jensenii NSC 683864 research buy derivatives (Figure 4). Again, MALP-2, in contrast to L. jensenii, induced a significant IL-8 upregulation in all three

models. Since the findings in the primary tissue model (Figure 4a) mirrored those in the immortalized epithelial monolayers (Figure 3b and 4b), as previously reported with other vaginal bacteria [20], we chose the immortalized cell line model for further analysis of immunity mediators and CFU counts based on its lower cost- and handling time efficiency. Figure 4 Cytokine profiles induced by bacteria or synthetic TLR2/6 ligand in cervicovaginal colonized epithelial model. Similar IL-8 levels measured in supernatants derived from primary and immortalized epithelial cells cultured with L. jensenii

1153–1666, 3666, gfp bioengineered and L. jensenii 1153 wild type (WT) strains or MALP-2 50 nM as a positive control. (Figure 4a) Two independent experiments with (VEC-100™) primary ectocervical originated tissue. (Figure 4b) Vaginal (Vk2/E6E7) and endocervical (End1/E6E7) epithelial colonized cells in one representative of three experiments. Bars represent mean and SEM from duplicate cultures. *** P<0.001 different from medium control, +++ P<0.001 different from L. jensenii WT. In further immune mediator analysis of L. jensenii colonized Vk2/E6E7 immortalized epithelial monolayers; MALP-2 induced significant increases over baseline levels of TNF-α (P<0.001) and IL-6 www.selleckchem.com/products/Fludarabine(Fludara).html (P<0.001), while the WT and derivatives had no significant effect on either (Figure

5a-b). IL-1α levels slightly increased (P<0.05) in the presence of the WT, however all derivatives maintained baseline levels (Figure 5c). No significant differences were observed in IL-1RA levels (Figure 5D). Figure BCKDHA 5 Absence of a pro-inflammatory cytokine response in L. jensenii colonized epithelial model. (Figure 5a) TNF-α, (Figure 5b) IL-6, (Figure 5c) IL-1α, (Figure 5d) IL-1RA cytokine levels measured in supernatants from vaginal (Vk2/E6E7) epithelium cultured for 24 h with L. jensenii 1153–1666, 3666, and gfp bioengineered strains and L. jensenii 1153 wild (WT) strain or MALP-2 (50 nM) as a positive control. Bars represent mean and SEM from duplicate and triplicate cultures in two independent experiments. *** P<0.001,* P<0.05 different from medium control, +++ P<0.001 different from L. jensenii 1153 WT. Sustained bacterial colonization by wild type and bioengineered L. jensenii does not alter levels of inflammation-associated proteins over time To determine if the homeostatic effect of L. jensenii on innate immunity proteins is sustained over time, despite NF-κB activation, we exposed the vaginal epithelial cells to wild type and bioengineered bacterial strains and MALP-2 and maintained the cultures for three days with supernatants harvested for protein measurement and replaced with plain KSFM medium at each 24 h interval.

The antisense fragment used in this study is identical to the corresponding region of porM1. While it displays a homology of 71.4% to porM2, the antisense fragment and porM2 still exhibit long stretches of identical nucleic acid sequences. Of particular importance is the similarity in the beginning of the antisense fragment covering the Shine-Dalgarno Sequence and the start codon (40 bp, 95% identity). We therefore are convinced that a down-regulation of both, porM1 as well as porM2, may be achieved using the strategy described in this study. Deletion- or insertion mutagenesis of either porM1 or porM2 might result in complementation PCI-32765 supplier of the deleted porin gene by the

remaining one. Such an effect has been observed in M. smegmatis, where the deletion of the mspA gene caused the activation of the transcription of mspB and/or mspD [28]. Mutagenesis of both porin genes in the same derivative, selleck screening library on the other hand, would

