The Cry8Ea1 toxin could be obtained by either of these two chromatographic methods (Fig. 2a). Two fractions containing the Cry8Ea1 toxin were obtained by elution of the ion-exchange chromatography column by Resource-Q using a gradient of NaCl. No

DNA could be detected in the toxin obtained in the first or the main elution peak from the Resource-Q column before or after phenol/chloroform extraction, but the small peak Thiazovivin clinical trial contained the toxin still together with DNA (data not shown), which is similar to published results from the purification of Cry1A (Bietlot et al., 1993). Agarose gel electrophoresis showed that the toxin obtained through the Superdex-200 column was also bound to DNA, which appears to be relatively homogeneous in size, about 20 kb (Fig. 2b, lanes 3 and 4). For the subsequent studies, we chose

the Superdex-200 column to obtain both the Cry8Ea1 toxin and the Cry8Ea1 toxin–DNA complex in order to exclude the possible effects of using different columns. Cry8Ea1 toxin–DNA was obtained in the first step, and it was further loaded onto the Superdex-200 column again after treatment with DNase I at 4 °C for 12 h. No DNA was detected after extraction by phenol/chloroform, which means that the toxin is DNA-free after digestion by DNase I (Fig. 2b, lane 5). The toxin without DNA was designated as the Cry8Ea1 toxin (Fig. 2a, lane 4). Then, the Cry8Ea1 toxin and the Cry8Ea1 toxin–DNA complex were obtained separately Regorafenib datasheet for further investigation into the role of the DNA binding for the Cry8Ea1 toxin. Two aliquots of the Cry8Ea1 toxin and of the Cry8Ea1 toxin–DNA complex – one newly purified and the other stored at 4 °C for 48 h – were loaded onto the Superdex-200 column. The elution profiles are shown in Fig. 3a and b. After storage, most of the Cry8Ea1 toxin aggregated into high-molecular-weight multimers, similar to other Cry proteins including Cry1Ac, while no aggregation occurred with the Cry8Ea1 toxin–DNA complex. The Gdm-HCl-induced Sclareol unfolding equilibrium

was used to investigate the stability of the Cry8Ea1 toxin with or without DNA. The unfolding curves of the Cry8Ea1 toxin and the Cry8Ea1 toxin–DNA complex at different Gdm-HCl concentrations and in three different pHs are shown in Fig. 4. Surprisingly, the stability of the Cry8Ea1 toxin in the Gdm-HCl solution was quite different from that of the Cry8Ea1 toxin–DNA complex at pH 4. As compared with the Cry8Ea1 toxin, the unfolding of the Cry8Ea1 toxin–DNA complex occurred at a relatively higher concentration of Gdm-HCl, about 4 M, at an acidic pH, but no huge difference was observed between the protein with or without DNA in a neutral or an alkaline pH, indicating that DNA binding to the protein may exert a protective effect on the protein against attack by a denaturant in an acidic pH. In an acidic pH, Cry8Ea1 has a positive charge because its isoelectric point occurs at pH 8.

8/100 PY (95% CI 66.5, 93.4/100 PY). For responders, the crude hospitalization rate declined statistically significantly during the 46 to 90-day time period, with a relative rate (RR) vs. the first 45 days of 0.71 (95% CI 0.51, 0.98). From 90 days to the end of the year, the hospitalization rate for responders stabilized at near 45/100 PY (RR for days 91–180 vs. the first 45 days, 0.56; 95% CI 0.40, 0.78). For nonresponders, there was no statistically significant change in all-cause

hospitalization rates across time periods, with the point estimates ranging from 78.7 to 99.7/100 PY (Fig. 1). Fewer than half of all subjects (34% of responders and 46% of nonresponders; P<0.001) were ever hospitalized over the entire period beginning 180 days before HAART initiation to 365 days afterwards. In multivariate analysis (Table 2), responders' hospitalization rates retained an identical selleck inhibitor pattern of statistically significant decrease in later time periods vs. earlier periods (RR 0.59; 95% CI 0.42, 0.82 for responders in days 91–180 vs. days 1–45). Having an increase in CD4 count of at least 101 cells/μL (the median increase in CD4 count in virological responders) had a borderline association with a decreased risk of hospitalization (RR 0.83; 95% CI 0.67, 1.03). Additional factors significantly associated with hospitalization included being a nonresponder in the 91–180 day

