2007), and were

2007), and were selleckchem therefore designated as saprophytes and endophytes, respectively. In the rubber tree, C. cassiicola has thus far been exclusively known as a necrotrophic pathogen that causes the Corynespora Leaf Fall (CLF) disease, which ranks among the most important fungal diseases in Asian and African rubber plantations. Initially, C. cassiicola was described as a minor pathogen capable of attacking

only budwood or seedling nursery plants (Newsam 1960; Chee 1988), but in 1975, the first epidemic outbreak on a plantation scale occurred in Indonesia. In the 1980s, several other countries in Southeast Asia were severely affected by disease outbreaks and thousands of hectares of rubber trees were uprooted in Malaysia, Indonesia, Thailand and Sri Lanka (Liyanage et al. 1986; Pongthep 1987; Chee 1988). By the end of the 1980s, African countries were also affected by CLF. The disease severity further increased until several important rubber tree cultivars considered to be tolerant or resistant to CLF during the first epidemic in the mid 1980s succumbed to the disease (Jayasinghe and Silva 1996; Shamsul and Shamsuri selleck compound 1996; Sinulingga et al. 1996; Wahounou et al. 1996). Currently, all Asian and African rubber-producing countries, which account for 98 % of the

natural rubber production in the world (94 and 4 % for each continent, respectively), are affected by the disease resulting in considerable economic losses. CLF is characterized by necrotic lesions that develop on both young and mature leaves and lead to extensive defoliation. The fungus typically causes areas of necrosis with a fish bone appearance due to the darkening of the veins adjacent to the lesions (Chee 1988; Liyanage and Liyanage 1986; Pongthep 1987). However, the symptoms vary depending on the age, type and location of the rubber tree (Jayasinghe et al. 1998). This symptom variability impedes diagnosis of the disease in a plantation. Additionally, C. cassiicola isolates within the same agroclimatic zone vary widely in morphology, colony color, growth, spore production, pathogenicity and

genetic diversity (Darmono et al. 1996; Jayasinghe and Silva 1996; Breton et al. 2000; Atan and Hamid 2003; Alanine-glyoxylate transaminase Romruensukharom et al. 2005; Dixon et al. 2009; Qi et al. 2009). Colonization of the rubber tree tissues by C. cassiicola involves the secretion of phytotoxic molecules (Onesirosan et al. 1975; Liyanage and Liyanage 1986; Purwantara 1987; Nugawela et al. 1989; Breton et al. 2000). A toxin called cassiicolin was purified and characterized from the culture filtrate of a rubber tree isolate (CCP) from the Philippines (Breton et al. 2000; Barthe et al. 2007; de Lamotte et al. 2007). The toxin is a small, secreted glycosylated protein that plays an important role in C. cassiicola pathogenicity. The cassiicolin-encoding gene encodes a precursor protein containing a signal peptide at the amino terminus that is predicted to target the protein for secretion (Déon et al. 2012).

J Antimicrob Chemother 2012, 67:849–856 PubMedCrossRef 15

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We did not find any peak that corresponds to the diffraction from

We did not find any peak that corresponds to the diffraction from Cu2O (111) or Cu (111) which would be located at 36.4° and 43.3°, respectively [18]. The XRD results are consistent with the TEM results that a pure CuO has been grown successfully on top of ZnO NWs. Figure 3 XRD patterns of ZnO (black line) and ZnO/CuO (red line). The inset shows the XRD patterns of ZnO (black line) and ZnO/CuO (red line) between 2θ = 35.5° and 40.5°. Transmission and spectral photoresponse of the ZnO-CuO are shown in Figure  4. With the light coming from the ‘back’ of the sample as shown in the Erismodegib solubility dmso inset of Figure  1, the ITO/glass substrate acts

as a ‘low-pass filter’ and will allow the light with a wavelength above 350 nm to pass without absorption [21]. As can be seen in the figure, the transmission spectrum of ZnO/CuO CH (blue line) shows two abrupt drops, one at about 420 nm and the other at about 800 nm, which correspond to the band-edge absorption of ZnO and CuO, respectively. Also shown in the figure are the photoresponse spectra of ZnO/CuO CH under MK-8669 supplier different reverse biases. We can identify two features located at 424 and 800 nm in the spectra. The huge response around 424 nm is below the typical band gap of ZnO. It could be due to the narrowing of the band gap of ZnO as a result of tensile stress in the coaxial structure

