Prophylaxis with nucleoside analogs is essential for preventing HBV reactivation in HBsAg positive patients. In contrast,

HBsAg negative with HBcAb and/or HBsAb positive patients should be monitored monthly for an increase in serum HBV DNA during and 12 months after completion of chemotherapy. Nucleoside analogs should be administrated immediately when HBV DNA becomes positive during this period. This strategy facilitates Cisplatin commencement of nucleoside analogs at an early stage of HBV reactivation and results in prevention of severe hepatitis. “
“Proton pump inhibitors (PPI) and H2-receptor antagonists (H2RA) are frequently prescribed in hospitalized patients with cirrhosis. There are conflicting reports regarding the role of acid-suppressive therapy in predisposing hospitalized patients with cirrhosis to spontaneous bacterial

peritonitis (SBP). The aim of this meta-analysis was to evaluate the association between acid-suppressive therapy and the risk of SBP in hospitalized patients with cirrhosis. We searched MEDLINE and four other databases for http://www.selleckchem.com/products/LDE225(NVP-LDE225).html subject headings and text words related to SBP and acid-suppressive therapy. All observational studies that investigated the risk of SBP associated with PPI/H2RA therapy and utilized SBP as an endpoint were considered eligible. Data from the identified studies were combined by means of a random-effects model and odds ratios (ORs) were calculated. Eight studies (n = 3815 patients) Vasopressin Receptor met inclusion criteria.

The risk of hospitalized cirrhotic patients developing SBP increased when using acid-suppressive therapy. The risk was greater with PPI therapy (n = 3815; OR 3.15, 95% confidence interval 2.09–4.74) as compared to those on H2RA therapy (n = 562; OR 1.71, 95% confidence interval 0.97–3.01). Pharmacologic acid suppression was associated with a greater risk of SBP in hospitalized patients with cirrhosis. Cirrhotic patients receiving a PPI have approximately three times the risk of developing SBP compared with those not receiving this medication. Prospective studies may help clarify this relationship and shed light on the mechanism(s) by which acid-suppressive therapy increases the risk of SBP in hospitalized patients with cirrhosis. “
“Background and Aim:  According to the Rome III definition, irritable bowel syndrome (IBS) has been a biopsychosocial dysfunction. We tried to know whether the IBS clinical manifestations were comparable to other countries. Method:  We have reviewed the IBS publications in Taiwan, thus its clinical significances are summarized and compared to others. Results:  Among a selected population of paid physical checkup, the Rome I & II criteria defined prevalences were 17.5% and 22.1%, respectively without an observed female predominance. However, female was a factor leading to constipation predominant IBS (C-IBS).

SC-43 act as a potent SHP-1 enhancer and was also docked in the same site. The trifluoromethyl group of SC-43 formed a hydrogen bond with Q529. In addition, the length of the phenylcyanyl group in SC-43 is shorter than pyridine-mehtylamide of sorafenib, which reduces the steric-hindering effect in the N-SH2 domain. Moreover, the meta connection of the phenyl ring between the urea and phenylcyanyl moiety in SC-43 reduces total length and results in a better fit in the pocket of N-SH2. The discrepancy in potency between sorafenib and SC-43 was likely attributable

to these two factors. We further modified see more SC-43 based on bioisosteric substitution. For example, SC-40, with the replacement of the urea and phenylcyanyl moiety in SC-43 by sulfonamide and nitroaniline, respectively, was able to activate SHP-1 activity. Also, SC-40 demonstrated that the sulfonamide moiety formed hydrogen bonds with R44 and Q529 in the docking model. Together, this discrepancy in binding ability may affect the potency

of pharmacological effect among sorafenib, SC-40, and SC-43 (Fig. 5F). Apoptosis was inhibited in myc-tagged STAT3-overexpressing Dabrafenib molecular weight HCC cells after exposure to SC derivatives for 24 h as evidenced by sub-G1 analysis (Fig. 6A). In addition, SHP-1 phosphatase-specific inhibitor (PTPIII) reversed SC-induced cell death and inhibition of p-STAT3 (Fig. 6B). Silencing SHP-1 markedly restored SC-43- and SC-40-induced apoptosis and inhibition of p-STAT3 (Fig. 6C). Conversely, overexpression of WT SHP-1 induced potent apoptosis and inhibited p-STAT3 as a result of SC-43 and 40 treatments in PLC5 cells (Fig. 6D). Titration of dN1 or D61A also gradually restored inhibition of p-STAT3 in SC-43-treated cells; and the apoptosis induced by SC-43 was abolished in dN1 and TCL D61A-expressing PLC5 cells (Fig. 6E,F). We established an HCC orthotopic model using luc2-expressed PLC5 cells inoculated into liver of nude

