The questionnaire was refined through email correspondence with focus-group participants. A draft of the questionnaire was piloted with care home managers (n = 3) with their feedback incorporated into the final version, which

was posted to care-home managers (59) in Buckinghamshire in July 2012 with a repeat Bortezomib order mailing (October 2012) and a reminder phone call to maximise the response rate (November 2012). Ethics approval was granted by the University of Reading Ethics Committee (March 2011). A total of 16 care-home managers (27%) responded to the questionnaire. On the whole, a GP or another healthcare professional performed the medication reviews with 10/16, (63%) stating that 80–100% of their residents received a medication review at least annually. Prompt supply

of medication for care-home residents (16/16, 100%), provision of pre-printed medication administration record charts (15/16, 94%) and providing medicines information (11/16, 69%) to care home staff and residents were the main functions carried out by community pharmacists, which matched the main requirements of care-home managers. Lower down the priorities selleck products were support with minimising waste medicines (9/16, 56%) and developing medication policy and procedures per se (5/16, 31%). Advice on medication errors and handling of adverse drug reactions, and auditing procedures and training on the safe handling of medication though were identified as potential areas of unmet need. Pharmacist involvement in care-home settings has returned mixed evidence of effectiveness but an increase in others’ knowledge and awareness about out medication2. Formal studies of pharmacist effectiveness are subject to normal constraints of quantitative methodology because they measure short-term, funded pharmacist input that might not be sustainable post-intervention. The current study although small does nonetheless

provide some interesting insight, suggesting that medication reviews are seen as an activity already covered by other healthcare professionals. The study highlights instead related perhaps more fundamental areas with potential for pharmacist involvement. Pharmacists could provide more training on safe handling of medicines, and give advice on medication errors and adverse drug reactions to meet perceived needs. Working in this way, pharmacists’ activities could be based on ‘wants’ and therefore be of greater value to care homes. 1. Barber ND, Alldred DP, Raynor DK, et al. Care homes’ use of medicines study prevalence, causes and potential harm of medication errors in care homes for older people. Qual Saf Health Care 2009; 18: 341–346 2. Verrue CLR, Petrovic, M, Mehuys E, Remon JP, Stichele RV. Pharmacists’ interventions for optimising medicines use in nursing homes. A systematic review. Drugs Aging 2009; 26: 37–49 Victoria Lea, Sarah Corlett, Ruth Rodgers Medway School of Pharmacy, Chatham, UK The aim was to explore how community pharmacists used delegation as a tool to manage workload.

“
“To evaluate the disease activity and current pharmacological interventions used to achieve remission in rheumatoid arthritis (RA) patients in Australia. Rheumatoid arthritis patients treated in participating Australian clinics were included in the study. Patient demographics, disease onset, medications and disease measures were analyzed. Data, de-identified to the patient, clinic and clinician were captured using an electronic www.selleckchem.com/products/Dasatinib.html clinical management program. The disease activity score

(DAS28) was used to classify patients into the disease activity states of remission, low disease activity (LDA), moderate disease activity (MDA) and high disease activity (HDA). Choice of therapy was at the discretion of the treating clinician. A total of 5686 patients, 72.9% female, 26.9% male, with mean age 61.1 (SD 13.6) years

and mean disease duration of 11.5 (SD 10.5) Fluorouracil years were analyzed. DAS28 ESR (erythrocyte sedimentation rate) scores were recorded for 2973 patients, with 41.6% in remission, 18.6% LDA, 31.6% MDA and 8.2% HDA. Of those in remission, 17% received a biological disease modifying anti-rheumatic drug (bDMARD), 73% methotrexate (MTX), 19% leflunomide (LEF) and 28% prednisolone. Of the patients with MDA, 20% received a bDMARD, 76% MTX, 24% LEF and 39% prednisolone. Of the patients in HDA, 27% received a bDMARD, 78% MTX, 31% LEF and 60% with prednisolone. Cross-sectional assessment of this large cohort of Australian RA patients found a large proportion remain in moderate or high disease activity; suggesting a considerable evidence–practice gap. Improvement in disease control in this group may reduce future health burdens. “
“To describe the clinical manifestations, disease activity and organ damage in Korean patients with systemic lupus erythematosus (SLE).