[22], which is consistent with our XRD and TEM results. Another response around 800 nm can be attributed to the photoresponse of CuO [23]. It is much smaller than that of the main peak at 424 nm because the CuO film is thin. We note that the optical responsivity of the devices is bias sensitive. The responsivity of the sample at 424 nm increases from 0.4 to 3.5 A W−1 when the reverse bias increases from 1 to 3 V. Figure 4 Transmission spectrum of ZnO/CuO

CH and its photoresponse spectrum at different reverse biases. The inset shows the photoresponse of ZnO NWs for comparison. The I-V curves of PR-inserted ZnO NWs/CuO with and without light illumination are shown in Figure  5. The inset shows that the I-V curves for the Ag-CuO film (black line) and ITO-ZnO NWs (blue line) are both linear, indicating the contacts are ohmic [24–26]. Hence, second the characteristic rectifying behavior is due to the ZnO/CuO CH p-n junction [26]. As can be seen in the figure, the leakage current is 12.6 μA at a reverse bias of −3 V, and it increases to 770 μA under light illumination, which is an increase of about 60-fold. As there is a large on/off ratio and the photoresponse is centered at around 424 nm, the experimental results suggest that the PR-inserted ZnO/CuO CH can be used as a good narrow-band blue light detector [27]. Figure 5 I – V characteristic curves of the ZnO/CuO CH with PR. In the dark (black line) and under light (424 nm) illumination (red line). The inset shows the I-V curves of the Ag-CuO film (black line) and ITO-ZnO NWs (blue line).

Cancer cells having a wild type p53 were sensitive while those wi

Cancer cells having a wild type p53 were sensitive while those with abnormal p53 (mutated or null) were resistant to bortezomib treatment. Consistent with

these findings, previous studies found that wild type p53 transcriptionally inhibits Vismodegib solubility dmso survivin expression in various cancer cell types [27–29] and bortezomib can stabilize wild type p53 in prostate cancer cells [40]. Here, we would like to point out that the bortezomib concentration used affects the results, suggesting the dose used in the clinic should be carefully considered. When high dose may kill cancer cells better in a short term, high dose will increase the possibility to generate bortezomib resistance, suggesting that in addition to p53 status-associated survivin expression,

other factors, such as other protein members in the IAP and Bcl-2 families may also play important roles in bortezomib resistance. Nevertheless, we have confirmed a role for survivin in bortezomib resistance by direct silencing of survivin expression using survivin-specific siRNA/shRNA. This finding is significant because our recent studies indicated that survivin may be a superior LY294002 cancer stem cell marker and possibly plays critical role in cancer stem cell expansion [41]. In this regard, cancer cells appear to have a higher percentage of subpopulation cells that are tumorigenic (cancer initiating/cancer

stem cells) in xenograft mouse Glutathione peroxidase models [42]. Therefore, consideration of both survivin expression and p53 status as interconnecting biomarkers and targets in cancer cells may not only be useful for predicting the outcome of bortezomib treatment, but may also provide pivotal criteria for rational drug combination. For example, bortezomib likely induces survivin expression in cancer cells with mutated or null p53 (this study), and it is known that paclitaxel rapidly induces survivin expression [43]. Thus, combination of bortezomib and paclitaxel likely obtained no good results in many cancer types with such as the mutated p53 background. Accordingly, a recent Phase II study in patients with metastatic esophageal, gastric, and gastroesophageal cancer showed poor results in the drug combination [44]. However, it is also possible that the poor results derived from such a drug combination involve other mechanisms of drug resistance in these tumors that are notoriously difficult to treat with chemotherapy. An important question that needs be answered for better application of the findings is the mechanism underlying bortezomib-mediated induction of survivin expression in mutated or null p53 cancer cells, while it showed downregulation of or minimal effect on survivin expression in wild type p53 cancer cells.

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94 mg g-1, respectively To understand how Hg2+ interacted with t

94 mg g-1, respectively. To understand how Hg2+ interacted with thiol-functionalized MGO, different adsorption isotherm models were used to fit the adsorption data. The data of Hg2+ adsorption

were fit with the Freundlich isotherm model, which can be expressed as [25] where K and n are the Freundlich adsorption 3-deazaneplanocin A price isotherm constants, which are related to the relative adsorption capacity of the adsorbent and the degree of nonlinearity between solution concentration and adsorption, respectively. K and 1/n values can be calculated from the intercept and slope of the linear plot between logC e and logQ e . Based on the plot shown in Figure  5a, n and K were calculated to be 1.02 and 10.54, respectively. However, the data did not fit the Langmuir isotherm model very well (Additional file 1: Figure S1b), indicating that the adsorption of Hg2+ by the adsorbent was not restricted to monolayer formations [26]. To test the reproducibility of the adsorbents, they Navitoclax price were immersed in an aqueous solution with an initial Hg2+ concentration of 100 mg l-1 for 48 h with oscillation. The adsorption capacity for the first-time immersion was calculated to be 289.9 mg g-1. After being washed with diluted HCl, thiol-functionalized MGO was applied to repeat the exact same adsorption test. The obtained adsorption capacities were 282.4, 276.8, and 258.1 mg g-1

