21,22 The increased risk of infection may also be due to the immunomodulatory effects of rheumatic disease.23,24 Indeed, in our study, 8 of 10 ISA with travel-related signs of skin infection had a rheumatic disorder, of which 4 (50%) used anti-TNF alpha drugs, opposed to 13 of 43 (30%) ISA with a rheumatic disorder without travel-related skin infection (p = 0.31). Because bacterial skin infection can be life-threatening, especially for immunocompromised persons, stand-by antibiotics for this may be useful for areas where the availability of proper treatment is poor. This Volasertib datasheet needs

further investigation. For IBD, the IR and the median number of days with diarrhea and abdominal pain were higher than among controls, both before and during travel. The incidence and burden of vomiting were higher among IBD, in particular during travel. The same was true for the burden of signs of skin infection, not the incidence. http://www.selleckchem.com/products/cx-5461.html No differences in travel-related fever, cough, rhinitis, and fatigue were found. Our study

design had distinctive strengths. Structurally specified data were obtained prospectively and on a daily basis. Data collection started before departure to gain insight into preexisting symptoms. It continued until 2 weeks after return from travel to encompass incubation periods of the most (acute) travel-related infectious diseases. With a travel companion serving as a matched control, situational specifics for the immunocompromised travelers and controls were comparable, which minimized any differences in exposure to infectious agents between the two groups. Both groups also matched for age and country of birth, but not for gender: both ISA and IBD were more often female. Yet, prospective new studies on travel-related infectious diseases found no association of symptoms of infectious diseases and gender.25–28 The prevalence of ISA and IBD among visitors of the travel clinic of the Public Health Service Amsterdam in 2008 was 0.5 and 0.4%, respectively, comparable with the general population in a developed country.10–12 Also, the ages of our subjects with rheumatoid

arthritis or IBD were comparable with the general population. Participants’ travel destinations were equally distributed across the four regions. Their median travel duration of 20 days corresponded well with the median travel duration of the average traveler.29,30 Thus, the study sample can be considered representative, and results can reasonably be applied to the average traveler with ISA or IBD to a developing country. Nevertheless, our findings represent immunocompromised persons who were well and confident enough to travel. This study also had some limitations. Sample size may not have been large enough to detect small differences. Secondly, some of the symptomatic illnesses could have been due to a non-infectious cause.

mutans, which is one of the principle causative agents of dental caries, has to be elucidated. MicroRNAs (miRNAs) are small noncoding RNAs that are c. 22 nt long. They are found in various species of plants, animals and viruses (Bushati & Cohen, 2007), and normally act as regulators in every major cellular event through inhibitory

mechanisms (He & Hannon, 2004). It has long been known that bacteria contain noncoding small RNAs (sRNAs) that have regulatory functions, other than miRNAs (Gottesman, 2005; Waters & Storz, 2009). sRNAs are usually between 50 and 200 nt in length and have been predicted by computational searches in a variety of bacterial species (Livny & Waldor, 2007). Like miRNAs, sRNAs usually act as post-transcriptional regulators by interacting with the target mRNAs through a variety of mechanisms, including changes in RNA conformation and modulation of the stability

of the specific targets (Waters & Storz, check details find more 2009). Smaller RNAs that have size similar to miRNAs are not well understood in bacteria, although many of them may be found among sequence reads registered in the transcriptome of Escherichia coli (Dornenburg et al., 2010). Streptococcus mutans is the major causative agent of human dental caries and is considered to be the most cariogenic of all of the oral streptococci (Ajdić et al., 2002). The disease occurs when ecologically driven changes in oral biofilms are perturbed and S. mutans is mainly responsible for the formation of the oral biofilms (Burne, 1998). The genome of S. mutans has been fully sequenced and contains c. 2 Mb and 1963 ORFs (Ajdić et al., 2002). This study examined the existence of small (c. 26 nt) RNAs in S. mutans that we subsequently isolated. For this purpose, a deep sequencing (next-generation sequencing) approach was used and more

