One of the S. aureus isolates that was positive for mecA gene by pentaplex PCR was found to be sensitive to oxacillin by the conventional MIC method. The diagnostic accuracy of a pentaplex PCR for 16S rRNA and femA genes was determined using 230 clinical isolates and found to have 100% sensitivity, specificity, and positive and negative predictive values. Selleck GSK1904529A However, the pentaplex PCR for the mecA gene detection showed 97.6% of sensitivity, 99.3% of specificity, and 98.8% of positive and 98.6% of negative predictive values in detecting methicillin-resistant staphylococci. Discussion The present study is believed to be the first to develop a combined molecular Selleck Lazertinib test for the rapid identification and discrimination

of the Staphylococcus genus from others, with simultaneous discrimination of methicillin-resistant from -susceptible staphylococcal strains, S. aureus from CoNS, and concomitant detection of PVL genes. Although there are numerous reports on PCR assays for the detection of methicillin resistance [15–17], only a few of them have incorporated internal controls in their assays to rule out false-negative results [18, 19]. According to guidelines for Molecular Diagnostic Methods for Infectious Diseases [20], incorporation of an internal control in the reaction is essential for the diagnostic test to exclude VX-809 price false-negative results or the presence of inhibitors

[21]. In the present study, the inclusion of a 759-bp internal control in the pentaplex PCR assay helped us

to rule out false-negative results or PCR inhibitors. To deal with applicability and accuracy, we further applied our pentaplex PCR assay to test a total of 53 MRSA, 125 MSSA, 22 methicillin-sensitive CoNS, and 30 methicillin-resistant Casein kinase 1 CoNS from routine clinical specimens obtained from Hospital Universiti Sains Malaysia. The Staphylococcus genus consists of at least 35 unique species, and only a few have been recovered from humans [6]. Previously published staphylococcal genus specific primers [22, 23] do not target wholly conserved regions in the staphylococcal 16S rRNA gene, which results in misdetection of some important CoNS. Therefore, we designed a new conserved Staphylococcus genus-specific primer and included it in our new pentaplex PCR assay, which allowed us to detect most species and strains of staphylococci (Table 1). The pentaplex PCR was found to be 100% sensitive and specific in detecting 16S rRNA genes among staphylococcal strains. Another gene, femA, has been characterized as essential for the expression of methicillin resistance in S. aureus and is universally present only in S. aureus isolates. This gene has been implicated in cell wall metabolism and is present in large amounts in actively growing cultures [24]. Specific primers for femA were designed and used in the pentaplex PCR to survey various staphylococcal isolates from our culture collection. All 178 S.

79 [0.70, 0.86] Scaling: k = 0.55 (0.44–0.66) Fissures: k = 0.65 (0.55–0.75) Sensitivity high, specificity moderate 13 Vermeulen et al. (2000) Hand eczema AZD8931 nmr Symptoms mTOR inhibitor ≥1 symptom, recurrent or lasted more than 3 weeks

– Moderate sensitivity and specificity depending on case definition of positive case SE = 0.46 [0.34, 0.58]; SP = 0.83 [0.75, 0.89] ≥12 symptoms, recurrent or lasted more than 3 weeks SE = 0.63 [0.50, 0.74]; SP = 0.75 [0.67, 0.82] ≥1 symptom SE = 0.23 [0.14, 0.34]; SP = 0.89 [0.83, 0.94] Symptoms at examination SE = 0.21 [0.13, 0.33]; SP = 0.85 [0.78, 0.90] 14 Demers et al. (1990) Respiratory disorders Symptoms SE = 0.99 [0.97, 1.00]; SP = 0.99 [0.98, 1.00] Sensitivity high, specificity high – – 15 Kujala et al. (1997) Latex allergy Symptoms Combining 1–3 skin with 1–3 mucosal symptoms: SE = 0.84 [0.67, 0.95]; SP = 0.98 [0.90, 1.00] Sensitivity moderate, specificity high – – 16 Choi et al. (2005) Hearing loss Symptoms Self-diagnosis Severity rating Self-reported screening questions: SE = 0.73 [0.60, 0.84] moderate; SP = 0.81 [0.69, 0.90] moderate – SE higher in younger age groups, SP higher in older age groups. Self-diagnosis (Rating Scale for Each Ear, RSEE): SE = 0.66 [0.52, 0.78] low; SP = 0.84 [0.73, 0.93] moderate Self-rating of severity (HEW-EHAS): SE = 0.54 [0.40, 0.67]

