Sigma-2 receptor ligands that have been investigated for efficacy in the treatment of cancer induce apoptosis in caspase-3 dependent and independent manners, but the exact mechanism of AZD4547 in vivo cell death is still not well characterized. For example, in SK-N-SH neuroblastoma cells caspase-3 was not activated by CB-64D [11], nor did caspase inhibitors afford protection against cell death in MCF-7 breast cancer cells [12]. Caspase-3 is however activated in MCF-7 [13] and in murine pancreatic adenocarcinoma Panc02cells [10] bysiramesine, though caspase-3 inhibitor did not rescue

viability in either case. With another compound, PB28, no caspase-3 activity was observed in MCF-7 [14] or SK-N-SH cells [15]. Thus, while various sigma-2 receptor ligands are capable of inducing apoptosis in tumor cells, the activation of caspase-3 and upstream signaling events leading to this appear to be specific to particular ligand and cell type. In this study, we sought to more closely study the apoptotic

pathway induced by a number of structurally distinct sigma-2 receptor ligands in pancreatic cancer, which have proven efficacious in preclincal models. With knowledge of chemotherapy resistance to apoptotic stimuli depending on different Selleck Caspase inhibitor mechanisms, we may more appopriately choose effective therapies. Results Structurally distinct sigma-2 receptor ligands inhibit growth of pancreatic Palbociclib ic50 cancer Multiple structurally distinct compounds (Figure 1) with high affinity for sigma-2 receptors were tested for cytotoxicity against multiple pancreatic cancer check details cell lines in vitro (Table1) and screened for efficacy in a mouse model of pancreatic cancer with Panc02 cells (Additional file 1: figure S1). Compounds were further tested in athymic nude mice bearing human Bxpc3 subcutaneous tumorsand treated daily with equimolar doses of these sigma-2 receptor ligands. These mice with established

tumors were treated for eleven days and compared to vehicle, SV119, SW43, PB28, and PB282 each significantly decreased tumor volume (Figure 2). Figure 1 Structures. Sigma-2 receptor ligands SW43 and SW120, derivatives of N-(9-(6-aminohexyl)-9-azabicyclo[3.3.1]nonan-3α-yl)-N-(2-methoxy-5-methylphenyl) carbamate hydrochloride (SV119), and PB282 and PB385, derivatives of 1-cyclohexyl-4-[3-(5-methoxy-1,2,3,4-tetrahydro-naphthalen-1-yl)propyl]-piperazine dihydrochloride (PB28). Affinity to sigma-1/2 (σ2) receptor given by Ki (nM). Figure 2 In vivo efficacy of sigma-2 receptor ligands. Athymic nude mice inoculated subcutaneously with 1×106 Bxpc3 cells were treated daily with sigma-2 receptor ligands SV119, SW43, PB28, or PB282 when tumors reached an average of 5 mm in diameter. Data represents mean ± SEM, n = 7–10 per group, * p < 0.05.

The oscillatory black curve shows coherent quantum beating of exciton 1. Figure reprinted with permission from Macmillan Publishers Ltd: Engel et al. (2007); Copyright 2007 The above 2D experiments illustrate that key mechanistic information can be extracted from spectra selleck measured using identical input pulses. Experimental strategies involving different polarizations

of the laser pulses may be used to probe an increased, or more specific, set of interactions. Such an approach SB202190 cell line is analogous to linear and circular dichroism methods in one-dimensional spectroscopy (see Garab and Van Amerongen, this issue), except with increased versatility as here four pulses can be independently controlled (Hochstrasser 2001; Zanni et al. 2001; Dreyer et al. 2003). The usefulness of rotating the pulse polarizations lies in the fact that in 2D spectra measured with parallel-polarized input pulses, diagonal peaks dominate the spectra (as evident in the T = 0

