapeutic applications. Although the hepatoprotection of IL-22 is well documented,12-14 the role of IL-22 in liver inflammation remains obscure. Liang et al20 reported that a single injection of IL-22 up-regulated expression of CXCL1 in the liver, followed by a transient increase in circulating neutrophils, Fulvestrant cell line suggesting IL-22 may promote liver inflammation. In contrast, blockage of IL-22

either through using a neutralizing antibody12 or genetic deletion13 exacerbated inflammation, whereas treatment with IL-2212 or overexpression of IL-22 (the current study) ameliorated ConA-induced liver inflammation, indicating IL-22 suppresses liver inflammation in this model. It is plausible that IL-22 plays dual roles in controlling liver inflammation: promoting liver inflammation by stimulating hepatocytes to produce

acute phase proteins and chemokines, and inhibiting liver inflammation by preventing hepatocyte damage and subsequently reducing necrosis-associated liver inflammation. The final effect of IL-22 on liver inflammation is likely determined by the balance between the proinflammatory and anti-inflammatory effects of IL-22 and is dependent on the types of liver diseases and liver injury models. A previous study reported that the expression of hepatic IL-22 messenger RNA was up-regulated in patients with viral hepatitis.23 Here we demonstrate that IL-22+ immune cells are accumulated in the livers of patients with viral hepatitis (Fig. 1); however, the types of inflammatory Vitamin B12 cells responsible for IL-22 production in viral hepatitis patients remain obscure. Because Th17, Th22, natural killer, and natural killer T cells, which are known to produce IL-22,2-4 are elevated in the livers in patients with viral hepatitis,24-26 these cells likely contribute to hepatic IL-22 expression in the patients. Further studies are needed to confirm this assessment. The next obvious question is how IL-22 up-regulation might affect the progression of viral hepatitis disease progression. First, it has been reported that IL-22 does not inhibit HCV replication in vitro,23 suggesting that elevated IL-22 may not affect HCV replication directly.

20 reported that injection of 5 × 1010 particles of IL-22 adenovirus resulted

in serum levels of 35,000-95,000 pg/mL IL-22 and causes hematological changes, loss of body weight, PLX4032 price and thymic atrophy, whereas we have previously shown that injection of 2 × 108 particles of IL-22 adenovirus resulted in serum levels of 5,000 pg/mL IL-22 (similar to those in liver-specific IL-22TG mice) and did not induce obvious adverse phenotypes.14 These findings suggest that only very high doses of IL-22 may cause severe adverse phenotypes. However, it is unlikely that therapeutic application of IL-22 will reach such high concentrations of IL-22 (35,000-95,000 pg/mL) in the serum reported in the study by Liang et al.20 Regardless, monitoring IL-22 levels will be important in any therapeutic applications. Although the hepatoprotection of IL-22 is well documented,12-14 the role of IL-22 in liver inflammation remains obscure. Liang et al20 reported that a single injection of IL-22 up-regulated expression of CXCL1 in the liver, followed by a transient increase in circulating neutrophils, X-396 ic50 suggesting IL-22 may promote liver inflammation. In contrast, blockage of IL-22

either through using a neutralizing antibody12 or genetic deletion13 exacerbated inflammation, whereas treatment with IL-2212 or overexpression of IL-22 (the current study) ameliorated ConA-induced liver inflammation, indicating IL-22 suppresses liver inflammation in this model. It is plausible that IL-22 plays dual roles in controlling liver inflammation: promoting liver inflammation by stimulating hepatocytes to produce

acute phase proteins and chemokines, and inhibiting liver inflammation by preventing hepatocyte damage and subsequently reducing necrosis-associated liver inflammation. The final effect of IL-22 on liver inflammation is likely determined by the balance between the proinflammatory and anti-inflammatory effects of IL-22 and is dependent on the types of liver diseases and liver injury models. A previous study reported that the expression of hepatic IL-22 messenger RNA was up-regulated in patients with viral hepatitis.23 Here we demonstrate that IL-22+ immune cells are accumulated in the livers of patients with viral hepatitis (Fig. 1); however, the types of inflammatory Dehydratase cells responsible for IL-22 production in viral hepatitis patients remain obscure. Because Th17, Th22, natural killer, and natural killer T cells, which are known to produce IL-22,2-4 are elevated in the livers in patients with viral hepatitis,24-26 these cells likely contribute to hepatic IL-22 expression in the patients. Further studies are needed to confirm this assessment. The next obvious question is how IL-22 up-regulation might affect the progression of viral hepatitis disease progression. First, it has been reported that IL-22 does not inhibit HCV replication in vitro,23 suggesting that elevated IL-22 may not affect HCV replication directly.