probably restrain the diffusion across the OM to an extent compromising cellular functions. The effects of an over-expression of porin in our M. fortuitum strains depended on characteristics of the strains as well as the amount of kanamycin added to the medium. The over-expression of porM1 and porM2 showed the most considerable influence on growth rate in strain 10851/03. Among the tested strains, 10851/03 has the slowest growth rate and produces least porin. Therefore, this strain probably benefits most from a better nutrient supply caused by porin over-production. Otherwise, the adverse effect of kanamycin on the growth rate was most pronounced in strain DSM 46621, which expresses the highest amount of porin among the analysed

strains. Disposing of a relatively high amount of porin, this strain probably takes less advantage of an ameliorated nutrient supply and instead suffers most from more kanamycin diffusion into the cells. When the kanamycin concentration in the plates was reduced to 25 μg ml-1, the over-expressing DSM 46621 derivatives did not show any growth inhibition compared to the control strain and even had a slight growth advantage. It seems that at this kanamycin concentration the beneficial effects of better nutrient influx slightly exceed the adverse effects of better antibiotic influx. The changes in growth behaviour in 10851/03 as well as in DSM acetylcholine 46621 were more pronounced upon over-expression of porM2 compared to over-expression of porM1. The down-regulation of the expression of PorM1 together with PorM2 by antisense-technology reduced the growth of both M. fortuitum strains to a similar and very low level suggesting that lack of porins in the knock-down strains strongly impairs the nutrient supply. Our observations point to a passage of kanamycin through the PorM porins. Studies performed with M. smegmatis gave rise to contrarious conclusions [29, 30]. Stephan et al. [29] observed no reduction of kanamycin resistance in a mspA mutant compared to the M.

J Exp Clin Cancer Res. 2012, 31:73.PubMedCrossRef”
“Introduction Glioma is the first commonly diagnosed types of intracranial tumors, accounting for more than 50% among all primary brain tumors [1]. Gliomas can be classified as astrocytomas, oligodendrogliomas, or tumors with morphological features of both two types of tumors above. According to their degrees of malignancy, gliomas are classified from graded I to IV. Glioblastoma, one subtype of aggressive gliomas, is the most common and lethal brain tumor, with widespread invasion in brain, poor differentiation, destruction of normal brain tissue, and resistance to traditional therapeutic approaches [1–3]. Sapanisertib in vivo Current

options for treatment of glioblastoma include surgical resection of the primary tumor to reduce the tumor size, followed by radiotherapy and adjuvant chemotherapy with temozolomide (TMZ) [4]. However, even with successful surgical resection and subsequent radiotherapy and chemotherapy, the prognosis remains poor, with a median survival of 12–15 months [5]. High tumor recurrence rate and mortality of patients is due to incomplete removal of primary ��-Nicotinamide supplier tumors after surgery and resistance to chemotherapy. The infiltrating characteristics of glioblastoma make complete removal of primary tumor virtually

impossible, and even cause normal brain tissue damage. Therefore, the limitation of current options for glioblastoma treatment suggests that it is urgently required to study mechanism of chemoresistance regulation of this cancer. MicroRNAs (miRNAs), a class of 22-nucleotide small non-coding RNAs, can regulate gene expression at post-transcriptional level. MiRNAs are evolutionarily conserved and negatively regulate gene expression. They

are transcribed by RNA polymerase II, spliced, and then poly-adenylated to generate primitive miRNAs (pri-miRNAs) [6]. The stem-loop structure of pri-miRNAs can be recognized and cleaved by the nuclear RNase III Drosha to generate hairpin precursor miRNAs (pre-miRNAs). Pre-miRNAs are rapidly exported to the cytoplasm by exportin-5, excised by the cytoplasmic RNase III Dicer to generate a 22-nucleotide miRNA duplex: one Avelestat (AZD9668) strand is a mature miRNA, whereas the other strand (miRNA*) is normally unstable and degraded. The mature miRNAs can suppress target gene expression by interaction with complementary sequences in the 3′-untranslated regions (3′-UTRs) of target mRNAs and trigger translation blockade or mRNA degradation depending on whether it is completely or partially matched with the target genes [7]. Multiple studies have shown that miRNAs are deregulated in various types of human cancers [8], including glioblastoma [9–11], breast cancer [12], lung cancer [13], colon cancer [14], and ovarian cancer [15]. MiRNAs may function as oncogenes or tumor suppressors, and also involve in chemoresistance [15, 16].

