One was an adult, 27-yr-old female dolphin with coccidioidomycosis confirmed by culture of fine-needle AZD1208 in vivo aspirate from a lung lesion. The second case was an adult, 12-yr-old male with a Mycoplasma infection of the lung confirmed by a polymerase catalyzed reaction (PCR) assay and immunohistochemical staining (IHC). Statistics were conducted using SAS Release 9.2 (SAS Incorporated, Cary, NC). NO was measured in triplicate from each sample,

and a Pearson correlation coefficient was used to determine the test-retest reliability among the three values. Once retest reliability was determined to be high (0.997), the mean value of the triplicate samples was used for subsequent statistical analyses. Repeated measures and Kruskal-Wallis nonparametric analyses were conducted to test for differences in NO, O2, and CO2 level by study (initial breath collection study and controlled feeding study); breath and outside air; breath hold time (30, 60, 90, and 120 s); and fasting/fed status. A P-value ≤0.05 was defined as significant. NO concentration in exhaled breath was higher compared to NO concentration in air (mean ± SD, 16.6 ± 14.2 ppb and 6.7 ± 5.4 ppb, respectively; P = 0.003). The percent O2 in air was higher than percent O2 in breath exhaled by dolphins in all groups after a 30 s breath hold (20.8%

± 0.4% and 11.9% ± 1.9%, respectively; P < 0.001); both of these groups had higher AZD1152-HQPA nmr percent O2 compared to breath exhaled after a 120 s breath hold (6.7% ± 2.2%, P < 0.001). The opposite was true for CO2; the amount of CO2 in air was lower than CO2 in breath exhaled after a 30 s breath

hold (1.2 ± 1.4 mmHg and 43.7 ± 7.3 mmHg, respectively; P < 0.001); As expected, CO2 was higher in breath exhaled after a 120 s breath hold (50.7 ± 6.7 mmHg, P < 0.001). The reliability coefficient among the triplicate readings of each breath sample was high (0.997, P < 0.001), demonstrating GNA12 that the instruments used in this study provided reliable readings among breath samples. A summary of NO breath measured among three healthy dolphins is provided (Table 1). Excluding an apparent outlier with NO measurements of 219 ppm, the range of the remaining 157 samples for NO concentration among the three dolphins was from 1.9 to 80.3 ppb. Using repeated measures analysis, there were no significant differences in NO concentration when comparing breath hold duration (30, 60, 90, and 120 s; P = 0.59). Dolphins had higher NO in breath after feeding compared to when they were fasted (P = 0.05). Nonparametric analyses using Kruskal-Wallis tests showed similar results for breath hold duration (P = 0.27) and fed vs. fasted (P < 0.0001), however, there was a significant difference in NO concentration when comparing individual animals (P = 0.01).

A total of 718 subjects were included in the analysis (mean age 71.6 ± 8.0 years, 40% men, 61% Hispanic). Using the TCV-adjusted DE definition, 19% of the sample had at least one dolichoectatic artery. In 7% of Peptide 17 cell line the subjects, two or more arteries were affected. The BA was the most common dolichoectatic artery. Reproducibility for arterial diameter measurements was good to excellent (.70–.95), while for visual assessment ranged from fair to good (.49–.79). A TCV-adjusted intracranial arterial diameter ≥2 SD is proposed as a useful DE definition. The variability in the prevalence of DE depending on the methods used underscores the need to agree

on a reliable, universal definition of DE. “
“Bilateral paramedian thalamic infarction is a rare subtype of stroke the etiology of which still remains undetermined in many patients. From a computed tomography (CT)/magnetic resonance imaging report database, we identified and analyzed 48 patients with bilateral paramedian thalamic infarction on diffusion-weighted imaging. Vascular pathologies were noted on CT angiography (CTA)/magnetic resonance angiography (MRA) and the P1 segments of the posterior cerebral artery (PCA) described as normal, hypoplastic, or absent. Vascular imaging revealed top of the basilar artery (BA) occlusion in 6 (12.5%), BA occlusion in 4 (8.3%), BA stenosis in 1 (2.1%), and BA hypoplasia in 3 (6.3%), PCA occlusion in 4 (8.3%), and PCA

stenosis in 4 (8.3%) patients. In 18 (37.5%) patients, one or both P1 segments of the PCA were hypoplastic or absent. Patients with hypoplastic/absent BMS-354825 price P1 segments were more likely to have exclusively bilateral paramedian thalamic lesions (P < .001). An embolic source could be identified in 25 (55.6%) patients; there were no significant differences between both groups. Vascular imaging is useful to determine underlying vascular pathologies and may support the diagnosis of small vessel disease in those patients with isolated bilateral paramedian thalamic infarction, hypoplastic/absent