mice. Long-term monitoring showed that SC-43 treatment had an evident anti-HCC effect and significant survival benefit, compared with mice treated with vehicle or sorafenib (Fig. 7A). In addition, SC PLC5 tumor-bearing mice were treated daily with vehicle, sorafenib, SC-43, or SC-40 at the dosage of 10 mg/kg/day orally. Compared to sorafenib, SC treatment had an inhibitory effect on tumor growth and the average tumor sizes of animals were less than half that of control mice at the end of treatment (Fig. 7B). To further correlate the molecular mechanism with the anticancer effect in vivo, p-STAT3 and SHP-1 activity in tumor extract from vehicle- and SC-treated mice was analyzed by immunoblotting. Down-regulation of p-STAT3 and elevation of SHP-1 activity were noted in SC-43/40-treated tumor lysate (Fig. 7C,D). The pharmacokinetics of SC-43 was determined (Fig. 7E). SC-43 exhibited a longer period of stability in vivo than that reported for sorafenib in a previous study.

Most information is derived from stranded animals and there has been no systematic study of their morphology. We present a multivariate analysis of the morphology of Gray’s beaked whales using 80 cranial measurements from 22 individuals and 13 external measurements from 50 individuals. Sparse principal component and linear discriminant function analyses were used to classify samples into sexes. Males and females have

markedly different cranial morphology. In particular, females have longer skulls with longer more slender rostra find more (beaks) in comparison to males. Two variables, depth of the rostrum at mid-length and tip of rostrum to the right temporal fossa, can classify sex with 100% accuracy. The external body measurements used in this study are more prone to error as they were recorded by a number of observers on carcasses in differing states of decomposition and this is reflected in the level of variance in most measurements.

However, analyses of these measurements showed a significant difference between sexes in the distance between (1) the tip of the rostrum to the genital slit, (2) the tip of the rostrum to the blowhole, as found in the cranial analyses and (3) tail fluke width where males have absolutely wider tail flukes than females. Differences in these same measurements were also found between animals stranded on the east and west coasts suggesting a degree of population separation Liothyronine Sodium across New Zealand. Finally, we present two linear models that enable the assignment of sex from either skull or

external measurements. These models will be www.selleckchem.com/products/MG132.html useful for future studies as well as the management of these whales and can be applied to archived data where genetic sex assignment is not possible. “
“Dispersal and philopatry are fundamental processes influencing the genetic structure and persistence of populations, and might be affected by isolation and habitat perturbation. Habitat degradation induced by human activities could have detrimental consequences on the genetic structure of populations. Therefore, it is crucial to understand the role of human impact in promoting or disrupting the genetic structure. Here, we conducted a genetic analysis using 12 polymorphic microsatellite markers of 70 lesser kestrels Falco naumanni from 10 breeding colonies of two subpopulations in Sicily (southern Italy). Genetic differentiation between the two subpopulations was negligible, and linear distances played no role in the level of genetic relatedness recorded in the two sites. Linear distances between nests also resulted in no effects on the relatedness recorded within and between colonies in the largest subpopulation. Clusters of more-versus less-related individuals resulted when the two-dimensional positions of colonies (i.e., latitude and longitude) were tested as predictors of genetic proximity instead of linear distances.

Most information is derived from stranded animals and there has been no systematic study of their morphology. We present a multivariate analysis of the morphology of Gray’s beaked whales using 80 cranial measurements from 22 individuals and 13 external measurements from 50 individuals. Sparse principal component and linear discriminant function analyses were used to classify samples into sexes. Males and females have

markedly different cranial morphology. In particular, females have longer skulls with longer more slender rostra selleck kinase inhibitor (beaks) in comparison to males. Two variables, depth of the rostrum at mid-length and tip of rostrum to the right temporal fossa, can classify sex with 100% accuracy. The external body measurements used in this study are more prone to error as they were recorded by a number of observers on carcasses in differing states of decomposition and this is reflected in the level of variance in most measurements.

