US can often diagnose an inflamed appendix and detects free fluid in the pelvis but this simple method is buy BIX 1294 influenced by the operator’s experience, the body built and co-operation of the patient. The wider use of CT scan for patients with suspected appendicitis has been shown to improve the accuracy of the diagnosis and decrease the negative laparotomy rates [3, 4, 17]. Recent studies reported a high sensitivity of 91-99% in this age group [20]. LDN-193189 manufacturer Storm-Dickerson TL et al. reported that the incidence of

perforation declined over the past 20 years from 72% to 51% in his patients due to the earlier use of CT scan [4]. In our patients, CT scan was only used in those with equivocal findings and in whom the diagnosis was not reached after repeated CA and US. We could not calculate the sensitivity and specificity of CA, US and CT scans in our patients because we studied the positive cases. PF477736 research buy However, we did not find any false positive result when the CT scan was used. Elderly patients have a higher risk for both mortality and morbidity following appendectomy. It was estimated to be around 70% as compared to 1% in the general population [1, 4, 9–11]. In our study, the overall post operative complication rate was 21%, a figure which is a bit lower than 27-60% reported by others [6, 20, 29]. As expected, complications were

three times more frequent in the perforated as compared to the nonperforated group. This finding is in consistency with several other studies that

have shown that perforation per se was the most predictive factor for post operative morbidity in the elderly patients with 3-mercaptopyruvate sulfurtransferase acute appendicitis [1, 7, 14, 20]. The mortality rate in elderly patients following perforated appendicitis was reported between 2.3%-10%. Death is often related to septic complications compounded by the patient’s co morbidities [3, 6, 7, 29, 30]. In this study, there were 6 (3%) deaths in both groups, four in the perforated and two in the nonperforated group. Three patients died due to septic complications while the others due to respiratory and cardiovascular causes. As compared to younger age groups, the length of the hospital stay is usually longer in the elderly patients. This is usually ascribed to the higher rate of complications, prolonged need of antibiotics, treatment of other comorbidities and difficulties in communication [6, 16, 31]. Our result of 7.4 and 4.2 days for perforated and nonperforated groups was found in agreement with these studies. When comparing our result to a previous study that was done in the same region 10 years back [32], we found that the incidence of appendiceal perforation did not decrease over the past ten years in spite of improved health care programs and diagnostic facilities. We think that this failure was due to the underestimation of the seriousness of the abdominal pain in this age group by both the patients and the primary health care providers.

1). Table 2 Commercial imports of live captive-bred CITES Appendix II-listed poison arrow frogs in 1987–2008 with Kazakhstan as reported origin, highlighting the role of Thailand as an importer and re-exporter and showing exports were restricted to the years 2004 and 2005 (ICG-001 purchase Lebanon is not party to CITES) Species Trade 1987–2003 2004 2005 2006 2007 2008 Exporter Importer Dendrobates

amazonicus Export 0 20 0 0 0 0 Lebanon Thailand Dendrobates auratus Export 0 100 100 0 0 0 Lebanon Thailand Re-export     10 20 0 0 Thailand Taiwan Dendrobates azureus Export 0 240 200 0 0 0 Lebanon Thailand         5 0 Thailand S Korea Dendrobates fantasticus Export 0 30 30 0 0 0 Lebanon Thailand Dendrobates galactonotus Export 0 100 100 0 0 0 Lebanon Thailand Re-export     30 7 0 0 Thailand Taiwan Dendrobates imitator Export 0 0 50 0 Proteasome inhibition assay 0 0 Lebanon Thailand check details Dendrobates lamasi Export 0 40 40 0 0 0 Lebanon Thailand Dendrobates leucomelas Export 0 100 100 0 0 0 Lebanon Thailand Dendrobates pumilio Export 0 100 100 0 0 0 Lebanon Thailand Dendrobates reticulatus Export 0 100 100 0 0 0 Lebanon Thailand Dendrobates tinctorius Export 0 200 200 0 0 0 Lebanon Thailand Re-export     18 20 0 0 Thailand Taiwan Re-export       6 0 0 Thailand Philippines         30 0 Thailand S Korea Dendrobates ventrimaculatus Export 0 20 40 0 0 0 Lebanon Thailand