P1 segment of the PCA, and lack of vascular pathology. selleck chemicals llc “
“Although transesophageal echocardiography (TEE) is the gold standard for right to left shunt detection, we observed that transcranial Doppler (TCD) was more sensitive and sought an explanation. We retrospectively evaluated results of TCD and TEE in 118 patients with cryptogenic stroke and transient ischemic attacks. TCDs were done as per modification of a published performance protocol and interpreted by a neurologist and radiologist. TEEs were performed and interpreted by five cardiologists without standardized protocol. Statistical methodology included χ2 tests, Fisher exact tests, and ANOVA. Overall agreement between TCD and TEE was found for 76 of 118 patients. Sensitivities of TCD and TEE were 93.8% and 53.1%. Sensitivities for TCD interpreters were 61.1% and 64.1%. Sensitivities for TEE operators varied from 46.7% to 75.7%.

Conclusion: These ITF2357 molecular weight findings indicate that autophagy plays a critical role in liver

regeneration and in the preservation of cellular quality, preventing hepatocytes from becoming fully senescent and hypertrophic. (Hepatology 2014;60:290–300) “
“Secretin stimulates ductal secretion by interacting with secretin receptor (SR) activating cyclic adenosine 3′,5′-monophosphate/cystic fibrosis transmembrane conductance regulator/chloride bicarbonate anion exchanger 2 (cAMPCFTRCl−/HCO AE2) signaling that is elevated by biliary hyperplasia. Cholangiocytes secrete several neuroendocrine factors regulating biliary functions by autocrine mechanisms. Melatonin inhibits biliary growth and secretin-stimulated choleresis in cholestatic bile-duct–ligated (BDL) rats by interaction with melatonin type 1 (MT1) receptor through down-regulation of cAMP-dependent signaling. No data exist regarding the role of melatonin synthesized locally by cholangiocytes in the autocrine regulation of biliary growth and function. In this study, we evaluated the (1) expression of arylalkylamine N-acetyltransferase (AANAT; the rate-limiting enzyme selleck chemicals llc for melatonin synthesis from serotonin) in cholangiocytes and (2) effect of local modulation of biliary AANAT expression on the autocrine proliferative/secretory responses of cholangiocytes. In the liver, cholangiocytes (and, to a lesser extent, BDL

hepatocytes) expressed AANAT. AANAT expression and melatonin secretion (1) increased in BDL, compared to normal rats and BDL rats treated with melatonin, and (2) decreased in normal and BDL rats treated with AANAT Vivo-Morpholino, compared to controls. The decrease in AANAT expression, and subsequent lower melatonin secretion by cholangiocytes, was associated with increased biliary proliferation and increased SR, CFTR, and Cl−/HCO AE2 expression. Overexpression of AANAT

in cholangiocyte cell lines decreased the basal proliferative rate and expression of SR, CFTR, and Cl−/HCO AE2 and ablated secretin-stimulated biliary secretion in these cells. Conclusion: Local modulation of melatonin synthesis may be important for management of the balance between biliary proliferation/damage Resminostat that is typical of cholangiopathies. (HEPATOLOGY 2013) Cholangiocytes modify canalicular bile before it reaches the duodenum through a series of secretory/absorptive events regulated by gastrointestinal hormones, including secretin.1, 2 Secretin stimulates bile secretion by interaction with secretin receptor (SR; expressed only by large cholangiocytes in the liver).3 Binding of secretin to its receptor induces an increase in cyclic adenosine 3′,5′-monophosphate (cAMP) levels,1, 4 activation of protein kinase A (PKA), which results in the efflux of Cl− through the cystic fibrosis transmembrane conductance regulator (CFTR),4 and subsequent activation of the chloride bicarbonate anion exchanger 2 (Cl−/HCO AE2)5 stimulating bicarbonate secretion.

