Indeed, in a large virulence plasmid of Shigella flexnery, an ast

Indeed, in a large virulence plasmid of Shigella flexnery, an astonishing 153 (53%) ORFs are related to known and putative IS elements; no known bacterial plasmid has been described previously with such a high proportion of IS elements, and four new IS elements have been definitively identified (Venkatesan et al., 2001). Additionally, metagenomic sequencing has yielded a flood of bacterial genome data that confirm the presence of increasing numbers of mobile elements in all analyzed bacterial genomes. This has naturally led to the development of evolutionary studies where consistent IS annotation across many different genomes has become necessary, and several

alternatives are now available for comparison and enhanced understanding of their evolutionary AZD2014 and functional roles (Siguier et al., 2006; Wagner et al., 2007). Piscirickettsia salmonis

is the etiologic agent of salmonid rickettsial septicemia, or piscirickettsiosis (Fryer et al., 1990), which is an aggressive infectious disease that has affected salmonid fish since the late 1980s (Bravo & Campos, 1989; Graggero et al., 1995; Marshall et al., 2007). Piscirickettsia salmonis is a facultative intracellular Gram-negative bacterium (Mauel et al., 2008; selleck chemicals Mikalsen et al., 2008; Gómez et al., 2009) that was initially described as a Rickettsia-like Niclosamide obligate intracellular Alphaproteobacteria. Recently, it was reclassified

as a Gammaproteobacteria that closely resembles Legionella and Francisella species (Fryer & Hedrick, 2003). This ambiguity misled researchers for more than a decade; therefore, its biology, epidemiology and genetics are almost totally unknown. Nevertheless, it is known that this bacterium persists in sea water (Olivares & Marshall, 2010), maintaining its infective potential under rough environmental conditions (Lannan & Fryer, 1994). This vitality suggests that its genetic background should be sufficiently versatile to adapt easily to changing stressful conditions. In fact, our laboratory has demonstrated that under limiting in vitro conditions, morphological and genetic changes are consistently observed (Rojas et al., 2008). Thus, the report of the first IS sequence in this genome strengthened the belief that the genome of P. salmonis might show a surprising degree of complexity and plasticity. As our laboratory can successfully grow this bacterium in liquid media (Gómez et al., 2009; E. González, F. Gómez, V. Henríquez, S. H. Marshall & C. Altamirano, unpublished data), based on increasing evidence of the adaptive potential of this bacterium (Rojas et al., 2008, 2009, 2010), we decided to evaluate the quality of the bacterial genome to determine whether the observed morphological changes and adaptability have a genetic background.

These cases were confirmed by serology at the Basel’s Swiss Tropi

These cases were confirmed by serology at the Basel’s Swiss Tropical Institute (Dr Hanspeter Marti, personal communication). Detailed epidemiological and clinical data of these patients are not available, but at least four of these cases were

diagnosed in immigrants from Africa, southeast Asia, and the Balkans. Reliable information on human Trichinella infection is not uniformly collected in Europe.1 In most European countries reporting BMN 673 of this infection is done on a voluntary basis and the information is fragmentary. In Germany, Italy, and Austria only the sylvatic cycle exists. Reliable epidemiological data from other Central European countries are PLX4032 supplier not available. Sporadic infections occur among people after consumption of wild boars. In Germany, the only country where trichinellosis is a reportable disease, in the period of 1996–2006, 95 human cases were diagnosed and 12 outbreaks were reported.6 The relationship between this parasitosis and displacement of the population is essential to characterize the dynamics of transmission

of the disease outside of endemic areas. In Switzerland, the foreign population constitutes 19% of the resident population and, since the 1970s, the percentage of immigrants from Eastern Europe has increased. More than 250,000 of these immigrants originate from the former Yugoslavia7 where Trichinella sp. infection is quite common in domestic pigs and wild animals.8 In nonendemic countries of Europe, trichinellosis has been documented in immigrants from endemic countries when they return home for holidays (Table 1).6,9,10–15 Furthermore, trichinellosis has been also documented in travelers else who visited endemic countries.16 In a study on eosinophilia among German tourists returning home from countries endemic for Trichinella sp. infection, Schulte et al.16 show that

1.2% of them were infected with Trichinella sp. This percentage is significantly higher among migrant populations from highly endemic areas visiting their relatives.6 Since the incubation period of trichinellosis can be highly variable (from few days up to 2–3 wk), the travel history is very important especially in nonendemic countries where physicians are not familiar with the clinical picture of trichinellosis. Furthermore, there are objective difficulties for migrants to access the health care system because of language barriers, cultural and legislative constraints.17 In addition to persons who acquire trichinellosis abroad and develop the disease at home, Trichinella sp. infections have also been documented among people of nonendemic countries who consumed infected meat (eg, pork from domestic pigs and wild boars, horse meat, bear meat) clandestinely imported from endemic countries as a gift to friends and relatives.

