This has been demonstrated by persistent elevation of pro-inflamm

This has been demonstrated by persistent elevation of pro-inflammatory cytokines like IL-6 among infertile women [12] and in tear fluid from selleck kinase inhibitor post-scarring trachoma populations [13]. One study identified IL-6 secretion via the TLR2 signaling pathway after C. trachomatis infections [14]. This TLR2 pathway has been shown to be associated with fallopian-tube pathology, potentially contributing to the immunopathogenesis associated with C. trachomatis infection [14]. The chemokine monocyte chemoattractant protein-1 (CCL2) has also been selleck chemicals identified in chronic chlamydial infections demonstrating elevated levels in post-scarring

trachoma populations [13]. Due to the high prevalence of worldwide trachoma, the World Health Organization (WHO) established and supports Alpelisib the use of the SAFE (surgery, antibiotics, facial cleanliness, and environmental improvements) strategy to reduce disease transmission in endemic areas. Mass antibiotic therapy has been a mainstay in this program resulting in

diminished prevalence of active chlamydial infections [15–17]. However, heightened recurrence rates of infection 6-24 months after termination of antibiotic therapy were evident in multiple studies [18–21]. Additionally, Burnham et al. saw an increase in chlamydia-associated STI Reinfection after a control program with antibiotic treatment was established [22]. The mass administration of antibiotics may lead to the development of antibiotic resistance in chlamydial species as well as other pathogenic bacteria. It is apparent ADAM7 that research into alternative treatments is warranted, and the use of phototherapy may be an attractive option. Phototherapy utilizing low power lasers or light emitting diodes (LEDs) has been

shown to reduce pain and chronic inflammation, and to promote tissue regeneration via a photochemical mechanisms (reviewed in [23]). Additionally, anti-bacterial effects due to the increased production of reactive oxygen species resulting in membrane instability and DNA damage have been evident with phototherapy [23–27]. Its use with several discrete wavelengths exhibits anti-bacterial activity requiring short treatment times without inducing anti-bacterial resistance subsequent to multiple treatment sessions [28]. In this study, we analyzed the effect of low-level 405 nm and 670 nm LED irradiation on the growth of C. trachomatis and the ensuing secretion of pro-inflammatory cytokines IL-6 and CCL2 from C. trachomatis-infected epithelial cells. Results Inhibition of chlamydial growth post – 405 nm irradiation This study assessed the use of 405 nm and 670 nm LEDs as an alternative treatment against chlamydial infections. In Figure 1A, HeLa cells were infected with C. trachomatis at a multiplicity of infection (MOI) of 5. Irradiation treatment with violet 405 nm LEDs demonstrated chlamydial growth inhibition at energy densities as low as 5 J/cm2 (Figure 1B, P < 0.005).

PubMedCrossRef 15 Haverkamp J, Charbonneau B, Ratliff TL: Prosta

PubMedCrossRef 15. Haverkamp J, Charbonneau B, Ratliff TL: Prostate inflammation and its potential impact on prostate cancer: a current review. J Cell Biochem 2008,103(5):1344–1353.PubMedCrossRef 16. Sutcliffe S, Platz EA: Inflammation in the CYT387 order etiology of prostate cancer: an epidemiologic perspective. Urol Oncol 2007,25(3):242–249.PubMed 17. De Marzo AM, Nakai Y, Nelson WG: Inflammation, atrophy, and prostate carcinogenesis. Urol Oncol 2007,25(5):398–400.PubMed 18. Al-Mously N, Eley A: Interaction of Chlamydia trachomatis serovar E

with male genital tract epithelium results in secretion of proCopanlisib in vitro inflammatory cytokines. J Med Microbiol 2007,56(Pt 8):1025–1032.PubMedCrossRef 19. Takeyama K, Mitsuzawa H, Shimizu T, Konishi M, Nishitani C, Sano H, Kunishima Y, Matsukawa M, Takahashi S, Shibata K, et al.: Prostate cell lines secrete IL-8 in response to Mycoplasma hominis through Toll-like receptor 2-mediated mechanism. Prostate 2006,66(4):386–391.PubMedCrossRef 20. Jugeau S, Tenaud I, Knol AC, Jarrousse V, Quereux G, Khammari A, Dreno B: Induction of toll-like receptors by Propionibacterium acnes. Br J Dermatol 2005,153(6):1105–1113.PubMedCrossRef 21. Kundu SD, Lee C, Billips BK, Habermacher GM,