American College of Rheumatology (ACR) criteria, SLE Disease Activity Index (SLEDAI), and Systemic Lupus International Collaborating Clinics/ACR damage index (SDI) were assessed in patients with SLE from 1998 to 2012. A total of 996 SLE patients were analyzed. The common accrual of ACR criteria included: immunologic (93%), hematologic (93%), arthritic (66%) and nephritic (50%). In the inception cohort over 10 years of follow-up Carbohydrate (n = 120), the number of ACR criteria increased significantly (5.0 ± 1.2 to 5.7 ± 1.3), and nephritis, serositis and neuropsychiatric symptoms tended to increase continuously over time. SLEDAI-2K decreased significantly (5.6 ± 3.4 to 4.1 ± 1.2), but the percentage of patients with SLEDAI scores ≥ 12 did not decrease over time. The common organ damages were musculoskeletal (14.9%) and renal (11.1%). The mean SDI score increased significantly (0.4 ± 0.8 to 1.1 ± 1.6) and renal damage had two peaks in 1 and 6–10 years, musculoskeletal and neuropsychiatric damage were predominant from 1 to 5 years, and ophthalmic damage increased sharply over 10 years.

The strain showed resistance to ampicillin, polymixin B, co-trimoxazole, trimethoprim, streptomycin, spectinomycin, furazolidone, tetracycline, ciprofloxacin and nalidixic acid. The sequencing of int, the SXT-specific integrase and attP attachment site indicated that it possessed a variant of SXT with trimethoprim (dfrA1), sulphamethoxazole (sul2) and streptomycin (strB) resistance genes. Its mobile nature was demonstrated PLK inhibitor by conjugation with rifampicin-resistant Escherichia coli. The emergence of

such an isolate should be closely monitored because it will improve our understanding of the evolution of the multidrug resistance phenotype. Vibrio cholerae, the causative agent of cholera, is still a major public health problem in many developing countries of Asia, Africa and Latin America. The emergence of resistance to multiple drugs is a serious clinical problem in the treatment and containment of the disease. The occurrence of multiple antibiotic resistance in V. cholerae is being reported with

increasing frequency (Garg et al., 2000; Ramamurthy et al., 2000; Das et al., 2005). The state of Kerala is considered as endemic to the disease cholera and outbreaks CP-673451 research buy involving multiple drug-resistant strains have been reported (Sabeena et al., 2001). The recently isolated Inaba strains from Kerala were resistant to multiple drugs (Sabu et al., 2007). The acquisition of antibiotic resistance genes is mediated by plasmids, integrons and conjugative transposons. The SXT, a conjugative element that forms a large class of mobile genetic elements, codes for genes conferring resistance to chloramphenicol (floR), streptomycin (strA and strB), sulphamethoxazole (sul2) and trimethoprim (dfrA1 and dfr18). This element can mobilize drug resistance Amisulpride genes from one strain to another (Waldor et al., 1996). SXT integrates into the 5′ end of prfC, a gene found on the large V. cholerae chromosome that encodes peptide chain release factor 3. The

SXT integrates into the chromosome through a recA-independent process involving site-specific recombination between a 17-bp nearly identical element (attP) and chromosomal sequences (attB) (Hochhut & Waldor, 1999). SXT integration into and excision from the chromosome requires an SXT-encoded tyrosine recombinase Int, which belongs to the λ family of site-specific recombinases (Burrus et al., 2006a). The fluoroquinolones possess excellent activity against V. cholerae O1 and O139 serogroups (Yamamoto et al., 1995). The single and multiple mutations in the quinolone-resistant determining region (QRDR) of gyrA, gyrB, parC and parE genes and overexpression of efflux pumps are associated with resistance to fluoroquinolones. In the present study, a clinical strain of V.

The RNA was adjusted to a concentration of 140 ng μL−1. A total quantity of 280 ng RNA was then used for one-step reverse transcription using High Capacity RNA-to-cDNA Master Mix (Applied Biosystems). For quantitative real-time PCR, amplification was performed with Power SYBR Green Master Mix in a Step One Plus Thermal Cycler (Applied Biosystems). Forty cycles were run with denaturation at 95 °C for 15 s,