These cases were confirmed by serology at the Basel’s Swiss Tropi

These cases were confirmed by serology at the Basel’s Swiss Tropical Institute (Dr Hanspeter Marti, personal communication). Detailed epidemiological and clinical data of these patients are not available, but at least four of these cases were

diagnosed in immigrants from Africa, southeast Asia, and the Balkans. Reliable information on human Trichinella infection is not uniformly collected in Europe.1 In most European countries reporting mTOR inhibitor of this infection is done on a voluntary basis and the information is fragmentary. In Germany, Italy, and Austria only the sylvatic cycle exists. Reliable epidemiological data from other Central European countries are AZD9668 molecular weight not available. Sporadic infections occur among people after consumption of wild boars. In Germany, the only country where trichinellosis is a reportable disease, in the period of 1996–2006, 95 human cases were diagnosed and 12 outbreaks were reported.6 The relationship between this parasitosis and displacement of the population is essential to characterize the dynamics of transmission

of the disease outside of endemic areas. In Switzerland, the foreign population constitutes 19% of the resident population and, since the 1970s, the percentage of immigrants from Eastern Europe has increased. More than 250,000 of these immigrants originate from the former Yugoslavia7 where Trichinella sp. infection is quite common in domestic pigs and wild animals.8 In nonendemic countries of Europe, trichinellosis has been documented in immigrants from endemic countries when they return home for holidays (Table 1).6,9,10–15 Furthermore, trichinellosis has been also documented in travelers 3-mercaptopyruvate sulfurtransferase who visited endemic countries.16 In a study on eosinophilia among German tourists returning home from countries endemic for Trichinella sp. infection, Schulte et al.16 show that

1.2% of them were infected with Trichinella sp. This percentage is significantly higher among migrant populations from highly endemic areas visiting their relatives.6 Since the incubation period of trichinellosis can be highly variable (from few days up to 2–3 wk), the travel history is very important especially in nonendemic countries where physicians are not familiar with the clinical picture of trichinellosis. Furthermore, there are objective difficulties for migrants to access the health care system because of language barriers, cultural and legislative constraints.17 In addition to persons who acquire trichinellosis abroad and develop the disease at home, Trichinella sp. infections have also been documented among people of nonendemic countries who consumed infected meat (eg, pork from domestic pigs and wild boars, horse meat, bear meat) clandestinely imported from endemic countries as a gift to friends and relatives.

These cases were confirmed by serology at the Basel’s Swiss Tropi

These cases were confirmed by serology at the Basel’s Swiss Tropical Institute (Dr Hanspeter Marti, personal communication). Detailed epidemiological and clinical data of these patients are not available, but at least four of these cases were

diagnosed in immigrants from Africa, southeast Asia, and the Balkans. Reliable information on human Trichinella infection is not uniformly collected in Europe.1 In most European countries reporting see more of this infection is done on a voluntary basis and the information is fragmentary. In Germany, Italy, and Austria only the sylvatic cycle exists. Reliable epidemiological data from other Central European countries are Ponatinib price not available. Sporadic infections occur among people after consumption of wild boars. In Germany, the only country where trichinellosis is a reportable disease, in the period of 1996–2006, 95 human cases were diagnosed and 12 outbreaks were reported.6 The relationship between this parasitosis and displacement of the population is essential to characterize the dynamics of transmission

of the disease outside of endemic areas. In Switzerland, the foreign population constitutes 19% of the resident population and, since the 1970s, the percentage of immigrants from Eastern Europe has increased. More than 250,000 of these immigrants originate from the former Yugoslavia7 where Trichinella sp. infection is quite common in domestic pigs and wild animals.8 In nonendemic countries of Europe, trichinellosis has been documented in immigrants from endemic countries when they return home for holidays (Table 1).6,9,10–15 Furthermore, trichinellosis has been also documented in travelers anti-PD-1 antibody inhibitor who visited endemic countries.16 In a study on eosinophilia among German tourists returning home from countries endemic for Trichinella sp. infection, Schulte et al.16 show that