Zhang Q, Liu V, Wong LY, Klumpp DJ, Thumbikat see more P: The toll-like receptor pathway: a novel mechanism of infection-induced carcinogenesis of prostate epithelial cells. Prostate 2008,68(2):223–229.PubMedCrossRef 22. Gatti G, Rivero V, Motrich RD, Maccioni M: Prostate

epithelial cells can act as early sensors of infection by up-regulating TLR4 expression and proinflammatory mediators upon LPS stimulation. J Leukoc Biol 2006,79(5):989–998.PubMedCrossRef Niclosamide 23. Takeda K, Kaisho T, Akira S: Toll-like receptors. Annu Rev Immunol 2003, 21:335–376.PubMedCrossRef 24. Chen Q, Koga T, Uchi H, Hara H, Terao H, Moroi Y, Urabe K, Furue M: Propionibacterium acnes-induced IL-8 production may be mediated by NF-kappaB activation in human monocytes. J Dermatol Sci 2002,29(2):97–103.PubMedCrossRef 25. Kishimoto T: Interleukin-6: from basic science to medicine–40 years in immunology. Annu Rev Immunol 2005, 23:1–21.PubMedCrossRef 26. Waugh DJ, Wilson C: The interleukin-8 pathway in cancer. Clin Cancer Res 2008,14(21):6735–6741.PubMedCrossRef 27. Hamilton JA: GM-CSF in inflammation and autoimmunity. Trends Immunol 2002,23(8):403–408.PubMedCrossRef 28. Gillitzer R, Berger R, Mielke V, Muller C, Wolff K, Stingl G: Upper keratinocytes of psoriatic skin lesions express high levels of NAP-1/IL-8 mRNA in situ. J Invest Dermatol 1991,97(1):73–79.PubMedCrossRef 29. Abd El All HS, Shoukry NS, El Maged RA, Ayada MM: Immunohistochemical expression of interleukin 8 in skin biopsies from patients with inflammatory acne vulgaris. Diagn Pathol 2007, 2:4.PubMedCrossRef 30.

The 48 h cell free fermented broth (CFB) of P pentosaceus

The 48 h cell free fermented broth (CFB) of P. pentosaceus strain IE-3 grown in anaerobic broth displayed antimicrobial activity against different indicator strains in well diffusion assay (Table 1). In contrast to typical narrow spectrum activity shown by pediocin-like bacteriocins [10], the antimicrobial peptide produced by strain IE-3 click here inhibited growth of Gram-positive and Gram-negative indicator strains. The most sensitive

strain among the test strains was Micrococcus luteus that showed a 26 mm zone of inhibition. There was no activity observed against other strains of Pediococcus, yeasts and fungi. A curve displaying Belinostat supplier antimicrobial production versus bacterial growth showed that the antimicrobial peptide production was initiated

during early log phase (6 h of incubation) which increased to a maximum level by initial stationary phase (14 h) and remained constant thereafter (Figure 1a). Antimicrobial activity was obtained when the P. pentosaceus strain IE-3 was grown in different media including minimal medium with optimal CHIR98014 supplier production obtained in media like anaerobic broth, MRS and reinforced clostridial broth, the latter containing reducing agents (Figure 1b). Significant delay was observed to reach exponential growth phase by strain IE-3 while growing in minimal media that resulted in slow antimicrobial production (data not shown). Table 1 Antimicrobial activity of the cell free fermented broth (CFB) of 48 h grown culture against various test strains (mean values of triplicate experiments) Test strain Inhibition zone using CFB (mm) Gram-positive   Listeria monocytogenes (MTCC 839) 13 Lactobacillus plantarum (MTCC 2621) 10 Clostridium bifermentas (MTCC 11273) 10 Clostridium sordelli (MTCC 11072) 12 Bacillus subtilis (MTCC 121) <10 Staphylococcus