LH3 spectrum of Fig. 5), obscuring off-diagonal peaks that report on chromophore interactions. The first example of 2D electronic spectroscopy using polarization techniques to uncover weak signals was also in an application to the FMO complex (Read et al. 2007). Extending techniques applied in the infrared regime (Hochstrasser 2001; Zanni et al. 2001), the polarization sequence (60°, −60°, 0°, 0°) for pulses (1, 2, 3, LO) was used to completely eliminate the diagonal peaks from the spectrum of FMO from Pelodictyon phaeum (Fig. 7). Fig. 7 The cross peak specific 2D and conventional 2D electronic spectra for FMO from Pelodictyon phaeum. The cross-peak L-gulonolactone oxidase specific spectrum reveals off-diagonal features click here obscured by the diagonal peaks in the conventional 2D spectrum. Both spectra are colored using a nonlinear ArcSinh coloration to emphasize smaller features, and the cross-peak specific coloration is inverted to facilitate direct visual comparison of the cross peaks to those in the conventional 2D spectrum. Diagonal peaks (DP i ) are shown with squares while cross peaks (CP ij ) are denoted with circles. The shape of the edge

of the cross peak regions agrees between the spectra, but significant additional structure is visible in the cross peak specific spectrum. Figure from Read et al. (2007); Copyright 2007, National Academy of Sciences, USA In addition to highlighting otherwise weak features, polarization techniques can be used to report on structures of photosynthetic complexes. The amplitude of a cross peak in a 2D spectrum, and the way that the amplitude changes with input pulse polarization, depends in part on the relative orientation between the coupled transition dipoles. In a measurement on the FMO complex from Prosthecochloris aestuarii using one set of pulse polarizations, a cross peak is only weakly visible in the spectrum at 400 fs (Fig. 8 (45°, −45°, 0°, 0°) spectrum), while under another polarization scheme (Fig. 8 (75°, −75°, 0°, 0°) spectrum) the cross peak appears strongly (Read et al. 2008).

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Table 2 Results from the Wingate test for judoists changes during their preparation period (mean ± SD, Median)   Pre Post RTW (J·kg-1) 285.6 ±

17.98; 283.1 283.3 ± 17.4; 286.7 C 294.9 ± 17.42; 296.4 284.1 ± 17.4; 280.8 T 276.3 ± 14.44; 270.4 282.5 ± 19.4; 292.4 RPP (W·kg-1) 12.28 ± 0.85; 12.02 12.52 ± 0.59; 12.76 C 12.17 ± 0.88; 12.04 12.12 ± 0.60; 11.98 FI (%) 46.33 ± 6.23; 44.40 44.83 ± 5.63; 44.55 C 43.42 ± 5.31; 43.28 40.99 ± 2.99; 40.39* T 49.23 ± 6.17; 51.61 48.67 ± 5.06; 46.10 toPP (s) 3.99 ± 0.71; 4.20 3.68 ± 0.77; 3.78# C 4.29 ± 0.28; 4.35 3.94 ± 0.52; 3.81 T 3.69 ± 0.92; 4.01 3.42 ± 0.95; 3.31 tuPP (s) 3.30 ± 0.93; 3.35 3.13 ± 0.55; 3.09 C 3.38 ± 0.64; 3.26 3.30 ± 0.51; 3.41 T 3.22 ± 1.24; 3.44 2.96 ± 0.60; 3.33 La (mmol·l-1) 14.35 ± 1.34; Small molecule library 4.31 14.73 ± 1.05; 15.08 C 14.44 ± 1.39; 14.61 14.99 ± 1.15;