for the second-, third-, and fourth-time immersion, respectively, which were corresponding to 97.4%, 95.5%, and 89.0% of initial adsorption capacity. It indicated that the adsorbents could be reused. Figure 4 Adsorption kinetics. (a) Hg2+ adsorption kinetics of GO, MGO, and thiol-functionalized MGO, respectively. (b) The adsorption Bay 11-7085 kinetics of thiol-functionalized MGO fits with the pseudo-second-order kinetics (initial concentration, 10 mg l-1). Figure 5 Adsorption isotherms and adsorption capacity. (a) Adsorption isotherms fitted with the Freundlich model (red line) for adsorption of Hg2+ on thiol-functionalized MGO and (b) adsorption capacity versus the

cycling number with the initial concentration of 100 mg l-1 Hg2+. Conclusion Thiol-functionalized MGO with magnetite nanoparticles was successfully synthesized using a two-step reaction. Thiol-functionalized MGO exhibited higher adsorption capacity compared to the bare graphene oxide and MGO. Its capacity reached 289.9 mg g-1 in the solution with an initial Hg2+ concentration of 100 mg l-1. The improved adsorption capacity could be attributed to the combined affinity of Hg2+ by magnetite nanocrystals and thiol groups. After being exchanged with H+, the adsorbent could be recycled. The adsorption of Hg2+ by thiol-functionalized MGO fits well with the Freundlich isotherm model and followed pseudo-second-order kinetics. The scheme reported here enables rational design of the surface properties of graphene oxide and can be used to synthesize other functionalized composites for environmental applications.

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Competing interests The authors declare that they have no competing interests. Authors’ contributions RRY designed parts of the experiments and sample preparations and drafted the manuscript. DLZ is the corresponding author and provided a great help for experimental designs. LZB, NNY, and LX took part in sample preparation and characterizations and discussed the results. All authors have read and approved the final manuscript.”
“Background Graphene has attracted global research interests across MAPK inhibitor a wide range of applications [1, 2]. However, graphene is highly sensitive to extraneous environmental influences. Thus, it was deemed worthwhile to deposit protective layers over graphene without impairing its properties. Hexagonal boron nitride (h-BN), a well-known dielectric material, may afford the necessary protection for graphene [3, 4]. As an analogue of graphene, h-BN shows a minimal lattice mismatch with graphene of about 1.7%, yet has a wide band gap [5–8] and lower environmental sensitivity [3, 4].

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proteomics: a paradigm shift in characterizing microbial activities at the molecular level. Microbiol Mol Biol Rev 2009,73(1):62–70.PubMedCrossRef 63. Imhoff JF: The phototrophic alpha-Proteobacteria. In Prokaryotes. Volume 5. Edited by: Dworkin M. Springer, New York; 2006:41–64.CrossRef 64. Wilson K: Preparation of genomic DNA from bacteria. In Current protocols in molecular biology. Edited by: Ausubel FM, Brent R, Kingston RE, Moore DD, Seidman JG, Smith JA, Struhl K.

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MN helped in the idea, drafting the first version of manuscript,

MN helped in the idea, drafting the first version of manuscript, and critically reading it. MA helped in the idea, and edited the manuscript. FAZ had the idea, designed the study protocol, collected and assessed the quality of the data, helped in writing the first draft of the paper, and repeatedly critically edited it. All authors have MI-503 read and approved the final version of the manuscript.”
“Introduction A pseudoaneurysm of the peripheral artery is very rare and is generally a late sequela of trauma, iatrogenic injury, and general

illness. It is more infrequent in the upper limb vasculature than in the lower limb vasculature. Although there are many reported causes of brachial artery pseudoaneurysms, to our knowledge, this is the first report of delayed rupture of a brachial artery pseudoaneurysm during the rehabilitation of a patient with burns of the upper extremity who underwent fasciotomy and musculocutaneous flap coverage. We also present a review of the brachial artery pseudoaneurysm. Presentation of case A 26-year old male patient