low; SP = 0.85 [0.72, 0.93] high 17 Gomez et al. (2001) Hearing loss Symptoms Hearing loss symptoms compared with audiometry (binaural mid-frequency) SE = 0.77 [0.68, 0.85]; SP = 0.82 [0.77, 0.86] Hearing loss symptoms compared with audiometry (binaural mid-frequency): overall agreement 80%, learn more k = 0.55 Self-report prevalence hearing loss 36%; audiometric hearing impairment prevalence 9% (low-frequency), 29% (mid-frequency) and 47% (high-frequency) Sensitivity moderate, specificity moderate In other frequencies lower agreement 18 Eskelinen et al. (1991) General Health Self-diagnosis

Overall SE = 0.82 [0.73, 0.89]; SP = 0.81 [0.71, 0.89] –   Coronary artery disease (male) SE = 95.2; SP = 87.2 Lower back pain (female) isothipendyl SE = 79.5; SP = 73.1 Sensitivity moderate to high, specificity moderate to high 19 Åkesson et al. (1999) MSD Symptoms Self-reported symptoms compared with clinical findings:   Higher sensitivity related to diagnoses, higher specificity related to clinical findings Neck/shoulders: SE = 73% and SP 81% moderate/moderate Elbows/wrists/hands SE 50% and SP 87% low/high Hips SE 45% and SP 97% low/high Self-reported symptoms compared with diagnoses Neck/shoulders SE 89% and SP 55% high/low Elbows/wrists/hands SE 67% and SP 71% low/moderate Hips SE 67% and SP 89% low/high 20 Bjorksten et al. (1999) MSD Symptoms Pain rating scale SE values 71–100; highest for shoulders (100%) and neck (92%)     SP values 21–66; highest for neck (62%) and thoracic spine (66%) Current ailment/pain: SE = 95% and SP = 88% Sensitivity moderate to high, specificity low to moderate 21 Kaergaard et al.

Detection of HSV-2-specific neutralization antibody Vorinostat ic50 titers Tucidinostat Blood was obtained from the saphenous veins and neutralization antibody titers were determined in the presence of complement as described previously [28, 30]. Clinical observations After challenge with wild-type HSV-2 strain MS, the animals were monitored daily until day 60. The number of lesions were counted and the progress of disease was scored using a modified method [31]: 0

= no disease; 1 = redness or swelling; 2 = a few small vesicles; 3 = several large vesicles; 4 = several large ulcers with maceration; 5 = paralysis; and 6 = death. Assay of acute and recurrent vaginal shedding of challenge virus After challenge with wild-type HSV-2 strain VS-4718 mouse MS, vaginal mucosae were swabbed with a moist calcium alginate swab (Fisher Scientific, Waltham, MA) on days 1, 2, 3, 5, 7 and 9. From days 30 to 60 post challenge swabs were taken daily. Swabs were kept in 1 ml DMEM and stored

at -80°C until assayed for infectious virus by standard plaque assay on Vero cell monolayers. Quantitative real-time PCR At day 60 after intravaginal challenge with HSV-2 strain MS, 12 lower lumbar and sacral dorsal root ganglia were collected from each of the surviving guinea pigs. Dorsal root ganglia were kept separately in 0.5 ml of normal growth medium and stored at -80°C for further processing. DNA was isolated from each dorsal root ganglion and assayed for viral DNA by quantitative real-time PCR as described previously [27]. Statistical analysis For statistical analysis unpaired Student’s t-tests were performed. Acknowledgements This work was supported by Public Health Service Grant 5RO1AI05088 from the National Institutes of Health. References 1. Paz-Bailey G, Ramaswamy M, Hawkes SJ, Geretti AM: Herpes simplex virus type 2: epidemiology