(RR vs. responders 2.14; 95% CI 1.41, 3.25) and 181–365 day (RR vs. responders 1.43; 95% CI 1.00, 2.04) time periods; female gender; African American race; IDU; and lower CD4 cell count at HAART initiation. CX-5461 purchase Hospitalization rates for the seven diagnostic categories with the highest

rates are shown in Fig. 2. Non-ADI infections (the three most frequent individual diagnoses being pneumonia, unspecified organism; lower limb cellulitis; and acute/subacute Immune system bacterial endocarditis) and ADIs (pneumocystosis, cryptococcosis and candidal esophagitis) were consistently the most common reasons for admission across all time periods for both responders and nonresponders. Psychiatric illness [major depression, recurrent episode; depressive disorder, not elsewhere classified (NEC); and drug-induced mood disorder] was the third most common category and was followed by gastrointestinal and hepatic disease (acute pancreatitis; chronic pancreatitis; and cirrhosis of the liver, NEC); cardiovascular disease (hypertensive end-stage chronic kidney disease; venous thrombosis, NEC; and cerebral artery occlusion with infarct); endocrine, nutritional, metabolic or immune disease (hypovolaemia, cachexia, and hypercalcaemia); and renal disease (acute renal failure, NEC; chronic renal failure; and lower nephron nephrosis). For responders, hospitalizations as a result of ADI and non-ADI infections revealed statistically significant decreases by the period starting 90 days after HAART initiation (Fig. 2a). In the 1–45 day period, IRIS hospitalizations (rate 10.9/100 PY; 95% CI 5.6, 21.

Thirty (79%) agreed that yes if they wanted to talk to the pharmacist then they are easy to contact. In response to being asked how they feel the pharmacist communicates concerns to staff, 27 (71%) viewed that

this is communicated in a helpful way, GSK2118436 clinical trial 5 (13%) felt that the communication was more of a reprimand, and 6 (16%) gave a neutral response. When asked in their experience do they think the pharmacist is assertive enough when communicating clinical issues that really matter, 32 (84%) were positive about the pharmacist trying hard to communicate the necessary message, and 6 (16%) were neutral. Of the 21 that responded to the question asking what would be the one thing that pharmacists on the ward can do to improve their communication skills, 10 related to a theme of more pharmacists on the ward spending more time with patients. One respondent replied ‘Don’t tell off juniors’. In general, the overall results of this small scale survey can be interpreted as suggesting that clinical pharmacists are considered approachable, the majority of clinical staff feel that issues are raised

appropriately by pharmacists, and they also feel the pharmacists are assertive. However, comments captured during the survey such as ‘… I am usually very busy and don’t always appreciate the interruption’, communication from the pharmacist ‘can feel rushed’, and ‘when I’m busy and stressed it can definitely feel like I’m being told off’ suggest there may be an opportunity to improve communication skills. This baseline assessment demonstrates that further research across more hospital selleck kinase inhibitor trusts and geographical locations is warranted to ensure that our results do not just reflect the culture in our trust, and to enable a fuller picture to emerge. 1. Howe H, Wilson K. Modernising Pharmacy Careers Programme Review of Post-Registration Career Development of Pharmacists and Pharmacy Technicians. Background

paper. Medical Education much England. July 2012. Veronica Smith University of Stirling, Stirling, UK What are the key barriers and facilitators for individual community pharmacists supporting people affected by dementia? When asked what they could do for people affected by dementia; most concerns were about medication management, followed by formal referral to the General Practitioner (GP). Community pharmacists may be the only health professional people affected by dementia regularly visit; they are ideally positioned to support them with medicines management and health advice. Recent policy initiatives are concerned with the role community pharmacists play, as part of the team of health professions providing support to people affected by dementia. The aims of this research are to identify what relationship community pharmacists have with people with dementia and their caregivers.