annealing at 55 °C for 30 s and extension at 60 °C for 45 s. rpsL was used as reference gene to normalize the relative amount of mRNA. The mRNA levels SCH772984 order of a specific gene were expressed by comparing with the expression of the reference gene on that strain and also in PAO1, and the expression levels were calculated on a standard curve (Oh et al., 2003). RT-PCR was carried out in triplicates. Primers used for RT-PCR investigations are described in Table S1. PAO1 and PAOMY-Mgm had similar growth rates in LB or in LB supplemented with 0.1 mg L−1 ciprofloxacin. Competition experiments were carried out in a Bioscreen (Labsystem C, Bie og Berntsen) with and without antibiotic. We attempted to start with a ratio 1 : 1 of PAO1 and PAOMY-Mgm in each well. The inoculums in the start of the experiment were 3.5 × 108 CFU mL−1 for PAO1 and 2.4 × 108 CFU mL−1 for PAOMY-Mgm. A total quantity of 140 µL of each strain culture was transferred in 2 × 10 wells in microtitre plate, the growth was carried out at 37 °C, continuously shaking, and OD600 nm

measurements were CX-5461 supplier performed every 30 min for 24 h. The experiment was carried out for 5 days (start day 0, end day 4), and in each day 1 : 1000 dilutions of the cultures were transferred to a new microtitre plate for exponential growth throughout very the experiment. Each day, the culture was serially diluted and plated on LB agar and on LB agar supplemented with 30 mg L−1 gentamicin, a concentration which is inhibitory for PAO1, but not for the PAOMY-Mgm mutant. The CFU mL−1 of PAOMY-Mgm was calculated on gentamicin plates and the PAO1 and PAOMY-Mgm mixture on LB plates. The

CFU of PAO1 was calculated by subtracting the number of CFU mL−1 on gentamicin plates from the number of CFU mL−1 on LB plates. The ratio of PAO1 : PAOMY-Mgm, PAO1 : PAOMYgm and PAO1 : PAOMMgm was followed for 4 days. The efflux pumps transcriptional regulators nfxB, mexR, mexZ and mexT, and the ciprofloxacin target genes gyrA, gyrB, parC and parE, were sequenced in selected isolates from the antibiotic resistance development study and from the growth competition study. DNA was purified using Promega Wisart purification kit (Promega). Polymerase Dynazyme EXT (Finnzymes, Espoo, Finland) was used for PCR amplification. The sequencing was done on an automatic DNA sequencer ABI3700 (Macrogen Inc., Seoul, South Korea). The numbers of reads were between two and four for each gene of each strain. The sequence results were compared with the strain PAO1 sequence (www.pseudomonas.com) with dnasis® max version 2.

Once virological failure is confirmed and a resistance result available, the regimen is changed as soon as possible to avoid accumulation of resistance mutations. The choice of the new ART regimen will primarily depend on the results of resistance testing and the patient’s preference. Additional considerations include the results of tropism and HLA-B*57 testing, DDIs/food interactions, co-morbidities and future therapy options. The goal of the new combination

is to re-establish a VL <50 copies/mL. In PLX3397 patients with ongoing viraemia and with few options to construct a fully suppressive regimen, referral for specialist advice and/or discussion in a multidisciplinary team ‘virtual’ clinic. Include at least two and preferably three fully active agents with at least one active PI/r (e.g. DRV/r) and one agent with a novel mechanism of action (CCR5 antagonist/integrase or fusion selleck kinase inhibitor inhibitor). Treatment interruption is not recommended. No resistance (WT virus). 3TC/FTC resistance (M184V/I) following any first-line therapy, including TDF/FTC or ABC/3TC. NNRTI resistance (e.g. K103N or Y181C/I/V) and/or 3TC/FTC resistance (following first-line therapy with NNRTI-based regimen, including TDF/FTC or ABC/3TC). INI resistance (e.g. Q148 or N155H) and/or 3TC/FTC

resistance (following first-line therapy with RAL-based regimen, including TDF/FTC or ABC/3TC). Extended RT resistance (e.g. K65R/L74V or thymidine analogue mutations) (following suboptimal regimens/patients with more extensive drug history associated with virological failure). Three-class resistance (indicating NRTI, NNRTI and PI) (following multiple failing regimens). Limited or no therapeutic options (following multiple failing regimens, including the newer drugs with novel actions). Record in patient’s notes of resistance result at ART initiation (if available) and at first VL >400 copies/mL and/or before switch. Record in patient’s oxyclozanide notes of adherence assessment and tolerability/toxicity to ART in patients experiencing virological failure or repeated

viral blips. Number of patients experiencing virological failure on current ART regimen. Proportion of patients experiencing virological failure switched to a new suppressive regimen within 6 months. Proportion of patients on ART with previously documented HIV drug resistance with VL <50 copies/mL. Record of patients with three-class virological failure with or without three-class resistance referred/discussed in multidisciplinary team with expert advice. In patients on ART: A single VL 50–400 copies/mL preceded and followed by an undetectable VL is usually not a cause for clinical concern (GPP). We recommend a single VL >400 copies/mL is investigated further, as it is indicative of virological failure (1C). We recommend in the context of repeated viral blips, resistance testing is attempted (1D). Optimal HIV control is ordinarily reflected by complete viral suppression with an undetectable VL.