and management options in developing countries. Sex Transm Infect 2007,83(1):16–22.PubMedCrossRef 2. Xu F, Sternberg MR, Kottiri BJ, McQuillan GM, Lee FK, Nahmias AJ, Berman SM, Markowitz LE: Trends in herpes simplex virus type 1 and type 2 seroprevalence in the United States. mafosfamide Jama 2006,296(8):964–973.PubMedCrossRef 3. Whitley RJ: Herpes simplex encephalitis: adolescents and adults. Antiviral Res 2006,71(2–3):141–148.PubMedCrossRef 4. Lafferty WE, Downey L, Celum C, Wald A: Herpes simplex virus type 1 as a cause of genital herpes: impact on surveillance and prevention. J Infect Dis 2000,181(4):1454–1457.PubMedCrossRef 5. Jin F, Prestage GP, Mao L, Kippax SC, Pell CM, Donovan B, Templeton DJ, Taylor J, Mindel A, Kaldor JM, et al.: Transmission of herpes simplex virus types 1 and 2 in a prospective cohort of HIV-negative gay men: the health in men study. J Infect Dis 2006,194(5):561–570.PubMedCrossRef 6. Roberts CM, Pfister JR, Spear SJ: Increasing proportion of herpes simplex virus type 1 as a cause of genital herpes infection in college students. Sex Transm Dis 2003,30(10):797–800.PubMedCrossRef 7.

01, except for pKL-1, with p < 0.05, and the pKLC conserved hypothetical protein, which does

not show a statistically significant correlation) [14]. The function of most of the genes belonging to this island has not been deciphered yet, but it is known that the PAPI-1/pKLC102-like members encode virulence factors, such as cytotoxins, pili, fimbriae and regulators of biofilm synthesis and antibiotic resistance [27]. Given the known functions of this island, the identified positive correlation to chronic infections was unexpected, as it has been demonstrated that P. aeruginosa reduces its acute virulence during the adaptation to the CF lung environment [28]. Nevertheless, Rakhimova and collaborators [14] showed that the pKL-3 gene was associated to a prolonged colonization time in a minority of P. aeruginosa strains in COPD patients [14], whose lung Lonafarnib manufacturer colonization click here pattern by Pseudomonas strains is comparable to the one observed in CF patients. Analysis of the AT-genotypes identified within the publicly available population studies An intrinsic feature of the AT technology is to be standardized and ARS-1620 research buy therefore to guarantee reliable data comparison between genotyping studies performed worldwide in different laboratories [7]. In order to gain further information on the

124-independent strains of our collection, we compared them with a global database, obtained by retrieving information from 4 publicly available AT-datasets, comprising a total of 698 isolates [7, 14, 15, 17]. These datasets comprised 240 strains of diverse Etofibrate habitat and geographic origin [7], 134 strains collected from patients affected by chronic obstructive pulmonary disease [14], 63 strains isolated from keratitis [15], and 381 environmental isolates from rivers [17]. Our 124-independent strain collection included 27 genotypes previously described [7, 14, 15, 17] and 14 which have never been previously reported (see Table 1). Among the 27 already described AT-genotypes, it is interesting to notice that 8 of them (D421, 3C2A, C40A,

2C1A, 239A, 0812, E429 and F429) were shared by all collections [7, 14, 15, 17] and were all among the 16 most abundant in the global P. aeruginosa population [7]. An eBURST analysis using 15 markers (13 SNPs, the multiallelic fliCa/fliCb locus and exoS/exoU) was performed to illustrate the similarities between SNP profiles of our and other collections, typed by the AT method. As shown in Additional file 6, the eBURST analysis revealed the presence of 2 main clusters of clones and 3 small ones (with 2–3 genotypes each). Most AT clones also previously described (25 out of 27) belonged to the 2 large clusters, 12 of which were among the 16 most abundant clones in the global P. aeruginosa population, namely D421, F469, 1BAE, 2C1A, 0C2E, 239A, 0812, C40A, E429, EC29, F429 and 3C2A [7]. All novel AT clones except one (1E1E) were part of the 2 large clusters or gave rise to a small cluster including a previously described strain (i.e.

