1, 3, 19, 26 The current standard of care therefore relates to decreasing either the absorption of ammonia by using nonabsorbable disaccharides or either its production by reducing urease-producing bacteria by nonabsorbable antibiotics.26, 27 Recent innovations, such as rifaximin or liver

dialysis, are either not universally licensed for use or hampered because of lack of direct applicability.28-30 The ultimate solution remains liver transplantation but this implies relentless liver and renal insufficiency to become priorized in the current MELD era. Recently, large SPSSs were described to be highly prevalent learn more (46%-71%) in patients with refractory HE. These latter might not only explain the refractoriness of HE but also serve as a therapeutic target.7-9, 12, 16, 31,

32 Nevertheless, the diagnosis of large SPSSs is often delayed and controversy still EGFR targets prevails whether SPSSs might be therapeutically targeted for HE.11, 15 To elaborate further on these issues, we pooled the datasets of six different European liver units concerning 37 patients whose data were collated into a preset standardized case-report form. Our analysis not only confirms a delayed diagnosis, as in our series the diagnosis of SPSS was made on average 13 months after onset of HE, but more importantly substantiates the therapeutic effectiveness of embolization of the considered culprit SPSSs once the diagnosis is made. More specifically, almost 50% of the treated patients became HE-free during an average follow-up of more than 2 years. Considering secondary parameters of success, defined as either improved autonomy (objectively using mRS20), or decreased number of hospitalizations or severity of the worst HE episode after embolization, an improvement was observed in three-quarters of the patients. More specifically, autonomy was improved 3-fold and as such the hospitalization rate and in-hospital stays were similarly significantly reduced. Even more important, the need for liver transplantation

selleck chemicals llc could theoretically be reduced in a large portion of these patients, as HE was the sole presenting symptom in a substantial proportion. It was impossible to retrospectively determine if all patients had been suitable for transplantation at the time of embolization. On the other hand, if eventually deemed necessary, as was the case in one patient, embolization did not technically compromise liver transplantation. If HE recurred nevertheless, it occurred either within days after index embolization (2-7 days, n = 15) or several months later (n = 4). Given angiographic confirmation of complete occlusion of the SPSS at the end of the procedure, the early occurrence presumably relates to insufficient remnant critical functional liver mass (cfr, the higher baseline MELD of nonresponders Fig.

There is no approved therapy for NASH. Weight reduction is typically recommended, but the efficacy of weight reduction for the treatment of NASH BIBW2992 order has not been carefully evaluated. We examined the relation of weight change and steatohepatitis by laboratory findings and unenhanced

CT. Methods: We enrolled the 85 patients that diagnosed for NASH clinically. NASH was established by the presence of hepatic ultrasonographic findings and elevated aminotrasnferase level (>40). Previous diagnosis of hepatic disease, serum creatinine level >1.5 mg/dl, other medical illness, pregnancy, use of drug (weight loss drug, diabetes medication), alcohol consumption >30 g per day were excluded. We measured the BMI (height and weight), see more AST/ALT, r-GTP, albumin, bilirubin and cholesterol level at 0 and 10 weeks. Each participant underwent two consecutive unenhanced CT for assessing the liver and visceral fat content at 0 and 10 weeks. Results: Seventy-five percent patients have decreased the body weight. The mean weight change over 10-week period was 2.3 kg. Percent weight reduction from baseline correlated significantly with improved liver chemistry (p = 0.008), improvements in the degree of hepatic steatosis by housfiled

unit (p < 0.001), and decreased visceral fat ratio (p < 0.001). Conclusion: Weight reduction leads to decreased the aminotrasferase levels, visceral fat ratio and improved the steatohepatitis in NASH. Key Word(s): 1. steatohepatitis; 2. weight reduction; Presenting Author: HU CHANGJIANG Additional Authors: HE SHI-MING Corresponding Author: HU CHANGJIANG, HE SHI-MING Affiliations: Department of Gastroenterology, XinQiao Hospital; Department of Biochemistry and Molecular Biology, College of Basic Medical Sciences Objective: Liver X receptors (LXRs), including LXRα and LXRβ isoforms, play important roles in the metabolic regulation of glucose, cholesterol and lipid. Moreover, activation of LXRs also represses the expression of Cyclin D1 and B1, and thus suppresses the proliferation of multiple cancer cells, but the relevant mechanism is not