Another obstacle to AAV-mediated gene transfer for HA gene therapy is the size of the FVIII coding sequence, which at 7.0 kb far exceeds the normal packaging capacity of AAV vectors. Packaging of large expression cassettes into AAV vectors has been reported but this is a highly inconsistent process resulting in low yields of vector particles with reduced infectivity [49, 50]. AAV vectors encoding the BDD-FVIII variant that is around 4.4 kb in size show promising results using canine FVIII but further evaluation of this approach using human BDD-FVIII is required. Other approaches include the co-administration

of two AAV vectors separately encoding the FVIII heavy- and light chains whose intracellular association in vivo leads to the formation of a functional molecule. The alternative two AAV vector approach exploits the tendency of these vectors MI-503 to

form head to tail concatamers. Therefore, by splitting the expression cassette such that one AAV vector contains a promoter and part of the coding sequence, as well as a splice donor site, whereas the other AAV vector contains the splice acceptor site and the remaining coding sequence. Following in vivo head to tail concatemerization a functional transcript is created that is capable of expressing full-length FVIII protein [51-53]. We have developed an AAV-based gene transfer approach that addresses both the size constraints and inefficient FVIII expression. Expression of human FVIII was improved 10-fold by re-organization of the wild-type tuclazepam cDNA of human PF-01367338 datasheet FVIII according to the codon usage of highly expressed

human genes [54-56]. Expression from B-domain-deleted codon optimized FVIII molecule was further enhanced by the inclusion of a 17 amino-acid peptide that contains the six N-linked glycosylation signals from the B domain required for efficient cellular processing. These changes have resulted in a novel 5.2 kb AAV expression cassette (AAV-HLP-codop-hFVIII-V3), which is efficiently packaged into recombinant AAV vectors and capable of mediating supraphysiological level of FVIII expression in animal models over the same dose range of AAV8 that proved to be efficacious in subjects with haemophilia B. Our novel AAV-HLP-codop-hFVIII-V3 cassette substantially improves the prospects of safe and effective gene transfer for haemophilia A. We are currently in the process of developing clinical grade AAV-HLP-codop-hFVIII-V3 for use in human subjects in the context of a clinical trial, which we hope will open in early 2015. The design of this clinical trial will be discussed in greater detail during the meeting. Recombinant retroviruses used in clinical gene therapy applications have been extensively engineered for efficient transfer of nucleic acid sequences into human cells. The most significant modification is the creation of replication incompetent viruses.

Doubling the IPS e.max Zirpress zirconia core from 0.4 mm to 0.8 mm increased the fracture resistance of this restorative system threefold. “
“The purpose of this study was to evaluate the effect of diamond-like carbon thin films doped and undoped with silver nanoparticles coating poly(methyl methacrylate) (PMMA) on Candida albicans biofilm formation. The control of biofilm formation is important to prevent oral diseases in denture users. Forty-five PMMA disks were obtained, finished, cleaned in an ultrasonic bath, and divided into three groups: Gc, no surface coating (control group); Gdlc, coated

with selleck inhibitor diamond-like carbon film; and Gag, coated with diamond-like carbon film doped with silver nanoparticles. The films were deposited using a reactive CH5424802 ic50 magnetron sputtering system (physical vapor deposition process). The specimens were characterized by optical profilometry, atomic force microscopy, and Rutherford backscattering spectroscopy analyses

that determined differences in chemical composition and morphological structure. Following sterilization of the specimens by γ-ray irradiation, C. albicans (ATCC 18804) biofilms were formed by immersion in 2 ml of Sabouraud dextrose broth inoculated with a standardized fungal suspension. After 24 hours, the number of colony forming units (cfu) per specimen was counted. Data concerning biofilm formation were analyzed using ANOVA and the Tukey test (p < 0.05). C. albicans biofilm formation was significantly influenced by the films (p < 0.00001), reducing the number of cfu, while not affecting the roughness parameters (p > 0.05). The Tukey test showed no significant difference between Gdlc and Gag. Films deposited were extremely thin (∼50 nm). The silver particles presented a diameter between

60 and 120 nm and regular distribution throughout the film surface (to Gag). Diamond-like carbon films, doped or undoped with silver nanoparticles, coating the base of PMMA-based PDK4 dentures could be an alternative procedure for preventing candidosis in denture users. “
“Purpose: Adequate preparation of abutment teeth for removable partial denture (RPD) rest seats allows appropriate masticatory force transmission, retention, and stability of supporting structures. It follows that careful preparation will be important for the longevity of the rehabilitation. The present study aimed to clinically evaluate rest seats and undercut areas of abutment teeth in RPD wearers after 2 years of use. Materials and Methods: A total of 193 occlusal, incisal, and cingulum rest seats were evaluated in terms of shape, rest adaptation, wear, caries, fractures, and surface type (enamel, composite resin, or amalgam). Two hundred and fourteen undercut areas were evaluated in terms of surface type (enamel or restoration) and integrity. This study was approved by the Research Ethics Committee of the Federal University of Rio Grande do Norte, resolution 196/1996, protocol number 11/05.