15.28 T 14.26 ± 1.44; 14.01 14.47 Tipifarnib research buy ± 1.00; 14.25 *differences T from C, #difference Post from Pre. Table 3 Indices which characterize aerobic power in judoists during their preparation period (mean ± SD; Median)   Pre Post VO2max (ml·kg-1·min-1) 59.04 ± 7.26; 61.1 58.49 ± 5.75; 58.7 C 63.98 ± 2.64; 63.4* 62.80 ± 4.23; 61.8* T 54.1 ± 7.10; 54.2 54.18 ± 3.16; 53.6 HRmax (bpm) 194.2 ± 10.6; 197 193.8 ± 9.31; 195 C 196.6 ± 8.44; 198 195.8 ± 11.19; 200 T 191.8 ± 12.93; 197 191.8 ± 7.73; 194 HRTDMA (bpm) 167.4 ± 6.04; 166 163.8 ± 11.49; 163 C 168.6 ± 7.83. C-X-C chemokine receptor type 7 (CXCR-7) 170 166.0 ± 2.75; 165 T 166.2 ± 4.15; 165 161.6 ± 11.06; 162 %HRmax (%) 86.37 ± 4.33; 87.1 84.66 ± 6.28; 85.4 C 85.79 ± 2.94; 86.9 84.9 ± 6.35; 85.9 T 86.94 ± 5.72; 87.3 84.42 ± 6.95; 84.8 %VO2max (%) 80.58 ± 10.59; 79.2 80.78 ± 6.88; 79.9

C 74.73 ± 5.03; 74.9 76.13 ± 3.48; 75.3* T 86.43 ± 11.89; 85.6 85.43 ± 6.35; 85.5 La (mmol·l-1) 11.65 ± 1.34; 12.0 12.39 ± 1.98; 11.6 C 11.43 ± 1.60; 11.8 10.39 ± 1.52; 12.4 T 11.86 ± 1.16; 12.2 11.39 ± 2.00; 11.2 *differences T from C, #difference Post from Pre. Mann–Whitney U test in the second measurement revealed no significant differences between medians of groups T and C in BM, indices of body build and composition, whereas in the first measurement a significant difference was learn more noticed only at FFM (Z = 2.09, P < 0.05).

CrossRef 37. Heczko U, Abe A, Brett Finlay B: Segmented Filamentous Bacteria Prevent Colonization of Enteropathogenic Escherichia coliO103 in Rabbits. J Infect Dis 2000,181(3):1027–1033.PubMedCrossRef 38. Kuehl CJ, Wood HD, Marsh TL, Schmidt TM, Young VB: Colonization of the cecal mucosa by Helicobacter hepaticusimpacts the diversity of the indigenous microbiota. Infect Immun 2005,73(10):6952–6961.PubMedCrossRef 39. Prakash S, Rodes L, Coussa-Charley M, Tomaro-Duchesneau C: Gut microbiota: next frontier in understanding human health and development of biotherapeutics.

Biologics: Targets and Therapy 2011, 5:71–86.CrossRef 40. Johnson-Henry KC, Nadjafi M, Avitzur Y, Mitchell DJ, Ngan BY, Galindo-Mata E, Jones NL, Sherman PM: Amelioration of the ��-Nicotinamide in vivo effects of Citrobacter rodentium infection in mice by pretreatment with probiotics. J Infect Dis 2005,191(12):2106–2117.PubMedCrossRef 41. Bergstrom KS, Guttman JA, Rumi M, Ma C, Bouzari

S, Khan MA, Gibson DL, Vogl AW, Vallance BA: Cediranib chemical structure Modulation of intestinal goblet cell function during infection by an attaching and effacing bacterial pathogen. Infect Immun 2008,76(2):796–811.PubMedCrossRef 42. Gareau MG, Wine E, Rodrigues DM, Cho JH, Whary MT, Philpott DJ, Macqueen G, Sherman PM: Bacterial infection causes stress-induced memory dysfunction in mice. Gut 2011,60(3):307–317.PubMedCrossRef 43. McCune B, Grace JB: Analysis of ecological communities. MjM Software Design, Oregon, USA; 2002. Authors’ contributions DMR carried out in vivo work, western blotting and gelatin zymography. AJS carried out the microbiome analysis. LV and SAK conducted the immunocytochemistry. click here DMR, AJS, SPH, LV, MGG, SAK, KCJH, and PMS conceived of the study, Carbohydrate participated in its design and coordination and writing of the manuscript. All authors read and approved the final manuscript.”
“Background Methicillin-resistant Staphylococcus aureus (MRSA)