1.2% of them were infected with Trichinella sp. This percentage is significantly higher among migrant populations from highly endemic areas visiting their relatives.6 Since the incubation period of trichinellosis can be highly variable (from few days up to 2–3 wk), the travel history is very important especially in nonendemic countries where physicians are not familiar with the clinical picture of trichinellosis. Furthermore, there are objective difficulties for migrants to access the health care system because of language barriers, cultural and legislative constraints.17 In addition to persons who acquire trichinellosis abroad and develop the disease at home, Trichinella sp. infections have also been documented among people of nonendemic countries who consumed infected meat (eg, pork from domestic pigs and wild boars, horse meat, bear meat) clandestinely imported from endemic countries as a gift to friends and relatives.

A univariate and a multivariate linear regression model were used

A univariate and a multivariate linear regression model were used to investigate factors RGFP966 correlated with ATV plasma concentration.

Receiver operating characteristic (ROC) curves were used to identify a plasma ATV concentration cut-off predictive of virological response and toxicity. Predictors of virological outcome were investigated using a logistic regression model: variables significantly associated with virological response in univariate analysis were subsequently evaluated in a multivariate model. Spearman correlation coefficients (r) were calculated to evaluate the correlation between ATV concentration and bilirubin levels. All analyses were performed using the spss version 13.0 software package (SPSS Inc., Chicago, IL, USA). A total of 115 plasma samples from 86 patients fulfilling the selection criteria were analysed. Baseline features of the studied population, also split according to the use of ritonavir boosting, are shown in Table 1. Groups of patients

taking boosted or unboosted ATV differed for time since ATV initiation [median 11 months (interquartile range (IQR) 5–20 months) vs. 7 months (IQR 2–12 months), respectively; P=0.041] and concomitant tenofovir use (87.9 vs. 25%, respectively; P<0.001). A MK-1775 mw genotypic resistance test was available in 49 patients (57%); the median interval between the genotypic resistance test and drug measurement was 30 months (IQR 16–42 months). ATV plasma concentrations showed high inter-individual variability both globally and in ritonavir-boosted or unboosted regimens (CV 83.1, 71.4 and 86.5%, respectively) (Fig. 1). Overall, the median ATV plasma concentration was 1.50 mg/L

(IQR 0.70–2.30 mg/L); it was higher in samples obtained from patients taking boosted regimens [1.91 mg/L (IQR 1.20–2.81 mg/L) vs. 1.00 mg/L (IQR 0.22–1.34 mg/L) for unboosted regimens; P<0.001] and not concomitantly receiving acid-reducing agents [1.64 mg/L (IQR 0.87–2.46 mg/L) vs. 0.28 mg/L (IQR 0.16–1.00 mg/L) in those receiving acid-reducing L-gulonolactone oxidase agents; P=0.007]. There were no significant differences in median ATV concentration between patients whose prescribed combination regimens contained tenofovir and those whose regimens did not [1.80 mg/L (IQR 0.90–2.57) for regimens containing tenofovir vs. 1.24 mg/L (IQR 0.38–2.00) for regimens not containing tenofovir; P=0.065]. However, when we considered only the subgroup of patients receiving unboosted ATV, median ATV concentration was lower when tenofovir was coadministered [0.22 mg/L (IQR 0.04–0.80 mg/L) vs. 1.07 mg/L (0.38–1.55 mg/L) when tenofovir was not coadministered; P=0.024]. When patients with ritonavir boosting were considered, no significant difference in ATV concentration was observed between those concomitantly receiving tenofovir and those not receiving tenofovir [median concentration 1.86 mg/L (IQR 1.20–2.81 mg/L) for those receiving tenofovir vs. 2.18 mg/L (IQR 0.59–3.19 mg/L) for those not receiving tenofovir; P=0.748].

