The advert appeared 388,630 times on Facebook, and there were 259

The advert appeared 388,630 times on Facebook, and there were 259 clicks on it (at a cost of £76). It was not possible to determine how much traffic came to the survey directly from the advert or from the use of selleck products Facebook generally via other means, but in total we received 754 completed surveys via Facebook (Fig. 3). Fig. 3 Facebook advert Advert in mumsnet and gransnet Mumsnet is the UK’s biggest online network of parents. According to the site there are 50 million page views and 9 million visits per month. selleck compound The Times newspaper reflects that it is ‘The country’s most popular meeting point for parents” (www.​mumsnet.​com). ‘Gransnet’ is a subsidiary website, particularly

targeted towards grandparents. We wrote a short advert that Mumsnet and Gransnet put onto one of their pages for regular followers. It appeared as this: We’ve been asked by the Wellcome Trust Sanger Institute to ask Mumsnetters to fill in a survey they’re running on genetic testing. Here’s what they say about the survey: “Your genes can tell you about your past, present and future medical health. Very soon, full genome testing (the ability

to look at all 20,000+ genes) will be available in the health service. Like Angelina Jolie, you could have a genetic test and find out what you are at risk Vorinostat molecular weight from. What would you want to know? Alzheimers? Cancer? Mental health issues? Or maybe you’d rather not know? Our research from Cambridge ( ) will have a direct impact on the way this testing is offered, find out about the possibilities and the ethical issues raised by this (no prior knowledge about genetics needed).” The survey is open to everyone so please take part and pass on to any friends/family you think might be interested.Please click here

to take part. Payment for the above advert cost £1,620, and we received 1,405 completed surveys; thus, each completed survey cost just over £1. Viral spread of survey Due to the nature of the World Wide Web it is impossible to control how another user chooses to re-report and debate issues that the Genomethics project initiated. Other websites chose to write blogs based on our press release and wrote commentaries on the research on Facebook sites and via Twitter; participants also emailed their friends PRKACG after completing the survey and ‘Liked’ it on Facebook and linked to it on Twitter. We had no influence on whether and how this was done, but the net effect was that a ‘viral’ or snowball process emerged whereby participants visited our website via routes completely unconnected to any of our active recruitment methods. For example, an online Polish newspaper ran an article on the study and provided a link to the survey (this was only discovered via an opportunistic google search). The net result of this was the direct recruitment of 90 new Polish research participants. Results Cleaning up of data The survey received 11,336 hits.

Diagn Microbiol Infect Dis 2004,50(4):237–245 PubMedCrossRef

Diagn Microbiol Infect Dis 2004,50(4):237–245.PubMedCrossRef MDV3100 in vivo 19. Maukonen J, Simoes C, Saarela M: The

currently used commercial DNA-extraction methods give different results of clostridial and actinobacterial populations derived from human fecal samples. FEMS Microbiol Ecol 2012,79(3):697–708.PubMedCrossRef 20. Bahl MI, Bergstrom A, Licht TR: Freezing fecal samples prior to DNA extraction affects the Firmicutes to Bacteroidetes ratio determined by downstream quantitative PCR analysis. FEMS Microbiol Lett 2012,329(2):193–197.PubMedCrossRef 21. RNAlater®: Preserving RNA Before Isolation TechNotes. 11(4): Life Technologies. Accessed 14 November 2013, http://​www.​lifetechnologies​.​com/​us/​en/​home/​references/​ambion-tech-support/​rna-isolation/​tech-notes/​rnalater-faqs.​html 22. Boesenberg-Smith KA, Pessarakli MM, Wolk DM: Assessment of DNA yield and purity: an overlooked detail of PCR troubleshooting. Clin Microbiol Newsl 2012,34(1):1–6.CrossRef PP2 order 23. U.S. Preventive Services Task Force: Guide to Clinical Preventive Services, 2008: recommendations of the U.S.