aureus (MTCC 1430) 10 Micrococcus luteus (MTCC 106) 26 Pediococcus acidilactici (MTCC 7442) – P. pentosaceus (MTCC 9484) – P. pentosaceus (MTCC 10308) – Gram-negative   Vibrio cholera (MTCC 3904) 15 Escherichia coli MYO10 (MTCC 1610) <10 Pseudomonas aeruginosa (MTCC 1934) 10 Serratia marcescens (MTCC 97) – Fungi   Candida albicans (MTCC 183) – Asperigillus flavus (MTCC 8188) – -, no activity. Figure 1 Antimicrobial production by P. pentosaceus strain IE-3. (a) Correlation between antimicrobial peptide production and growth of strain IE-3. Growth measured as OD at 600 nm (dotted lines), bacteriocin production as zone of inhibition (continuous line). Error bars shows ± SD for triplicate experiments. Culture was grown in anaerobic broth under anaerobic conditions at 30°C on a shaker incubator. (b) Antimicrobial assay of 24 h cell free fermented broth obtained by growing strain IE-3 on different media. Purification of antimicrobial peptide The crude extract obtained by Diaion HP20 chromatography showed significant increase in antimicrobial activity compared to CFB.

PCR products for both assays were separated by gel electrophoresi

PCR products for both assays were separated by gel electrophoresis and visualised using a UV transmilluminator. Negative controls (dH2O) were included in each amplification round to control for PCR contamination. PCR products were purified with an Invitrogen PureLink™ PCR purification kit and sent to the Australian Genome Research Facility (AGRF) for sequencing using the Sanger dideoxy method [30]. Gene sequence names from each C. pecorum positive sample were derived from the population SCH 900776 mw from which the koala originated and the ID name assigned by the veterinarians (i.e. ‘Bre/Ned’ = Brendale population; animal name ‘Ned’). Sequence and

statistical analysis Alignments for each sequenced gene were produced using ClustalW Gefitinib supplier [31] and RevTrans [32] was used to reverse-translate all alignments. Non-coding genes were aligned based on their nucleotide sequence. The software package DnaSP 5.0 [33] was used to analyse the extent of sequence variation by calculating the number

of polymorphic and parsimony-informative sites, the average nucleotide diversity (p-distance) and Tajima’s test for neutrality (D-value). The Molecular Evolutionary Genetics Analysis (MEGA) [34] software package was used to calculate the number of synonymous and non-synonymous sites and subsequent dN/dS ratio using the Repotrectinib purchase Nei-Gojobori method [35]. The discrimination index (D.I.), based on Simpson’s index of diversity [36], was calculated to determine the differentiating and discriminatory capacity of each gene: where D = index of discrimination, N = number of strains in the sample, and n i = number of strains in group i. The index ranges from 0 to 1, with a value close to 0 indicating low genetic diversity and a value close to 1 indicating high genetic diversity [36]. Calculation of the D.I. requires at least three nucleotide sequences for analysis. Criteria for identifying genetic markers In order to select the most appropriate candidate

genes for further investigation, a shortlist of three genes, ORF663, incA and tarP (in addition to ompA), were selected based on their application in previous C. pecorum typing studies [21], in addition to several empirical criterions: Clomifene The average proportion of nucleotide distances (p-distance) should be ≥ 0.02 before intra-species differentiation may be attempted [37, 38], which can be calculated from an alignment containing two or more sequences [39, 40]. Furthermore, both highly constrained, slowly-changing molecular markers and highly variable genes under diversifying selection each have their advantages, disadvantages, and advocates [41], implying the importance of selecting genes under both positive and negative selection. Finally, the discrimination index (D.I.) for candidate markers should be > 0.