microarray.org). DNA microarrays contained 41,125 cDNA clones and represented approximately 24,473 unique genes. The cDNAs were amplified and spotted on glass slides in duplicate by using a robotic arrayer. Total RNA (100μg) was labeled by reverse transcription in the presence of Cy5(red)-labeled or Cy3(green)-labeled SCH772984 nmr nucleotides (Amersham Biosciences, Piscataway, NJ). Two labeled RNAs were competitively hybridized to the microarray, and the signals were analyzed

by using a GenePix 4000A scanner (Axon Instruments, Molecular Devices, Palo Alto, CA). Quantitation was performed by using GenePix Pro 5.0 (Axon Instruments). Chromatin immunoprecipitation (ChIP) assay was performed on Hep3B cells, infected

by 75 MOI Ad-PPARγ or Ad-LacZ as control using EZ-Magna ChIP A kit (Millipore, Billerica, MA). Chromatin DNA fragments were precipitated with 10 μg PPARγ antibody (Santa Cruz Biotechnology). The DNA BMN673 was then de-crosslinked and extracted from the DNA-protein complex. The immunoprecipitated DNA was subjected to ChIP-PCR validation. To confirm the presence of PPARγ binding on promoter targets, we performed ChIP-PCR using four known PPARγ-responsive targets, including Acyl-coenzymeA oxidases (ACOX), phosphatase and tensin homolog (PTEN), fibronectin (Fn), and thromboxane A2 receptor (TBXA2R). Immunoprecipitated DNAs were amplified with primers (Supporting Table 1) flanking the consensus sequences of the PPARγ-responsive elements. After confirming that PPARγ binds to the above promoters, we demonstrated the success of ChIP against PPARγ. Expression of growth differentiation factor 15 (GDF15) promoter was detected in ChIP DNA samples with primer sequences listed

in Supporting Table 1. The final PCR products were electrophoresed on 1.5% agarose gels and photographed under ultraviolet light. GDF15 and Ki-67 were detected in paraffin-embedded Bcl-w liver sections using the specific antibodies and an avidin-biotin complex immunoperoxidase method.14 The proliferation index was determined by counting the numbers of cells staining positive for Ki-67 as percentages of the total number of tumor cells. At least 1000 tumor cells were counted each time. Total RNA was extracted from frozen liver tissues and cell pellets with RNA Trizol reagent (Invitrogen, Carlsbad, CA). The messenger RNA (mRNA) expression level of the target gene was determined by reverse transcription PCR (RT-PCR).7 Data were expressed as mean ± standard deviation (SD). Nonparametric data between two groups was computed by chi-squared test or Fisher Exact test. Multiple group comparisons were made by one-way analysis of variance after Bonferroni’s correction or Kruskal-Wallis test where appropriate. The difference for two different groups was determined by Mann-Whitney U test. A P value of less than 0.05 was considered statistically significant.

This consensus process was not directly sponsored by any commercial companies. The first face-to-face meeting in Kuala Lumpur was sponsored by the Steering Committee of ANMA and the Depsipeptide molecular weight second face-to-face meeting

in Beijing was sponsored by the Organizing Committee of ANMA 2011 Beijing Congress. No consensus team member has any financial disclosure to declare in relationship with this consensus process. “
“The liver architecture plays an important role in maintaining hemodynamic balance, but the mechanisms that underlie this role are not fully understood. Hepsin, a type II transmembrane serine protease, is predominantly expressed in the liver, but has no known physiological functions. Here, we report that hemodynamic balance in the liver is regulated through hepsin. Deletion of hepsin (hepsin−/−) in mice resulted in enlarged hepatocytes and narrowed liver sinusoids. Using fluorescent microbeads GDC-973 and antihepsin treatment, we demonstrated that metastatic cancer cells preferentially colonized the hepsin−/− mouse liver as a result of the retention of tumor cells because of narrower sinusoids. The enlarged hepatocytes expressed increased levels of connexin, which

resulted from defective prohepatocyte growth factor (pro-HGF) processing and decreased c-Met phosphorylation in the livers of hepsin−/− mice. Treatment of hepsin−/− mice with recombinant HGF rescued these phenotypes, and treatment of wild-type Amrubicin mice with an HGF antagonist recapitulated the phenotypes observed in hepsin−/− mice. Conclusion: Our findings show that the maintenance of hepatic structural homeostasis occurs through HGF/c-Met/connexin signaling by hepsin, and hepsin-mediated changes in liver architecture significantly enhance tumor metastasis to the liver. (HEPATOLOGY 2012;56:1913–1923) Type II transmembrane serine proteases (TTSPs) have important physiological functions and pathological implications in iron metabolism,1 blood pressure regulation, and metastasis of cancers.2 More than 20 TTSPs exist and they are

divided into four subfamilies. Among these families, the hepsin/enteropeptidase subfamily is recognized structurally by a scavenger receptor cysteine-rich domain linked to a serine protease domain contained within an extracellular stem region. Although hepsin may be involved in the progression of several human cancers,3 its physiological function has not yet been fully characterized. Hepsin is predominantly expressed in the liver.4 Antisense-oligonucleotide blockade of hepsin affects cell growth and enlarges and flattens hepatoma cells.5 Several in vitro studies have identified substrates for hepsin, including coagulation factor VII,6 prohepatocyte growth factor (pro-HGF),7 and prourokinase-type plasminogen activator.8 In addition, hepsin colocalizes with desmoplakin at the sites of desmosomal junctions.9 Previously, Wu et al.