Services Task Force. Rockville, MD: Agency for Healthcare Research and Quality; 2008. [AHRQ Publication No. 08–05122] 24. Allison JE: Review article: faecal occult blood testing for colorectal cancer. Aliment Pharmacol Ther 1998,12(1):1–10.PubMedCrossRef Competing interests The authors declare that they have no competing interests. Authors’ contributions CD performed the statistical analysis and drafted the manuscript. JW carried out the sequencing assays and drafted the manuscript. RBH participated in the design of the study and helped to draft the manuscript. JA conceived the study, participated in its design and coordination, and helped to draft manuscript. All authors read and approved the final manuscript.”
“Background Bio-aerosols are airborne particles Org 27569 that originate from living microorganisms such as bacteria, fungi, and viruses generally found as part of the patient’s endogenous flora. Their components have negative effects

especially on the health of immuno-compromised people [1]. The infectious aerosols are small and may remain suspended and viable in the air stream over long periods of time. Attributable to the above-mentioned facts, the risk of airborne infections especially in hospitals and other health-care settings can be high as there can be confined spaces in which aerosols may build up to infectious MK 8931 price levels [1]. The buildup of infectious aerosols exacerbates healthcare challenges in developing countries as the role of bio-aerosols in hospital-acquired infections (HAIs) has been recognized; studies have uncovered increasing evidence regarding the spread of disease via the aerial route [2]. Consequently, the presence of bio-aerosols in health-care settings needs to be monitored and controlled to limit their dispersal.

A balanced relationship, therefore, must exist between bacteria a

A balanced relationship, therefore, must exist between bacteria and their human hosts. A disruption in this homeostasis threatens the state of immune tolerance and may result in gut inflammation. Several lines of evidence suggest a role for gut bacteria in the pathogenesis of IBD. Faecal stream diversion induces remission in CD [13],

animal models of colitis require the presence of gut bacteria to initiate inflammation (reviewed in [14]), an increased mucosal bacterial load is observed in IBD patients [15, 16], genome-wide IBD association studies have identified polymorphisms in genes involved in bacterial recognition and clearing (reviewed in [17]) and broad-spectrum antibiotics have some efficacy in the treatment of CD [18, 19]. With CD in particular, individual species such as Mycobacterium avium subspecies paratuberculosis or Escherichia coli have Emricasan clinical trial been implicated in disease aetiology [20, 21] while check details the emerging “”dysbiosis”" hypothesis implicates multi-species assemblages in an overall imbalance between harmful and protective bacteria [22, 23]. Numerous studies have attempted to characterise the microbial

communities in IBD and to compare these with healthy individuals. Results indicate that individuals with IBD have reduced bacterial diversity, temporal stability and cluster separately when compared to healthy controls [24–28]. Compositional comparisons have generated inconsistent results Evodiamine but have generally identified reductions in components of the Firmicutes phylum in IBD, often, but not always, with LY2835219 solubility dmso concurrent increases in Bacteroidetes and facultative anaerobes such as Enterobacteriaceae [12, 22, 29–31]. Faecal/luminal bacterial communities have repeatedly been shown to be distinct from mucosal communities [32–37], meaning that study of the IBD mucosa-associated microbiota and comparison with those from healthy individuals

should provide the best insight into whether or not a particular microbial signature is disease specific. In addition, within IBD-affected intestines disease-causing agents might be enriched at sites of active inflammation relative to comparatively unaffected mucosa. We have therefore used in-depth bacterial 16S rRNA gene cloning and sequencing technology to compare the mucosa-associated microbiota from inflamed and non-inflamed sites of the colon in CD and UC patients and in non-IBD controls. Our findings indicate that mucosal microbial diversity and composition is disturbed in IBD and that there are significant differences in microbial community structure between inflamed and non-inflamed mucosa. Results Twenty-nine mucosal biopsies were collected from a total of seventeen patients, including paired biopsies of inflamed and non-inflamed tissue from six patients with active CD (n = 12), paired biopsies from six patients with active UC (n = 12) and five biopsies from non-IBD controls (n = 5).