e tumor resections into healthy surrounding tissue, would no lon

e. tumor resections into healthy surrounding tissue, would no longer be determined by the morphology of the cells only, but also by the subcellular (Dibutyryl-cAMP protein-based, epigenetic and genetic) status of the normal-appearing cells surrounding the primary tumor and/or metastasis, respectively. The consequence therefrom

would be more precise surgical resections (guided by prior subcellular analysis) which in turn should reduce the rate of local recurrence of primary tumors, e.g. of advanced stage (colo)rectal carcinomas. Furthermore, given the loss of function of tumor suppressor proteins LY2874455 molecular weight coinciding with an oncoprotein metastasis and its (epi)genetic correlates (Fig. 2b), drug treatment of cancer disease could NVP-BGJ398 cost equally undergo a paradigm shift through the application of cell-permeable tumor suppressor peptides that enter both morphologically normal, yet likely premalignant cells and cancer cells (Fig. 2c), as previously envisaged [17, 18, 39, 40, 44]. This potential pharmacological rationale would address not only the primary tumor, but also its distant metastases in an appropriate fashion, specifically

by disrupting oncoprotein-tumor suppressor protein heterodimers and thereby reactivating tumor suppressor function in the entire organism. Hence, the survival of the cancer patient which depends primarily on the extent of successful eradication of tumor metastasis would be predictably increased. The above-proposed therapeutic approach by means of antineoplastic, cell-permeable peptides would have bionic features as it would reflect some properties of natural molecules which combine antiproliferative properties with a propensity to shuttle in and out of cells such as interferons [39], e.g. γ-interferon [45], insulin-like growth factor binding protein (IGFBP) 3 [46, 47] and the IGFBP-related HtrA1 gene product [48]. In the same way as these defensive proteins contribute to the homeostasis of cell growth, so would their artificial peptide mimetics whereby these synthetic molecules could be titrated such that the growth acceleration

excess would be curtailed, yet not the entire Epothilone B (EPO906, Patupilone) proliferative process per se ablated, consistent with a previously proposed artificial induction of homeostatic defense mechanisms [49] and also a more recent view cautioning against the side effects of a complete abrogation of a given disease target [50]. Ramifications for biophysics It is furthermore interesting to note that non-malignant cells in which tumor suppressor function is compromised by a) putatively oncoprotein metastasis along with oncoprotein-tumor suppressor protein complex formations, b) epigenetic silencing through hypermethylation of the promoters of tumor suppressor genes or, respectively, c) tumor suppressor gene LOH may be regarded as (energetically) distinct quantum states of a (morphologically) normal cell whereby an intrinsic (premalignant) evolution of this cell towards the latter state, i.e.

2003) It is hypothesized

2003). It is hypothesized #see more randurls[1|1|,|CHEM1|]# that the decrease of work capacity of the ageing worker

will result in increasing need for recovery levels if the workload remains the same. As such need for recovery might be considered an instrument to assess potential imbalance between demands of work and the functional capacities of the ageing worker. So far, only few studies have reported on the association between age and need for recovery. Sluiter et al. (Sluiter et al. 2001) observed that age was not significant in the prediction of need for recovery. A study by Jansen et al. (2002) showed that employees aged 46–55 scored somewhat higher on need for recovery compared to employees aged 36–45. Kiss et al. (2008) observed significantly higher mean recovery scores in older workers (≥45 years) when compared to younger workers (<45 years). Whereas cross-sectional studies gain insight into the magnitude of the problem at a specific point in time, and may reveal associations between work demands, age and need for recovery, longitudinal studies are necessary

to investigate the net-effect of age on need for recovery. To date, we are not aware of studies investigating the longitudinal relationship between age (categories) and need for recovery from work. When studying the relationship between age and need for recovery over time various factors should be taken into account, such as demographics, work environment, IWR 1 health, lifestyle and characteristics of the private situation. Some studies have found gender differences in the need for recovery, with men reporting higher levels of need for recovery when compared to women (Jansen et al. 2002). Also differences in need for recovery are observed when comparing different educational levels, with employees with a lower educational level reporting higher need for recovery scores (Jansen et al. 2002). High psychological job demands, low decision latitude, physically demanding work and work–family conflict have been found to be associated with elevated need for

recovery (Jansen et al. 2002, 2003a; Eriksen et al. 2006). Need for recovery further substantially varies when different working hours, patterns or schedules are considered (Jansen et al. SPTLC1 2003b; De Raeve et al. 2007). Therefore, in this study, need for recovery will be studied in day workers exclusively. The aim of the present prospective study was to investigate whether increasing age is related to higher need for recovery from work over time, while taking into account demographic, work-related factors and characteristics of the private situation. Methods Sampling and procedures The present study is based on data of the first six questionnaires of the Maastricht Cohort Study on “Fatigue at Work” (Kant et al. 2003), that is, a total follow-up of 2 years. Employees were followed by means of self-administered questionnaires, which they received every 4 months.