These appeared randomly within the block. Trials containing electrical stimuli were excluded from off-line analysis of MEPs and intracortical excitability in order to eliminate an unlikely direct impact of the sensory input. However, previous studies have shown that only strong (2–3 × PT) stimuli, but not around the PT, can change SICI (Kobayashi selleck chemicals llc et al., 2003). The visual tasks were presented on the screen of a PC at a resolution of 1024 × 768 pixels (Fig. 2). The eye–monitor distance was ~57 cm. Vision was corrected by individual glasses if necessary. Head movement was unnecessary to see the target and only minimal gaze movements were required. Two different visual search tasks, conjunction (Fig. 2A)

and feature (Fig. 2B), were used (series 1). The array was 660 × 660 pixels. selleck inhibitor Ten search elements were placed at random within a (not visible) 6 × 6 grid in this area, then jittered within the ‘square’ in which they were placed. The elements were 60 × 60 pixel red or blue diagonals. In the conjunction search, the distractors were red and blue diagonals in opposite orientations and the target was a blue diagonal pointing in the same direction as the red distractors. In the feature search, a blue diagonal was the target and only red distractors were present. The display

duration was 700 ms and blue and red stimuli were isoluminant (~20 cd/m3 on the monitor). The target was present on 50% of the trials. Intracortical excitability was recorded using paired pulses as previously described (Kujirai et al., 1993) with a subthreshold conditioning pulse preceding a suprathreshold selleckchem test stimulus. Four different interstimulus intervals (ISIs) were tested: 2 and 3 ms to evaluate SICI, and 12 and 15 ms to evaluate ICF. The first series of experiments was performed under three different experimental conditions: (i) at rest, (ii) during a block involving the detection of cutaneous electrical stimulation to a skin area on the dorsum of the hand, and (iii) during a block during which participants performed the visual attention protocol. The stimulus intensity of the test pulse was adjusted to 130% of the resting motor

threshold, which is known to often produce an MEP of ~1 mV. The intensity of the conditioning stimulus was set at 80% of the active motor threshold. The active motor threshold was defined as the lowest intensity able to evoke an MEP of more than 200 μV during a minimal background contraction of 5–10% of the maximal voluntary contraction. The resting motor threshold was defined as the lowest intensity to evoke an MEP of more than 50 μV at rest. For each experimental condition, five randomly intermixed conditions were used (four double pulses presented 12 times each, single test pulses presented 20 times). The intertrial interval was ~5 s. For MEP recordings under different experimental conditions, 20 trials (at 130% resting motor threshold) per condition were recorded using single TMS pulses in series 1.

Therefore, the confirmation of ALA is based on laboratory diagnostic methods: serological tests are the most helpful especially in an emergency context, thanks to rapid and specific E histolytica antibody LY2109761 tests.[1, 4] A 27-year-old French male had returned 6 months

earlier from a 6-month journey through Nepal and had spent 6 months in Senegal 2 years previously. He was complaining of night and day sweats and lower-thoracic pain for the previous 7 days. His physical examination only revealed a body temperature of 37.5°C. Laboratory studies of blood showed elevated white blood cell (WBC) count, 35,000/μL (85% neutrophils), an inflammatory syndrome, and alkaline phosphatase level at 1.5 times the normal value. Blood culture remained sterile. An abdominal computerized tomography (CT) scan revealed a single hypodense

lesion in the right lobe of the liver (diameter 9.2 cm) consistent with a hepatic abscess. An amebic etiology was suspected, but latex agglutination test (LAT) (Bichro-Latex Amibe, Fumouze, Levallois-Perret, France) on serum was negative on day 1 (threshold at 1 : 5). The patient was given a first standard course of empiric intravenous antibiotherapy against pyogenic organisms and ameba: co-amoxiclav (3 g/day) and metronidazole (1.5 g/day). Because of risk of spontaneous rupture, drainage of the liver abscess was performed as an emergency (Figure 1). Microscopic examination of the chocolate brown aspiration fluid revealed neither cysts and trophozoites of Entamoeba Talazoparib solubility dmso Interleukin-3 receptor sp. nor bacteria after Gram coloration. Quantitative indirect hemagglutination assay test (IHAT) (Amibiase HAI, Fumouze)