Dendrobates spp Re-export 0 50 0 0 0 0 Lebanon Thailand Phyllobates bicolor Export 0 100 100 0 0 0 Lebanon Thailand         10 0 Thailand S Korea Phyllobates terribilis Export 0 100 100 0 0 0 Lebanon Thailand Epipedobates tricolor Export 0 50 50 0 0 0 Lebanon Thailand Re-export       5 0 0 Thailand South Korea Cryptophyllobates azureiventris Export 0 0 40 0 0 0 Lebanon Thailand Fig. 1 Trade routes of dendrobatid frogs from Kazakhstan and Lebanon Adenosine triphosphate to Thailand and thence to South Korea, Taiwan Province of China and the Philippines. Size of arrows are proportional (log10-transformed) to the volumes traded. The dotted line indicates a minimum number of individuals

following an assumed route from range States Discussion This analysis shows high levels of international trade in dendrobatid frogs, six times higher than reported by Gorzula (1996) more than a decade ago. Compared to the late 1980s–early 1990s (Gorzula 1996), 12 species were no longer reported to be in international trade whereas 18 new ones appeared in recent years. There are large differences between numbers of captive-bred versus wild-caught dendrobatid frogs. Gorzula (1996) reported 14% of the total international trade to be captive-bred, whereas currently 91% of the individuals are reported as such (with an additional 5% comprising ranched or F1 captive-born individuals).

gingivalis [106] either, and so their substrate specificity cannot be assigned at present. In G. metallireducens, duplicate kup genes, predicted to encode low-affinity potassium/proton symporters, are found in one place (Gmet_0038 = GSU3342; Gmet_0039 = GSU2485, 29% and 31% identical to the E. coli protein [108]), apart from the kdpABCDE genes (Gmet_2433-Gmet_2437 = GSU2480-GSU2484, 38–49% identical

to ITF2357 clinical trial the homologs in E. coli [109, 110]) encoding an osmosensitive potassium-translocating ATPase complex. In G. sulfurreducens, one of these kup genes (GSU2485) is located 3′ of the kdp gene cluster, apparently under control of an osmosensitive riboswitch (GSU2484.1, sequence coordinates 2728254 to 2728393), and there is a third kup gene (GSU2350, 49% identity to E. coli) not found in other Geobacteraceae. G. sulfurreducens also has at least two

potassium/proton antiporters (GSU1203, 34% identical to CvrA of Vibrio parahaemolyticus [111]; GSU2759, 31% identical to KefB of E. coli [112]) and a sodium/proton antiporter complex (mrpABCDEFG GSU2344-GSU2338, 29–48% identical to the homologs in B. subtilis [113]) that are not found in G. metallireducens. Three mechanosensitive ion channels are common to the two species (Gmet_1942 = GSU1633; Gmet_2581 = GSU2316; and Gmet_2522 = GSU2794); two more are unique to G. sulfurreducens (GSU1557; GSU1723). Thus, control of monovalent cation homeostasis appears to be more complex in G. sulfurreducens. Several heavy metal efflux pumps are conserved between the two species, but their substrate specificity is uncertain. Transporters present GDC-0449 research buy in G. sulfurreducens but not G. metallireducens include that for uracil (GSU0932, 48% identical to the Bacillus caldolyticus protein [114]). Transporters present in G. metallireducens but not G. sulfurreducens include those for nitrate/nitrite

(Gmet_0333-Gmet_0334) and chromate (Gmet_2732-Gmet_2731), which are each present as two paralogous genes rather than gene fusions such as their homologs that have been characterized in other bacteria [36, 115]. Signalling, chemotaxis and Celecoxib global regulation G. metallireducens possesses orthologs of the six sigma factors of RNA polymerase identified in G. sulfurreducens (Table 3), as well as a seventh factor (Gmet_2792) not found in other Geobacteraceae, related to the extracytoplasmic sigma-Z factor of B. subtilis [116]. Intriguingly, a particular anti-anti-sigma factor gene is frameshifted in both genomes: GSU1427 has frameshifts in the phosphatase Stem Cells inhibitor domain, resulting in an in-frame protein, whereas the homologous Gmet_1229 is shifted out of frame in the kinase domain. These differences imply that global regulatory networks may be different in the two species. Table 3 Sigma factors of G. metallireducens and G. sulfurreducens. Locus Tag Annotation G. metallireducens gene G.