well known. Forkhead Box M1 (FOXM1) selleck compound is a proliferation-specific member of forkhead box family, which is highly expressed in proliferating normal cells and numerous cancer cells. FOXM1 directly activates transcription of Cyclin D1 and B1, resulting in the enhancement of cell cycle progression and cell proliferation. However, it is unclear whether LXRs are involved in the regulation of FOXM1. In the present study, we demonstrated that specific LXRs agonists downregulated expressions of FOXM1, Cyclin D1 and B1 in hepatocellular carcinoma (HCC) cells, which led to cell cycle and cell proliferation arrest. Methods: We used knockdown of FOXM1, Reporter assays, electrophoretic mobility shift assay (EMSA) and chromatin immunoprecipitation (ChIP) assays. FOXM1 expression in liver tissues was also inhibited in the mice fed with LXRs agonists.

There is no approved therapy for NASH. Weight reduction is typically recommended, but the efficacy of weight reduction for the treatment of NASH AZD3965 supplier has not been carefully evaluated. We examined the relation of weight change and steatohepatitis by laboratory findings and unenhanced

CT. Methods: We enrolled the 85 patients that diagnosed for NASH clinically. NASH was established by the presence of hepatic ultrasonographic findings and elevated aminotrasnferase level (>40). Previous diagnosis of hepatic disease, serum creatinine level >1.5 mg/dl, other medical illness, pregnancy, use of drug (weight loss drug, diabetes medication), alcohol consumption >30 g per day were excluded. We measured the BMI (height and weight), Sirolimus AST/ALT, r-GTP, albumin, bilirubin and cholesterol level at 0 and 10 weeks. Each participant underwent two consecutive unenhanced CT for assessing the liver and visceral fat content at 0 and 10 weeks. Results: Seventy-five percent patients have decreased the body weight. The mean weight change over 10-week period was 2.3 kg. Percent weight reduction from baseline correlated significantly with improved liver chemistry (p = 0.008), improvements in the degree of hepatic steatosis by housfiled

unit (p < 0.001), and decreased visceral fat ratio (p < 0.001). Conclusion: Weight reduction leads to decreased the aminotrasferase levels, visceral fat ratio and improved the steatohepatitis in NASH. Key Word(s): 1. steatohepatitis; 2. weight reduction; Presenting Author: HU CHANGJIANG Additional Authors: HE SHI-MING Corresponding Author: HU CHANGJIANG, HE SHI-MING Affiliations: Department of Gastroenterology, XinQiao Hospital; Department of Biochemistry and Molecular Biology, College of Basic Medical Sciences Objective: Liver X receptors (LXRs), including LXRα and LXRβ isoforms, play important roles in the metabolic regulation of glucose, cholesterol and lipid. Moreover, activation of LXRs also represses the expression of Cyclin D1 and B1, and thus suppresses the proliferation of multiple cancer cells, but the relevant mechanism is not

well known. Forkhead Box M1 (FOXM1) selleck inhibitor is a proliferation-specific member of forkhead box family, which is highly expressed in proliferating normal cells and numerous cancer cells. FOXM1 directly activates transcription of Cyclin D1 and B1, resulting in the enhancement of cell cycle progression and cell proliferation. However, it is unclear whether LXRs are involved in the regulation of FOXM1. In the present study, we demonstrated that specific LXRs agonists downregulated expressions of FOXM1, Cyclin D1 and B1 in hepatocellular carcinoma (HCC) cells, which led to cell cycle and cell proliferation arrest. Methods: We used knockdown of FOXM1, Reporter assays, electrophoretic mobility shift assay (EMSA) and chromatin immunoprecipitation (ChIP) assays. FOXM1 expression in liver tissues was also inhibited in the mice fed with LXRs agonists.

18–20 Interestingly, in humans, amplification of the chromosomal region containing the YAP gene (11q22) has been reported in several tumor types.21, 22 On the basis of these findings, we investigated

whether (1) the Hippo pathway plays a critical role in the termination of the xenobiotic-induced liver overgrowth and (2) this pathway is defective in cancer cells arising in hyperplastic livers. AFP, alpha-fetoprotein; BrdU, 2-bromodeoxyuridine; CAR, constitutive androstane receptor; cDNA, complementary DNA; CTGF, connective tissue growth factor; Cyp2b10, cytochrome 2b10; DENA, diethylnitrosamine; HSP cancer HCC, hepatocellular carcinoma; miR-375, microRNA 375; mYAP, YAP mutated in Ser127 and Ser381; PCNA, proliferating cell nuclear antigen; PCR, polymerase chain reaction; TCPOBOP, 1,4-bis(2-(3,5-dichloropyridyloxy)benzene; YAP, Yes-associated protein. C3H or CD-1 female mice (8 weeks old) were obtained from Charles River (Milano, Italy). All experiments were performed in accordance with the Universities Federation for Animal Welfare Handbook on the Care and Management of