However, no association with viral load has been identified [16]. In contrast with Ahonkai and Saif et al., Jacobsen et al. found no association between CD4 cell count and risk of VTE, but still suggested an association between VTE

and advanced HIV disease [15]. This agrees with Sullivan’s finding of an association between VTE and cytomegalovirus infection as well as other AIDS-defining opportunistic infections, but no association between VTE and low CD4 cell count [12]. Our study showed a trend towards a higher risk of VTE with a low CD4 count (<200 cells/μL), although the association was not statistically significant. IDU has been identified as a strong risk factor for community-acquired VTE in young adults [48,49], mainly because of the venous damage induced by the drug abuse [12,16,22]. IDU accounts for nearly 10% of all community-acquired VTE and almost 50% of episodes in patients aged ≥40 years [48]. This learn more is corroborated by our study, which found the risk of VTE to be nearly 15 times higher in IDU HIV-infected patients, mainly attributable to unprovoked VTE, and is in accordance with the fact that IDU is not included in the definition of provoked VTE. To our knowledge, our study is the first to show the impact

of IDU on risk of VTE in HIV-infected patients. The recent study of Sørensen et al. found that patients with venous thromboembolism have a substantially increased long-term risk of subsequent arterial cardiovascular events [34]. Furthermore, Brækkan et al. found that family history of myocardial infarction was a risk Ipatasertib order factor for overall as well as unprovoked VTE, independent of classical cardiovascular risk factors [50]. We and others have observed an increased risk of myocardial infarction after HAART initiation [9,10]. Accumulating evidence thus indicates that HIV infection and HAART may be associated with considerable arterial as well as venous side effects. We

found that HIV-infected patients Monoiodotyrosine are at increased risk of unprovoked and provoked VTE, especially in the IDU population. HAART and potentially low CD4 cell count further increase the risk. We are grateful to the staff of our clinical departments for their continuous support and enthusiasm. We thank Preben and Anna Simonseńs Foundation, the NOVO Foundation, the University of Southern Denmark and the Clinical Institute of Copenhagen University for financial support. Centres in the Danish HIV Cohort Study Departments of Infectious Diseases at Copenhagen University Hospitals, Rigshospitalet (J. Gerstoft and N. Obel) and Hvidovre (G. Kronborg), Odense University Hospital (C. Pedersen), Aarhus University Hospitals, Skejby (C. S. Larsen) and Aalborg (G. Pedersen), Herning Hospital (A. L. Laursen), Helsingør Hospital (L. Nielsen) and Kolding Hospital (J. Jensen). Conflicts of interest: N.

However, no association with viral load has been identified [16]. In contrast with Ahonkai and Saif et al., Jacobsen et al. found no association between CD4 cell count and risk of VTE, but still suggested an association between VTE

and advanced HIV disease [15]. This agrees with Sullivan’s finding of an association between VTE and cytomegalovirus infection as well as other AIDS-defining opportunistic infections, but no association between VTE and low CD4 cell count [12]. Our study showed a trend towards a higher risk of VTE with a low CD4 count (<200 cells/μL), although the association was not statistically significant. IDU has been identified as a strong risk factor for community-acquired VTE in young adults [48,49], mainly because of the venous damage induced by the drug abuse [12,16,22]. IDU accounts for nearly 10% of all community-acquired VTE and almost 50% of episodes in patients aged ≥40 years [48]. This Fer-1 manufacturer is corroborated by our study, which found the risk of VTE to be nearly 15 times higher in IDU HIV-infected patients, mainly attributable to unprovoked VTE, and is in accordance with the fact that IDU is not included in the definition of provoked VTE. To our knowledge, our study is the first to show the impact

of IDU on risk of VTE in HIV-infected patients. The recent study of Sørensen et al. found that patients with venous thromboembolism have a substantially increased long-term risk of subsequent arterial cardiovascular events [34]. Furthermore, Brækkan et al. found that family history of myocardial infarction was a risk check details factor for overall as well as unprovoked VTE, independent of classical cardiovascular risk factors [50]. We and others have observed an increased risk of myocardial infarction after HAART initiation [9,10]. Accumulating evidence thus indicates that HIV infection and HAART may be associated with considerable arterial as well as venous side effects. We