J Bacteriol 2007, 189:3414–3424.PubMedCrossRef 42. Balasubramanian S, Kannan TR, Baseman JB: The surface-exposed carboxyl region of Mycoplasma pneumoniae elongation factor Tu interacts with fibronectin. Infect Immun 2008, 76:3116–3323.PubMedCrossRef 43. Dallo SF, Kannan TR, Blaylock MW, Baseman JB: Elongation factor Tu and E1 beta subunit of pyruvate dehydrogenase complex act as fibronectin binding proteins in Mycoplasma pneumoniae . Mol Microbiol 2002, 46:1041–1051.PubMedCrossRef 44. Alonso JM, Prieto M, Parra F: Genetic and antigenic characterisation of elongation factor buy Adriamycin Tu from Mycoplasma mycoides subsp. mycoides SC. Vet Microbiol 2002, 89:277–289.PubMedCrossRef 45. Bercic RL, Slavec

B, Lavric M, Narat M, Bidovec A, Dovc P, Bencina D: Identification of major immunogenic proteins

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72 kDa lipoprotein of Mycoplasma mycoides subsp. mycoides small colony type. Microbiology 1996, selleck antibody 142:3515–3524.PubMedCrossRef 50. Reverchon S, Rouanet C, Expert D, Nasser W: Characterization of Indigoidine Biosynthetic Genes in Erwinia chrysanthemi and Role of This Blue Pigment in Pathogenicity. J Bacteriol 2002, 184:654–665.PubMedCrossRef 51. Tola S, Idini G, Manunta D, Galleri G, Angioi A, Rocchigiani AM, Leori G: Rapid and specific detection of Mycoplasma agalactiae by polymerase chain reaction. Vet Microbiol 1996, 51:77–84.PubMedCrossRef 52. Ferrer-Navarro M, Gómez A, Yanes O, Planell R, Avilés FX, Piñol J, Pérez J, Pons A, Querol E: Proteome of the bacterium Mycoplasma penetrans . J Proteome Res 2006, 5:688–694.PubMedCrossRef 53. Chevallet M, Luche S, Rabilloud T: Silver staining of proteins in polyacrylamide gels. Nat Protoc 2006, 1:1852–1858.PubMedCrossRef 54. Laemmli UK: Cleavage of structural proteins during the assembly of the head of bacteriophage T4. Nature 1970, 227:680–685.PubMedCrossRef 55. Addis MF, Tanca A, Pagnozzi D, Crobu S, Fanciulli G, Selleckchem Fedratinib Cossu-Rocca P, Uzzau S: Generation of high-quality protein extracts from formalin-fixed, paraffin-embedded tissues. Proteomics 2009, 9:3815–3823.PubMedCrossRef 56. Addis MF, Tanca A, Pagnozzi D, Rocca S, Uzzau S: 2-D PAGE and MS analysis of proteins from formalin-fixed, paraffin-embedded tissues. Proteomics 2009, 9:4329–4339.PubMedCrossRef 57.

: Genome sequence of CX-5461 price the dissimilatory metal ion-reducing bacterium Shewanella oneidensis. Nat Biotechnol 2002,20(11):1118–1123.PubMedCrossRef 26. Andrews SC, Robinson AK, Rodriguez-Quinones F: Bacterial iron homeostasis. FEMS Microbiol Rev 2003,27(2–3):215–237.PubMedCrossRef 27. Wilderman PJ, Sowa NA, FitzGerald DJ, FitzGerald PC, Gottesman S, Ochsner UA, Vasil ML: Identification of tandem duplicate regulatory small RNAs in Pseudomonas aeruginosa involved in iron homeostasis. Proc Natl Acad Sci USA 2004,101(26):9792–9797.PubMedCrossRef 28. Zhang Y: miRU: an automated plant miRNA target prediction

server. Nucleic Acids Res 2005, (33 Web Server):W701–704. 29. Tjaden B, Goodwin SS, Opdyke JA, Guillier M, Fu DX, Gottesman S, Storz G: Target prediction for small, noncoding RNAs in bacteria. Nucleic Acids Res 2006,34(9):2791–2802.PubMedCrossRef 30. Vecerek B, Moll I, Blasi U: Control of Fur synthesis by the non-coding RNA RyhB and iron-responsive decoding.