Indicating another intra-mitochondrial pool of creatine, which seems to play an essential role in the phosphate-transport system from the mitochondria to the cytosol [13]. Myopathy patients have demonstrated reduced levels of total creatine and phosphocreatine as well as lower levels of CreaT1 protein, which is thought to be a major contributor to these decreased levels [14]. Documented effects of creatine supplementation on physical performance The majority of studies focusing on creatine supplementation report an increase in the

body’s’ creatine pool [15–17]. There is a positive relationship between muscle creatine uptake and exercise performance [17]. Volek et al [18] observed a significant find more increase in strength performance after 12 weeks creatine supplementation with a concurrent periodized heavy resistance training protocol. The creatine supplementation

protocol consisted of a weeklong loading period of 25 g/d followed by a 5 g maintenance dose for the remainder of the training. These positive effects were attributed to an increased total creatine pool resulting in more rapid adenosine triphosphate (ATP) regeneration between resistance training sets allowing athletes to maintain a higher training intensity and improve the quality of the workouts along the entire see more training period. It is regularly reported that creatine supplementation, when combined with heavy resistance training leads to enhanced physical performance, fat free mass, and muscle morphology [18–22]. A 2003 meta analysis [8] showed individuals ingesting creatine, combined with resistance training, obtain on average +8% and +14% more performance on maximum (1RM) or endurance strength (maximal repetitions at a given percent of 1RM) respectively than the placebo groups. However, contradicting studies have reported no effects of creatine supplementation on strength performance. Jakobi et al

[23] found no effects of a short term creatine loading protocol upon isometric elbow flexion force, muscle activation, and recovery process. However, this study did not clearly state if creatine CYTH4 supplementation was administered concurrent with resistance training. Bemben et al [24] have shown no additional benefits of creatine alone or combined with whey protein for improving strength and muscle mass after a progressive 14 weeks (3 days per week) resistance training program in older men. These conflicting results can be explained by the possibility that the supplemented groups were formed by a greater amount of non-responders or even because creatine supplementation was administered on the training days only (3 times a week). This strategy has not been adequately tested as effective in middle aged and older men for maintaining post loading elevated creatine stores [5].

This process was carefully observed to prevent any loss of potentially discriminatory peaks at both ends of the derivative curves. To prevent excessive simplification and loss of informative data, smoothing was performed only if it undoubtedly resulted in a distinct amelioration of peaks’ discrimination. Electrophoresis and analysis of banding patterns After melting analysis was performed, each sample was also subjected to gel electrophoresis in 2% agarose gel at 5 V/cm for 3 hours. The gels were stained by ethidium bromide

VRT752271 research buy added into them during preparation at the final concentration of 1 μg/ml and resulting banding patterns were photographed. Comparison of fingerprints was performed using GelCompar II software (Applied Maths, Sint-Martens-Latem, Belgium) applying the Jaccard coefficient at 1.5% positioning tolerance. Dendrograms were constructed using the UPGMA algorithm. Acknowledgements Ministry of Health (NR8365-4/2005), Czech Republic, supported this work. Dr. Mine Yücesoy

from Dokuz Eylül University, Izmir, Turkey and Dr. Jozef Nosek from Comenius University in Bratislava, Slovakia kindly gifted this website some of the strains. Technical assistance of Mrs. Jana Novotna, Mrs. Jitka Cankarova, and Mrs. Ivana Dosedelova is highly acknowledged. Electronic supplementary material Additional file 1: Similarity coefficients. Listing of similarity coefficients obtained upon automated comparison of normalized melting curves within each species. (XLS 250 KB) Additional file 2: Dendrogram of RAPD fingerprints. Dendrogram based on RAPD fingerprints of all strains included in the study. Analysis of RAPD fingerprinting patterns always provided accurate identification except for 2 strains showing quite unique fingerprints (marked by arrows). For comparison of strain clustering between conventional RAPD and McRAPD, the strains of different species are color-coded by ground tint colors and their specific McRAPD genotypes