found that HIV-infected patients Dimethyl sulfoxide are at increased risk of unprovoked and provoked VTE, especially in the IDU population. HAART and potentially low CD4 cell count further increase the risk. We are grateful to the staff of our clinical departments for their continuous support and enthusiasm. We thank Preben and Anna Simonseńs Foundation, the NOVO Foundation, the University of Southern Denmark and the Clinical Institute of Copenhagen University for financial support. Centres in the Danish HIV Cohort Study Departments of Infectious Diseases at Copenhagen University Hospitals, Rigshospitalet (J. Gerstoft and N. Obel) and Hvidovre (G. Kronborg), Odense University Hospital (C. Pedersen), Aarhus University Hospitals, Skejby (C. S. Larsen) and Aalborg (G. Pedersen), Herning Hospital (A. L. Laursen), Helsingør Hospital (L. Nielsen) and Kolding Hospital (J. Jensen). Conflicts of interest: N.

Conclusions. Analysis of the results revealed significant deficits in travel medicine knowledge among health-care providers. Emphasis on continuing medical education for disease vector behavior, prophylactic drug prescription, and preventative vaccination is important to travel safety. Health professionals in Taiwan should actively participate in the International Society of Travel Medicine to follow the international standard of travel

medicine practitioners. This type of survey should be adopted in other countries which would be helpful in improving the quality of care selleck compound for travelers. Health-care providers play an essential role in ensuring healthy and safe travel. Although the International Society of Travel Medicine (ISTM) had tried to encourage the global professional development of travel medicine by promoting the ISTM Certificate of Knowledge Program, many countries, including Taiwan, are still not actively participating in the ISTM.1,2 The frequency of international travel has

increased dramatically, making pre-travel health advice and post-travel health issues the subject of frequent office visits for many health-care professionals.3 Therefore, Adriamycin mw health-care providers should have a general knowledge of travel medicine and be able to provide both adequate pre-travel consultation and post-travel care.4 In Taiwan, pre-travel health advice such as yellow fever vaccination and antimalaria drugs are mainly given in 11 hospitals contracted with Center for Disease Control of Taiwan. PIK3C2G The health professionals

in these hospitals are the main population of travel health providers in Taiwan. The field of travel medicine includes knowledge regarding numerous diseases, epidemiology, and vaccination issues.5,6 The scope of the travel medicine becomes increasingly more complex when factors such as patients’ chronic health issues, changes in disease vectors due to climate and environment change, new medication and vaccine developments, and rising drug resistance are taken into account. Education for health-care providers may not provide adequate training prior to initiating travel-related consultations. As a result, physicians, nurses, pharmacists, and other health-care professionals may require updates in their knowledge when advising travelers. Many questionnaire survey studies assessed the knowledge, attitude, and practices of travelers,7–9 but there are relatively few studies which aim to assess the knowledge of health-care professionals.10,11 The information obtained from such a study would provide invaluable data for governments and international organizations that could be used to promote the development of travel health profession. Mosquito-transmitted diseases such as malaria, yellow fever, and dengue fever, are commonly discussed during pre-travel counseling.12–15 Basic knowledge about the diseases, vaccines, and preventative medications is important for health professionals.

Haloarchaeal genomes encode the complete set of enzymes

of the TCA cycle (Falb et al., 2008). Furthermore, activity of all enzymes of the cycle was detected in Hbt. salinarum (Aitken & Brown, 1969). Field studies on a hypersaline cyanobacterial mat have shown metabolic interactions between haloarchaea and the primary producer Coleofasciculus (Microcoleus) chthonoplastes. This cyanobacterium excretes acids of the citrate cycle into the medium, and aerobic halophilic Selleckchem ACP-196 Archaea further utilizes these as the major carbon and energy source (Zvyagintseva et al., 1995). The existence of a functional glyoxylate cycle has been demonstrated in Haloferax volcanii (Serrano et al., 1998) and in Natronococcus occultus (Kevbrina & Plakunov,