Embo J 2007,26(4):965–975.PubMedCrossRef 31. Saffarini DA, Schultz R, Beliaev A: Involvement of cyclic AMP (cAMP) and cAMP receptor protein in anaerobic respiration of Shewanella oneidensis. J Bacteriol 2003,185(12):3668–3671.PubMedCrossRef 32. Maier TM, Myers CR: AZ 628 research buy Isolation and characterization of a Shewanella putrefaciens MR-1 electron transport regulator etrA mutant: reassessment of the role of EtrA. J Bacteriol 2001,183(16):4918–4926.PubMedCrossRef 33. Beliaev AS, Thompson DK, Fields MW, Wu L, Lies DP, Nealson KH, Zhou J: Microarray transcription profiling of a Shewanella oneidensis etrA mutant. J Bacteriol 2002,184(16):4612–4616.PubMedCrossRef 34. Yang Y, Meier UT: Genetic interaction between a chaperone of small nucleolar ribonucleoprotein particles and cytosolic serine hydroxymethyltransferase. J Biol Chem 2003,278(26):23553–23560.PubMedCrossRef Carnitine palmitoyltransferase II 35. Gralnick JA, Brown CT, Newman DK: Anaerobic regulation by an atypical Arc system in Shewanella oneidensis. Mol Microbiol 2005,56(5):1347–1357.PubMedCrossRef 36. Myers CR, Nealson KH: Respiration-linked proton translocation coupled to anaerobic reduction of

manganese(IV) and iron(III) in Shewanella putrefaciens MR-1. J Bacteriol 1990,172(11):6232–6238.PubMed 37. Saltikov CW, Newman DK: Genetic identification of a click here respiratory arsenate reductase. Proc Natl Acad Sci USA 2003,100(19):10983–10988.PubMedCrossRef 38. Littell RC, Milliken GA, Stroup WW, Wolfinger RD: SAS system for mixed models. Cary, NC: SAS Institute; 1996. 39. Edgar RC: MUSCLE: multiple sequence alignment with high accuracy and high throughput. Nucleic Acids Res 2004,32(5):1792–1797.PubMedCrossRef Authors’ contributions YY conceived the study, implemented experiments to identify ryhB and drafted the manuscript. LAM performed bioinformatics analyses and manuscript editing. ABP carried out quantitative RT-PCR and growth experiments and performed manuscript editing. SF performed statistical analyses.

Determination of invasiveness HeLa S3 cell line (ATCC CCL-2.2) between passages 8 and 15 was grown in F12K medium containing 10% HI-FBS at 37°C with 5% CO2. Twenty-four hours prior to infection, the cells were suspended and cultured in 25 cm2 culture flasks (Corning, Corning, NY) at a concentration of 2 × 106 cells/flask and replaced in the incubator. Before infection, cells from 1 flask were detached and counted. For infection with B. melitensis 16 M or its

derivatives, selleckchem the medium overlying the HeLa monolayers was replaced by a bacterial inoculum grown overnight in F12K cell culture media, at a multiplicity of infection of 1,000 bacteria per cell (MOI 1,000:1). Bacteria were centrifuged onto the cells at 800 × g for

10 min, followed by 30 min of incubation at 37°C with 5% CO2. Then, cells were washed once with phosphate buffer solution (PBS) to remove extracellular bacteria and subsequently re-incubated for 1 h in F12K media supplemented with 100 μg ml-1 of gentamicin solution (Sigma, St. Louis, MO). To determine the viable number of intracellular bacteria, infected cultures were washed 3× with PBS and then lysed with 0.1% Triton X-100 (Sigma). Lysates were serially diluted and cultured on TSA plates for quantification of CFU. Isolation of total RNA from B. melitensis 16 M Total RNA was isolated by phenol-chloroform extraction from 4 different cultures of B. melitensis 16 M grown in F12K supplemented with 10% HI-FBS at late-log and stationary MGCD0103 order www.selleckchem.com/products/p5091-p005091.html growth phases, as previously described [66]. Briefly, ice-cold ethanol/phenol solution was added to the B. melitensis culture, and the bacteria were recovered by centrifugation. The media was then removed and the pellet suspended in TE buffer-lysozyme solution containing 10% SDS (Ambion, Austin, TX). After 2 min of incubation, acid water-saturated phenol (Ambion) was added to the lysate and mixed, and the sample was subsequently

incubated for 6 min at 64°C. Tubes were kept on ice for at least 2 min and then centrifuged at maximum speed. The upper layer, containing the RNA, was transferred to a new tube, mixed Amylase with an equal volume of chloroform (Sigma) and then separated by centrifugation. The aqueous phase was mixed with 100% cold ethanol and stored at -20°C. After at least one hour of incubation, RNA was pelleted by centrifugation, washed in 80% ethanol and suspended in DEPC-treated water (Ambion) containing 2% DTT and 1% RNase inhibitor (Promega, Madison, WI). Contaminant genomic DNA was removed by RNase-free DNase I treatment (Ambion) according to the manufacturer’s instructions, and samples were stored at -80°C until used. RNA concentration was quantified using the NanoDrop® ND-1000 (NanoDrop, Wilmington, DE), and quality was determined using the Agilent 2100 Bioanalyzer (Agilent, Palo Alto, CA). Isolation and labeling of B.