are indicated by different saturation of colors. In case a strain was not assigned to a specific McRAPD genotype, it is not color-coded. (PNG 3 MB) Additional file 3: Average derivative curves. Plots of average McRAPD first negative derivative curves of species and genotypes included in the study. (XLS 1 MB) Additional file 4: Listing of clinical isolates and reference strains included in this study. (PDF 93 KB) References 1. Hobson RP: The Tyrosine-protein kinase BLK global epidemiology of invasive Candida infections – is the tide turning? J Hosp Infect 2003, 55:159–168. quiz 233CrossRefPubMed 2. Warnock DW: Trends in the epidemiology of invasive fungal infections. Nippon Ishinkin Gakkai Zasshi 2007, 48:1–12.CrossRefPubMed 3. Krcmery V, Barnes AJ: Non- albicans Candida spp. causing fungaemia: pathogenicity and antifungal resistance. J Hosp Infect 2002, 50:243–260.CrossRefPubMed 4. Freydiere AM, Guinet R, Boiron P: Yeast identification in the clinical microbiology laboratory: phenotypical methods. Med Mycol 2001, 39:9–33.PubMed 5.

For competition between 345-2RifC(RP1) and P1 or P2 agar contained ampicillin at 25 μg/ml. For competition between wild-type plasmids and CP-690550 price their respective host strains it contained ampicillin for RP1 carrying strains, and tetracycline for the pUB307 and N3 carrying strains. Six replicates of each competition experiment were performed. Average per generation fitness (W) was calculated as W = 1 – b, where b is equal to t he gradient of the graph

of ln(strain x count/strain y count) per transfer, divided by the number of generations per transfer (T). T was calculated as ln(dilution factor)/ln(2). The students t-test was used to estimate the statistical significance of results. Investigation of in vitro reversion to resistance The recovery of resistance by isolates with intact but silent RP1 encoded resistance genes was investigated by spreading undiluted and serially diluted overnight nutrient broth cultures onto IsoSensitest agar containing the appropriate antibiotic (ampicillin, 25 μg/ml; kanamycin 30 μg/ml; tetracycline, 25 μg/ml). To calculate reversion frequencies, total cell counts were obtained following plating serial dilutions of the same culture onto antibiotic-free medium. Animal experiments Animal experiments were carried out using a modified method of that described previously [24]. For each experiment, six organic piglets

from two litters of Saddleback-Duroc cross, weaned at five weeks of age, were housed as a single group for two weeks, to allow the animals to acclimatize to their AZD0156 mw surroundings. They were then randomly separated into two groups of three into pens with individual HEPA filtration and fed a standard organic feed (Organic feed company, grower/finisher pellets, UK) ad libitum. All procedures complied with the Animals (Scientific Procedures) Act 1986 and were performed under Home Office License. Briefly, bacterial strains (E. 5-FU coli 345-2RifC(pVE46), 345-2RifC(RP1), L5 and P1) were inoculated separately into six piglets as a single dose of 1010 cfu per animal by oral gavage. Faecal samples were collected from

each animal by digital manipulation on day 3, 5, 7, 10, 12, 14, 17, 19 and 21 post-inoculation and analysed within 24 hours. One gram of faeces was suspended in nine millilitres of saline and plated at appropriate dilutions onto six MacConkey agar plates containing 50 μg/ml rifampicin (detection limit 2 cfu/g). They were incubated overnight at 37°C and colonies obtained replica plated onto MacConkey agar containing 50 μg/ml rifampicin with ampicillin (25 μg/ml), tetracycline (25 μg/ml), sulfamethoxazole (500 μg/ml) or streptomycin (25 μg/ml) for L5, and rifampicin with ampicillin, tetracycline or kanamycin (30 μg/ml) for P1, followed by replica plating onto MacConkey agar with rifampicin only. Nucleotide sequence accession number The N3 DNA sequence has been submitted to EMBL under the accession number FR850039.