Laboratory Animals and the guidelines www.selleckchem.com/GSK-3.html of the animal ethics committee of the University of Cagliari. In experimental protocol 1 (Fig. 1A), hepatocyte proliferation was induced by 1,4-bis[2-(3,5-dichloropyridyloxy)]benzene (TCPOBOP) (3 mg/kg body weight, dissolved in dimethyl sulphoxide–corn oil solution; Sigma-Aldrich, Milan, Italy). Controls received an equivalent amount of the vehicle. To determine the proliferative response of the liver to TCPOBOP, mice were given 2-bromodeoxyuridine (BrdU) dissolved in drinking water (1 mg/mL; Sigma-Aldrich, selleck chemicals llc Milan, Italy) and sacrificed 1 week later. In experimental protocol 2 (Fig. 2A), mice were treated as in protocol 1 except that they were sacrificed 24 hours, 36 hours, and 1 week after one dose or 24 and 36 hours after two doses of TCPOBOP. BrdU dissolved in drinking water was given as shown in Fig. 2A. The p2xFlag CMV-YAP vector

(a kind gift from M. Sudol) was digested with EcoRI, blunted, and the entire YAP complementary DNA (cDNA) was moved in the EcoRV site of the lentiviral vector p156RRLsin.PPTh CMV.MCS.pre. Lentiviruses were produced as described.23 The concentration of viral p24 antigen was assessed using the HIV-1 p24 core profile enzyme-linked immunosorbent assay kit (NEN Life Science Products) according to the manufacturer’s instructions. For in vivo studies, viral particles of mutated YAP (mYAP) (Ser127Ala and Ser381Ala) and control vector were purified by way of ultracentrifugation and suspended in sterile, endotoxin-free phosphate-buffered saline. Viral particles (20 μg of purified p24/mice in 400 μL phosphate-buffered saline) were injected into the tail vein of CD-1 mice 3 days after the first and 4 days prior to the second TCPOBOP administration (Fig. 3A).

18–20 Interestingly, in humans, amplification of the chromosomal region containing the YAP gene (11q22) has been reported in several tumor types.21, 22 On the basis of these findings, we investigated

whether (1) the Hippo pathway plays a critical role in the termination of the xenobiotic-induced liver overgrowth and (2) this pathway is defective in cancer cells arising in hyperplastic livers. AFP, alpha-fetoprotein; BrdU, 2-bromodeoxyuridine; CAR, constitutive androstane receptor; cDNA, complementary DNA; CTGF, connective tissue growth factor; Cyp2b10, cytochrome 2b10; DENA, diethylnitrosamine; buy MLN0128 HCC, hepatocellular carcinoma; miR-375, microRNA 375; mYAP, YAP mutated in Ser127 and Ser381; PCNA, proliferating cell nuclear antigen; PCR, polymerase chain reaction; TCPOBOP, 1,4-bis(2-(3,5-dichloropyridyloxy)benzene; YAP, Yes-associated protein. C3H or CD-1 female mice (8 weeks old) were obtained from Charles River (Milano, Italy). All experiments were performed in accordance with the Universities Federation for Animal Welfare Handbook on the Care and Management of

Laboratory Animals and the guidelines PD0325901 molecular weight of the animal ethics committee of the University of Cagliari. In experimental protocol 1 (Fig. 1A), hepatocyte proliferation was induced by 1,4-bis[2-(3,5-dichloropyridyloxy)]benzene (TCPOBOP) (3 mg/kg body weight, dissolved in dimethyl sulphoxide–corn oil solution; Sigma-Aldrich, Milan, Italy). Controls received an equivalent amount of the vehicle. To determine the proliferative response of the liver to TCPOBOP, mice were given 2-bromodeoxyuridine (BrdU) dissolved in drinking water (1 mg/mL; Sigma-Aldrich, selleck inhibitor Milan, Italy) and sacrificed 1 week later. In experimental protocol 2 (Fig. 2A), mice were treated as in protocol 1 except that they were sacrificed 24 hours, 36 hours, and 1 week after one dose or 24 and 36 hours after two doses of TCPOBOP. BrdU dissolved in drinking water was given as shown in Fig. 2A. The p2xFlag CMV-YAP vector