Pretreatment of the PUFs The pretreatment of PUFs was investigate

Pretreatment of the PUFs The pretreatment of PUFs was investigated to activate the material. First, foams were washed with acetone and then with distilled water to eliminate the possible commercial treatments applied to the material. Different pretreatments were applied to

1 cm3 of foam samples, which were immersed in 25 ml of the pretreatment reagent solution (1 M HNO3, 3 M HNO3, 1 M NaOH, and selleck chemicals 3 M NaOH) for 2 h under agitation. Afterwards, the samples were washed several times with distilled water. In order to determine the possible effect of the pretreatments in the chemical structure of the PUFs, attenuated total reflectance Fourier transform infrared (FTIR-ATR) spectra were recorded with a Perkin Elmer Spectrum GX spectrometer (Norwalk, CT, USA). Moreover, for determining the concentration of the functional groups before and after the pretreatment of the matrix, two titration methods were applied to calculate IEC (in meq/g) of the material [16]: 1 For determining cation exchange groups: 1 cm3 of PUF was immersed in 100 ml of NaOH 0.1 M and shaked at room temperature for 48 h, time enough to ensure a complete neutralization of the acidic groups. Then, an aliquot of 10 ml was titrated with standardized

HCl 0.1 M (3 replicates).   2 For determining anion exchange groups a similar procedure was used, but immersing the sample in 100 ml of HCl 0.1 M, and using standardized NaOH 0.1 M to titrate the 3 aliquots of 10ml.   Synthesis of AgNPs The synthesis of AgNPs in the polymeric matrices by the IMS methodology ATR inhibitor consisted of the following: (1) loading of the material with the metal ions (AgNO3 0.4 M solution) and (2) reduction of metal ions to zero-valent MNPs through reaction (by using NaBH4 0.5M solution). The reactions

involved are as follows: (1) (2) Although equations depict a pure ion exchange mechanism, the generation of coordination bonds between species may also result in the immobilization of the ionic species in old the polymeric matrix. In addition, the entry of metal ions into the see more matrix could be significantly affected by the synthetic conditions (i.e., temperature) which can affect the structural organization of the polymer matrices thus making the matrix temporarily accessible to the metal ions by opening their structure; after the synthesis, the fibers revert back to their closely packed state thus trapping the MNPs within the polymer structure. For the PUFs, the procedure described above was performed at room temperature; whereas in the case of the textile fibers, synthesis using different temperatures (25°C, 40°C, and 80°C) were applied. Nanocomposite characterization In order to determine the exact metal content in the prepared nanocomposites, samples of known weight were digested with concentrated HNO3. The resulting solutions (two replicates) were diluted and analyzed by inductively coupled plasma mass spectrometry (ICP-MS).

aureus 43300(106 CFU/ml) intranasally Group 2: Mice were administ

aureus 43300(106 CFU/ml) intranasally Group 2: Mice were administered S. aureus 43300, left for a period of 48 hours to allow

nasal colonisation followed by intranasal administration of BIBF 1120 in vivo 50 μl of phage (107 PFU/ml) given twice (at an interval of 24 hours). Group 3: Mice were administered S. aureus 43300, left for a period of 48 hours to allow nasal colonisation followed by intranasal administration of 50 μl of mupirocin (5 mg/kg dissolved in water; given once) the next day. Group 4: Mice were administered S. aureus 43300, left for a period of 48 hours to allow nasal colonisation followed by intranasal administration of phage as well as mupirocin (5 mg/kg) the next day. The parameters used to monitor colonization included a) Bacterial load (CFU/ml) in nares b) Phage counts in nares c) Nasal myeloperoxidase (MPO) levels and e) Histopathological examination Nasal bacterial GSK2245840 load Four mice from each of group were taken and sacrificed on day 2, 5, 7, 10, 12 post treatment by cervical dislocation. The nasal region was wiped

externally with 70% ethanol, nose was removed along with nasal bone. The entire nasal tissue was excised using sterile scissors and homogenized. The homogenates were plated quantitatively on nutrient agar containing 20 μg/ml of ampicillin to select S. aureus 43300 after overnight incubation at 37°C. Nasal homogenates were also processed to determine the phage titer by modified double layer agar method [20]. Myeloperoxidase (MPO) estimation Mice from each group (same groups as those categorized for phage protection studies with 20 animals per group) were killed