Esherichia coli RNase III that is encoded by the rnc gene recogni

Esherichia coli RNase III that is encoded by the rnc gene recognizes its substrates through specific structural and sequence features (reactivity epitopes) that are Opaganib concentration contained within a double-helical structure of at least one full turn (11 bp), a primary reactive epitope (Dunn, 1982; Robertson, 1982; Court, 1993; Nicholson, 1999, 2003). Internal loops or bulges in the helix can limit the cleavage

of a target site to a single phosphodiester (Robertson, 1982; Court, 1993; Nicholson, 1999). In addition, a bulge–helix–bulge motif has been identified that allows binding of E. coli RNase III, but inhibits cleavage (Calin-Jageman & Nicholson, 2003). While a number of identified bacterial RNase III substrates

have no sequence conservation as positive recognition determinants, it has been proposed that specific base pair sequences can be excluded from two discrete double-helical segments, termed the proximal box (pb) and the distal box (db) (Zhang & Nicholson, 1997). Introduction of one or more of the excluded base pairs into either box within a model substrate inhibits RNA binding by E. coli RNase III (Zhang & Nicholson, 1997). Based on these findings, it was proposed that reactive E. coli RNase III sites are identified by the absence of inhibitory base pairs within the pb and db (Zhang & Nicholson, 1997; Nicholson, 1999). While positive sequence recognition determinants for

cleavage site selection check details by RNase III are not known, nonetheless, such elements Montelukast Sodium may exist and may be common features of the diverse substrates for bacterial RNases III, which have not yet been discovered. In this study, to investigate determinants for cleavage site selection by RNase III, we performed a genetic screen for mutant sequences at the RNase III cleavage sites present in bdm mRNA that resulted in altered RNase III cleavage activity using a transcriptional bdm′-′cat fusion construct (Sim et al., 2010). Based on analyses of the isolated mutant sequences that altered RNase III cleavage activity, we show that base compositions at scissile bond sites play an important role in both RNA-binding and cleavage activity of RNase III, which may explain the ability of bacterial RNase III to carry out site-specific cleavage of cellular RNA substrates despite its ability to degrade long double-stranded RNAs of broad sequence into short duplex products in a largely base pair sequence-independent manner under in vitro conditions (Xiao et al., 2009). DNA fragments containing random mutations at the cleavages sites 3 and 4-II in bdm mRNA (Sim et al., 2010) were amplified using overlap extension PCR, were digested with NcoI and NotI, and were cloned into the same sites in pBRS1 (Sim et al., 2010).

59 (039, 088)

59 (0.39, 0.88) EMD 1214063 and 0.52 (0.37, 0.72), respectively, after adjusting for age, gender and calendar year of starting HAART. When the effect of HBV or HCV coinfection on the probability of developing elevated levels of individual lipids was examined, HBV was found to have a stronger effect and HCV had a somewhat weaker effect than in the analysis classifying patients as HBV- or HCV-coinfected if they had a positive laboratory test

or a note in the medical chart. It was not possible to assess the effects of all individual antiretroviral medications in these analyses, as a consequence of the fact that the outcome was the occurrence of a grade 3 or 4 elevation in lipid measurements or use of lipid-lowering drugs at any time during follow-up and antiretroviral use changed over time. However, we did specifically assess the effects of ever having used tenofovir given the dual antiviral activity against HIV and HBV and of ever having used nevirapine given the relatively ‘lipid friendly’ characteristics of this medication. The proportions of participants who had ever used tenofovir was greater in HIV/HBV-coinfected patients (64%) compared with HIV-monoinfected patients (47%) (P<0.0001) but similar in HIV/HCV-coinfected individuals (51%) compared with

monoinfected individuals (P=0.22). Tenofovir use was not associated with hyperlipidaemia or lipid-lowering drug use (unadjusted OR 1.05; 95% CI 0.88, 1.24; P=0.62). The proportions of participants who had ever used nevirapine was lower in HIV/HBV-coinfected patients (19%) compared with HIV-monoinfected patients (27%) (P=0.02) but similar in Crizotinib HIV/HCV-coinfected individuals (24%) compared with monoinfected individuals (P=0.27). Nevirapine use was associated with hyperlipidaemia or lipid-lowering drug use (adjusted OR 1.41; 95% CI 1.14, 1.74; P<0.01). Methocarbamol This may reflect a selection bias or the concurrent nucleosides administered with nevirapine. Other previously reported predictors remained unchanged

with the inclusion of nevirapine in our models. Chronic HCV infection has been associated with lower total and LDL cholesterol levels in patients with and without advanced liver disease [8–13,15]. Lower serum triglyceride and cholesterol levels have been reported in those with chronic HCV infection [16]. Our analysis suggests that this perturbation of the lipid profile extends to HAART-treated, HIV/HCV-coinfected patients. This is consistent with our previous work [8] and an analysis specifically focused on an HIV/HCV-coinfected Hispanic population [17]. HBV may have a much smaller effect on lipid profile. However, this effect was inconsistently demonstrated by our analysis. HIV/HCV coinfection was found to protect against grade 3 and 4 lipid events following the initiation of HAART. This effect was consistent over the entire period of evaluation.