are versatile and highly adaptive bacteria that are a major cause of hospital-associated (HA) infections, and are emerging to be a common cause of community-associated (CA) and livestock-associated (LA) infections. Resistance to every antibiotic commonly prescribed is reported, and therefore the treatment and control of MRSA populations is difficult; this is of global concern. Resistance and virulence genes are often carried on mobile genetic elements (MGEs), such as bacteriophage, plasmids and transposons [1, 2]. Dissemination of these genes through S. aureus populations by horizontal gene transfer (HGT) will lead to strains that are both more resistant and more virulent [1]. Plasmids carry a diverse range of antimicrobial and biocide resistance genes and can carry toxin genes [2–4]. Resistances to antimicrobial agents carried by S. aureus plasmids include aminoglycosides, β-lactams and macrolides. Recently, the sequencing of S.

41 protein at the cell surface in the heterologous host L. lactis (Figure 5c, red trace). This protein was absent at the surface of WT MG1363 (black

trace) and MG1363::pJRS525 transformant (green trace). Figure 5 Scl1 expression in L. lactis promotes biofilm formation. L. lactis was transformed with the plasmid construct pSL230 to express Scl1.41 surface protein or with pJRS525 vector. (a) PCR analysis of L. lactis transformants using scl1.41-gene-specific GW786034 primers; lanes: (1) MG1363 wild-type (WT) cells; (2) MG1363::pJRS525 vector-only control; (3) MG1363::pSL230 transformant; (4) control pSL230 plasmid DNA. (b) Scl1.41 expression by western blot analysis of cell-wall extracts prepared from transformed L. lactis and control GAS strains using anti- P176 (rScl1.41) antibodies; lanes: (1) purified recombinant P176 protein (truncated Scl1.41); (2) MG1363 WT strain; (3) MG1363::pJRS525 vector; (4) MG1363::pSL230 Lazertinib order transformant; (5) MGAS6183 (M41) control. (c) Analysis of Sc1.41 expression by flow cytometry with anti-P176 (rScl1.41) rabbit polyclonal antibodies on the surface

of MGAS1363 WT strain (black trace), MGAS1363::pJRS525 vector-only control (green trace) and MG1363:pSL230 transformant (red trace). (d) Crystal violet staining of 24 h biofilms formed by L. lactis WT strain, MG1363::pJRS525 vector-only control or MG1363::pSL230 transformant (top) with visual representation of the corresponding wells (bottom). Statistical significance is denoted as **P ≤ 0.001. (e) CLSM analysis of 24 h biofilms from same experiment shown in (d). Images are X-Y orthogonal Z-stack views representative of ten images within a single experiment. Average vertical biofilm thickness is indicated in micrometers (top right). The capacity of L. lactis expressing Scl1.41 to form biofilm was evaluated spectrophotometrically following crystal violet staining. As shown in Figure 5d, the MG1363::pSL230

transformant demonstrated a significant increase in NCT-501 biofilm-associated biomass at 24 h, as compared to wild type L. lactis or L. lactis-containing pJRS525 vector (P ≤ 0.001). Crystal violet stained wells PD184352 (CI-1040) were photographed for visual representation of biofilm formation prior to spectrophotometric assay. Biofilm thickness and architecture were evaluated by CLSM (Figure 5e; Additional file 1: Figure S2a-c). The MG1363::pSL230 transformant produced a substantially thicker biofilm (14 μm) as compared to both MG1363 WT (6 μm) and the vector-only transformant MG1363::pJRS525 (6 μm). The MG1363::pSL230 cells formed highly aggregated structures, thus, acquiring a phenotype consistent with biofilm formation. As shown in Table 2, the MG1363::pSL230 transformant, expressing Scl1.41 surface protein, had significantly enhanced cell surface hydrophobicity (hydrophobicity index of ~137% vs. 100% WT, P ≤ 0.001) with an actual value of 82.0 ± 2.6, when compared to the MG1363 WT (59.7 ± 7.2) and the vector-only MGAS1363::pJRS525 control (56.6 ± 5.5).