≡ Sphaeria compressa Pers., Syn. meth. fung. (Göttingen) 1: 56 (1801). Platystomum was introduced by Trevisan in 1877, and has been considered a synonym of Lophidium, as the ascospores of Platystomum have both transverse and vertical

septa (Barr 1990a, b; Chesters and Bell 1970). However, the boundary between Lophiostoma and Platystomum is not clear (Chesters and Bell 1970). Holm and Holm (1988) treated Platystomum as a synonym of Lophiostoma, and concurrently, the Platystomaceae should be treated as a synonym of Lophiostomataceae. Based on a phylogenetic analysis, however, the generic type of Platystomum (P. compressum) separated from other species of Lophiostoma, and nested with the clade of Platystomaceae Geneticin (Mugambi and Huhndorf 2009b) which may be S63845 order closely related to species in the Testiduniaceae (Plate 1). Polyplosphaeria Kaz. Tanaka & K. Hirayama, Stud. Mycol. 64: 192 (2009). Type species: Polyplosphaeria fusca Kaz. Tanaka & K. Hirayama, Stud. Mycol. 64: 193 (2009). Polyplosphaeria is characterized by globose ascomata surrounded by numerous brown hyphae and a reddish pigment on the host surface around the ascomata (Tanaka et al. 2009). Asci are cylindro-clavate with fissitunicate dehiscence and ascospores are narrowly fusoid surrounded by a sheath. The anamorph is Piricauda-like

(Tanaka et al. 2009). The cylindro-clavate asci, narrowly fusoid ascospores as well as its thin and numerous pseudoparaphyses are comparable with those of Massarina sensu lato, especially Lentithecium (Zhang et al. 2009a). The terrestrial and bambusicolous habitat of Polyplosphaeria and Piricauda anamorph readily distinguishes the genus from Lentithecium. out Pontoporeia Kohlm., Nova

Hedwigia 6: 5 (1963). Type species: Pontoporeia biturbinata (Durieu & Mont.) Kohlm., Nova Hedwigia 6: 5 (1963) ≡ Sphaeria biturbinata Durieu & Mont., Flora Algéricae 1: 497 (1849). Pontoporeia was introduced by Kohlmeyer in 1963, and is monotypified by P. biturbinata. Pontoporeia was treated as a synonym of Zopfia (Malloch and Cain 1972), which is followed by Hawksworth and Booth (1974). Based on its asci originating at the periphery of the subglobose locus, filaments occupying the center of the ascocarps, the irregular peridial structure, the ascospores having 2-layered walls with a germ pore at each end and its marine habitat, Pontoporeia was kept as a separate genus within see more Pleosporaceae (Kohlmeyer and Kohlmeyer 1979). A DNA based phylogeny placed an isolate on a long branch in relationship with other marine species, Halotthia posidoniae and Mauritiana rhizophorae, but a familial placement awaits further resolution (Suetrong et al. 2009). Pseudotrichia Kirschst., Annls mycol. 37: 125 (1939). Type species: Pseudotrichia stromatophila Kirschst., Annls mycol. 37: 125 (1939).

Localization

of liposomes in the tumor tissue was directly observed by fluorescence microscopy in live tumor-bearing mice. Conclusions Intratumoral injection is an effective method for liposome-mediated drug delivery into tumor tissues. The use of DOX-loaded DSPE-PEI cationic liposomes was found to result in significantly increased in vitro click here intracellular uptake compared with control liposomes. Notably, the conjugation of PEI to the liposomal membrane effectively improved the localization of drug-loaded liposomes at the tumor site through electrostatic interaction, which occurred in the tumor tissue of tumor-bearing mice treated with intratumorally injected liposomes. Our results demonstrate a promising approach to improve the intracellular uptake and localization effect of cationic liposomes. Although DSPE-PEI liposomes check details exhibit enhanced intracellular uptake, additional studies on the localization, injection route, and stability of these carriers is required for validation of their potential clinical application.