Previous

Previous find more midline laparotomy incision and multiple previous episodes of ASBO with estimated PAI score of > =2 in more than 3 abdominal regions, were significantly associated in this series with increased risk of conversion and longer operative times. Prevention We do need to prevent ASBO (LOE 2b GoR B). In view of the incidence of adhesions and recurrence rates of ASBO as well as of the magnitude of the medical problems and financial burden related to adhesions, prevention or reduction of postoperative

adhesions in an important priority. Hyaluronic acid-carboxycellulose membrane and icodextrin are able to reduce adhesions (respectively LOE 1a GOR A and LOE 1b GOR A). Icodextrin may reduce the risk of re-obstruction for ASBO (LOE 1 b GOR A). Hyaluronic acid-carboxycellulose can not reduce the need of surgery for ASBO (LOE 1a GOR A). Most of Peptide 17 order the available literature is based on gynecologic patients. For general surgical

patients no recommendations or guidelines exist. Any prevention strategy should be safe, effective, practical, and cost effective. A combination of prevention strategies might be more effective [78]. In the same review the authors recommend a laparoscopic approach if possible, the use of bioabsorbable barriers, a meticulous hemostasis, XAV-939 mw avoiding excessive tissue dissection and ischemia and reducing remaining surgical material [78]. In the long term follow up study from Fevang et al. [79] the surgical treatment itself decreased the risk of future admissions

for ASBO, even though the risk of new surgically treated ASBO episodes was the same regardless of the method of treatment (surgical vs conservative). Intraoperative techniques such as avoiding unnecessary peritoneal dissection, avoiding spillage of intestinal contents or gallstones [80], and the use of starch-free gloves [81–83] are basic principles that should be applied to all patients. In most abdominal procedures the laparoscopic approach is associated with a significantly lower incidence of adhesive SBO or adhesion-related re-admission [79, 83]. There is some class I evidence in obstetrics supporting the theory that from suturing the peritoneum increases the risk of adhesions [84]. Concerning mechanical barriers no progresses has been made in the last 6 years. The authors remain convinced that the absorbable adhesion barrier Interceed reduces the incidence of adhesion formation following laparoscopy and laparotomy [85–90]. Gore-Tex may be superior to Interceed in preventing adhesion formation but its usefulness is limited by the need for suturing and later removal [91]. There was no evidence of effectiveness of Seprafilm and Fibrin sheet in preventing adhesion formation [92–99]. Chemical/fluid agents have the theoretical advantage of covering more potential sites of adhesion formation than mechanical barriers. In the newest P.O.P.A. study Catena et al. randomized 91 patients to have 2000 cc of icodextrin 4% and 90 to have the traditional treatment.

Radiat Res 1993, 134:63–70 PubMedCrossRef 44 O’Sullivan B, Levin

Radiat Res 1993, 134:63–70.PubMedCrossRef 44. O’Sullivan B, Levin W: Late radiation-related fibrosis: pathogenesis, manifestations, and current management. Semin Radiat Oncol 2003, 13:274–289.PubMedCrossRef 45. Zhao W, Diz DI, Robbins ME: Oxidative damage pathways in relation to normal tissue injury. Br J Radiol 2007, 80:23–31.CrossRef 46. Tew KD, Ronai Z: GST function in drug and stress response. Drug Resist Updat