The historic 027 isolate CD196 exhibits a similar level of tolerance to strain 630 [18]. This increase in tolerance to www.selleckchem.com/products/brigatinib-ap26113.html p-cresol in the modern hypervirulent 027 isolates may be linked to increased virulence. In addition, the hypervirulent PCR-ribotype 027 strain has a higher capacity to convert tyrosine to p-HPA resulting in a higher overall yield of p-cresol. Analysis of the decarboxylase mutants revealed that although

C. difficile can tolerate p-cresol, high selleck products levels have a deleterious effect on the growth rate of C. difficile, as the mutants grow better in-vitro than their respective parent strains. Although it is evident that the 027 ribotype R20291 is more tolerant to p-cresol and produces significantly more p-cresol

than other strains, the mechanism of tolerance to p-cresol does not appear to be linked to its production. These results indicate that there is an intricate balance between optimal p-cresol production buy C646 and deleterious effects on growth. Conclusions The hypervirulent R20291 strain produces high levels of p-cresol, and has an elevated tolerance, which may contribute to the colonisation and dissemination of the 027 clonal lineage by providing a selective advantage. There is a delicate interplay between relative p-cresol production and growth rate, whereby R20291 may have reached an advantageous compromise. Materials and methods Bacterial strains and culture C. difficile strains used in this study were 630, 630Δerm and R20291. Strain 630, PCR-ribotype 012, was originally isolated from a patient with severe PMC in Zurich, Switzerland in 1982. 630Δerm is an erythromycin sensitive strain that was isolated after passage of the original sequenced strain 630 [19]. Erythromycin sensitivity is required Rutecarpine for the construction of C. difficile

gene inactivation mutants. R20291, a hypervirulent PCR-ribotype 027 strain was isolated from an outbreak at Stoke Mandeville hospital in 2006 and was provided by Jon Brazier (Anaerobe reference laboratory, Cardiff, UK). Strains were stored at -80°C and were cultured on BHI Agar (Oxoid), supplemented with 0.05% L-cysteine and cycloserine/cefoxitin antibiotic supplement (Fluka) at the recommended concentrations for 1 to 2 days under anaerobic conditions, in a Modular Atmosphere Control System 500 (Don Whitney Scientific) at 37°C. Liquid cultures were grown in BHI broth (Oxiod) supplemented with 0.05% L-cysteine and cycloserine/cefoxitin antibiotic supplement (Fluka) with and without 0.1% p-HPA (Sigma), or in yeast peptone (YP) broth, 16 gL-1 peptone (Sigma), 5 gL-1 yeast (Sigma), and 5 gL-1 NaCl2 (Sigma). E. coli strain CA434, the conjugation donor, was grown in Luria-Bertani (LB) broth or agar supplemented with 12.5 μg/ml chloramphenicol. Para-cresol tolerance assays Primary cultures were inoculated with three single colonies into pre-equilibrated media, shaking at 50 rpm on an orbital shaker. At an OD600 nm of 0.3-0.

To maintain telomere length of telomerase is necessarily to indefinite proliferation of human cells. The

human telomerase complex consists of human telomerase-associated this website RNA (hTR), providing the template for telomeric repeat synthesis, and human telomerase reverse transcriptase (hTERT), representing the catalytic subunit of the complex [22]. One Chinese study reported that hTERT mRNA positive expression was 96.6% (28/29) of ESCC, 48.9% (23/47) of dysplasia, and 7.5% (2/29) of Necrostatin-1 mouse normal tissues [23]. In our study, the positive rates of hTERT mRNA expression in peripheral blood mononuclear cells increased with the progressive stages of the esophageal carcinogenesis. However, it is clear that the positive expression rate of hTERT in peripheral blood mononuclear cells of the normal controls in our study is higher than that in the normal tissues of the above paper reported. Accordingly, Lord reported on higher hTERT levels in histological normal squamous esophagus tissues from cancer patients compared with hTERT levels VX-680 cell line found in normal esophageal tissues from patients with no cancer [24]. Most interestingly, results of the studies of esophagus adenocarcinoma also showed that hTERT not only expressed in all cancer tissues but also in all adjacent non-cancerous tissues. Moreover, the trend toward longer