and their nasal tissue was excised and homogenised in 50 mM PBS (pH 7.4). Nasal samples were processed for MPO determination as per the method of Greenberger et al. [21]. The absorbance was read immediately at 490 nm over a period of 4 minutes. MPO was calculated as the change in optical density (O.D) x dilution factor (D.F). Histopathological examination Extent of injury caused by S. aureus and healing of the colonized mouse nose following therapy with phage or antibiotic was assessed on the basis of histopathological analysis of the injured and recovered nose according to the method of Brans et al. [22]. The sections were picked (-)-p-Bromotetramisole Oxalate on separate slides, stained with hematoxylin and eosin (Hi-Media, Mumbai) and the slides then examined under a microscope to evaluate the extent of damage. Statistical methods The data is expressed as mean ± standard deviation of replicated values where indicated. The statistical significance of differences between groups was determined by Student’s t-test (two groups),one-way ANOVA followed by a Tukey test using Sigma Stat, Graph pad prism (Graph pad software, San Diego, CA). p value of less than 0.05 and 0.01 was considered statistically significant for a confidence interval of 95% and 99% respectively. Results The nasal epithelial cells were isolated from mouse nasal tissue and cultured at 37°C in presence of 5% CO2.

The transformation of DON and the significant reduction in its to

The transformation of DON and the significant reduction in its toxicity was demonstrated by a pig feeding experiment [9]. Both in vitro and in vivo studies have also shown that DON can be transformed to DOM-1 by intestinal microorganisms of other animal species including cow, rat, sheep, and pig [10, 15–18]. Although mixed microorganisms from animal intestines often demonstrated the ability to transform DON to DOM-1, isolation of DON-transforming microorganisms to a pure culture has been a great challenge. There have been only a few reports on DON transformation by a pure bacterial culture [5]; only one of these cases thus far, Eubacterium sp., isolated from the

rumen [19], has been systematically studied. It appears that the lack of pure cultures of transforming bacteria has limited the full implementation of biological

detoxification STA-9090 order strategies. The present research was conducted to select DON-transforming bacteria from the chicken intestines with potential application in the management of mycotoxin risks. Results In vivo enrichment The effect of feeding DON-contaminated wheat on the enrichment of DON-transforming bacteria in the chicken intestines was initially investigated. Digesta samples from the large intestine (LIC) of layers fed DON-contaminated wheat were able to completely transform DON in the medium to DOM-1 after incubation. However, only 80% DON on average (standard deviation = 16.4) was transformed by the digesta samples from the layers fed clean wheat. Similar results were obtained with the digesta samples

from the small intestine (SIC). Effect of media selleck chemical p38 MAPK cancer Different media were O-methylated flavonoid examined initially for their effect on the activity of DON transformation and also on the bacterial growth of digesta samples. Among the tested media including AIM, AIM+CecExt, L10, MRS, RB, VL, and DAM, only L10 and AIM+CecExt fully supported the transformation of DON to DOM-1 (100%). While bacterial cultures could be rapidly established in L10 broth, the growth of bacteria in AIM + CecExt was minimal. These two media were therefore used for subsequent selection for DON-transforming bacteria, depending on the aim of particular experiments. DON-transforming activity of digesta samples and their subcultures The level of DON-transforming activity in the digesta samples collected from the crop, small and large intestines of chickens fed DON-contaminated or clean wheat was determined. Among 12 chickens examined, 92% LIC (11 out of 12) and 50% SIC (5 out of 10) samples transformed DON to DOM-1 completely after 72 hr incubation. However, only 25% (1 out of 4) samples from the chicken crop demonstrated a partial activity in transforming DON to DOM-1 (conversion = 26%) after 72 hr incubation. The LIC digesta samples collected from the chickens fed DON-contaminated or clean wheat were also examined for their activity of DON transformation during subculturing (6 passages, 72 hr per subculture) in L10 broth.

Conclusion Complicated intra-abdominal infections remain an impor

Conclusion Complicated intra-abdominal infections remain an important source of patient morbidity and are frequently associated with poor clinical prognoses, particularly for patients in high-risk categories. Given the sweeping geographical distribution of the participating medical

centers, the CIAOW Study gives an accurate description of the epidemiological, clinical, microbiological, and treatment profiles of complicated intra-abdominal infections worldwide. References 1. Menichetti F, Sganga G: Definition and classification of intra-abdominal infections. J Chemother 2009,21(Suppl 1):3–4.PubMedCrossRef 2. Marshall JC, Maier RV, Jimenez M, Dellinger EP: NVP-BSK805 solubility dmso Source control in the management of severe sepsis and septic shock: an evidence-based review. Crit Care Med 2004,32(11 Suppl):S513-S526.PubMedCrossRef 3. Pieracci FM, Barie PS: Management of severe sepsis of abdominal origin. Scand J Surg 2007,96(3):184–196.PubMed 4. Sartelli M, Catena F, Ansaloni L, Leppaniemi A, Taviloglu K, Goor H, Viale P, Lazzareschi DV, Coccolini F, Corbella D, Werra C, Marrelli D, Colizza S, Scibè R, Alis H, Torer N, Navarro