However, analyses of these measurements showed a significant difference between sexes in the distance between (1) the tip of the rostrum to the genital slit, (2) the tip of the rostrum to the blowhole, as found in the cranial analyses and (3) tail fluke width where males have absolutely wider tail flukes than females. Differences in these same measurements were also found between animals stranded on the east and west coasts suggesting a degree of population separation CYTH4 across New Zealand. Finally, we present two linear models that enable the assignment of sex from either skull or

external measurements. These models will be 3Methyladenine useful for future studies as well as the management of these whales and can be applied to archived data where genetic sex assignment is not possible. “
“Dispersal and philopatry are fundamental processes influencing the genetic structure and persistence of populations, and might be affected by isolation and habitat perturbation. Habitat degradation induced by human activities could have detrimental consequences on the genetic structure of populations. Therefore, it is crucial to understand the role of human impact in promoting or disrupting the genetic structure. Here, we conducted a genetic analysis using 12 polymorphic microsatellite markers of 70 lesser kestrels Falco naumanni from 10 breeding colonies of two subpopulations in Sicily (southern Italy). Genetic differentiation between the two subpopulations was negligible, and linear distances played no role in the level of genetic relatedness recorded in the two sites. Linear distances between nests also resulted in no effects on the relatedness recorded within and between colonies in the largest subpopulation. Clusters of more-versus less-related individuals resulted when the two-dimensional positions of colonies (i.e., latitude and longitude) were tested as predictors of genetic proximity instead of linear distances.

They concluded that younger age, Asian race, injection drug use, and a greater number of lifetime sexual partners are risk factors for HBV-HCV dual infection. An interesting and clinically important finding is the marked difference in the severity of liver disease. Compared with patients monoinfected with HCV, patients dually infected with HBV and HCV have higher alanine aminotransferase levels and necroinflammatory scores, more advanced fibrosis, and faster fibrosis progression rates.

In particular, patients with dual infection have a greater severity of hepatic steatosis, which has never been evaluated in this population before. To further elucidate the association between HBV-HCV dual infection and hepatic steatosis, we conducted a study enrolling 100 consecutive dually infected patients [59 males and 41 females, 52.5 ± learn more 11.3 years old, with 31% positive for HBV DNA by the COBAS Amplicor HBV monitor (Roche Diagnostics, Dasatinib Branchburg, NJ) and 100% positive for HCV RNA by Amplicor (Roche Diagnostics)] and 100 age-matched, sex-matched, and body mass index (BMI)–matched individuals with chronic hepatitis C in Taiwan, in which both viruses are endemic.2-4 Patients with HBV-HCV

dual infection and patients with HCV monoinfection were similar with respect to the ratio of diabetes mellitus, HCV genotype, alanine aminotransferase levels, and necroinflammatory scores, although patients with dual infection had more advanced fibrosis scores (F3 and F4; P = 0.041) and lower platelet counts (P = 0.045) than those with HCV monoinfection. Based on the Metavir classification system,5 the prevalence of hepatic steatosis was comparable between the two groups; however, dually infected patients had a higher severity of steatosis (grade 2 or 3) than those infected with HCV alone (P = 0.025; Fig. 1). Among dually infected patients, factors associated with the presence of steatosis by multivariate analysis were advanced fibrosis [odds ratio (OR) = 3.703, 95% confidence interval (CI) = 1.527-9.009, P = 0.004] and BMI (OR = 1.191, 95% CI

= 1.037-1.368, P = 0.014). Likewise, independent variables associated with advanced through fibrosis were the platelet count (104/μL; OR = 0.818, 95% CI = 0.725-0.923, P = 0.001), grade 2 or 3 steatosis (OR = 6.695, 95% CI = 1.911-23.45, P = 0.003), and higher necroinflammatory scores (OR = 2.880, 95% CI = 1.084-7.647, P = 0.034). Hepatic steatosis, a frequent histological feature of chronic HCV infection, has been recognized as a cofactor influencing the presence and progression of fibrosis.6, 7 In contrast, the association between HBV infection and hepatic steatosis is controversial.8, 9 In this case-control study, our data, in keeping with the findings of Bini et al.,1 confirm that patients dually infected with HBV and HCV have more severe steatosis than those with HCV monoinfection.

The present multigene phylogenetic analyses resolved that the three species of Gloeomonas belong to the Chloromonas lineage or Chloromonadinia of the Volvocales, and Chloromonas insignis (Anakhin) Gerloff et H.