pylori from the Chinese to the Malay population. Another potential source of H. pylori for non-aboriginal Malays is the Orang Asli population, who originated from early human migration out of Africa. The Orang Asli is likely to have taken the “”Southern Route”" into South East Asia to reach Malaysia by traveling along the Indian Ocean Coast line 50–65,000 years ago [31–33]. Therefore the Orang Asli H. pylori, if it exists, may share common ancestry with the Indian H. pylori, leading to the observed similarity of Malay isolates to Indian isolates. However given that other earlier

H. pylori populations such as the Maori and American Indian populations can be readily identified [12], one would expect that the Orang Asli H. pylori population would be unique and identifiable Epacadostat in vivo after such a long period of separation, arguing against acquisition from Orang Asli population and in favour of acquisition

learn more from the Indian population. Flow of H. pylori genes/genotypes among the Malaysian population and from other populations Apart from the Malay population who appear to have gained the majority of its H. pylori isolates from the Indian population as discussed above, there was also gene flow from other populations. In particular the Indian and Malay populations have higher levels of inflow of genes. Thirteen of the 51 (25.5%) Malaysian Indian/Malay isolates were found grouped with the hpEurope population: six isolates grouped with AE1 and seven with AE2 (Additional file 1). One Malay isolate was found to be grouped with hpAfrica1, and one Indian and one Malay isolates grouped with hspMaori. MycoClean Mycoplasma Removal Kit The Malaysian Chinese population seems to have little inflow of genes from other populations with the exception of one Chinese isolate which grouped with AE2. The low frequency of Chinese isolates with other population affinity indicates that this isolate was more likely to have been acquired by its current or most recent host directly from an AE2 H. pylori host. In contrast, the Indian/Malay isolates with ancestral European

history (Table 2) are more likely to represent greater heterogeneity in the Indian/Malay H. pylori population and not direct transmission of isolates from the current European population or from early British or Portuguese colonization as these strains have genes from the Indian H. pylori gene pool. These isolates contain 8% to 40% hspIndia genes based on STRUCTURE analysis. By population segregation sites, 14 segments with at least two PSSs identical to the Indian/Malay population were identified (data not shown). Three isolates have one identical (PSSs) allele (FD542i in atpA, FD550i in mutY, FD540i in ureI). In contrast, the only Chinese isolate (FD493c) with a European ancestry showed almost no signal of Indian or Chinese ancestry. Such a diversity of isolates in the Malaysian population is interesting and warrants further studies.

It was previously found that by controlling the initial size of the gold sulfide particles, the resonance shift can be correlated with a theoretical model that includes both quantum confinement and the resonance effects (the so-called surface plasmon resonance) [22]. Ultra-smooth

surfaces from template-stripping procedures can be also used for periodic structures preparation [23], which can induce effects of surface plasmon resonance. The behavior of annealed gold nanolayers prepared by evaporation is rather different. The peak of plasmon resonance can be found for the annealed samples of thicknesses up to 7 nm (see Figure 5). In addition, the shift of the peak of plasmon resonance towards higher wavelengths as described earlier [5] was observed. selleck chemicals The suppressed diffusion of the evaporated gold nanolayers during the annealing process may be the leading cause in the plasmon peak appearance. Figure 5 UV–vis spectra of gold structures evaporated on glass

– before (RT) and after annealing (annealing). The numbers of the curves are Au thicknesses in nanometers. The difference in absorbancies in extinction spectra of evaporated structures under RT and evaporated onto substrate heated to 300°C can be determined from Figure 6. The surface plasmon peak has been observed for the layer thickness up to 10 nm. The absolute value of the absorbance is higher in comparison to annealed structures, GM6001 which is probably caused by the changes in structure morphology, density