telomeres with increasing depth of tumor invasion not only suggested for telomere lengths in cancer tissue but also for telomere Lengths in adjacent non-cancerous Barrett mucosa [25]. It is the first time report the positive rate of hTERT in peripheral blood mononuclear cells of the normal controls in our study. The mechanism is not clear. The main discovery in the present study was EYA4 mRNA

expression in peripheral blood mononuclear cells increased with the stages of progressive carcinogenesis of esophagus. Although the positive expression Florfenicol rates were relative low, using a positive cut-off value of 0.47, testing sensitivities were 4% and 16% for ESCD and ESCC, respectively, but the testing specificity increased to 100%, where no false positive cases were existed in the study. Because there was a low degree of correlation between hTERT and EYA4 mRNA expression in the present study, both of them were dependent biomarkers. The discriminating ability between positive and negative status with either hTERT or EYA4 is too low to predict the high-risk persons. In the study, we try to use the discriminating regression model to increase the power of predicting high-risk persons. Comparing with that in the discriminate models including independent variables of sex, age, smoking, drinking, family history of ESCC, in the model including the variables of hTERT, EYA4 and the five variables in the models increased the sensitivities and specificities of predicting ESCD and ESCC increased. This knowledge may be useful in identifying high-risk persons who need to take part in the endoscopic test.

Bladé J, Kyle RA: Nonsecretory myeloma, immunoglobulin D myeloma, and plasma cell leukemia. ematol Oncol Clin North Am 1999, 13:1259–1272.CrossRef 2. Jancelewicz Z, Takatsuki K, Sugai selleck inhibitor S, Pruzanski W: IgD multiple myeloma. Review of 133 cases. Arch Intern Med 1975, 135:87–93.www.selleckchem.com/products/nu7026.html PubMedCrossRef 3. Fibbe WE, Jansen J: Prognostic factors in IgD myeloma: study of 21 cases. Scand J Haematol 1984, 33:471–475.PubMedCrossRef 4. Bladé J, Lust JA, Kyle RA: Immunoglobulin D multiple myeloma presenting features response to therapy, and survival in a series of 53 cases. J Clin Oncol 1994, 12:2398–2404.PubMed 5. Sinclair D: IgD myeloma: clinical, biological and laboratory features. Clin Lab 2002, 48:617–622.PubMed 6. Shimamoto

Y, Anamy Y, Yamaguchi M: A new risk grouping for IgD myeloma based on analysis of 165 Japanese patients. Eur J Haematol 1991, 47:262–267.PubMedCrossRef 7. Bemelmans RH, van Toorn DW, van Leeuwen L, Schaar CG: Long-term complete remission in IgD-myeloma. Eur J Haematol 2006, 76:339–341.PubMedCrossRef 8. Bladé J, Kyle RA: IgD monoclonal gammopathy with long-term follow-up. Br J Haematol 1994, 88:395–396.PubMedCrossRef 9. Kyle RA: IgD multiple myeloma: a cure at 21 years.

Am J Hematol 1988, 29:41–43.PubMedCrossRef 10. Hiyoshi M, Hashimoto S, Ota T, Nakao T, Takubo T, Tagawa S, Tatsumi N: Long-term survival in a case of high-risk type IgD myeloma: a possibility JQ-EZ-05 ic50 of effectiveness of interferon-alpha and erythropoietin. Haematologia (Budapest) 1997, 28:177–180. 11. Wechalekar