Ettl NIES-447 and C. rubrifilum SAG 3.85, both of which selleck kinase inhibitor have pyrenoids without associated starch grains, were positioned basally to the clade composed of the three species of Gloeomonas. Therefore, Gloeomonas might have evolved from such a Chloromonas species through reduction in pyrenoid matrix size within the chloroplast and by separating their two flagellar bases. “
“The culture of microalgae using organic carbon sources decreases the cost of operation in closed systems. The effect of carbon sources on microalgae is thus an interesting problem in not only theoretical research but also practical production. The short-term effects of acetate and microaerobic conditions on the

growth, photosynthesis, and respiration of the green microalga Chlorella sorokiniana I. Shihira & R.W. Krauss GXNN 01 were described Selleckchem GDC-0980 after acetate addition to autotrophic cultures. As the acetate concentration increased, cells needed a longer lag phase to grow, and 243.8 mM acetate completely inhibited growth. Acetate addition induced an immediate response in photosynthesis and respiration. The activity of PS II and PS I were impaired and declined with different rates, and then recovered compared with autotrophic cells. Carbonic anhydrase and Rubisco activities were also inhibited at the beginning, and respiration was SDHB increased. We propose that ATP consumption for acetate assimilation results in surplus NADPH, and then accumulated reducing power over-reduces inter-photosystem components and raises the transthylakoid proton gradient, which

redistributes energy between PS I and PS II, and leads to a decrease in the PS II/PS I ratio and O2 evolution. An apparent cyclic electron flow was also observed, which may be mainly mediated by NAD(P)H dehydrogenase-dependent pathway since NADPH was in excess. These observations pointed to an acclimation process after acetate addition, and suggested the interaction between photosynthesis and respiration involving ATP and reducing power. “
“Blooms of Microcystis aeruginosa (Kützing) Kützing occur frequently in many freshwater ecosystems around the world, but the role of environmental factors in promoting the growth and determining the proportion of toxic and non-toxic strains still requires more investigation. In this study, four strains (toxic CPCC299 & FACHB905 and non-toxic CPCC632 & FACHB315) were exposed to high light (HL) condition, similar to light intensity found at the surface of a bloom, to evaluate their sensitivity to photoinhibition. We also estimated their capacity to recover from this HL stress. For all strains, our results showed an increased inhibition of the photosynthetic activity with HL treatment time.

Disclosures: Fabio Marra – Advisory Committees or Review Panels: Abbott; Consulting: Bayer Healthcare; Grant/Research Support: ViiV Massimo Pinzani – Advisory Committees or Review Panels: Intercept Pharmaceutical, Silence Therapeutic, Abbot; Consulting: UCB; Speaking and Teaching: Gilead, BMS The following

people have nothing to disclose: Jose Macias-Barragan, Jose Vera-Cruz, Jesus Garcia-Banuelos, David A. Lopez-de la Mora, Cibeles San-chez-Roque, Krista Rombouts, Juan Armendáriz-Borunda Background: Nonalcoholic Fatty Liver Disease (NAFLD) is a heritable and prevalent disease, affecting about 30% of the population. A characteristic feature of NAFLD is hepatic steatosis, the presence of excess fat (mostly triglycerides (TG)) in the liver. Using genome wide association analysis (GWAS) we identified genetic variants in PNPLA3 and NVP-BKM120 GCKR, and near LYPLAL1 that associate with population based hepatic steatosis. How these variants result in increased liver steatosis is not known. Here we aim to characterize the genetic mechanism by which genetic variants at

these loci may affect nearby genes to result in hepatic triglyceride accumulation. Methods: HuH-7 and HepG2 liver cell lines were infected with lentiviruses expressing wildtype PNPLA3, this website GCKR, and LYPLAL1 as well as the mutants PPP1R3B(I148M) and GCKR(P446L) or with shRNAs to PNPLA3, GCKR, and LYPLAL1 and stably expressing cell lines were selected. Overexpression/knockdown was quantified using Western/Northern blotting analysis. Stable cell lines were loaded with oleic acid, hepatic steatosis was measured using LipidTOXTM Methamphetamine (Life Technology), and total cellular triglyceride was quantified using a Triglyceride Determination Kit (Sigma-Aldrich). Results: Overexpression of wildtype and to a larger

extent mutant PNPLA3 but not knockdown of PNPLA3 resulted in increased steatosis/TG accumulation. Over-expression of wildtype GCKR but not mutant GCKR resulted in increased steatosis/TG accumulation whereas knockdown of GCKR also resulted in increased steatosis/TG accumulation. Overexpression of LYPLAL1 resulted in decreased steatosis/TG accumulation and knockdown in increased steatosis/TG accumulation. Conclusions: These results suggest that variants in PNPLA3 exert their effect through an increase/gain-of-function mechanisms, those in GCKR and near LYPLAL1 likely through a loss-of-function mechanism. Disclosures: The following people have nothing to disclose: Yue Chen, Andrew W. Tai, Elizabeth K. Speliotes Background and aims: We developed an optimized diet-induced mouse model that produces robust inflammation and fibrosis. Using this model we investigated the changes of proin-flammatory transcripts expressed in liver and fat tissues.