(a kind gift from M. Sudol) was digested with EcoRI, blunted, and the entire YAP complementary DNA (cDNA) was moved in the EcoRV site of the lentiviral vector p156RRLsin.PPTh CMV.MCS.pre. Lentiviruses were produced as described.23 The concentration of viral p24 antigen was assessed using the HIV-1 p24 core profile enzyme-linked immunosorbent assay kit (NEN Life Science Products) according to the manufacturer’s instructions. For in vivo studies, viral particles of mutated YAP (mYAP) (Ser127Ala and Ser381Ala) and control vector were purified by way of ultracentrifugation and suspended in sterile, endotoxin-free phosphate-buffered saline. Viral particles (20 μg of purified p24/mice in 400 μL phosphate-buffered saline) were injected into the tail vein of CD-1 mice 3 days after the first and 4 days prior to the second TCPOBOP administration (Fig. 3A).

In lineages with plasticity, there were five parallel paths of evolution, each toward the optimal morphology for one of the habitats. For these simulations, species distinguishability was drastically less than for the previous simulations (48.6% for the simpler organisms, 69.7% for the

more complex organisms; Fig. 3). In other words, plasticity has a strongly negative Erlotinib effect on the potential to recognize species based on their morphology. Any advantages brought about by habitat selection (i.e., subdivision of the species distinguishability problem into subproblems) are completely wiped out by the presence of species that have distinctive morphologies in the different habitats they inhabit. There are three main messages we can take home from this simulation exercise. First, there are substantially fewer unique morphologies than there are species in lineages with simple structures. In other words, we can expect cryptic diversity to abound

and indeed, this appears to be the case in algal taxonomy. As such, for any given algal taxon, we should expect to be unable to distinguish between at least some and possibly many of its species based on morphology alone. The second conclusion is that these problems are more pronounced in simple organisms than in more complex organisms, but PD-1/PD-L1 inhibition even in complex organisms there are generally much fewer distinct morphologies than there are species. Third, habitat-induced plasticity drastically reduces the

likelihood that one can distinguish between species based on morphology, even in complex organisms. These simulation results, in combination with what we have learned from empirical studies over click here the last few decades, have clear consequences for how species-level taxonomy is best approached in algae. Most importantly, morphological features have lost credibility as the primary species delimitation criterion. They can still play an important role in the initial discovery of unknown entities in the field or in collections, but should not be trusted to be informative about species boundaries without verification by other methods (preferably DNA-based). Importantly, the results also suggest that one should not assume that because two individuals look alike, they are going to belong to the same species because a substantial proportion of species can be expected to be cryptic. This has consequences for how field-work is carried out. Rather than sampling one or a few individuals of each morphological type, we should move to a sampling design where many individuals of similar morphology are investigated in detail. So how should species be delimited? Neutral DNA markers are an obvious and easily obtainable alternative source of information.

In lineages with plasticity, there were five parallel paths of evolution, each toward the optimal morphology for one of the habitats. For these simulations, species distinguishability was drastically less than for the previous simulations (48.6% for the simpler organisms, 69.7% for the

more complex organisms; Fig. 3). In other words, plasticity has a strongly negative selleck effect on the potential to recognize species based on their morphology. Any advantages brought about by habitat selection (i.e., subdivision of the species distinguishability problem into subproblems) are completely wiped out by the presence of species that have distinctive morphologies in the different habitats they inhabit. There are three main messages we can take home from this simulation exercise. First, there are substantially fewer unique morphologies than there are species in lineages with simple structures. In other words, we can expect cryptic diversity to abound

and indeed, this appears to be the case in algal taxonomy. As such, for any given algal taxon, we should expect to be unable to distinguish between at least some and possibly many of its species based on morphology alone. The second conclusion is that these problems are more pronounced in simple organisms than in more complex organisms, but Stem Cell Compound Library in vitro even in complex organisms there are generally much fewer distinct morphologies than there are species. Third, habitat-induced plasticity drastically reduces the

likelihood that one can distinguish between species based on morphology, even in complex organisms. These simulation results, in combination with what we have learned from empirical studies over selleck screening library the last few decades, have clear consequences for how species-level taxonomy is best approached in algae. Most importantly, morphological features have lost credibility as the primary species delimitation criterion. They can still play an important role in the initial discovery of unknown entities in the field or in collections, but should not be trusted to be informative about species boundaries without verification by other methods (preferably DNA-based). Importantly, the results also suggest that one should not assume that because two individuals look alike, they are going to belong to the same species because a substantial proportion of species can be expected to be cryptic. This has consequences for how field-work is carried out. Rather than sampling one or a few individuals of each morphological type, we should move to a sampling design where many individuals of similar morphology are investigated in detail. So how should species be delimited? Neutral DNA markers are an obvious and easily obtainable alternative source of information.