and immunofluorescence assay test (IFAT) (Amoeba-Spot IF, bioMérieux) for the detection of antibodies to E histolytica were both positive: IHAT 1 : 640 (threshold at 1 : 320) and IFAT 1 : 640 (threshold at 1 : 160). The negative result with LAT was confirmed by a new analysis done with a new lot of the same kit and a prozone phenomenon was excluded. Serology was controlled on day 6. The results of serological tests on day 6 compared with day 1 in the same run were respectively 0 (day 1) and 1 : 20 (day 6) for LAT, 1 : 640 and >1 : 2560 for IHAT, and 1 : 320 and 1 : 640 for IFAT. The result of real-time polymerase chain reaction (PCR) to detect E histolytica DNA directly in pus was positive. Co-amoxiclav was stopped, metronidazole was maintained for 10 days and tiliquinol was added for 10 days. The patient left the hospital on day 7. Three weeks after his arrival in Tchad, a 45-year-old French male suffered from a sudden pain in the right hypochondrium, hyperthermia (40°C), and cholestatic jaundice. Abdominal ultrasound revealed a liver abscess compressing bile ducts. Empiric parenteral antibiotherapy was started (day 1): cefotaxim (3 g/day), gentamicin (200 mg/day), and metronidazole (1.5 g/day). On day 10, the patient was repatriated back to France.

The reporter plasmid pHxk1-EGFP was constructed by cloning a full-length copy of the H. jecorina hxk1 including its own promoter and terminator region into pIG1783, which contains the EGFP expression cassette. Genomic DNA (gDNA) of H. jecorina, prepared as described previously (Seiboth et al., 2004), was used as template. The hxk1 sequence was obtained from the genomic database of H. jecorina QM6a (http://genome.jgi-psf.org/Trire2/Trire2.home.html) and the hxk1 was amplified using primers HexF (5′-CCGAAGCTTTCGCCCTGCTTGGAGCTTTC-3′) and HexR (5′-GCGAAGCTTTGCGGACCTTCATCATGGAGTG-3′), which introduced two HindIII restriction sites (underlined) at the ends. The amplified 3791-bp fragment was cloned

into the HindIII-restricted plasmid pIG1783, resulting in the plasmid pHxk1-EGFP (Supporting Information, Fig. S1a). Plasmid pHxk1-EGFP was verified by sequencing around the cloning sites. Palbociclib clinical trial Preparation of protoplasts and DNA-mediated transformation with pHxk1-EGFP were performed essentially as described (Gruber et al., 1990). For fungal

transformation, 1 M d-mannitol or 1 M d-sorbitol was separately used for osmotic stabilization and sole carbon source in a glucose-free MM. After transformation, aliquots of protoplast suspensions were spread onto selective medium using an overlay technique. The plates were incubated at 30 °C for 5–7 days. Visible colonies were transferred Selleck Veliparib to MM containing 10 g L−1d-mannitol instead of d-glucose as the sole carbon source. After sporulation of these colonies, homokaryotic Histidine ammonia-lyase transformants were prepared by single spore isolation. gDNA isolated from selected transformants was analyzed by PCR using the primers GfpF (5′-ATGGTGAGCAAGGGCGAGGA-3′) and GfpR (5′-CGGCCGCTTTACTTGTACAGCTC-3′) for amplification of a 728-bp DNA fragment of the egfp gene, and using primers HexF and HxkRR (5′-CATCCTCGGCTGCCAGAATC-3′) for amplification of a 3153-bp fragment of the hxk1 marker, respectively. For Southern blot analysis, total gDNA was digested with SalI, size-fractionated by