SP, SZ, AG, DF and DP participated in the experiments of cell culture and molecular biology. MM participated in statistical analysis and interpretation. SN, NS and AS participated in the design of the experiments. All authors read and approved the final manuscript.”
“Introduction Invasive ductal carcinoma is the most common breast

malignancy and a leading cause of cancer-related death in women worldwide.[1] Despite developments in surgical methods, cytotoxic chemotherapy, and agents targeted against estrogen receptor (ER) and HER2, a subset of patients with advanced stage invasive ductal carcinoma may experience tumor recurrence or metastasis within several years after treatment. It has been estimated that 11% of women with invasive ductal carcinoma will experience a

CP673451 solubility dmso recurrence within five years after surgery, including 8% of women with luminal A OICR-9429 datasheet breast cancers and 15% of women with tumors having basal-like features.[2, 3] The cancer stem cell hypothesis was proposed to explore breast cancer heterogeneity and the risk of breast cancer recurrence, and these cell subpopulations may contribute to drug resistance that drives tumor recurrence or metastasis [4]. Using keratin profiling, Hoechst dye efflux, and flow cytometry analysis of cell surface markers such as CD44, CD24, CD133, epithelial cell adhesion molecule, and mucin-1,[5] normal human breast stem-cell like cells have been independently identified AZD2281 datasheet as showing elevated expression of CD44 and no expression of CD24 (CD44+/CD24-), as well as elevated levels of stem cell enriched genes.[6] The CD44+/CD24- subpopulation MG-132 datasheet was believed

to be putative stem cells in human breast tissue, enriched for basal cells and motility genes, which could be generated during the epithelial-mesenchymal transition. Moreover, these cells were negative for mucin 1, estrogen receptor (ER), and v-erb-b2 erythroblastic leukemia viral oncogene homolog 2 (erbB2) receptor.[7, 8] More importantly, high expression of CD44+/CD24- cancer cells was associated with poor patient prognosis.[9] These cells had the phenotype of cancer cells during the epithelial to mesenchymal transition, [10] indicating that the gene expression pattern of CD44+/CD24- cells in breast cancers resembled more closely the pattern observed in CD44+/CD24- cells in normal breast than that of CD44-/CD24+ cells isolated from the same tumor.[6] Taken together, these findings indicated that CD44+/CD24- cells, especially those expressing epithelial cell adhesion molecule, were breast cancer stem cells (CSCs).[11] In contrast, breast cancer cells expressing elevated levels of aldehyde dehydrogenase 1 (ALDH1) were also described as breast CSCs, with ALDH1+/CD44+/CD24- cells displaying strong tumorigenic potential.[12] Moreover, breast CSCs were believed to constitute up to 35% of the cancer cells in a tumor, whereas these cells constituted only about 1% of stem and progenitor cells present in normal breast [13].

e. Ad.null, Ad.hTERT-E1A-TK, Ad.hTERT-E1A-TK plus GCV and PBS plus GCV, and each group contained at least 7 animals. About 1 × 109 PFU of 3-MA in vivo Ad.null orAd.hTERT-E1A-TK in 100 μl PBS or 100 μl PBS alone were injected into tumors respectively. On the 3rd day post virus injection, GCV (100 mg/kg/day) was intraperitoneally administered for 14 consecutive days. The tumor growth was assessed by measuring bi-dimensional diameters twice a week with calipers. The tumor volumes (V) were calculated according to the formula V = 1/2ab2 (a represents

the largest diameter and b represents the smallest diameter). All animals were killed 4 weeks later after treatment and then the tumors were removed and weighed. Histopathologic examination of tumors The resected tumors were fixed with 10% formalin and embedded in paraffin. The tumor sections were stained with hematoxylin-eosin and evaluated by two individual pathologists. Statistical analysis All numerical data were expressed as mean ± SD. A comparison of means among two or more groups was performed using one-way analysis of variance or nonparametric test, and further confirmed by post-hoc analyses with S-N-K or Games-Howell test. All statistical analyses were conducted using SPSS 11.5 software (SPSS, Chicago, IL). Differences with p