1999, 2:143–147.PubMedCrossRef 47. Martin M, Vozenin MC, Gault N, Crechet F, Pfarr CM, Lefaix JL: Coactivation of Protein Tyrosine Kinase inhibitor AP-1 activity and TGF-b1 gene expression in the stress response of normal skin cells to ionizing radiation. Oncogene 1997, 15:981–989.PubMedCrossRef 48. Andreassen CN, Alsner J, Overgaard J: Does variability in normal tissue reactions after radiotherapy have a genetic basis-where and how to look for it? Radiother Oncol 2002, 64:131–140.PubMedCrossRef 49. West CM, Elliott RM, Burnet NG: The genomics revolution and radiotherapy. Clin Oncol 2007, 19:470–480.CrossRef 50. Filippi AR, Franco P, Ricardi U: Is clinical radiosensitivity a complex genetically buy CCI-779 controlled event? Tumori 2006, 92:87–91.PubMed 51. Andreassen CN, Alsner J, Overgaard M, Sorensen FB, Overgaard J: Risk of radiation-induced subcutaneous fibrosis in relation to single nucleotide polymorphisms

in TGFB1, SOD2, XRCC1, XRCC3, APEX and ATM-a study based on DNA from formalin fixed paraffin embedded tissue samples. Int J Radiat Biol 2006, 82:577–586.PubMedCrossRef 52. Andreassen CN, Alsner J, Overgaard J, Herskind C, Haviland J, Owen R, Homewood J, Bliss J, Yarnold J: TGFB1 polymorphisms are associated with risk of late normal tissue complications in the breast after radiotherapy for early breast cancer. Radiother Oncol 2005, 75:18–21.PubMedCrossRef 53. Chang-Claude J, Ambrosone CB, Lilla C, Kropp S, Helmbold I, von GNS-1480 price Fournier D, Haase Farnesyltransferase W, Sautter-Bihl ML, Wenz F, Schmezer P, Popanda O: Genetic polymorphisms

in DNA repair and damage response genes and late normal tissue complications of radiotherapy for breast cancer. Br J Cancer 2009, 100:1680–1686.PubMedCrossRef 54. Alsbeih G, Al-Harbi N, Al-Hadyan K, El-Sebaie M, Al-Rajhi N: Association between normal tissue complications after radiotherapy and polymorphic variations in TGFB1 and XRCC1 genes. Radiat Res 2010, 173:505–511.PubMedCrossRef 55. Andreassen CN, Alsner J, Overgaard M, Overgaard J: Prediction of normal tissue radiosensitivity from polymorphisms in candidate genes. Radiother Oncol 2003, 69:127–135.PubMedCrossRef 56. Damaraju S, Murray D, Dufour J, et al.: Association of DNA repair and steroid metabolism gene polymorphisms with clinical late toxicity in patients treated with conformal radiotherapy for prostate cancer. Clin Cancer Res 2006, 12:2545–2554.PubMedCrossRef 57.

The typical

The typical check details thickness of as-cut CNT membrane is 5 μm (Figure 1B). The membranes (approximately 0.6 × 0.6 cm2) were glued over a 3-mm diameter hole in polycarbonate plate (1-mm thick) to act as mechanical support. The top of the membrane was referring to the surface in the recess

of the hole in the polycarbonate support, while the bottom of the membrane was on the bottom plane of the polycarbonate support. Pd/Au (30 nm) was sputter-deposited on the bottom of the membrane to give electrical contact to the CNT membrane and to act as Alisertib in vitro effective working electrode. Figure 1 TEM and SEM images of DWCNT and schematic diagram of functionalized anionic dye. (A) TEM image of DWCNTs (purchased from Sigma-Aldrich). (B) SEM image of as-made DWCNT membrane in the cross-sectional

view. (C) Schematic diagram of functionalized anionic dye on the CNT tip playing as gatekeeper (gray, C; red, O; blue, N; yellow, S). Modification of DWCNT membranes To avoid grafting in the inner core of CNTs, CNT membranes were placed in U-tube fittings under a 2-cm inner solution column pressure. In two-step functionalization, as-prepared DWCNT membranes were first www.selleckchem.com/products/byl719.html modified by flow electrochemical grafting with 5-mM 4-carboxy phenyl diazonium tetrafluoroborate/0.1-M KCl solution at −0.6 V for 2 min. In the next step, Direct Blue 71 dye (Sigma-Aldrich) was coupled with the carboxyl group on the tip of CNTs with carbodiimide chemistry: 10 mg of ethyl-(N′,N′-dimethylamino) propylcarbodiimide hydrochloride and 5 mg of N-hydroxysulfosuccinimide were dissolved into 4 ml of 50-mM Direct Blue 71 dye in 0.1 M 2-(N-morpholino) ethane sulfonic acid buffer for 12 h at ambient temperature. In one-step functionalization, Direct Blue 71 dye, which Clomifene has a primary amine, was directly grafted to CNT by electrooxidation of amine. Electrografting was carried out under a