than 19 million sRNA clones were read. To differentiate these very sRNAs from the bacterial sRNAs (50–250 nt) and well-studied eukaryotic miRNAs, we suggest the term ‘miRNA-size, Transmembrane Transproters inhibitor small RNA’ (msRNA). Their origin and putative functional significance are discussed. Streptococcus mutans (ATCC 25175) were inoculated into brain heart infusion broth (three independent cultures) and total RNA was extracted from the cultured S. mutans after pooling using the miRNeasy Mini kit (Qiagen, CA) according to the manufacturer’s protocol. RNA was processed and used for deep sequencing by LC Sciences (Houston, TX). An sRNA library was generated from the S. mutans RNA according to Illumina’s sample preparation instructions for Illumina Genome Analyzer IIx (Ilumina Inc., San Diego, CA). The following gives a brief summary of the procedures performed. The total RNA sample was size-fractionated on a 15% Tris–borate–EDTA (TBE)–urea polyacrylamide gel. The RNA fragments of c. 15–50 nt in length were eluted and ethanol-precipitated.

PERIOD1 antibody was the generous gift of Shimon Amir. This project was funded by grants from the Natural Sciences and Engineering Research Council of Canada (NSERC) and the Canadian Funds for innovation (CFI) awarded to A.A. E.W.L. was supported by postdoctoral fellowship from the Fonds de la recherche en santé du Québec (FRSQ). Abbreviations ARC arcuate nucleus CT circadian time DD constant darkness DMH dorsomedial nucleus of the hypothalamus GHSR growth hormone secretagogue Staurosporine clinical trial receptor KO

knockout LD 12 h of light and 12 h of darkness LH lateral hypothalamus LL constant light PER1 PERIOD1 PER2 PERIOD2 PVN paraventricular nucleus of the hypothalamus PVT paraventricular nucleus of the thalamus RF restricted feeding SCN suprachiasmatic

nucleus SPVZ subparaventricular buy MG-132 zone VMH ventromedial hypothalamus ZT zeitgeber time Table S1. Summary data of period and acrophase (in hours) for individual animals under LD, LL with ad libitum feeding and 10 and 30 days, and LL with temporally restricted access to food (LLRF). Table S2. Summary data of period and acrophase (hours) for individual animals under DD with ad libitum feeding and DD with temporally restricted access to food (DDRF). “
“The neurotransmitter dopamine (DA) plays a critical role in both priming-and cue-induced reinstatement of extinguished drug-seeking behavior, but its role in stress-induced reinstatement is less clear. Our laboratory has recently demonstrated that systemic administration of the DA D1-like

receptor antagonist, SCH 23390, attenuates acute food deprivation (FD) stress-induced reinstatement. The current study was designed to elucidate the brain regions critical to the effect of SCH 23390 on FD stress-induced reinstatement. Rats were trained to press a lever to self-administer heroin (0.1 mg/kg/inf) over a period of 10 days. Following training, heroin was removed leading to an extinction of lever pressing. Next, rats were tested for reinstatement twice, under extinction conditions: once following 21–48 h FD; and once under sated conditions. Prior to testing, SCH 23390 was administered into the nucleus accumbens (NAc) shell (0.0, 0.3, 0.6 μg/side), NAc core (0.0, 0.3, 0.6 μg/side), dorsomedial prefrontal cortex (dmPFC; 0.0, 0.2, 2.0 μg/side), ventromedial HAS1 prefrontal cortex (vmPFC; 0.0, 2.0 μg/side) or basolateral amygdala (BLA; 0.0, 1.0, 2.0 μg/side). An attenuation of FD-induced reinstatement of heroin seeking was seen in rats injected with SCH 23390 into the NAc shell, dmPFC or BLA, but not into the NAc core or the vmPFC. These findings support the hypothesis that DA transmission through the DA D1-like receptors plays a critical role in stress-induced reinstatement of heroin seeking. “
“Eye blinks, typically occurring 15–20 times per minute, rarely capture attention during face-to-face interaction.