A, Amato D, Chen C, Keith SA, Reece D: IgD multiple myeloma- a clinical profile and outcome with chemotherapy and autologous stem cell transplantation. Ann Hematol 2005, 84:115–117.PubMedCrossRef 12. Sharma M, Qureshi SR, Champlin RE, Popat U, Giralt S, Qazilbash MH: The outcome of IgD myeloma after autologous hematopoietic stem cell transplantation is similar to other oxyclozanide Ig subtypes. Am J Hematol 2010, 85:502–504.PubMedCrossRef 13. Maisnar V, Hájek R, Ščudla V, Gregora E, Büchler T, Tichý M, Kotouček P, Bláha V, Malý J: High-dose chemotherapy followed by autologous stem cell transplantation changes prognosis of IgD multiple myeloma. Bone Marrow transplantation 2008, 41:51–54.PubMedCrossRef 14. Reece DE, Vesole DH, Shrestha S, Zhang MJ, Pérez WS, Dispensieri A, Milone GA, Abidi M, Atkins H, Bashey A, Bredenson CN, Boza WB, Freytes CO, Gale RP, Gajewski JL, Gibson J, Hale GA, Kumar S, Kyle RA, Lazarus HM, Mccarthy PL, Pavlovsky S, Roy V, Weisdorf DJ, Wiernik PH, Hart PN: Outcome of patients with IgD and IgM multiple myeloma undergoing autologous hematopoietic stem cell transplantation: a retrospective CIBMTR study. Clin Lymphoma myeloma Leuk 2010, 10:458–463.PubMedCrossRef 15. Morris C, Drake M, Apperly MJ, Iacobelli S, van Biezen A, Bjorkstrand B, Goldschmidt H, Harousseau JL, Morgan G, de Witte T, Niederwieser D, Gahrton G: Efficacy and outcome of autologous transplantation in rare myelomas. Haematologica 2010, 95:2126–2133.PubMedCrossRef 16.

Bolivia, located in the center of South America, includes representative examples of most major terrestrial biomes present on this continent, ranging from tropical rainforest to thorny Chaco scrub and the arid Puna of the high Andes (Ibisch et al. 2003) (Fig. 1). It is an important center for the origin of domestic plant species and of wild

relatives of many important food plants, such as potatoes (Solanum spp.), groundnuts (Arachis spp.), cassava (Manihot esculenta), beans (Phaseolus spp.), and hot peppers (Capsicum spp.) (Beck 1998). Fig. 1 Map Staurosporine datasheet of Bolivia showing the distribution of the ten major ecoregions modified after Ibisch et al. (2003) and the study sites (white dots). AM amazonian rain forest, BSI seasonally

deciduous inter-Andean forest, BSC seasonally deciduous Chiquitano forest, BTB subtropical Tucumano-Boliviano forest, CE Cerrado of the Brazilian shield, CHS seasonally deciduous montane Chaco forest, GCH Gran Chaco thorn forest, PN humid northern Puna, SB seasonally flooded savanna, and YU humid montane Yungas forest The rural population in many parts of the country still actively BIBW2992 price uses the natural flora as sources of human and animal foods, medicines, construction materials, and fibers. Therefore, much information on the potential uses of many native species can be gathered (Boom 1987). Phosphatidylinositol diacylglycerol-lyase Bolivia has about 135 species of Araceae (Kessler and Croat 1999; Croat and Acebey 2005) and approximately 323 species of selleck screening library Bromeliaceae (Krömer et al. 1999; Krömer, unpublished data). Compared to other plant groups, both families have a good status of knowledge in Bolivia due to intensive research on their distribution, diversity, and ecology in recent decades (Ibisch 1996; Bach et al. 1999; Ibisch and Vásquez 2000; Kessler and Krömer 2000; Acebey and Krömer 2001; Kessler 2001, 2002; Krömer et al. 2005, 2006, 2007). The aim of this study was to gather information on the potential use of species of Araceae and Bromeliaceae in Bolivia for the different ecoregional units of the country. The underlying question

was how the potentially useful species of these plant families are distributed in different ecosystems, as a guideline for the prioritization of regional activities aimed at developing their economically and ecologically sustainable use. Because the major ecoregions differentiated here occur throughout the Neotropics, this study is of relevance for the entire continent. Materials and methods A thorough literature search, including numerous unpublished reports, was conducted to compile information on past and current uses of the native species of Araceae and Bromeliaceae in Bolivia, as well as for other neotropical countries (Acebey 2003). A full list of references is available from the first author on request.