constant potential of 1.0 V using a potentiostat (E-corder 410, eDAQ, Denistone East, Australia) in the three-electrode cell. The CNT membrane, with sputtered Pd/Au film (approximately 30-nm thick) on the membrane’s back side, was used as the working electrode; Pt wire was the counter electrode, and the reference electrode was Ag/AgCl. Before electrografting, the ethanol solution of 0.1 M LiClO4/1 mM direct blue was purged by argon gas for 15 min to remove adsorbed oxygen in the solution. Rectification experimental setup The schematic of the ionic rectification setup is shown in Additional file 1: Figure S1. Both U-tube sides were filled with potassium ferricyanide solution. The working electrode (W.E) was DWCNT membrane coated with 30-nm-thick Pd/Au film; the reference electrode (R.E) was Ag/AgCl electrode. Voltage was controlled using an E-Corder 410 potentiostat. The counter electrode was a sintered Ag/AgCl electrode purchased from IVM Company (Healdsburg, CA, USA). The membrane area was approximately 0.07 cm2. Linear scan was from −0.60 to +0.60 V with the scan rate at 50 mV/s.

We draw special attention to institutional upscaling, which is pe

We draw special attention to institutional upscaling, which is perceived as a collective process, and bring in insights from the literature on system innovations, especially strategic niche management SYN-117 nmr (SNM). The section ends with a new typology of upscaling. ‘Analytical approach and data collection’

is devoted to data collection methods. ‘Results’ Acalabrutinib concentration introduces the five Indian initiatives and contains the empirical analysis. The paper ends with ‘Conclusions’ and sets out relevant elements for future research. Theoretical building blocks Upscaling in social entrepreneurship and development studies Within the entrepreneurship field as a whole, ‘social entrepreneurship’ deserves special attention here. Social entrepreneurship encompasses the activities and processes undertaken to discover, define, and exploit opportunities in order to enhance social wealth by creating new ventures or managing existing organizations in an innovative manner. Social wealth may be defined broadly to include economic, societal, health, and environmental aspects of human welfare. Essentially, then, one can conceive of social entrepreneurs as key players in sustainability transitions

(Witkamp et al. 2011). According to Witkamp et al. (2011), social entrepreneurship is pitted against two extant ‘regimes’, i.e., the business regime where profit maximization and increasing shareholder value is the ATM Kinase Inhibitor major goal, and the civil-society regime where societal objectives take a major role and profit maximization takes a back seat. Social entrepreneurship, therefore, continuously faces tensions between private profit-making and fulfilling

societal objectives. Most social entrepreneurs have an ability to create new connections among people and organizations for new paths, or business models, in which these tensions are managed and societal value is created. In so doing, (social) entrepreneurs also create and develop the institutions and infrastructures needed for development (Garud et al. 2007; Dees 2009; Mair and Marti 2009; Chowdhury and Santos 2010; Zahra et al. 2008, 2009). According to Mair and Marti (2006), Robben (1984), and Sud et al. (2008), entrepreneurs can leverage resources to create new institutions and norms or transform existing ones. Maguire et al. (2004) Galactosylceramidase speak about entrepreneurs’ leading efforts to identify political opportunities, frame issues, and induce collective efforts to infuse new beliefs and norms into social structures. In other words, social entrepreneurs can foster development in many different ways: by getting new legislation or regulations passed; getting old legislation or regulations enforced; shifting social norms, behaviors, and attitudes among fellow citizens, corporations, and government personnel; changing the way markets operate; and finding ways to solve problems or meet previously unmet needs.