and size of Au clusters on the examined surface. The shift of the plasmon peak for lower thickness of Au was observed. This is probably caused by the interaction of gold nanoparticles, which may arise from a different mechanism of gold nanostructure growth when compared to the annealed one and when the layer is deposited on non-heated substrate. Figure 6 UV–vis spectra of gold structures evaporated on glass heated to 300°C (300°C). The numbers of the curves are Au thicknesses in nanometers. Surface plasmon resonance (SPR) can be described before as a collective oscillation of electrons in solid or liquid stimulated by incident light. The condition for the resonance appearance is established when the frequency of light photons matches the frequency of surface electrons oscillating against the restoring force of the positive nuclei. This effect when occurring in nanometer-sized structures is called localized surface plasmon resonance. Surface plasmons have been used to enhance the surface sensitivity of several spectroscopic measurements including fluorescence, Raman scattering, and second harmonic generation. Also, SPR reflectivity measurements can be used to detect molecular adsorption, such as polymers, DNA or proteins, and molecular interaction studies [24]. The shift of the curves in extinction spectra can be explained by the coupling of the electromagnetic field between surface plasmons excited in gold nanoparticles of different densities and sizes.

The majority of trials (24)[9, 12, 13, 15–18, 25, 27, 29, 30, 32, 34–36, 40, 46, 47, 49–54] included patients with stage II or more advanced cancers. Additional file 1 displays the study characteristics and formulations along with the TCM philosophy for the preparation. All studies employed transcatheter arterial chemoembolization (TACE) as adjunct therapy. No placebo was used as the control group in any study. TCM Interventions The TCM interventions identified in this study were principally combinations of different herbal medicines or animal/insect

extracts (Additional file EPZ-6438 research buy 1). A brief outline on the oncologic and immunologic pharmacology of the most commonly used ingredients is presented below. Astragalus Astragalus appears CB-839 mw to have a number of immunomodulatory properties [55–57]. Astragalus appears to have anti-tumour activity where its potentiates

LAK cell activity in vitro when used in combination with IL-2[58]. Astragalus appears to restore in vitro T-cell function, which is suppressed in cancer patients[59]. Panax ginseng Panax ginseng and its chemical constituents were found to have inhibitory effects on putative carcinogenesis mechanisms, e.g., cell proliferation and apoptosis, immunosurveillance and angiogenesis[60]. Ginsenosides from Panax ginseng have been shown to inhibit tumor cell invasion and to suppress sister chromatid exchanges in human lymphocytes[61]. Toad skin secretions (bufotoxin) The toad skin secretion bufalin was found to induce apoptosis in human-leukemia cells by altering expression of apoptotic genes c-myc and bcl-2[62]. Other toad skin secretions like 3-formyloxyresibufogenin, 19-oxobufalin, 19-oxodesacetylcinobufagin, 6-hydroxycinobufagin and 1-hydroxybufalin were found to exert inhibitory effects on KB, HL-60 and MH-60 cancer cell lines[63]. Beetle extracts (Mylabris) An extract from Mylabris phaleratais, the dried body of the Chinese blister beetle, was shown to have anti-cancer activity via inducing cancer cell apoptosis and was associated with little toxicity[64].

Atractylodes Atractylodes appears to have anticancer activity by inducing apoptosis and cytotoxic effects against leukemia and other cancer cell lines[65]. Bupleurum Saikosaponins from Bupleurum falcatum were shown to exhibit Clomifene potent anti-cell adhesive activity on solid tumour cells and to have strong hemolytic action[66]. Curcuma Curcuma longa may have immunostimulatory activity[67]. Meta-analysis Complete Response We analyzed data from 37 trials[10, 12, 13, 15–18, 20, 21, 23, 25–30, 32, 33, 35, 36, 38–41, 44–54, 68, 69] reporting on RECIST CR score. Our pooled analysis indicates an RR of 1.26 (95 CI, 1.04–1.52, P = 0.01, I2 = 0%, P = 0.99). See figure 2. Applying meta-regression, we found that products containing ginseng, astragalus and mylabris had a larger treatment effect (OR 1.34, 95% CI, 1.04–1.71, P = 0.01) than the pooled broad estimate and that any product containing astragalus also had this effect (OR 1.35, 95% CI, 1.001–1.80. P = 0.048).

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