S, Sakakushev B, Massalou D, Augustin G, Catani M, Kauhanen S, Pletinckx P, Kenig J, Saverio S, Jovine E, Guercioni G, Skrovina M, Diaz-Nieto R, Ferrero A, et al.: Complicated intra-abdominal infections in Europe: a comprehensive review of the CIAO study. World J Emerg Surg 2012,7(1):36.PubMedCentralPubMedCrossRef 5. Sartelli M, Catena F, Ansaloni L, Moore Selleck MEK inhibitor E, Malangoni M, Velmahos G, Coimbra R, Koike K, Leppaniemi A, Biffl W, Balogh Z, Bendinelli C, Gupta S, Kluger Y, Agresta F, Di Saverio S, Tugnoli Fenbendazole G, Jovine E, Ordonez C, Gomes CA, Junior GA, Yuan KC, Bala M, Peev MP, Cui Y, Marwah S, Zachariah S, Sakakushev B, Kong V, Ahmed A, et al.: Complicated intra-abdominal infections in a worldwide context: an observational prospective study (CIAOW

Study). World J Emerg Surg 2013,8(1):1.PubMedCentralPubMedCrossRef 6. Oliak D, Yamini D, Udani VM, Lewis RJ, Arnell T, Vargas H, Stamos MJ: Initial nonoperative management for periappendiceal abscess. Dis Colon Rectum 2001, 44:936–941.PubMedCrossRef 7. Brown CV, Abrishami M, Muller M, Velmahos GC: Appendiceal abscess: immediate operation or percutaneous drainage? Am Surg 2003, 69:829–832.PubMed 8. Andersson RE, Petzold MG: Nonsurgical treatment of appendiceal abscess or phlegmon: a systematic review and meta-analysis. Ann Surg 2007, 246:741–748.PubMedCrossRef 9. Lau H, Lo CY, Patil NG, Yuen WK: Early versus delayed-interval Vorinostat in vivo laparoscopic cholecystectomy for acute cholecystitis. A Meta Anal Surg Endosc 2006,20(1):82–87.CrossRef 10. Papi C, Catarci M, D’Ambrosio L, Gili L, Koch M, Grassi GB, Capurso L: Timing of cholecystectomy for acute cholecystitis: a meta-analysis. Am J Gastroenterol 2004,99(1):147–155.PubMedCrossRef 11. Gurusamy KS, Samraj K: Early versus delayed laparoscopic cholecystectomy for acute cholecystitis. Cochrane Database Syst Rev 2006,18(4):CD005440. 12.

Since aerial mycelia of S avermitilis begin to emerge after 48 h

Since aerial mycelia of S. avermitilis begin to emerge after 48 h

of incubation on YMS, we transferred mycelia of bald mutants grown for 3 days by streaking on YMS plates. Genomic DNA was analyzed by PFGE as described above. Acknowledgements This work was supported by grants from the National Natural Science Foundation of China (Grant No. 30670037) and the National Basic Research Program of China (Grant No. 2009CB118905). Electronic supplementary material Additional file 1: Supplementary Fig. S1. AseI restriction patterns of genomic DNA of spontaneous bald mutants from 76-9. Supplementary Fig. S2. Southern hybridization analysis of the left (A) and right end (B) of the SA1-8 chromosome. Supplementary Fig. S3. Southern selleck kinase inhibitor hybridization analysis of AseI macrorestriction fragments of the SA1-6 chromosome with probe N4. Supplementary Fig. S4. Generational stability analysis

of bald mutants. (PDF 413 KB) Additional file 2: Complete data for HSP inhibitor cancer deletion extent of fragment G1. (XLS 22 KB) References 1. Demain AL: Pharmaceutically active secondary metabolites of microorganisms. Appl Microbiol Biotechnol 1999,52(4):455–463.PubMedCrossRef buy GSK1904529A 2. Bentley SD, Chater KF, Cerdeno-Tarraga AM, Challis GL, Thomson NR, James KD, Harris DE, Quail MA, Kieser H, Harper D, Bateman A, Brown S, Chandra Urease G, Chen CW, Collins M, Cronin A, Fraser A, Goble