No serious complications occurred in either group. Conclusions: 

In this retrospective and small case series, guidewire cannulation after needle-knife fistulotomy increased the success rate of selective bile duct cannulation in patients with difficult bile duct access. “
“Cyclin G1 deficiency is associated with reduced PLX4032 mouse incidence of carcinogen-induced hepatocellular carcinoma (HCC), but its function in HCC progression remains obscure. We report a critical role of cyclin G1 in HCC metastasis. Elevated expression of cyclin G1 was detected in HCCs (60.6%), and its expression levels were even higher in portal vein tumor thrombus. Clinicopathological analysis revealed a close correlation of cyclin G1 expression with distant metastasis and poor prognosis of HCC. Forced expression of cyclin G1 promoted epithelial-mesenchymal transition (EMT) and metastasis of HCC cells in vitro and in vivo. Cyclin G1 overexpression enhanced Akt activation through interaction with p85 (regulatory subunit of phosphoinositide 3-kinase [PI3K]), which led to subsequent phosphorylation of glycogen

synthase kinase-3β (GSK-3β) and stabilization of Snail, a critical EMT mediator. TSA HDAC clinical trial These results suggest that elevated cyclin G1 facilitates HCC metastasis by promoting EMT via PI3K/Akt/GSK-3β/Snail-dependent pathway. Consistently, we have observed a significant correlation between cyclin G1 expression and p-Akt levels in a cohort of HCC patients, and found that combination of these two parameters is a more powerful predictor of poor prognosis. Conclusions: Cyclin G1 plays a pivotal role in HCC metastasis and may serve as a novel prognostic biomarker and therapeutic target. (HEPATOLOGY 2012;55:1787–1798) Cyclin G1 was first

identified serendipitously in screening for Src kinase family in rat fibroblasts.1 It has been categorized as a cyclin on account of possessing a well-conserved cyclin box, although it lacks a destruction box or PEST (Pro, Glu, Ser and Thr)-rich sequences that are responsible for cyclin degradation.1 Cyclin G1 has been well documented as a p53-responsive gene and could be transcriptionally activated by p53 or p73.2, 3 In fact, p53 is the selleckchem major factor regulating cyclin G1 expression upon DNA damage.4 Cyclin G1 was reported to interact with the B′ regulatory subunit of protein phosphatase 2A, which in turn dephosphorylated MDM2 followed by p53 degradation.5 A feedback regulation of p53 by cyclin G1 was also observed in cyclin G1-null mouse embryo fibroblasts, which exhibited increased p53 levels.6, 7 Additionally, cyclin G1 was found to interact with certain proteins involved in cell cycle regulation, such as cyclin G–associated kinase and cyclin-dependent kinase 5, but the physiologic significance of these interactions remains elusive.8 Cyclin G1–deficient mice have been reported to be viable without any apparent phenotype.

No serious complications occurred in either group. Conclusions: 

In this retrospective and small case series, guidewire cannulation after needle-knife fistulotomy increased the success rate of selective bile duct cannulation in patients with difficult bile duct access. “
“Cyclin G1 deficiency is associated with reduced selleck chemicals incidence of carcinogen-induced hepatocellular carcinoma (HCC), but its function in HCC progression remains obscure. We report a critical role of cyclin G1 in HCC metastasis. Elevated expression of cyclin G1 was detected in HCCs (60.6%), and its expression levels were even higher in portal vein tumor thrombus. Clinicopathological analysis revealed a close correlation of cyclin G1 expression with distant metastasis and poor prognosis of HCC. Forced expression of cyclin G1 promoted epithelial-mesenchymal transition (EMT) and metastasis of HCC cells in vitro and in vivo. Cyclin G1 overexpression enhanced Akt activation through interaction with p85 (regulatory subunit of phosphoinositide 3-kinase [PI3K]), which led to subsequent phosphorylation of glycogen