After initiation of IL-6 therapy the patient was followed over ti

After initiation of IL-6 therapy the patient was followed over time to monitor the hemodynamic changes in pulmonary vasculature. Following treatment with Tocilizumab, the patient showed dramatic improvement in her clinical symptoms and remains in remission, through combination of tocilizumab (8 mg/kg), methotrexate and prednisone. Improvement of systemic symptoms, right heart catheterization (RHC) findings and the VECTRA-DA score served as a measure of treatment PXD101 order response. Tocilizumab has been effective in demonstrating marked improvement in both the clinical and laboratory parameters. Tocilizumab is an effective novel treatment for AOSD with PAH. This is

the first documented report of successful use of tocilizumab in AOSD patients presenting with PAH. Prospective comparative studies could help validate its efficacy and safety. “
“To assess parental stress levels of mothers of children with juvenile idiopathic arthritis (JIA) aged between 2–12 years and compare with those reported for other chronic childhood illnesses. Mothers of children aged between 2–12 years with

JIA were recruited from hospital-based outpatient clinics. Maternal stress was measured by using the Parenting Alectinib cell line Stress Index Long Form (PSI). The physician assessing the child completed an active joint count, a physician’s global assessment and recorded the C-reactive protein and/or erythrocyte sedimentation rate if one was clinically indicated. The mothers recruited had children with a mean age of 6 years. The mean total stress score of mothers of children with science JIA measured by the PSI was 235.4 (95% CI 218.5–252.3)

was greater than the mean total stress scores for mothers of normal children at 222.8 (95% CI 221.4–224.2). It was also greater than children with other chronic disorders such as insulin-dependent diabetes mellitus (IDDM), 218.1 (95% CI 204.7–231.6) and profound deafness, 221.7 (95% CI 206.4–237.0). One third of mothers had total PSI scores that were in the clinical range (Total PSI > 260), indicating a need for intervention. JIA should be regarded as a significant illness in which maternal stress is at least equivalent to that associated with the care of children with other chronic diseases of childhood. Juvenile idiopathic arthritis (JIA) is a chronic childhood illness characterized by inflammatory arthritis of one or more joints for at least 6 weeks in a child 16 years or younger.[1] The reported prevalence of JIA is as high as 1–2/1000,[2] with the disease being further classified into seven sub-types: oligoarticular, polyarticular rheumatoid factor positive and negative, systemic arthritis, enthesitis-related arthritis and psoriatic arthritis.

AOB were traditionally considered to be responsible for most ammo

AOB were traditionally considered to be responsible for most ammonia oxidation in natural environments, but AOA amoA genes are now known to be ubiquitous and to outnumber those of AOB in many environments, including soils MAPK Inhibitor Library nmr (Leininger et al., 2006), oceans (Wuchter et al., 2006), streams (Merbt et al., 2011) and alpine lakes (Auguet et al., 2011). Although AOA and AOB coexist in many ecosystems, differential sensitivities to pH (Nicol et al., 2008), temperature (Tourna et al., 2008) and ammonium concentration

(Martens-Habbena et al., 2009; Verhamme et al., 2011) appear to control their relative abundances and activities, suggesting distinct physiological adaptations for each group. Photoinhibition of ammonia oxidation has been investigated in laboratory cultures of AOB (e.g. Hooper & Terry, 1974, Guerrero & Jones, 1996a, b). Hyman & Arp (1992) found that light may completely inhibit nitrite production and de novo synthesis of ammonia monooxygenase is required after exposure of cultures to light, leading to suggestions that light may be responsible for the inhibition of nitrification in ocean surface waters (Horrigan et al., 1981), coastal areas (Olson, 1981), estuaries (Horrigan &