, 1995) was identified in the six pneumococcal strains, and its single-nucleotide variant TATGATAgAAT was found in the rest of the 23 genome sequences analyzed. Changes in this nucleotide are not critical Vincristine mouse for the binding of the σ subunit of the

RNA polymerase (Sevostyanova et al., 2007). A Shine- and Dalgarno-like sequence (SD) (AGGAGG) is located five nucleotides upstream of the gpdA start codon (AUG). As expected, the polycistronic transcript has a putative transcription start site within a purine (A) nucleotide located seven nucleotides downstream of the −10 extended promoter element. The putative promoter sequence consists of an extended −10 element without a −35 site and is situated 30 nucleotides upstream of the ATG initiation codon of the gpdA gene. Regarding pneumococcal promoters, we compared similar extended −10 elements of sulA (dihydropteroate synthase), murB (UDP-N-acetylenolpyruvoylglucosamine reductase), pcrA (ATP-dependent DNA helicase), comCDE operon, and fcsR (regulator of fucose operon) with the gpdA-galU promoter described herein (Chan et al., 2003; Ware et al., 2005; Ruiz-Masó et al., 2006 and Martin et al., 2010). These sequences match the consensus extended −10 region previously JNK inhibitor described by Sabelnikov et al. (1995) (TnTGnTATAAT). The nucleotides in the canonical −10 hexamer TATAAT are conserved in murB, pcrA, comCDE, fcsR,

and gpdA-galU (six strains). Moreover, −10 extended promoter element of comCDE showed an alteration of the T-TG extension. Also, −10 and −35 promoter elements found in fcsK (fuculose kinase),

yefM-yoeB (toxin–antitoxin), relB2 (antitoxin), and tts (βglucosyltransferase) genes were compared, and most of them showed −10 canonical element (TATAAT) and the −35 box (TTGACA) with minor differences (Llull et al., 2001; Chan et al., 2003, 2011; Nieto et al., 2006). On the other hand, ung (DNA-uracil glycosylase) and spxB (pyruvate oxidase) exhibit −10 extended promoter element and a −35 box (Ramos-Montañez et al., 2008; Ruiz-Cruz et al., 2010), (Fig. 3b). Semi-quantitative real-time reverse transcription PCR (RT-PCR) was used to compare relative transcriptional Dolichyl-phosphate-mannose-protein mannosyltransferase abundance of galU transcripts at different points of the growth curve of S. pneumoniae R6. The results showed that galU-specific transcript levels in the exponential phase were 14-fold higher than during the other phases (Dunnet’s test, P < 0.05; Table 2), in agreement with that previously suggested for metabolic genes involved in biosynthetic processes whose expression is probably down-regulated in the stationary phase (Navarro Llorens et al., 2010). However, our results contrast with those carried out in Bacillus subtilis (Varón et al., 1993) and Lactobacillus casei (Wu et al., 2009) where the expression of the corresponding galU genes increased in the stationary phase.

The potential drug–drug interactions that may occur in HIV-infected individuals with comorbidities such as diabetes, hypertension, dyslipidaemia and hyperuricaemia are a subject of much debate. There is clearly a risk of impaired drug tolerance and efficacy. PIs ALK signaling pathway and nonnucleoside reverse transcriptase inhibitors (NNRTIs) are all metabolised in the liver by the cytochrome (CYP) 450 system, a common metabolic pathway for many other drugs, including statins. Some PIs and NNRTIs inhibit statin excretion and therefore a lower starting dose is required. Conversely, others