1992). Inquiries effectuated on the 13 complete halophilic genomes present in the HaloWeb data base (DasSarma et al., 2010) did not find any simultaneous positive matches for the glyoxylate cycle key enzymes: isocitrate lyase and malate synthase (with the exception of previous mentioned species Hfx. volcanii). A blastp (Altschul et al., 1997) search made on NCBI using the amino acid sequences of the Hfx. volcanii isocitrate lyase and malate synthase showed that Proteasome inhibitor these enzymes are present also in Haladaptatus paucihalophilus strain DX253. Recently, a novel pathway for the synthesis of malate from acetyl-CoA was discovered

in Hfx. volcanii and in Har. marismortui, in which acetyl-CoA is oxidized to glyoxylate via methylaspartate as key intermediate (Khomyakova et al., 2011). Although most halophilic Archaea preferentially use amino acids as carbon and energy source, there are carbohydrate-utilizing species such as Haloarcula marismortui, Halococcus saccharolyticus, and Hfx. mediterranei. These species have the capacity to metabolize pentoses (arabinose, xylulose), hexoses (glucose, fructose), sucrose, and lactose (Rawal et al., 1988; Altekar & Rangaswamy, Paclitaxel solubility dmso 1992; Johnsen et al., 2001). Comparative analysis of ten haloarchaeal genomes showed that Halorhabdus utahensis and Haloterrigena turkmenica encode over forty glycosyl hydrolases each and may break down complex carbohydrates. Hrb. utahensis has specialized in growth on carbohydrates and has few amino acid degradation pathways. It uses the nonoxidative pentose phosphate cycle and a transhydrogenase instead of the oxidative pathway, giving it a great deal of flexibility in the metabolism of pentoses (Anderson et al., 2011). Hrb. utahensis degrades xylan and can grow on xylose (Wainø & Ingvorsen, 2003). Many species of Halobacteriaceae also produce exoenzymes such as proteases, lipases, DNAses, and amylases to degrade organic polymeric substances extracellularly, making small organic molecules available as carbon and energy source.

Haloarchaeal genomes encode the complete set of enzymes

of the TCA cycle (Falb et al., 2008). Furthermore, activity of all enzymes of the cycle was detected in Hbt. salinarum (Aitken & Brown, 1969). Field studies on a hypersaline cyanobacterial mat have shown metabolic interactions between haloarchaea and the primary producer Coleofasciculus (Microcoleus) chthonoplastes. This cyanobacterium excretes acids of the citrate cycle into the medium, and aerobic halophilic RG7204 manufacturer Archaea further utilizes these as the major carbon and energy source (Zvyagintseva et al., 1995). The existence of a functional glyoxylate cycle has been demonstrated in Haloferax volcanii (Serrano et al., 1998) and in Natronococcus occultus (Kevbrina & Plakunov,

1992). Inquiries effectuated on the 13 complete halophilic genomes present in the HaloWeb data base (DasSarma et al., 2010) did not find any simultaneous positive matches for the glyoxylate cycle key enzymes: isocitrate lyase and malate synthase (with the exception of previous mentioned species Hfx. volcanii). A blastp (Altschul et al., 1997) search made on NCBI using the amino acid sequences of the Hfx. volcanii isocitrate lyase and malate synthase showed that CAL-101 datasheet these enzymes are present also in Haladaptatus paucihalophilus strain DX253. Recently, a novel pathway for the synthesis of malate from acetyl-CoA was discovered

in Hfx. volcanii and in Har. marismortui, in which acetyl-CoA is oxidized to glyoxylate via methylaspartate as key intermediate (Khomyakova et al., 2011). Although most halophilic Archaea preferentially use amino acids as carbon and energy source, there are carbohydrate-utilizing species such as Haloarcula marismortui, Halococcus saccharolyticus, and Hfx. mediterranei. These species have the capacity to metabolize pentoses (arabinose, xylulose), hexoses (glucose, fructose), sucrose, and lactose (Rawal et al., 1988; Altekar & Rangaswamy, Farnesyltransferase 1992; Johnsen et al., 2001). Comparative analysis of ten haloarchaeal genomes showed that Halorhabdus utahensis and Haloterrigena turkmenica encode over forty glycosyl hydrolases each and may break down complex carbohydrates. Hrb. utahensis has specialized in growth on carbohydrates and has few amino acid degradation pathways. It uses the nonoxidative pentose phosphate cycle and a transhydrogenase instead of the oxidative pathway, giving it a great deal of flexibility in the metabolism of pentoses (Anderson et al., 2011). Hrb. utahensis degrades xylan and can grow on xylose (Wainø & Ingvorsen, 2003). Many species of Halobacteriaceae also produce exoenzymes such as proteases, lipases, DNAses, and amylases to degrade organic polymeric substances extracellularly, making small organic molecules available as carbon and energy source.