The cationic liposome delivery strategy presented here has considerable potential as a drug delivery platform for the treatment of a broad range of human diseases and can be adapted for other injection applications in various therapeutic fields. Acknowledgements This work was supported by the National Research Foundation of Korea (NRF) grant funded by the Korea government (MEST) (No. 2009–0078434) (BCS) and Basic Science Research Program through the National Research Foundation of Korea (NRF) funded by the Ministry of Education (NRF-2013R1A1A2059167) (HDH). This work

was supported by Ulixertinib Basic Research Laboratory Program through the National Research Foundation of Korea (NRF) funded by the Ministry of Science, ICT & Future Planning (No. 2013R1A4A1069575) (HDH). References 1. Allen TM, Cullis PR: Liposomal drug delivery systems: from concept to clinical applications. Adv Drug Deliv Rev 2012, 65:36–48.CrossRef 2. Safinya CR, Ewert KK: Materials chemistry: liposomes derived from molecular vases. Nature 2012, 489:372–374.CrossRef 3. Petersen AL, Hansen AE, Gabizon A, Andresen TL: Liposome imaging agents in personalized medicine. Adv Drug Deliv this website Rev 2012, 64:1417–1435.CrossRef 4. Moghimi SM, Szebeni J: Stealth liposomes and long circulating nanoparticles: critical issues in pharmacokinetics, opsonization and protein-binding properties. Prog Lipid Res 2003, 42:463–478.CrossRef 5. Drummond DC, Meyer O, Hong K, Kirpotin DB, Papahadjopoulos D: Optimizing liposomes for delivery of chemotherapeutic agents to solid tumors. Pharmacol Rev 1999, 51:691–743. 6. Jung SH, Kim SK, Kim EH, Cho SH, Jeong KS, Seong H, Shin BC: Increased stability in plasma and enhanced cellular uptake of thermally denatured albumin-coated liposomes. Colloids Surf B Biointerfaces 2010, 76:434–440.CrossRef 7. Han HD, Mora EM, Roh JW, Nishimura M, Lee SJ, Stone RL, Bar-Eli M, Lopez-Berestein G, Sood AK: Chitosan hydrogel for localized gene silencing.

), ultrastructural (sites of NO synthesis, immunohistochemistry), and cell communication (co-culture of isolated symbionts, NO donors, c-PTIO) studies of NO, with the aim of clarifying the role of this multifaceted molecule. Acknowledgements This project was funded by the Spanish Ministry of Education and Science [project numbers

CGL2006-12917-C02-0 and CGL2009-13429-C02-01], project Prometeo 2008/174 of the Generalitat Valenciana and the project AECID PCI/A/024755/09 of the Spanish Ministry of Foreign Affaires. We are grateful to F. Gasulla, J. Gimeno-Romeu, E. Barreno, (ICBIBE, University of Valencia) and A. Guéra (Plant Biology, University of Alcalá) for communicating unpublished data, to Dr. R. Catalá (CIB, Madrid), Dr. P. D’Ocón (UVEG, Valencia) and Dr. J. Medina (INIA, Madrid) for critical revision of the manuscript, and J.L. Rodríguez Gil for MDA protocol optimization. English revision FHPI cost was done by Wendy Ran. References 1. Demmig-Adams B, Adams WW III: Harvesting sunlight safely. Nature 2000, 403:371–374.PubMedCrossRef 2. Kranner I, Beckett R, Hochman A, Nash TH: Desiccation-Tolerance in Lichens: A Review. The Bryologist 2008, 111:576–593.CrossRef 3. Kranner I:

Glutathione status correlates with different degrees of desiccation tolerance Selonsertib research buy in three lichens. New Phytologist 2002, 154:451–460.CrossRef 4. Kranner I, Zorn M, Turk B, Wornik S, Beckett RR, Batic F: Biochemical traits of lichens differing in relative desiccation tolerance. New Phytologist 2003, 160:167–176.CrossRef 5. Kranner I, Birtic F: A modulatin role for antioxidants in desiccation tolerance. Integr Comp Biol 2005, 45:734–740.CrossRef 6. Kranner I, Cram WJ, Zorn M, Wornik S, Yoshimura I, Stabentheiner E, et al.: Antioxidants and photoprotection in a lichen as compared with its isolated symbiotic partners. PNAS USA 2005, 102:3141–3146.PubMedCrossRef 7. Gasulla F, de Nova PG, Esteban-Carrasco A, Zapata JM, Barreno E, Guera A: Dehydration rate and time of desiccation affect recovery of the lichen alga Trebouxia erici :

alternative and classical protective mechanisms. Planta 2009, 231:195–208.PubMedCrossRef 8. Halliwell Tryptophan synthase B, Cross CE: Oxygen-derived species: their relation to human disease and environmental stress. YM155 datasheet Environ Health Perspect 1994,102(Suppl 10):5–12.PubMedCrossRef 9. Courtois C, Besson A, Dahan J, Bourque S, Dobrowolska G, Pugin A, et al.: Nitric oxide signaling in plants: interplays with Ca 2+ and protein kinases. J Exp Bot 2008, 59:155–163.PubMedCrossRef 10. Palmieri MC, Sell S, Huang X, Scherf M, Werner T, Durner J, et al.: Nitric oxide-responsive genes and promoters in Arabidopsis thaliana : a bioinformatics approach. J Exp Bot 2008, 59:177–186.PubMedCrossRef 11. Wilson ID, Neill SJ, Hancock JT: Nitric oxide synthesis and signaling in plants. Plant Cell Environ 2008, 31:622–631.PubMedCrossRef 12. Darley-Usmar VM, Pate RP, O’Donell VB, Freeman BA: Antioxidant actions of nitric oxide.

J Bacteriol 2002, 184:2857–2862.CrossRefPubMed 45. Carattoli A, Bertini A, Villa L, Falbo V, Hopkins KL, Threlfall EJ: Identification of plasmids by PCR-based replicon typing. J Microbiol Methods 2005, 63:219–228.CrossRefPubMed Authors’ contributions CC designed, instructed and supervised most aspects of this project. CSC did PFGE analysis and prepared the manuscript. JML and SWC performed the experiments and data analysis. CHC, BCW and JGT assisted in the design of the study and helped to prepare the manuscript. CLC, CHC, and CHL gave useful comments and critically read the manuscript. YFC edited and revised the manuscript. All authors read and approved the final manuscript.”
“Background

Serratia marcescens Akt inhibitor is widely distributed in natural environments and has emerged in the last two decades as an important nosocomial pathogen, mainly in immunocompromised patients [1, 2]. Although S. marcescens pathogenicity is poorly understood, Berzosertib chemical structure its extracellular secreted enzymes, including several types of proteases, are candidates for virulence factors [2]. Other factors (e.g., fimbria for adhesion, lipopolysaccharide (LPS), and ShlA hemolysin) have also been suggested as virulence factors [2, 3]. Hemolysins are produced

by various pathogenic bacteria and have been proposed to be responsible for their pathogenesis [4–6]. These hemolysins, including S. marcescens ShlA, also have cytolytic activity [7]. One type of hemolysin/cytolysin is a group of pore-forming toxins. This type of toxin typically forms a homo-10058-F4 datasheet oligomer integrated into its target cell Urease membrane, thereby changing the cell permeability and leading to cell death. ShlA has been shown to increase cell membrane permeability, but not to form an oligomer [3]. Another type of hemolysin