reduce the efficacy of the statin, meaning that a higher dose may be needed [5]. Regular monitoring and dose titration are therefore essential in patients taking ART and statin therapy. Fibrates are not considered to potentially interact with ritonavir, or PIs in general [40]. The challenge of treating diabetes and dyslipidaemias in HIV-infected patients receiving ART, including PIs, and especially ritonavir, has been reviewed by Fantoni [41]. Drug–drug interactions may occur between ritonavir and rosiglitazone in the management of diabetes, leading to a reduced metabolism and potential overdosage of the anti-diabetic drug. Knowledge of when to refer to other specialist colleagues has become very important; similarly, proactive communication of the need for lifestyle changes related

to diet, smoking, alcohol use and physical activity is paramount. Clinicians Afatinib order should be given the opportunities to educate each other, within their own hospitals, and HIV physicians should be discouraged from working in isolation. Programmes such as the ongoing HIV and the Body initiative (http://www.hivandthebody.com) can help address some of these issues. As well as a programme of international and national medical education meetings, expert-led treatment and management algorithms are available for physicians

to download from http://www.hivandthebody.com and use in everyday practice. There is an increasing Protirelin need for ongoing monitoring of interventions that aim to reduce the risk of development and progression of comorbidities in individuals infected with HIV. Awareness of the findings of clinical endpoint studies, such as fracture prevalence studies, and the use of surrogate markers in CVD are important in achieving a clear picture of the impact of the intervention. Risk stratification tools are not sufficient to demonstrate the effectiveness of an intervention. Patient-related outcomes and the evaluation of quality of life are also important, particularly in the assessment of interventions to address comorbidities that affect body image, such as lipodystrophy [9]. An ageing HIV-infected population demands a new approach to the management of HIV infection.

The inhibitory effect of LOV has been investigated in detail. LOV induced apoptosis-like

cell death in Mucor racemosus (Roze & Linz, 1998) and inhibited the growth of different Rhizomucor species (Lukács et al., 2004). The fungistatic effect of LOV has been demonstrated in Candida albicans (Gyetvai et al., 2006), and the antifungal activities of SIM and ATO have been observed against Aspergillus fumigatus and various Candida species (Macreadie et al., 2006). The growth-inhibitory effect of statins is probably based on their negative influence on membrane fluidity (Gyetvai et al., 2006). They also indirectly affect cell signaling (Cordle et al., 2005), proliferation and differentiation through inhibition of the synthesis of important terpenoids (Miida et al.,

2004). Because of the fungus-specific or immunomodulating Selleckchem Bleomycin actions of statins, it has been hypothesized that the widespread use of statins by patients with diabetes has led to lower rates of zygomycoses in developed countries since the 1990s (Kontoyiannis, 2007). Some published work has suggested the possibility Selleck Everolimus of the combined application of statins and different antimycotics (Chin et al., 1997; Chamilos et al., 2006; Galgóczy et al., 2007; Natesan et al., 2008; Nyilasi et al., 2010). Azoles are a class of antifungal drugs that target the fungal cell membrane by inhibiting the cytochrome P450-dependent 14α-lanosterol demethylase, which catalyzes a critical step of ergosterol biosynthesis. Imidazoles, such as miconazole (MCZ) and ketoconazole (KET), are generally used topically, whereas triazoles, such as fluconazole (FLU), itraconazole (ITR) and voriconazole, are applied orally or PI-1840 intravenously against systemic mycoses. The aim of our study was to examine the inhibition of fungal growth by pairs of drugs, in order to find effective drug combinations. Each pair contained a statin (LOV, SIM, FLV, ATO, ROS or PRA) and an azole

compound (MCZ, KET, ITR and FLU). The in vitro interactions of the effects of these compounds against some opportunistic pathogenic yeasts and filamentous fungi were examined using a standard chequerboard broth microdilution method. Clinically important Candida (C. albicans and Candida glabrata) and Aspergillus species (A. fumigatus and Aspergillus flavus) and Rhizopus oryzae, the most frequent causative agent of zygomycoses (Ribes et al., 2000), were included in the study. All fungal isolates were collected from clinical sources. The A. fumigatus and A. flavus strains were isolated in Indian hospitals, and the C. albicans and C. glabrata strains in Hungarian hospitals. These strains were deposited in the Szeged Microbial Collection (SZMC) at the University of Szeged, Szeged, Hungary. Eleven C.