A, Hidalgo J, Hornsby T, Howarth S, Huang CH, Kieser T, Larke L, Murphy L, Oliver K, O’Neil S, Rabbinowitsch E, Rajandream MA, Rutherford K, Rutter S, Seeger K, Saunders D, Sharp S, Squares R, Squares S, Taylor K, Warren T, Wietzorrek A, Woodward J, Barrell BG, Parkhill J, Hopwood DA: Complete genome sequence of the model actinomycete Streptomyces coelicolor A3(2). Nature 2002,417(6885):141–147.PubMedCrossRef 3. Lin YS, Kieser HM, Hopwood DA, Chen CW: The chromosomal DNA of Streptomyces lividans 66 is linear. Mol Microbiol 1993,10(5):923–933.PubMedCrossRef 4. Omura S, Ikeda H, Ishikawa J, Hanamoto A, Takahashi C, Shinose M, Takahashi Y, Horikawa H, Nakazawa H, Osonoe T, Kikuchi H, Shiba T, Sakaki Y, Hattori M: Genome sequence of an industrial microorganism Streptomyces avermitilis : deducing the ability of producing secondary metabolites. Proc Natl Acad Sci USA 2001,98(21):12215–12220.PubMedCrossRef 5. Volff JN, Altenbuchner J: Genetic instability of the Streptomyces chromosome. Mol Microbiol 1998,27(2):239–246.PubMedCrossRef 6.


Bowling selleck chemicals llc pin-like nanostructures are the main morphological structures

shown in Figure 1c. The diameter of the bottom part of stem of the nanostructures was between 40 and 80 nm. The nanostructures in Figure 1b,c also had particles at the tip. Figure 2 shows the corresponding XRD patterns of the various In-Sn-O nanostructure samples shown in Figure 1. The XRD results showed several Bragg reflections that corresponded to the cubic bixbyite of the In2O3-based phase. Several small Bragg reflections from metallic Sn appear in Figure 2a, but not in Figures 2b,c, suggesting that a high degree of metallic Sn might have been present in sample 1. NSC 683864 Figure 1 SEM images of In-Sn-O nanostructures: (a) sample 1, (b) sample 2, and (c) sample 3. Figure 2 XRD patterns of In-Sn-O nanostructures: (a) sample 1, (b) sample 2, and (c) sample 3. The Sn atomic percentages and chemical GSK458 price binding states of the constitutive elements of the samples were characterized using the narrow scan XPS spectra. The Sn atomic percentages of samples 1, 2, and 3 were 6.9%, 3.8%, and 3.4%, respectively. Sample 1 had a relatively large Sn content. The XPS spectra of Sn 3d 5/2 showed an asymmetric curve. The

detailed Gaussian-resolved results show that the two components were centered on 486.5 and 485.0 eV (Figure 3a,b,c). The relatively high binding energy component (SnI) was ascribed to a Sn4+ valence state and that with a low binding energy (SnII) was associated with metallic Sn [18, 19]. The intensity ratio of SnII/(SnI + SnII) increased as the total Sn atomic percentages of the samples increased. Differences in morphology, particularly the dimension of the tip particles and the density of the nanostructures, might account for the various contents of metallic Sn in the samples. The composition and structure of the tip particles are identified in the following sections using TEM-EDS

measurements. Figure 4a,b,c shows that the binding energies of In 3d 5/2 were centered on 444.6 to 444.7 eV; these energies were associated with the In3+ bonding state from In2O3[20, 21]. No small shoulder was observed at the lower binding energy side of the In 3d peaks, indicating Selleck Pazopanib that no In-In bonds existed in the In-Sn-O nanostructures [20]. Figure 5a,b, c shows the asymmetric O 1 s peaks of the samples. Two Gaussian-resolved peaks were centered on approximately 529.5 and 530.8 eV. The lower binding energy component (OI) was associated with oxygen in the oxide crystal, whereas the higher binding energy component (OII) represented the oxygen ions in the oxygen-deficient regions. Oxygen vacancies usually form in oxide nanostructures manufactured using thermal evaporation in an oxygen-deficient environment [22]. The oxygen vacancy content in the crystalline In-Sn-O nanostructures was defined as an intensity ratio: OII/(OI + OII). The ratios for samples 1, 2, and 3 were 0.39, 0.28, and 0.21, respectively.