has phospholipase C (PLC) activity. The α-toxin produced by Clostridium perfringens is the most thoroughly investigated PLC, but the molecular mechanism for its disruption of red blood cells (RBC) is not fully understood [8]. The pathogenic effects of other types of phospholipases, such as phospholipase A (PLA), have been studied in various bacteria, including Helicobacter pylori (PldA) [9], Legionella pneumophila (PlaA) [10], Campylobacter coli (PldA) [11], and Yersinia enterocolitica (YplA) [12]. Two extracellular PLAs, PhlA and PlaA, have been described previously in Serratia species [13, 14]. PlaA is produced in Serratia sp. strain MK1 isolated from Korean soil [14]. The amino acid sequence of PlaA was found to have significant similarity (80%) to PhlA from S. marcescens MG1, which was originally classified as S. liquefaciens [13–15]. However, the cytotoxic and hemolytic activities of these enzymes have remained unclear, and the importance of PLA in bacterial virulence is not well understood. S.

Best Practice & Research Clinical Obstetrics and Gynaecology 2002,16(1):81–98.CrossRef 12. Roberts WE: Emergent Obstetric Management of Postpartum Hemorrhage. Obstetrics and Gynecology Clinics

of North America 1995,22(2):283–302.PubMed 13. Bonnar J: Major Obstetric Hemorrhage. Baillieres Best Practice & Research. Clinical Obstetrics & Gynaecology 2000,14(1):1–18.CrossRef 14. Moore M, Morales JP, Sabharwal T, Oteng-Ntim E, O’Sullivan G: Selective Arterial Embolisation: A First Line Measure for Obstetric P505-15 molecular weight Haemorrhage. International Journal of Obstetric Anesthesia 2008, 17:70–73.CrossRefPubMed 15. Golan A, Lidor AL, Wexler S, David MP: A New Method in the Management of Retained Placenta. American Journal of Obstetrics and Gynaecology 1983,146(6):708–709. selleck kinase inhibitor 16. Hughey MJ: Postpartum Hemorrhage. [http://​www.​brooksidepress.​org/​Products/​Military_​OBGYN/​Home.​htm] Military Obstetrics & Gynecology Brookside Elafibranor mw Associates 2006. 17. O’Keeffe T, Refaai M, Tchorz K, Forestner JE, Sarode R: A Massive Transfusion Protocol to Decrease Blood Component Use and Costs. Archives of Surgery 2008,143(7):686–691.CrossRefPubMed 18. Gunter OL, Au BK, Isbell JM, Mowery NT, Young PP, Cotton BA: Optimizing Outcomes in Damage Control Resuscitation: Identifying Blood Product Ratios Associated With Improved Survival. The Journal of Trauma 2008, 65:527–534.CrossRefPubMed 19. Fuller AJ, Bucklin B: Blood

Component Therapy in Obstetrics. Obstetrics and Gynecology Clinics of North America 2007, 34:443–458.CrossRefPubMed

20. Munn MB, Owen J, Vincent R, et al.: Comparison of Two Oxytocin Regimens to Prevent Uterine Chlormezanone Atony at Cesarean Delivery: A Randomized Controlled Trial. Obstet Gynecol 2001, 98:386.CrossRefPubMed 21. Oyelese Y, Scorza WE, Mastrolia R, et al.: Postpartum Hemorrhage. Obstetrics and Gynecology Clinics of North America 2007, 34:421–441.CrossRefPubMed 22. Gilstrap LC, Ramin SM: Postpartum Hemorrhage. Clinical Obstetrics and Gynecology 1994,37(4):824–830.CrossRefPubMed 23. O’Brien P, El Refaey H, Gordon A, Geary M, Rodeck CH: Rectally Administered Misoprostol for the Treatment of Post-Partum Haemorrhage Unresponsive to Oxytocin and Ergometrine: A Descriptive Study. Obstetrics and Gynaecology 1998,92(2):212–214. 24. Gulmezoglu AM: Prostaglandins for Prevention of Postpartum Hemorrhage. Cochrane Database Syst Rev 2000, CD000494. 25. Lurie S, Appleman Z, Katz Z: Subendometrial Vasopressin to Control Intractable Placental Bleeding. The Lancet 1997, 349:698. Drucker M, Wallach RC: 1979, Uterine Packing: A Reappraisal. The Mount Sinai Journal of Medicine. 46(2). 191–194CrossRef 26. Drucker M, Wallach RC: Uterine Packing: A Reappraisal. The Mount Sinai Journal of Medicine 1979,46(2):191–194. 27. Katesmark M, Brown R, Raju KS: Successful Use of Sengstaken-Blakemore Tube to Control Massive Post-Partum Haemorrhage. British Journal of Obstetrics and Gynaecology 1994, 101:259–260.PubMed 28.