The inhibitory effect of LOV has been investigated in detail. LOV induced apoptosis-like

cell death in Mucor racemosus (Roze & Linz, 1998) and inhibited the growth of different Rhizomucor species (Lukács et al., 2004). The fungistatic effect of LOV has been demonstrated in Candida albicans (Gyetvai et al., 2006), and the antifungal activities of SIM and ATO have been observed against Aspergillus fumigatus and various Candida species (Macreadie et al., 2006). The growth-inhibitory effect of statins is probably based on their negative influence on membrane fluidity (Gyetvai et al., 2006). They also indirectly affect cell signaling (Cordle et al., 2005), proliferation and differentiation through inhibition of the synthesis of important terpenoids (Miida et al.,

2004). Because of the fungus-specific or immunomodulating Pexidartinib datasheet actions of statins, it has been hypothesized that the widespread use of statins by patients with diabetes has led to lower rates of zygomycoses in developed countries since the 1990s (Kontoyiannis, 2007). Some published work has suggested the possibility Erastin molecular weight of the combined application of statins and different antimycotics (Chin et al., 1997; Chamilos et al., 2006; Galgóczy et al., 2007; Natesan et al., 2008; Nyilasi et al., 2010). Azoles are a class of antifungal drugs that target the fungal cell membrane by inhibiting the cytochrome P450-dependent 14α-lanosterol demethylase, which catalyzes a critical step of ergosterol biosynthesis. Imidazoles, such as miconazole (MCZ) and ketoconazole (KET), are generally used topically, whereas triazoles, such as fluconazole (FLU), itraconazole (ITR) and voriconazole, are applied orally or Carbohydrate intravenously against systemic mycoses. The aim of our study was to examine the inhibition of fungal growth by pairs of drugs, in order to find effective drug combinations. Each pair contained a statin (LOV, SIM, FLV, ATO, ROS or PRA) and an azole

compound (MCZ, KET, ITR and FLU). The in vitro interactions of the effects of these compounds against some opportunistic pathogenic yeasts and filamentous fungi were examined using a standard chequerboard broth microdilution method. Clinically important Candida (C. albicans and Candida glabrata) and Aspergillus species (A. fumigatus and Aspergillus flavus) and Rhizopus oryzae, the most frequent causative agent of zygomycoses (Ribes et al., 2000), were included in the study. All fungal isolates were collected from clinical sources. The A. fumigatus and A. flavus strains were isolated in Indian hospitals, and the C. albicans and C. glabrata strains in Hungarian hospitals. These strains were deposited in the Szeged Microbial Collection (SZMC) at the University of Szeged, Szeged, Hungary. Eleven C.

These companies had no input into the study design, the data collection and analysis, or the interpretation Lumacaftor of the results. Appendix S1. D:A:D Study Group. Please note: Wiley-Blackwell is not responsible for the content or functionality of any supporting materials

supplied by the authors. Any queries (other than missing material) should be directed to the corresponding author for the article. “
“Conflicting results have been reported regarding the ability of valproic acid (VPA) to reduce the size of HIV reservoirs in patients receiving suppressive highly active antiretroviral therapy (HAART). In a randomized multicentre, cross-over study, we assessed whether adding VPA to stable HAART could potentially reduce the size of the latent viral reservoir in CD4 T cells of chronically infected patients. A total of 56 virologically suppressed patients were randomly assigned