< 0.05 were considered as significant. Results and discussion Tumor specific replication click here and killing effect of Ad.hTERT-E1A-TK In the present study we generated a novel oncolytic adenoviral vector, Ad. hTERT-E1A-TK, in which tumor selective replication was mediated by the hTERT promoter and HSV-TK gene expression was controlled by CMV promoter. Given Ad.hTERT-E1A-TK contained a suicide gene HSV-TK, we first examined TK expression in Ad.hTERT-E1A-TK infected cells by Western blot. Our results showed that TK expression could be detected in Ad.hTERT-E1A-TK-infected tumor cells but not in control cells (Additional file 2). We next examined Ad.hTERT-E1A-TK/GCV Ketotifen high throughput screening compounds induced cytopathic effect. As shown as crystal violet staining in Fig. 1A and Additional file 3, Ad.hTERT-E1A-TK/GCV was able to kill different type of tumor cells including

NCIH460, SW1990, SMMC-7721 and Hela. Its tumor killing effect was comparable with other oncolytic adenoviral vector such as Ad.hTERT-E1A-CD/5-FC, and even superior to Ad.hTERT-E1A as well as wild type adenovirus dl309 in most tested cell lines. Furthermore, Ad.hTERT-E1A-TK killed tumor cell in dose dependent manner. Ad.hTERT-E1A-TK induced tumor cell killing effect was further confirmed by CCK-8 assay. As shown in Fig. 1B, two NSCLC cell lines, NCIH460 and A549, and one human cervical carcinoma cell line Hela showed significant reduction in surviving cells after Ad.hTERT-E1A-TK infection, and GCV could further enhance Ad.hTERT-E1A-TK induced tumor cell killing effect. Figure 1 Tumor cell killing effect of Ad.hTERT-E1A-TK on NSCLC NCIH460 cells. A.

vaginae and G. vaginalis specific primers obtained for 50 neovaginal samples.     Gardnerella vaginalis     + – Total Atopobium vaginae + 12 17 29   – 3 18 21   Total 15 35 50 The samples that were PCR positive for G. vaginalis were selected for amplification with bacterial vaginosis associated

bacteria (BVAB) primers. All 15 specimens were PCR negative for BVAB1 and BVAB3 and only one specimen, positive for both A. vaginae and G. vaginalis, was PCR positive for BVAB2. Remarkably, 41 of 50 neovaginal specimens showed an amplicon after amplification with M. curtisii primers (Table 3). Of these, 36 (88%) could be confirmed using Mobiluncus genus specific primers. Table 3 Detection of Mobiluncus curtisii in 30 neovaginal samples: comparison between Gram stain, culture and species specific primers.   C+P+ C+P- C-P+ C-P- Total G+ 6 H 89 0 6 1 13 G- 4 0 10 selleck screening library 3 17 G+/-: Presence or absence of Mobiluncus cell types on Gram stain. C+/-: Presence of absence of M. curtisii after anaerobic incubation on Columbia-based blood agar. P+/-: Presence or absence of an amplicon after amplification with M. curtisii specific primers. After amplification of the neovaginal DNA extracts with primers that target the ITS2-region

of the rRNA Selleckchem BI 10773 cistron of Fungi and size determination of the amplified ITS2 by means of capillary electrophoresis, 6 specimens revealed an amplicon. Three specimens could not be sequenced and the remaining three sequences were identified as molds (resp. Davidiella tassiana, Lycoperdon perlatum and Phaeosphaeria sp.). The PCR assay for Chlamydia on urine was negative for all participants. Discussion The pH of the neovagina of the transsexual women in our study was consistently elevated (mean 5.8; range 5.0–7.0) as compared to that of the biological vagina. This is not unexpected as the acidic pH (3.8–4.5) of the vagina results primarily

from lactic acid production by the resident lactobacilli [9, 10] and is Galactosylceramidase further enhanced through acidification by an active proton pump action of the vaginal epithelium – a mechanism upregulated by oestrogen [11]. In our patient series however, lactobacilli were consistently lacking, with only one transsexual woman with a penile skin-lined neovagina displaying some lactobacilli. As expected, and although these women show serum oestradiol levels comparable to those in substituted postmenopausal women, the environment of this penile skin-lined neovagina, does not support the growth of lactobacilli. This might be due to the absence of glycogen rich epithelial cells and to the absence of lactobacillus epithelial binding sites that are upregulated by oestrogen in the normal vaginal mucosa. Our study indicates that the microflora of the neovagina is characterized by bacterial species from the skin and the intestinal microflora, somewhat similar to what is observed with premenarchal girls, who also lack a Lactobacillus dominated microflora, eliciting colonisation resistance.