Doubling the IPS e.max Zirpress zirconia core from 0.4 mm to 0.8 mm increased the fracture resistance of this restorative system threefold. “
“The purpose of this study was to evaluate the effect of diamond-like carbon thin films doped and undoped with silver nanoparticles coating poly(methyl methacrylate) (PMMA) on Candida albicans biofilm formation. The control of biofilm formation is important to prevent oral diseases in denture users. Forty-five PMMA disks were obtained, finished, cleaned in an ultrasonic bath, and divided into three groups: Gc, no surface coating (control group); Gdlc, coated

with SCH772984 order diamond-like carbon film; and Gag, coated with diamond-like carbon film doped with silver nanoparticles. The films were deposited using a reactive selleck inhibitor magnetron sputtering system (physical vapor deposition process). The specimens were characterized by optical profilometry, atomic force microscopy, and Rutherford backscattering spectroscopy analyses

that determined differences in chemical composition and morphological structure. Following sterilization of the specimens by γ-ray irradiation, C. albicans (ATCC 18804) biofilms were formed by immersion in 2 ml of Sabouraud dextrose broth inoculated with a standardized fungal suspension. After 24 hours, the number of colony forming units (cfu) per specimen was counted. Data concerning biofilm formation were analyzed using ANOVA and the Tukey test (p < 0.05). C. albicans biofilm formation was significantly influenced by the films (p < 0.00001), reducing the number of cfu, while not affecting the roughness parameters (p > 0.05). The Tukey test showed no significant difference between Gdlc and Gag. Films deposited were extremely thin (∼50 nm). The silver particles presented a diameter between

60 and 120 nm and regular distribution throughout the film surface (to Gag). Diamond-like carbon films, doped or undoped with silver nanoparticles, coating the base of PMMA-based others dentures could be an alternative procedure for preventing candidosis in denture users. “
“Purpose: Adequate preparation of abutment teeth for removable partial denture (RPD) rest seats allows appropriate masticatory force transmission, retention, and stability of supporting structures. It follows that careful preparation will be important for the longevity of the rehabilitation. The present study aimed to clinically evaluate rest seats and undercut areas of abutment teeth in RPD wearers after 2 years of use. Materials and Methods: A total of 193 occlusal, incisal, and cingulum rest seats were evaluated in terms of shape, rest adaptation, wear, caries, fractures, and surface type (enamel, composite resin, or amalgam). Two hundred and fourteen undercut areas were evaluated in terms of surface type (enamel or restoration) and integrity. This study was approved by the Research Ethics Committee of the Federal University of Rio Grande do Norte, resolution 196/1996, protocol number 11/05.

After transfection, cells were treated with MMP-9 inducer 12-O-tetradecanoylphorbol-13-acetate (TPA), and then luciferase activities selleck chemicals were

determined. HBx or AIB1 alone can induce MMP-9 promoter activity to 5- or 3-fold, whereas the coexpression of HBx and AIB1 dramatically increased MMP-9 promoter activity to more than 10-fold (Fig. 6C). These results suggest that HBx can cooperate with AIB1 to increase MMP-9 promoter activity. To determine whether the cooperative effect of HBx and AIB1 on MMP-9 promoter activity is simply the result of elevated AIB1 protein levels, MMP-9 promoter/reporter assays were performed after HBx was transfected along with WT AIB1, AIB1-S505A, and AIB1-S509A, respectively. Similar to WT AIB1, HBx could cooperate with AIB1-S505A and AIB1-S509A to promote MMP-9 promoter activity (Fig. 6D). These results exclude the possibility that the cooperative effect of HBx and AIB1 on MMP-9 promoter activity is solely dependent on the elevation of AIB1 protein levels, because the protein levels of