16. Drudy D, Mullane NR, Quinn T, Wall PG, Fanning S: Enterobacter sakazakii : An emerging pathogen in powdered infant formula. Food Safety 2006, 42:996–1002. 17. Kothary MH, McCardell BA, Frazar CD, Deer D, Tall BD: Characterization of the zinc-containing metalloprotease (zpx) and development of a species-specific detection method for Enterobacter sakazakii . Appl Environ Microbiol 2007, 73:4142–4151.PubMedCrossRef 18. Chap J, Jackson P, Siqueria R, Gasper N, Quintas C, Park J, Osaili T, Shaker R, Jaradat Z, Hartantyo SHP, Abdullah Sani N, Estuningsih

S, Forsythe SJ: International survey of Cronobacter sakazakii selleck chemicals llc and other Cronobacter spp. in follow up formulas and infant foods. Int J Food Microbiol 2009, 136:185–188.PubMedCrossRef 19. Jaradat ZW, Ababneh QO, Saadoun IM, Samara NA, Rashdan MA: Isolation of Cronobacter spp. (formerly Enterobacter sakazakii ) from infant food, herbs and environmental samples and the subsequent identification and confirmation of the isolates using biochemical, chromogenic assays, PCR and 16S rRNA sequencing. BMC Microbiol 2009, 9:225.PubMedCrossRef 20. Molloy M, Cagney C, O’Brien S, Iversen C, Fanning S, Duffy G: Surveillance and characterization by pulse-field gel Smoothened Agonist electrophoresis

of Cronobacter spp. in farming and domestic selleck screening library environments, food production animals and retail foods. Int J Food Microbiol 2009, 136:198–203.PubMedCrossRef 21. Lai KK: Enterobacter sakazakii infections among neonates, infants, children and adults. Medicine 2001, 80:113–122.PubMedCrossRef 22. Gurtler JB, Kornacki JL, Beuchat LR: Enterobacter sakazakii A coliform

of increased concern to infant health. Int J Food Microbiol 2005, 104:1–34.PubMedCrossRef 23. Jaradat Z, Zawistowski J: Production and characterization of monoclonal antibodies against the O5 antigen of Salmonella typhimurium lipopolysaccharide. Appl Environl Microbiol 1996, 62:1–5. 24. Pupo E, Aguila A, Santana H, Nunez J, Castellanos-Serra L, Hardy E: Mice immunization with gel electrophoresis-micropurified bacterial lipopolysaccharides. Electrophoresis 1999, 20:458–461.PubMedCrossRef 25. Banada PP, Bhunia AK: Antibodies and immunoassays for detection of bacterial pathogens. In Principles of Bacterial Detection: Biosensors, Recognition Receptors and Microsystems. Volume Chapter 21. Edited by: Nintedanib (BIBF 1120) Zourob M, Elwary S, Turner A. Springer, New York; 2008:567–602.CrossRef 26. Davies RL, Wall RA, Borriello SP: Comparison of methods for the analysis of outer membrane antigens of Neisseria meningitis by western blotting. J Immunol Methods 1990, 134:215–25.PubMedCrossRef 27. Liddell JE, Cryer A: A practical guide to monoclonal antibodies. John Wiley and Sons, Chichester, UK; 1991. 28. Harlow ED, Lane D: Antibodies; A laboratory manual. Cold Spring Harbor, USA; 1988. 29. Friguet B, Djavadi-Chaniance L, Golberg M: A convenient enzyme linked immunosorbent assay for testing whether monoclonal antibodies recognize the same antigenic site. In Immunoenzymatic techniques.