PubMed 14 Smith GL, Bunker GB, Dinneen MD: Fournier’s gangrene

PubMed 14. Smith GL, Bunker GB, Dinneen MD: Fournier’s gangrene. BJU 1998, 81:347–355.PubMedCrossRef 15. Fournier JA: Citarinostat mouse gangrene foudroyante de la verge. Medecin Practique 1883, 4:589–597. 16. Unalp HR, Kamer E, Derici H, Atahan K, Balci U, Demirdoven C, Nazli O, Onal MA: Fournier’s gangrene: Evaluation of 68 patients and analysis of prognostic variables. J Postgrad Med 2008, 54:102–105.PubMedCrossRef 17. Tuncel A, Aydin O, Tekdogan U: Fournier’s Gangrene: Three years of experience with 20 patients and validity of the Fournier’s gangrene severity index score. Eur Urol 2006, 50:838–843.PubMedCrossRef 18. Czymek R, Frank P, Limmer S, Schmidt A, Jungbluth T, Roblick U, Bürk C,

Bruch HP, Kujath P: Fournier’s gangrene: is the Emricasan cell line female gender a risk factor? Langenbecks Arch Surg 2010, 395:173–180.PubMedCrossRef 19. Malik AM, Sheikh S, Pathan R, Khan A, Sheikh U: The spectrum of presentation and management of Fournier’s gangrene-An Experience LY2090314 chemical structure of 73 Cases. J Pak Med Assoc 2010, 60:617–619.PubMed 20. Sallami S, Maalla R, Gammoudi A, Ben Jdidia G, Tarhouni L, Horchani A: Fournier’s Gangrene: What are the prognostic factors? Our experience with 40 patients. La Tunisie Medicale 2012, 90:708–714.PubMed 21. Yilmazlar T, Ozturk E, Ozguc H: Fournier’s Gangrene: An analysis of 80 patients and a novel scoring system. Tech Coloproctol 2010, 14:217–223.PubMedCrossRef

22. Ruiz-Tovar J, Córdoba L, Devesa JM: Prognostic Factors in Fournier Gangrene. Asian J Surg 2012, 35:37–41.PubMedCrossRef 23. García A, Martín J, Vaquero A, Sánchez T, de Tomás J, Lago J, Turégano F: Fournier’s gangrene: analysis of prognostic variables in 34 patients. European Journal of Trauma and Emergency Surgery 2011, 37:141–145.CrossRef 24. Jarboui S, Jarraya H, Daldoul S, Zaouche A: Étude clinique et thérapeutique et analyse pronostique des gangrènes du périnée. Presse Med 2008, 37:760–766.PubMedCrossRef

25. Dahm P, Roland FH, Vaslef SN, Moon RE, Price DT, Georgiade GS, Vieweg J: Outcome analysis in patients with primary necrotizing fasciitis of the male genitalia. Urology 2000, Dolichyl-phosphate-mannose-protein mannosyltransferase 56:31–35.PubMedCrossRef 26. Nisbet AA, Thompson IM: Impact of diabetes mellitus on the presentation and outcomes of Fournier’s gangrene. Urology 2002, 60:775–779.PubMedCrossRef 27. Laor E, Palmer LS, Tolia BM, Reid RE, Winter HI: Outcome prediction in patients with Fournier’s gangrene. J Urol 1995, 154:89–92.PubMedCrossRef 28. Martinschek A, Evers B, Lampl L, Gerngroß H, Schmidt R, Sparwasser C: Prognostic aspects, survival rate, and predisposing risk factors in patients with Fournier’s gangrene and necrotizing soft tissue infections: evaluation of clinical outcome of 55 patients. Urol Int 2012, 89:173–179.PubMedCrossRef 29. Ersoz F, Sari S, Arikan S, Altiok M, Bektas H, Adas G, Poyraz B, Ozcan O: Factors affecting mortality in Fournier’s gangrene: experience with fifty-two patients. Singapore Med J 2012, 53:537–540.PubMed 30.