A hobnail-like appearance is often characteristically observed. Unlike those of cervical and vaginal origin, the corpus CCA is not related to exposure

to diethylstilbestrol. The biological behavior of CCA is similar to or worse than that of G3 EMA,[11] but is more favorable than that of SEA. Based on the immunohistochemical expression profiles of ER, PgR, Ki-67 and p53, CCA can be regarded as intermediate between EMA and SEA for the following reasons: the labeling index is usually lower than that of SEA, overexpression of p53 is often observed but not as strongly as SEA, and low expression of ER and PgR Veliparib purchase is common in CCA.[22] CCA frequently has PIK3C and ARID1A mutations,[77, 78] and shows an ARID1A loss, with ER and PgR

expressions. E-cadherin is also significantly less expressed in CCA than in EMA. As similarly seen in the ovarian CCA, although not highly specific, hepatocyte nuclear factor (HNF)-1β as a marker related to glycogen metabolism is positive in most of the corpus CCA.[79] The differential diagnostic considerations include SEA, EMA of a secretory variant and EMA mimicking CCA due to a solid structure with a clear cell appearance. EIC as a putative precursor of SEA also may develop into CCA.[74] Even though rarely encountered, CCA may arise from adenomyosis[80] and from endometrial see more polyps.[81-83] The differential diagnoses for the above-mentioned three types of endometrial carcinomas are commonly confounding and challenging because their components are overlapping, fused and/or ambiguous to characterize.[84] Adenosine triphosphate Therefore, it may be basically impossible to distinguish among these cases using the historically established diagnostic criteria. With them, the designation

of ‘hybrid carcinoma’ has been successfully proposed.[84] On the other hand, endometrial carcinomas of mixed histology, including a variable proportion of EMA, SEA, CCA and undifferentiated carcinoma, often may be encountered. By definition, currently, the mixed carcinoma should be comprised of clearly different histological components of both type I and II carcinomas in which either one is required to constitute at least 10% of the total tumor volume.[85] Mixed histology, namely, a combination of EMA, CCA and SEA, can be seen in 11% of endometrial carcinomas.[86] This type of endometrial carcinoma is divided into two patterns: predominantly type I with minor type II versus predominantly type II with minor type I. It is suggested that EMA with the pattern of predominantly type I with minor type II takes a clinical behavior comparable to pure type II endometrial carcinoma. Some CCA have a minor counterpart of usual EMA. Therefore, the idea that CCA is an aggressive setting of EMA may be reasonably explained by these histological features. It is reported that EMA mixed with at least 25% of CCA shows a poorer clinical behavior.

Although these fitness trade-off scenarios are commonly observed in natural and experimental systems, few studies have focused on their underlying mechanisms. Some of these trade-off scenarios are observed in drug-resistant isolates of C. albicans. Evidence of AP in drug-resistant mechanisms was observed in a single isolate from our recent evolutionary study of C. albicans (Huang et al., 2011). In this study, cell populations were evolved under the selective pressures of fluconazole and limiting carbon source (glucose). An adaptive clone isolated from one population (DP-1-M5) showed a significant increase in the relative fitness compared to the parental strain in the presence

of Romidepsin mw drug, but the increased drug resistance had a fitness cost, as the mutant showed a lower relative fitness in the absence of the drug (Table 1), demonstrating a clear case of AP. However, the majority of the isolates from this study fall in the IA or CA categories described above, where mutations that are beneficial in the presence of the drug are either neutral or beneficial in the absence of the drug (see Table 1). This is contrary to results from Cowen et al. (2001); in their study, most isolates with Sorafenib increased fitness

in the presence of the drug compared with the parental strain showed neutral or negative fitness in the absence of the drug (AP or IA). Possible explanations for the difference in our observations may be due to the differences in C. albicans strains used for the evolution experiments, the media used for the evolution (yeast nitrogen base vs. RPMI 1640), and the population size and evolution system used (chemostat vs. serial batch transfer). The use of serial batch transfer involves a larger bottleneck effect during each transfer. Thus, it is likely that the majority of the beneficial mutations that arise are lost in the process. In a continuous system, on the other hand, beneficial mutants have a higher probability of being retained in the system for further evolution. However, the exact mechanisms for the fitness trade-offs will require further studies