Key Word(s): 1. gemcitabine; 2. HSP27; 3. Snail; 4. ERCC1; Presenting Author: ZHAO JIA-JUN Additional Authors: GUO XIAO-ZHONG, LI HONG-YU, SHAO XIAO-DONG Corresponding Author: GUO XIAO-ZHONG Affiliations: General Hospital of Shenyang Military Area Command Objective: To study the expression

of p73 protein and mRNA in pancreatic carcinoma and its clinical significance. Methods: Surgical specimens of tissue were from 26 cases of surgically resected pancreatic cancer, 12 cases of pancreatic tissue adjacent to carcinoma and 8 cases of normal pancreas tissue. p73 protein JQ1 concentration and mRNA were detected by immunohistochemical assay and in situ hybridization. Results: The result of immunohistochemical detection showed in 26 cases of pancreatic carcinoma P73 was positive in 11 patients (42.3%). There was no significant relationship between the clinical characteristics (age, gender) and the expression of p73 protein. In situ hybridization results showed that P73 mRNA had no significant positive expression in pancreatic cancer and paracancerous normal pancreatic tissue. Conclusion: The p73 gene has an important role in human pancreatic cancer development. The data suggest that expression of p73 gene is also associated with the development of pancreatic cancer. Key Word(s): 1. p73; 2. Pancreatic Cancer; 3. mRNA; Presenting

Author: WU CHUN-YAN Additional Authors: GUO XIAO-ZHONG, LI HONG-YU, SHAO XIAO-DONG Corresponding Author: GUO XIAO-ZHONG Affiliations: General Hospital of Shenyang Military Area Command Objective: Our previous findings revealed that KAI1, a metastasis suppressor gene, inhibited human pancreatic cancer metastasis and see more proliferation in vitro. Furthermore, MiaPaCa-2 cells learn more with overexpression of KAI1/CD82 subcutaneous injection into nude mice significantly

reduced metastases without affecting primary tumor growth in vivo. However, the reason why KAI1 can not affect primary tumor growth is unclear. To explore the reason why KAI1 can not affect primary tumor growth. Methods: Human pancreatic cancer cells MiaPaCa-2 were cultured under the condition of hypoxia and serum-free to simulate the hypoxic-ischemic microenvironment within solid tumors to a certain degree. Results: The study showed that both hypoxia and serum-free can effectively reduce the apoptosis and proliferation inhibition caused by the KAI1. Meanwhile, both hypoxia and serum-free can induce autophagy. 3-MA, one of the inhibitors of autophagy, was used to inhibit autophagy. 3-MA pretreatment significantly aggravated KAI1-induced apoptosis and proliferation inhibition. Blocking autophagy can Alpha effectively block the protective effect of hypoxia and serum-free on cells. Conclusion: It is the autophagy induced by hypoxia and serum-free in the microenvironment within solid tumors that protects MiaPaCa-2 cells from apoptosis and proliferation inhibition induced by KAI1.

g. recombinant or plasma-derived FVIII or FIX – to treat haemophilia A or B, respectively, prothrombin complex concentrates, fibrogamin for FXIII deficiency

and recombinant activated factor VII for haemophilia patients with inhibitors, FVII deficiency or Glanzmann thrombasthenia), cryoprecipitate (for haemophilia A, Von Willebrand and fibrinogen disorders – in case specific concentrates are not available), platelet transfusions for platelet function disorders and adjunct antifibrinolytic therapy for all infants with bleeding disorders during acute bleeding episodes or surgical procedures [35]. Off label use of recombinant factor VIIa (rFVIIa) SAHA HDAC in vitro has been attempted in neonates with severe acute bleeding or presence of ICH [36]. Prenatal diagnosis FK506 price of most congenital severe factor deficiencies or severe congenital inherited platelet function disorders is currently possible in families with a history of inherited coagulation deficiency. Foetal DNA, obtained through amniocentesis or chorionic villi biopsy, can be tested for presence of known mutations