AIB1-S505A and AIB1-S509A were almost not affected by HBx (Fig. 4D). We previously showed that AIB1 could be recruited to the MMP-9 promoter.17 Therefore, it is possible that HBx and AIB1 can co-occupy the MMP-9 promoter if these two proteins are stably associated. To test this hypothesis, ChIP assays were performed. Results Tamoxifen solubility dmso showed that HBx Nintedanib (BIBF 1120) was recruited to the MMP-9 promoter, and that recruitment was enhanced after the overexpression of AIB1 (Fig. 6E, lane 6 versus lane 5); similarly, AIB1 was recruited to the MMP-9 promoter, and recruitment was enhanced by HBx (Fig. 6F, lane 6 versus lane 5). These results indicate that both HBx and AIB1 are recruited to the MMP-9 promoter to cooperatively enhance MMP-9 promoter activity. To further confirm the cooperative role of HBx and AIB1 in MMP-9 expression, HepG2 cells, which highly express AIB1 (AIB1WT), but do not contain the HBx gene, were stably transfected with AIB1-knockdown (AIB1KD) plasmids to establish AIB1KD/HBx−

cell lines, HBx expression plasmids to establish AIB1WT/HBx+ cell lines, both AIB1-knockdown plasmids and HBx expression plasmids to establish AIB1KD/HBx+ cell lines, and control plasmids to establish AIB1WT/HBx− cell lines, respectively. The expression of AIB1 protein was dramatically reduced in AIB1KD/HBx− cells, compared to AIB1WT/HBx− cells; ectopic expression of HBx significantly up-regulated AIB1 protein levels in both AIB1KD/HBx+ and AIB1WT/HBx+ cells, compared to AIB1KD/HBx− and AIB1WT/HBx− cells, respectively (Fig. 7A). The protein levels of HBx in AIB1KD/HBx+ and AIB1WT/HBx+ cells were comparable to that in human HBx-positive HCC tissues (Supporting Fig. 1).

After transfection, cells were treated with MMP-9 inducer 12-O-tetradecanoylphorbol-13-acetate (TPA), and then luciferase activities RAD001 in vivo were

determined. HBx or AIB1 alone can induce MMP-9 promoter activity to 5- or 3-fold, whereas the coexpression of HBx and AIB1 dramatically increased MMP-9 promoter activity to more than 10-fold (Fig. 6C). These results suggest that HBx can cooperate with AIB1 to increase MMP-9 promoter activity. To determine whether the cooperative effect of HBx and AIB1 on MMP-9 promoter activity is simply the result of elevated AIB1 protein levels, MMP-9 promoter/reporter assays were performed after HBx was transfected along with WT AIB1, AIB1-S505A, and AIB1-S509A, respectively. Similar to WT AIB1, HBx could cooperate with AIB1-S505A and AIB1-S509A to promote MMP-9 promoter activity (Fig. 6D). These results exclude the possibility that the cooperative effect of HBx and AIB1 on MMP-9 promoter activity is solely dependent on the elevation of AIB1 protein levels, because the protein levels of

AIB1-S505A and AIB1-S509A were almost not affected by HBx (Fig. 4D). We previously showed that AIB1 could be recruited to the MMP-9 promoter.17 Therefore, it is possible that HBx and AIB1 can co-occupy the MMP-9 promoter if these two proteins are stably associated. To test this hypothesis, ChIP assays were performed. Results DNA Damage inhibitor showed that HBx Tacrolimus (FK506) was recruited to the MMP-9 promoter, and that recruitment was enhanced after the overexpression of AIB1 (Fig. 6E, lane 6 versus lane 5); similarly, AIB1 was recruited to the MMP-9 promoter, and recruitment was enhanced by HBx (Fig. 6F, lane 6 versus lane 5). These results indicate that both HBx and AIB1 are recruited to the MMP-9 promoter to cooperatively enhance MMP-9 promoter activity. To further confirm the cooperative role of HBx and AIB1 in MMP-9 expression, HepG2 cells, which highly express AIB1 (AIB1WT), but do not contain the HBx gene, were stably transfected with AIB1-knockdown (AIB1KD) plasmids to establish AIB1KD/HBx−

cell lines, HBx expression plasmids to establish AIB1WT/HBx+ cell lines, both AIB1-knockdown plasmids and HBx expression plasmids to establish AIB1KD/HBx+ cell lines, and control plasmids to establish AIB1WT/HBx− cell lines, respectively. The expression of AIB1 protein was dramatically reduced in AIB1KD/HBx− cells, compared to AIB1WT/HBx− cells; ectopic expression of HBx significantly up-regulated AIB1 protein levels in both AIB1KD/HBx+ and AIB1WT/HBx+ cells, compared to AIB1KD/HBx− and AIB1WT/HBx− cells, respectively (Fig. 7A). The protein levels of HBx in AIB1KD/HBx+ and AIB1WT/HBx+ cells were comparable to that in human HBx-positive HCC tissues (Supporting Fig. 1).