either to receive VPA plus HAART for 16 weeks followed by HAART alone for 32 weeks (arm 1; n = 27) PF-01367338 research buy or to receive HAART alone for 16 weeks and then VPA plus HAART for 32 weeks (arm 2; n = 29). VPA was administered at a dose of 500 mg twice a day (bid) and was adjusted to the therapeutic range. A quantitative culture assay was used to assess HIV reservoirs in CD4 T cells at baseline and at weeks 16 and 48. No significant reductions in the frequency of CD4 T cells harbouring replication-competent HIV after 16 and 32 weeks of VPA therapy were observed. In arm 1, median (range) values of IU per Protirelin log10 billion (IUPB) cells were 2.55 (range 1.20–4.20), 1.80 (range 1.0–4.70) and 2.70 (range 1.0–3.90; P = 0.87) for baseline, week 16 and week 48, respectively. In arm 2, median values

of IUPB were 2.55 (range 1.20–4.65), 1.64 (range 1.0–3.94) and 2.51 (range 1.0–4.48; P = 0.50) for baseline, week 16 and week 48, respectively. Our study demonstrates that adding VPA to stable HAART does not reduce the latent HIV reservoir in virally suppressed patients. Despite its ability to sustain durable inhibition of viral replication, highly active antiretroviral therapy (HAART) does not eliminate HIV-1 infection even after years of therapy [1]. The persistence of replication-competent virus in resting memory CD4 T cells has emerged as a major obstacle to eradication of HIV-1 [2, 3]. Mechanisms that allow HIV-1 to establish and maintain latency are still poorly understood, but recent evidence suggests that the modulation of chromatin architecture within the viral promoter plays a key role in this process [4, 5].

A region containing the blaSHV-5 gene is flanked by two IS26 copies

and its copy number multiplies spontaneously within p1658/97 and RecA-deficient E. coli strains. Here, we demonstrate that the amplified IS26-blaSHV-5 units were arranged in tandems, containing up to more than 10 units, which could raise ceftazidime MICs for host strains from 4 μg mL−1 to more than 128 μg mL−1. Successive deletions within p1658/97, located outside the amplifiable module and encompassing even as little as c. 15% of the plasmid, click here blocked the amplification. Moreover, the complementing re-introduction of the deleted fragments in trans did not restore the process. Similarly, insertions of a 1-kb DNA fragment into the amplicon inhibited its self-multiplication ability. The module was able to transmit into another IS26-containing plasmid by recombination. The results prompted us to speculate that local DNA structure, especially favorable in p1658/97, might have been responsible for the IS26-blaSHV-5 multiplication ability. “
“The Streptococcus mutansComX-regulon encompasses > 200 mostly uncharacterized AZD8055 order genes, including

cinA. Here we report that cinA is regulated by ComX in the presence of the competence stimulating peptide (CSP), wherein loss of CinA (strain SmuCinA) results in reduced transformability with or without added CSP by 74- and 15-fold, respectively (P < 0.003). In CSP-supplemented cultures, a two-fold increase in cell viability was noted for SmuCinA relative to UA159 (P < 0.002), suggesting

CinA’s involvement in the CSP-modulated cell killing response. Relative to UA159, loss of CinA also rendered the mutant hypersensitive to killing by methyl methanesulfonate (MMS), which impairs homologous recombination. Despite our use of a non-polar mutagenesis strategy to knockout cinA, which is the first gene of the multicistronic operon harboring cinA, we noted a drastic reduction in recA expression. By using a Fossariinae CinA-complemented mutant, we were able to partially, but not completely restore all phenotypes to UA159 levels. Complementation results suggested that although cinA participates in modulating competence, viability and MMS tolerance, genes downstream of the cinA transcript may also regulate these phenotypes, a finding that warrants further examination. This is the first report that describes a role for S. mutans’ CinA in contending with DNA damage, genetic transformation and cell survival. Genetic competence is a transient physiological state that facilitates horizontal gene transfer that enables recipient bacteria to acquire novel genes by the uptake of exogenous DNA from the environment (Claverys & Martin, 1998).

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 CFTR activator 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 PD-0332991 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, Chloroambucil 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.