Springer, 1990) and eutrophic rivers (Lipschultz et al., 1985). The low availability of laboratory cultures has restricted physiological studies of photoinhibition in AOB and, particularly, AOA. This has prevented assessment of the role of light exposure in niche separation and distribution of AOA and AOB in natural environments. Recent observations of the distribution Panobinostat concentration of archaeal amoA genes in stream biofilms exposed to light and dark conditions (Merbt et al., 2011) and along a vertical profile in the Atlantic Ocean (Church et al., 2010) suggest, however, that AOA could also be sensitive to light and that sensitivity of AOA and AOB may differ. The aims of this study were to determine the effects of different light intensities on

bacterial and archaeal ammonia oxidation using several science laboratory cultures of AOA and AOB and to assess their potential to explain AOB and AOA differential distribution and activity in aquatic ecosystems. Photoinhibition of two AOB (Nitrosomonas europaea ATCC19718 and Nitrosospira multiformis ATCC25196) and two AOA (Nitrosopumilus maritimus and Nitrosotalea devanaterra) strains was investigated during growth in batch culture. Nitrosomonas europaea and N. multiformis were obtained from NCIMB (http://www.ncimb.com/). Nitrosopumilus maritimus and N. devanaterra were obtained from existing laboratory cultures (Könneke et al., 2005; Lehtovirta-Morley et al., 2011). All strains were grown aerobically in 100-ml quartz flasks containing 50 mL inorganic growth medium. AOB were grown in Skinner & Walker (1961) medium containing 1.78 mM ammonia sulphate, adjusted to pH 8.0 with Na2CO3 (5% w/v). Nitrosopumilus maritimus was grown in HEPES-buffered, synthetic medium (pH 7.

, 2002) However, regulatory studies of the atz were not performe

, 2002). However, regulatory studies of the atz were not performed for a decade, likely due to the remarkable resistance of the host strain to genetic manipulation (in addition to the remarkable instability of the pADP-1 plasmid). In recent years, the use of P. putida KT2442 as a surrogate host for in vivo gene expression analysis, along with in vitro tools, has led to an indepth understanding of the regulation of the atzR-atzDEF system. This work has been a source of new insights into the previously unexplored general

nitrogen control in learn more the genus Pseudomonas, and the molecular details of transcriptional regulation by the LTTR family. The intricacy of the regulation of the cyanuric acid degradative genes and its seamless integration in the bacterial physiology is in stark contrast to the apparently accidental and unregulated expression of the genes in the upper atrazine pathway, highlighting the notion that the atrazine-degradative Lenvatinib solubility dmso pathway is a patchwork assembly of newly acquired genes added to a pre-existing, mature pathway. We wish to thank Ana Belén Hervás, Inés Canosa, Manuel García-Jaramillo and Claudia Lucía Millán for their contribution to the atrazine degradation project.

Our work on the regulation of atrazine degradation has been supported by grants QLK3-CT-1999-00041 (European Union), BIO2004-01354 and BIO2007-63754 (Ministerio de Educación y Ciencia, Spain), and fellowships from the I3P (CSIC/Ministerio de Educación y Ciencia, Spain) and FPU (Ministerio de Educación y Cultura, Spain) programs, awarded to O.P. Inositol monophosphatase 1 and V.G.-G., respectively. “
“Clostridium difficile is the leading cause of bacterial antibiotic-associated diarrhoea in hospitals in the developed world. Despite this notoriety, the complex mechanisms employed by this pathogen to overcome innate host defences and induce fulminant disease are poorly understood. Various animal models have been used extensively for C. difficile research to study disease pathogenesis. Until recently, the most commonly used C. difficile disease model has utilised hamsters; however,

mouse and pig models have now been developed that unravel different aspects of C. difficile pathology. This review summarises key aspects of the small animal models currently used in C. difficile studies with a specific focus on major differences between them. Furthermore, this review highlights the advantages and disadvantages of each model and illustrates that careful consideration is required when selecting models for use in C. difficile research. “
“A defence response can be induced by nonpathogenic Fusarium oxysporum CS-20 in several crops, but the molecular mechanism has not been clearly demonstrated. In the present study, we analysed the defence mechanism of a susceptible cucumber cultivar (Cucumis sativus L. 9930) against a pathogen (F. oxysporum f. sp. cucumerinum) through the root precolonization of CS-20.