presented ABT-888 mw to the hospital with wound dehiscence and oozing of the left axilla that had commenced two days earlier while undergoing rehabilitative therapy for postburn joint ankylosis and brachial plexus palsy of the upper extremity (Figure 1). According to the patient’s history, he had undergone escharectomy and latissimus dorsi musculocutaneous flap coverage of a neurovascular bundle exposed in the medial upper arm due to a contact burn of the left upper extremity six months earlier, in addition to a split-thickness skin graft for a lesion (Figure 2). At the time of the hospital visit, the patient’s blood pressure was 130/74 mmHg, and his heart rate was 98 bpm. The hemoglobin

value was 12.8 g/dl. The examination revealed no other specific findings. The wound was approximately 1 × 1 cm wide, with Galeterone bleeding in an oozing pattern. Distal pulsation and circulation had been maintained. Under the assumption that wound dehiscence had occurred during the rehabilitative treatment, a moderate compression gauze dressing was applied. The wound gradually healed, but wound rupture occurred again at the site of the posterior axilla on day 14 of hospitalization. The new site of wound dehiscence was due to a hematoma, which was accompanied by profuse bleeding. A gauze compression bandage was applied again, and a computed tomography angiography (CTA) was conducted. The CTA images revealed a pseudoaneurysm in the brachial artery (Figure 3). Due to the profuse bleeding from wound, the patient’s blood pressure was decreased to 90/50 mmHg, and the heart rate was increased up to 108 bpm. The hemoglobin value was also dropped to 8.2 g/dl. The patient underwent immediate surgical exploration and the pseudoaneurysm was approached through the marginal side of the previously performed latissimus dorsi musculocutaneous flap.

8% agarose gel in 1X Tris/Borate/EDTA (TBE) buffer [18] and visua

8% agarose gel in 1X Tris/Borate/EDTA (TBE) buffer [18] and visualized to assess their integrity, then stored at 4°C prior to PCR amplification. BOX-PCR, ERIC-PCR and the molecular identification of selected Nutlin-3a chemical structure bacterial strains Amplification reactions using the primers BOXA1R [19] and ERIC1R and ERIC2F [20] were performed in the following mix: 1 μl (50–100 ng) of target DNA; 5 μl of 5X PCR buffer (Promega, RJ, Brazil); 2.5 mM (ERIC) or 3.75 mM (BOX) MgCl2; 0.5 mM dNTP; 0.4 μM

and 1 μM of the primers ERIC1R – ERIC2F or BOXA1R, respectively; and 0.5 U (ERIC) or 1.25 U (BOX) of Taq polymerase in a 25 μl final volume. The cycle applied was 1 × [7 min at 95°C], 35 × [1 min at 94°C, 1 min at 52°C (with ERIC primers) or 53°C (with BOXA1R primer), 8 min at 65°C] and a final extension of 16 min at 65°C. Negative controls (without DNA) were run during all amplifications. Agarose gel electrophoresis of PCR products was performed using 1.4% agarose in 1X TBE buffer at 90 V for 4 h at room temperature. The BOX and ERIC-PCR results were collected into matrices indicating the presence or absence (scored as 1 or 0, respectively) of bands. Dendrograms were constructed using Dice similarity coefficients and the unweighted pair group method with

arithmetic mean (UPGMA) through the BioNumerics software package (Applied Maths, Ghent, Belgium). For molecular identification find more of the selected isolates, their 16S rRNA coding gene was amplified by PCR using the pair of universal primers pA and pH and the

conditions described in Massol-Deya et al. [21]. The PCR products were then sequenced by Macrogen (South Korea). The partial 16S rRNA gene sequences (~800 bp) were identified using the BLAST-N tool (http://​blast.​ncbi.​nlm.​nih.​gov/​) on the National Center for Biotechnology Information (NCBI) website using the GenBank non-redundant database. A phylogenetic tree was constructed Silibinin based on partial 16S rRNA gene sequences using the neighbor-joining method. MEGA 5.1 software was used to calculate Jukes-Cantor distances. Bootstrap analyses were performed with 1,000 repetitions, and only values higher than 50% are shown in the phylogenetic tree. Susceptibility of the bacterial isolates to the essential oil obtained from L. sidoides genotypes LSID006 and LSID104 The determination of the minimum inhibitory concentration (MIC) was performed using a serial dilution technique in 0.2 ml thin-walled 8 strip cap microtubes as recommended by CLSI M7-A4 for bacteria [22]. Bacterial isolates from the four genotypes were tested for susceptibility. The investigated essential oils containing contrasting amounts of thymol and carvacrol (Table 1) were diluted seven times using doubling dilution, from 4 to 0.03 mg ml-1, and 1 μl of each dilution was added to 189 μl TSB with 10 μl of the bacterial suspension (cells grown to a O.D. = 0.09 at 625 nm, then diluted 50X in TSB). The microtubes were incubated for 48 h at 32°C.