gel electrophoresis and transferred to a Hybond N+ nylon membrane (Amersham Biosciences, Piscataway, NJ). The 3791-bp hxk1 fragment obtained by PCR using primers HexF and HexR was labeled as a probe to detect the target DNAs. DNA labeling, hybridization and detection were performed according to the manufacturer’s recommendations for the use of the DIG High Primer DNA Labeling and Detection Starter Kit I (Roche Applied Science, Mannheim, Germany). The RNA isolation was mainly performed as described (Seiboth et al., 2004). Total RNA was extracted using Tripure reagent (Bioteke). Reverse transcription was carried out using Reverse Transcriptase XL (Takara). Hxk1-specific cDNAs were amplified by PCR with primer pair HxkFR (5′-GTTCGAGGCTGCGATTGCTAA-3′) and HxkRR (5′-CATCCTCGGCTGCCAGAATC-3′) spanning two introns of hxk1 gene.

[9] The ulnaropathy could also be explained by an eosinophilic

vascular mononeuropathy multiplex, but after electromyographic analysis, is more likely to be a pressure neuropathy due to the marked weight loss. Symptoms of a chronic hookworm infection are usually caused by the characteristic iron-deficient anemia and hypoproteinemia, due check details to a sustained intestinal blood loss. Infection occurs when naked skin is put into contact with warm, wet soil contaminated with larvae.[1] This can cause a local dermatitis, which the patient had not noticed.[5] The larvae penetrate the skin and are hematogenously transported to the lungs, where they travel through the airways into the digestive tract. The larvae mature in the small intestines, where they start to produce eggs.[1] Acute infection among selleck products travelers can cause gastrointestinal

symptoms with nausea, vomiting, abdominal pain, and sometimes diarrhea.[6] High eosinophilia (>1.5 × 109/L) is a hallmark characteristic of this infection, typically surfacing 5 to 9 weeks after infection.[3] The latter is consistent with the increase in diarrhea 5 to 7 weeks after the infection in the Philippines. The patient’s stool also tested positive for LH. In 2001, LH was first isolated from blood and pus of empyema of a 54-year-old man admitted to a Hong Kong hospital with liver cirrhosis complicated by sepsis.[10] The seagull-shaped (lat. Larus), gram-negative rods were classified via 16S rRNA gene sequencing as being both a new species

and new genus.[10] Eating raw infected fish will cause infection in humans. Most frequent symptoms are watery or bloody diarrhea (resp. 80%/20%), abdominal pain (75%), and vomiting (35%).[11] The disease is self-limiting with a median duration of symptoms of 4 days. A large multicenter case-control next trial in Hong Kong did not find LH in its control group (n = 1,894), suggesting causal relationship between gastroenteritis and LH.[12] However, studies fulfilling Koch’s postulates for causality have not been performed, making this bacterium of questionable significance in the patient’s history.[13] Cysts of the protozoa B hominis are often found in stool samples, especially in returning travelers (up to 30%).[14] There is considerable controversy about its role as a pathogenic organism. If decided to treat, first choice would be metronidazole. After making the hypothesis of a reactive hypereosinophilic syndrome-like reaction, it should be noted that one cannot exclude the direct pathogenic role of any of the microorganisms found in the patient’s feces. Especially the role of LH is uncertain, because little is known about the pathogenic nature of this bacterium. It could very well have had a significant or additive role in the gastrointestinal symptoms of the patient for a prolonged period of time.