to identify all the underlying adaptive mutations and to characterize their exact fitness effects. Both in vivo and in vitro data have shown C. albicans populations to be heterogeneous and that clonal interference plays Pyruvate dehydrogenase lipoamide kinase isozyme 1 an important role in the population structure during exposure to antifungal agents. With the development of VERT, we can now track the population dynamics during adaptive evolution to readily estimate the frequency at which drug-resistant mutants arise in the population and to isolate mutants in a systematic manner. While clinical isolates from patients throughout the course of treatment would be the ideal system to study the emergence of antifungal drug resistance, it is difficult and often not practical to control. In vitro systems using bioreactors offer controlled and more reproducible environments.

05, P < 0.0001; Fig. 7A). Tukey post hoc analysis revealed that the severe lesion was significantly different from the intermediate lesion (P < 0.05) and highly significantly different from the mild lesion (P < 0.0001), while the intermediate lesion was significantly different from the mild lesion (P < 0.05). Apomorphine-induced rotation was also able to differentiate between the three subgroups (Group, F2,33 = 15.09, P < 0.0001; Fig. 7B). The post hoc analysis revealed that the severe lesion was significantly different from the intermediate lesion (P < 0.05) and

highly significantly different from the mild lesion (P < 0.0001), while the intermediate lesion was significanly different from the mild lesion (P < 0.05). Amphetamine

rotation was clearly less informative and could only differentiate between the animals with a mild lesion and those with > 60% striatal denervation (Group, F2,33 = 10.69, Protease Inhibitor Library manufacturer P < 0.0001; Fig. 7C); Tukey post hoc analysis revealed that the mild lesion was significantly different check details from both the intermediate and the severe lesions (P < 0.001 and P < 0.05, respectively). By contrast, neither the stepping test nor the cylinder tests were able to distinguish between any of the lesion types (Group, F2,33 = 2.08, P = 0.15, n.s; Group, F2,27 = 1.31, P = 0.29, n.s, respectively; Fig. 5D and E). A subset of seven severely lesioned mice was followed long-term in four of the tests that showed profound deficits at the early post-lesion time-point (6–7 weeks), and were compared to a group of seven intact control animals (Fig. 8A–D). In all four tests the two groups showed stable

performance over the entire test period (20–23 weeks), and the lesioned and intact mice performed significantly different from one another in all four tests, including the corridor test (Group, χ21,48 = 827.14, P < 0.0001; Fig. 8A), apomorphine-induced rotation (Group, χ21,48 = 159.69, P < 0.0001; Fig. 8B), amphetamine-induced rotation (Group, χ21,48 = 26.91, P < 0.0001; Fig. 8C) and the stepping test (Group, χ21,36 = 208.26, P < 0.0001; Fig. 8D). There was no significant effect aminophylline of time measured in any of the behavioural tests, thus confirming the stability performance in both the intact and lesioned groups (data not shown). The results show that intranigral 6-OHDA lesions can be used to induce profound loss of midbrain dopaminergic (DAergic) neurons, accompanied by extensive denervation of the striatum and behavioural impairments in a range of drug-induced and spontaneous motor tests. Based on the extent of striatal TH+ denervation we allocated the mice into three subgroups, exhibiting severe, intermediate and mild lesions of the mesostriatal pathway. From the behavioural impairments seen in these subgroups, it was possible to predict the severity of the lesion, i.e.

, 2002; Gorby et al., 2006); (2) nonreductive dissolution of metal oxides to form more readily reducible organic metal complexes (Taillefert et al., 2007; Fennessey et al., 2010; Jones et al., http://www.selleckchem.com/screening/anti-diabetic-compound-library.html 2010); and (3) delivery of

electrons to external metals via endogenous or exogenous electron shuttles (Hernandez et al., 2004; Marsili et al., 2008; Roden et al., 2010). Shewanella oneidensis contains an electron transport chain that consists of IM-localized primary dehydrogenases, menaquinone, and CymA, a menaquinol-oxidizing c-type cytochrome that functions as a central branch point in electron transport to Fe(III), Mn(IV), nitrate (), nitrite (), dimethyl sulfoxide (DMSO), and fumarate (Myers & Myers, 1997). CymA transfers electrons to the periplasmic c-type cytochrome MtrA (Schuetz et al., 2009), which interacts with outer membrane (OM)-localized protein complexes composed of transmembrane β-barrel protein MtrB (Beliaev & Saffarini, 1998; Myers & Myers,