synthase kinase-3β (GSK-3β) and stabilization of Snail, a critical EMT mediator. BGB324 order These results suggest that elevated cyclin G1 facilitates HCC metastasis by promoting EMT via PI3K/Akt/GSK-3β/Snail-dependent pathway. Consistently, we have observed a significant correlation between cyclin G1 expression and p-Akt levels in a cohort of HCC patients, and found that combination of these two parameters is a more powerful predictor of poor prognosis. Conclusions: Cyclin G1 plays a pivotal role in HCC metastasis and may serve as a novel prognostic biomarker and therapeutic target. (HEPATOLOGY 2012;55:1787–1798) Cyclin G1 was first

identified serendipitously in screening for Src kinase family in rat fibroblasts.1 It has been categorized as a cyclin on account of possessing a well-conserved cyclin box, although it lacks a destruction box or PEST (Pro, Glu, Ser and Thr)-rich sequences that are responsible for cyclin degradation.1 Cyclin G1 has been well documented as a p53-responsive gene and could be transcriptionally activated by p53 or p73.2, 3 In fact, p53 is the selleck chemicals llc major factor regulating cyclin G1 expression upon DNA damage.4 Cyclin G1 was reported to interact with the B′ regulatory subunit of protein phosphatase 2A, which in turn dephosphorylated MDM2 followed by p53 degradation.5 A feedback regulation of p53 by cyclin G1 was also observed in cyclin G1-null mouse embryo fibroblasts, which exhibited increased p53 levels.6, 7 Additionally, cyclin G1 was found to interact with certain proteins involved in cell cycle regulation, such as cyclin G–associated kinase and cyclin-dependent kinase 5, but the physiologic significance of these interactions remains elusive.8 Cyclin G1–deficient mice have been reported to be viable without any apparent phenotype.

A multilocus sequence typing method was developed for H. suis, revealing that H. suis is a genetically diverse bacterial species on the pig herd level [46]. In addition, strain typing revealed that the H. suis strain colonizing the pig veterinarian described above [3] showed a very close relationship

to porcine H. suis strains. Moodley et al. [47] described how the H. pylori phylogeny splits into 2 primary superlineages, after which the closely related H. acinonychis originated from a host jump from the San people to large felines approximately 43,000–56,000 years ago. The complete genome sequence of H. cinaedi strain PAGU611 isolated in a case of human bacteremia was reported [48]. The PAGU611 genome is comprised of a 2,078,348-bp chromosome and a 23,054-bp plasmid Romidepsin cell line (pHci1) with average G+C contents of 38.6% and 31.6%, respectively. Synteny plots identified a unique H. cinaedi genomic island (HciGI1)

containing 173 protein-coding sequences including 147 hypothetical protein genes and 12 genes to assemble a type VI secretion system (T6SS). Okoli et al. [49] reported the effects of human and porcine bile on the proteome of H. hepaticus, Opaganib manufacturer revealing that 46 proteins of H. hepaticus were differentially expressed in human bile, and 32 proteins were differentially expressed in porcine bile. These data suggest that bile is an important factor that determines

the virulence, host adaptation, localization, and colonization of specific niches within the host environment. Kaakoush et al. [50] identified 104 proteins of H. trogontum that were bioinformatically predicted to be secreted, including 11, 11, 3, and 3 proteins involved in the response to oxidative stress or redox reactions, motility, virulence, and the T6SS, respectively. An apoprotein form of the Helicobacter mustelae iron urease, encoded by ureA2B2 genes, was shown to be activated with ferrous ions in the absence of auxiliary proteins, but not with nickel ions, as goes for the “standard” gastric Helicobacter ureAB, which also needs accessory proteins click here for its proper activity [51]. Schur et al. [52] cloned and expressed HAC1267 and HAC1268, 2 sialyltransferase enzymes of the GT-42 family from H. acinonychis strain ATCC 51104, revealing that HAC1268 is the first member of this family showing α2,6-sialyltransferase activity. The construction and characterization of a nikR mutant strain of H. hepaticus was reported [53]. Disruption of this gene, encoding the nickel-responsive regulator NikR, led to increased activities of two Ni-requiring enzymes: urease and hydrogenase. In addition, the mutant strain had a two- to threefold lower growth yield than the wild-type strain, suggesting that the regulatory protein might play additional roles in this mouse liver pathogen.