Recent fatal stings in Thailand were first attributed to “global warming.”28 However, severe stings and fatalities have long been present in Thailand and surrounding waters. What is “new,” however, is the widespread recognition

of the problem and a whole-of-government approach to managing it. In December 2008 and April 2009, Australian experts gave seminars and workshops in Thailand to educate the Government and tourism bodies how to reduce stings in line with the current advice in Australia. Commencing in July 2009, a grant from the Australian Government (through the Australia–Thailand Institute—Department of Foreign Affairs) is funding Thai scientists and physicians to visit Australia to learn state-of-the-art marine stinger prediction, prevention, and treatment from a variety CP-868596 mouse of experts around the country. These proactive safety measures will enable the standard to be set for other countries in the Indo-Pacific. These cases demonstrate a need to update sting prevention strategies, targeting the highest risk populations and activities. Prevention is better than cure”—tourists must be made aware of the danger and alternates made available to them. Honest and accurate educational material must be freely available and provided by tourism agencies arranging holidays in Thailand and other Indo-Pacific Countries where the problem

exists, and be freely available at the airports and resorts. Beaches need restricted access, Trichostatin A concentration with walkways to them having signs mafosfamide warning of possible dangerous jellyfish presence. These signs must be multilingual and/or with translation easily available by digital access—including phonetic language. Vinegar should be freely available on all beaches together with provision of stinger-resistant nets, where the beach profile allows, with suitably trained lifeguards to reduce sting possibilities. In areas where nets cannot be fitted, swimming pools make excellent substitutes. Provision of protective clothing by tourism operators should be mandatory in areas of swimming, snorkeling, diving, or other in-water activities.

Stings and even fatalities will never be prevented completely; however, such measures would greatly reduce the possibility of serious envenomations and will not detract from tourism; they will enhance it, secondary to improved safety. We would like to acknowledge Andrew Jones, a journalist, whose young son was badly stung while on holidays in Thailand; in response to the sting, Mr Jones has personally spent much time and effort to make Thai beaches safer, including coordinating efforts to present the problem to the Thai authorities, and arranged for Dr Lisa Gershwin and her medical colleagues to present educational seminars in Thailand. Mr Jones and Dr Gershwin were flown to Thailand courtesy of Jetstar Airlines of Australia and accommodated in Le Meridien Phuket, in the interest of Thai–Australian interests.

Qualitative variables were analysed using the χ2 test. Student’s t-test and one-way analysis of variance (ANOVA) with a post hoc Bonferroni test were used to compare selleck compound continuous variables between two groups and more than two groups, respectively, and the Mann–Whitney U-test and the Kruskal–Wallis test were used to compare variables that did not have a Gaussian distribution. Associations between quantitative variables were evaluated by Pearson correlation analysis or Spearman correlation

for nonnormally distributed variables. The independence of the associations was evaluated by linear regression analysis. In all statistical tests, P-values < 0.05 were considered significant. The main clinical and metabolic characteristics of healthy controls and HIV-1-infected patients are shown in Table 1. UCs presented a higher BMI compared with HIV-1-infected patients (P < 0.001). Inflammatory parameters (sTNFR2 and IL-6; P < 0.001 for both) and TG (P < 0.001) were higher in HIV-1-infected patients, whereas HDLc was lower (P = 0.021). In contrast, sTNFR1 and adiponectin did not show any significant differences between groups. With respect to ZAG, overall, HIV-1-infected patients had lower plasma ZAG levels than UCs (P < 0.001). When we categorized patients and controls in different age subsets (18–39, 40–59 and 60–89 years), ZAG levels were

significantly lower in infected subjects from the youngest subset only: 48 μg/mL (40–60 μg/mL) in infected patients Rapamycin vs. 67 μg/mL (53–92 μg/mL) in uninfected controls (P < 0.001). In the older groups, ZAG was always lower in infected patients, but the differences were nonsignificant (full data not shown). Otherwise, no significant correlation was observed between plasma ZAG level and viral load Nintedanib (BIBF 1120) or age. Table 2 shows plasma carbohydrate and lipid metabolism parameters and plasma adipokine levels for the HIV-1-infected patients included in the study, categorized according to the presence or absence of lipodystrophy. Of the 166 HIV-1-infected subjects,