or analysed to compare linkage and sequences against the sick proband and his parents. Early diagnosis allows for termination of pregnancy or proceeding towards early intervention and therapy, as indicated. In special cases pregenetic determination may be used together with IVF, enabling selection of healthy embryos only at very early stages, prior to actual pregnancy [37]. The authors are grateful and would

like to thank Dr Bruce Evatt, retired director Division of Blood Disorders, for reviewing the manuscript and all the HTC directors and staff for the UDC data. Disclaimer:  The findings and conclusions in this report are those of the authors and do not necessarily represent the views of the Centers for Disease Control and Prevention. The authors stated that they had no interests which might be perceived as posing a conflict or bias. “
“Head-on comparative studies of factor IX (FIX) concentrates performed under standardized conditions are rarely conducted regardless of being a valuable instrument guiding health care providers towards better informed and cost-effective decisions. This study is an extension of a multicentre study that assessed the efficacy, safety and pharmacokinetics (PK) of oxyclozanide AlphaNine® in 25 previously treated patients with severe haemophilia B (FIX:C ≤ 2%). After a washout period ≥7 days following the last PK performed with AlphaNine® after a dose of 65–75 IU kg−1, an identical PK study was performed with BeneFIX® on 22 of the same patients. Venous blood samples for analysis were taken at baseline and at 0.25, 0.5, 1, 3, 6, 9, 24, 48, 72 and 74 h post infusion. The outcomes of the comparison of the PK parameters were as follows: Mean (±SD) in vivo recovery (IVR) was 1.3 ± 0.4 IU dL−1 per IU kg−1 for AlphaNine® and 1.0 ± 0.3 IU dL−1 per IU kg−1 for BeneFIX® (P < 0.01).

g. recombinant or plasma-derived FVIII or FIX – to treat haemophilia A or B, respectively, prothrombin complex concentrates, fibrogamin for FXIII deficiency

and recombinant activated factor VII for haemophilia patients with inhibitors, FVII deficiency or Glanzmann thrombasthenia), cryoprecipitate (for haemophilia A, Von Willebrand and fibrinogen disorders – in case specific concentrates are not available), platelet transfusions for platelet function disorders and adjunct antifibrinolytic therapy for all infants with bleeding disorders during acute bleeding episodes or surgical procedures [35]. Off label use of recombinant factor VIIa (rFVIIa) AZD9291 manufacturer has been attempted in neonates with severe acute bleeding or presence of ICH [36]. Prenatal diagnosis Selleck GSK3235025 of most congenital severe factor deficiencies or severe congenital inherited platelet function disorders is currently possible in families with a history of inherited coagulation deficiency. Foetal DNA, obtained through amniocentesis or chorionic villi biopsy, can be tested for presence of known mutations

or analysed to compare linkage and sequences against the sick proband and his parents. Early diagnosis allows for termination of pregnancy or proceeding towards early intervention and therapy, as indicated. In special cases pregenetic determination may be used together with IVF, enabling selection of healthy embryos only at very early stages, prior to actual pregnancy [37]. The authors are grateful and would

like to thank Dr Bruce Evatt, retired director Division of Blood Disorders, for reviewing the manuscript and all the HTC directors and staff for the UDC data. Disclaimer:  The findings and conclusions in this report are those of the authors and do not necessarily represent the views of the Centers for Disease Control and Prevention. The authors stated that they had no interests which might be perceived as posing a conflict or bias. “
“Head-on comparative studies of factor IX (FIX) concentrates performed under standardized conditions are rarely conducted regardless of being a valuable instrument guiding health care providers towards better informed and cost-effective decisions. This study is an extension of a multicentre study that assessed the efficacy, safety and pharmacokinetics (PK) of Bortezomib mouse AlphaNine® in 25 previously treated patients with severe haemophilia B (FIX:C ≤ 2%). After a washout period ≥7 days following the last PK performed with AlphaNine® after a dose of 65–75 IU kg−1, an identical PK study was performed with BeneFIX® on 22 of the same patients. Venous blood samples for analysis were taken at baseline and at 0.25, 0.5, 1, 3, 6, 9, 24, 48, 72 and 74 h post infusion. The outcomes of the comparison of the PK parameters were as follows: Mean (±SD) in vivo recovery (IVR) was 1.3 ± 0.4 IU dL−1 per IU kg−1 for AlphaNine® and 1.0 ± 0.3 IU dL−1 per IU kg−1 for BeneFIX® (P < 0.01).