2002) and decaheme c-type cytochrome MtrC (Shi et al., 2006; Ross et al., 2007). Purified MtrC reduces Fe(III) (Hartshorne et al., 2007; Eggleston et al., 2008), and in proteoliposomes, purified MtrB, MtrC, and MtrA form a lipid-embedded ‘porin–cytochrome’ complex (Richardson FK228 clinical trial et al., 2012) that transfers electrons from internal reduced methyl viologen to external Fe(III) substrates (Hartshorne et al., 2009; White et al., 2013). Previous nucleotide sequence analyses indicated that the N-terminus of S. oneidensis MtrB contained a unique CXXC motif (Beliaev & Saffarini, 1998). The identification of a CXXC motif in S. oneidensis MtrB was unusual because CXXC motifs are generally not found in OM β-barrel else proteins, most likely to avoid protein-folding problems caused by redox-reactive cysteines during passage across the intermembrane space in eukaryotes or the periplasmic space in bacteria (Tamm et al., 2004; Schleiff & Soll, 2005; Denoncin et al., 2010). The identification of an unusual CXXC motif in the N-terminus of MtrB led us to

hypothesize that this motif may represent a molecular signature unique to metal-reducing γ-proteobacteria. To test this hypothesis, nucleotide sequence analyses were carried out to correlate dissimilatory metal reduction capability with the presence of MtrB homologs containing an N-terminal CXXC motif. Site-directed mutational analyses were performed to determine whether the N-terminal CXXC motif of MtrB was required for metal reduction by the representative metal-reducing γ-proteobacterium S. oneidensis. The ability to predict dissimilatory metal reduction by a γ-proteobacterium with unknown metal reduction capability was then tested with Vibrio parahaemolyticus, a human pathogen whose genome encodes an MtrB homolog with an N-terminal CXXC motif. Bacterial strains and plasmids used in this study are listed in Table 1. For genetic manipulations, all Escherichia coli and S.

In a symbiotic host system, collagen degradation could benefit the bacteria, but would be harmful for the eukaryotic host. Using a polyphasic approach, we investigated the presence of

collagenolytic activity in the bacterial community hosted by the marine sponge Cymbastela concentrica. Functional screening for collagenase activity using metagenomic library clones (227 Mbp) and cultured isolates of sponge’s bacterial community, as well as bioinformatic analysis of metagenomic shotgun-sequencing data (106 679 predicted genes) were used. The results show that the abundant members of the bacterial community contain very few genes encoding for collagenolytic enzymes, while some low-abundance learn more sponge isolates possess collagenolytic activities. These findings indicate that collagen is not a preferred nutrient source for the majority of the members of the bacterial community associated with healthy C. concentrica, and that some low-abundance bacteria have collagenase activities that have the potential to harm the sponge through tissue degradation. Collagen is the major component of extracellular matrices of all metazoan life and represents an important protein conferring integrity and the physical form of eukaryotic organisms

(Harrington, 1996; Exposito et al., 2008). Sponges are among the oldest Metazoa and often contain collagen, which is either dispersed as AC220 thin fibrils or organized as bundles, termed spongin, in the intercellular matrix (Simpson, 1984; Brusca & Brusca, 1990). The expression of collagen is known to be essential for the development and structural integrity of sponges (Garrone et al., 1975; Shimizu & Yochizato, 1993; Krasko et al., 2000). Sponges harbour specific bacterial communities in different

cellular compartments, often for an extended period of time, and hence close associations between the microorganisms and the sponge host have been established (Taylor et al., 2007). Collagen is an essential and abundant part of the internal mesohyl structure of most sponges Liothyronine Sodium (and in particular the Demospongia), where many microorganisms reside. As a rich source of nitrogen and carbon, collagen could provide nutrients for the sponge-associated microorganisms, and this may potentially have implications for the structural integrity of the host. A few cases of sponge diseases have been attributed to the presence of bacterial pathogens (Gaino & Pronzato, 1989; Webster et al., 2002; Mukherjee et al., 2009) and collagenolytic enzymes have been speculated to lead to tissue necrosis in sponges. Generally, bacterial collagenases, including the well-characterized enzymes from Clostridium sp. (Matsushita et al., 1994) and Vibrio sp. (Yu & Lee, 1999; Vaitkevicius et al., 2008), have been linked to pathogenicity and are regarded as virulence factors in human disease.