77 had lipodystrophy (46.4%) and 89 (53.6%) did not have lipodystrophy. Among the lipodystrophy subset, 27 had pure lipoatrophy and 50 had a mixed form (lipoatrophy plus lipohypertrophy). With respect to the analytical parameters, the two groups had similar glucose levels. In contrast, the lipodystrophy subset had higher plasma levels of insulin (P < 0.001), HOMA-IR (P < 0.001), TG (P < 0.001), total cholesterol (P = 0.005) and LDLc (P = 0.038) and lower HDLc (P < 0.001) compared with the nonlipodystrophy individuals. Circulating levels of sTNFR1, sTNFR2 and IL-6 were similar in the two HIV-1-infected subgroups. Patients with lipodystrophy had significantly lower adiponectin (P < 0.001) and significantly higher leptin (P = 0.008) plasma levels compared with the nonlipodystrophy subset.

1 400 aa 2610–3623 YP_004831123.1 337 aa 47 083–48 171 YP_004556205

362 aa 45 685–46 887 YP_004556204 400 aa 44 624–45 637 YP_004556203.1 337 aa 10 225–11 319 YP_004842390 364 aa 6087–6737 YP_004842384 216 aa 3757–4413 YP_667820.1 218 aa 648–1541 YP_667821.1 297 aa 2644–3567 YP_003858293.1 307 aa 1855–2562 YP_195758.1 235 aa For CHIR99021 some other degradative plasmids from sphingomonads, currently, only the sequence data deposited in public databases are available, for example, for plasmid pSWIT02 from the dibenzo-p-dioxin degrading strain Sphingomonas wittichii RW1 (coding for the dibenzo-p-dioxin dioxygenase) or plasmids pISP0, pISP1, pISP3 and pISP4 from the γ-hexachlorocyclohexane-degrading isolate Sphingomonas sp. MM-1 (Table 1). These sequenced plasmids belong to a much larger number of degradative plasmids, and plasmids are also involved in the degradation of several Antidiabetic Compound Library order PAHs, naphthalenesulphonates

or polymeric polyethylenglycols and polyvinyl alcohols by sphingomonads (Fredrickson et al., 1999; Shuttleworth et al., 2000; Cho & Kim, 2001; Basta et al., 2004; Tani et al., 2007; Hu et al., 2008). It has been demonstrated for many sphingomonads with the ability to degrade xenobiotic compounds that they contain multiple plasmids. Thus, in S. aromaticivorans F199, S. wittichii RW1 and Novosphingobium pentaaromativorans US6-1, two plasmids each were found. In the γ-hexachlorocyclohexane-degrading strain, Sphingobium japonicum UT26 and the PAHs-degrading isolate Novosphingobium sp. strain PP1Y three plasmids, in the naphthalenesulphonates-degrading strain Sphingobium xenophagum BN6 and the organophosphates-degrading

click here Sphingobium fuligines ATCC27551 four plasmids and in the γ-hexachlorocyclohexane-degrading strain Sphingomonas sp. MM-1 even five plasmids have been detected (Table 1; Romine et al., 1999; Basta et al., 2004; D’Argenio et al., 2011; Luo et al., 2012; Pandeeti et al., 2012; Tabata et al., 2013). Furthermore, for some sphingomonads, the presence of a ‘second chromosome’ has been described. These ‘second chromosomes’ are often only slightly larger than some of the ‘megaplasmids’ and resemble in various traits (e.g. the mechanism of replication) the ‘megaplasmids’. Therefore, it appears that these ‘second chromosomes’ might have been evolved by the uptake of some essential genes by certain ‘megaplasmids’ (Copley et al., 2012; Nagata et al., 2011). The ability of sphingomonads to host several different plasmids in a single cell is essential for the degradation of many organic compounds. Thus, it has been shown for S. japonicum UT26 and also for Sphingomonas sp. MM-1 that the genes encoding for the mineralization of γ-hexachlorocyclohexane are scattered on at least three replicons in these strains (Nagata et al., 2010, 2011; Tabata et al., 2013). Similarly, in S. wittichii RW1, only the genes coding for the initial ‘dibenzo-p-dioxin dioxygenase’ have been located on plasmid pSWIT02 (Colquhoun et al., 2012).