Overall, (1) low quantities of soil-derived N in combination with

Overall, (1) low quantities of soil-derived N in combination with (2) high contents of easy available N result in rapid plant litter decomposition of L. corniculatus compared with C. epigejos due to (3) high C/N ratios and hence lower microbial degradation of C. epigejos. The application of plant

litter resulted in a significant stimulation (P<0.05) of the total microbial biomass in all treatments, irrespective of the method used (Fig. 2a and b). The highest biomass values were found in the L. corniculatus treatments 4 weeks after litter application. Surprisingly, microbial biomass at later sampling times decreased in L. corniculatus treatments and was not significantly different from that of C. epigejos. The relative content of litter-derived 13C in the microbial biomass followed the same trend. The results of the present study agree with the findings of recent EPZ-6438 chemical structure studies, which postulated

a stimulation of the microbial biomass as a result of the fast decomposition of attractive and easily available C (Xiao et Autophagy activator al., 2007; Poll et al., 2008; Jin et al., 2010). In the L. corniculatus treatment, within 4 weeks, the available plant litter nutrients were incorporated by the soil microbial biomass, whereas higher amounts of available compounds in L. corniculatus can be directly linked to a higher stimulation of the soil microbial biomass due to the increased 13C incorporation. After 12 weeks of incubation,

a decline in microbial biomass in the L. corniculatus treatment indicated a second phase in the litter much decomposition process. This process could be characterized by an increasing complexity of the available substrate, causing a shift in the microbial community structure towards slow-growing k-strategists in a community that was initially dominated by fast-growing r-strategists (Poll et al., 2008). In C. epigejos treatments, the slightly increased contents of total PLFA and the corresponding litter-derived 13C proportions at the 4-week sampling time indicated the use of easily available litter compounds; however, the maximum measured was significantly lower compared with L. corniculatus treatments. Overall, these results are in accordance with our hypothesis and show the important role of N in the microbial biomass during the decomposition process. A PCA (Fig. 3) based on individual PLFA mol% (Table S1) indicated that the litter type applied had a clear influence on the structure of microbial litter degraders. After 4 weeks, a small shift along PC1 occurred, mainly as a result of the high proportions of fungi (18:2ω6,9 and 18:3) in both litter treatments. This finding was in accordance with Poll et al. (2008), who found that an increase in fungi was detected between 2 and 4 weeks after litter application, based on ergosterol measurements.

, 1985), different virulence factors (Mekalanos,

, 1985), different virulence factors (Mekalanos, MAPK Inhibitor Library 1992; Bajaj et al., 1996) and several other genes (Weber et al., 2006; Gunasekera et al., 2008). Hitherto, most of the well-characterized osmoregulated genes correspond to genes that are upregulated following an osmotic upshift (Cairney et al., 1985; Han et al., 2005; Weber et al., 2006; Gunasekera et al., 2008). Nevertheless, adaptation

to low-osmolarity conditions must also result in regulation of genes that are specifically required to cope with these conditions. In this work we designed a genetic strategy focused on identifying genes that are optimally expressed at low osmolarity in Salmonella enterica serovar Typhimurium (S. Typhimurium). We report here the identification of a novel LysR-type transcriptional regulator (LTTR) that shows osmolarity-dependent expression. Bacterial strains, plasmids and phages used are listed in Table 1. Cells were routinely grown in Luria–Bertani (LB) medium. For some experiments, LB was modified by adding NaCl up to 0.5 M (LB 0.5 M NaCl) or by not including NaCl (LB 0 M NaCl). When required, X-Gal (40 μg mL−1) was added to the culture medium. Antibiotics were used at the following concentrations: kanamycin

(Km) 50 μg mL−1; ampicillin (Ap) 25 and 50 μg mL−1; tetracycline (Tc) 15 μg mL−1. The growth temperature was 37 °C unless noted otherwise. To obtain phage-free isolates, transductants were purified by streaking on EBU plates (LB agar MK-2206 research buy supplemented with 0.25% glucose, 0.25% KH2PO4, 12.5 mg L−1 Evans Blue and 25 mg L−1

fluorescein). Restriction digestion, ligation, transformation, agarose gel electrophoresis and DNA manipulations were performed using standard procedures. For plasmid DNA preparations, the Wizard® Plus SV Minipreps kit (Promega) was used. DNA was recovered GPX6 from agarose gels by electroelution or Qiaquick® gel extraction kit (Qiagen). The Wizard® Clean-Up System (Promega) was used for purification of DNA fragments. PCR experiments were performed in the Perkin Elmer GeneAmp PCR System 2400 according to standard protocols, using DynaZyme™ (Finnzyme). Oligonucleotides used are listed in Table 1. DNA sequencing reactions were carried out according to the instructions of the BigDye® Terminator v3.1 Cycle Sequencing Kit from Applied Biosystems. A lysate of P22HTint4 phage grown on S. Typhimurium strain TT10288 (hisD9953∷MudJ) was used to transduce strain TT1704, selecting Km resistance (Kmr). The recipient strain carried the nontransducible deletion his-9953, which avoids homologous recombination with MudJ from donor lysate. To identify the gene in which MudJ was inserted, Sau3A-partially digested TT1704-OS chromosomal DNA was ligated with BglII-digested cosmid pLA2917. The ligation was packed following instructions from Gigapack III (Stratagene) and used to infect E. coli HB101.

van de Fliert,

bedrijfsarts, reizigersgeneeskundige, DMCC

van de Fliert,

bedrijfsarts, reizigersgeneeskundige, DMCC, MPH, EMPH, CEMG, Cluster Public Health en Epidemiologie; Willeke P. J. Franken, Department of Infectious Diseases, Leiden University Medical Center, Leiden, the Netherlands; Dr Paul Jung, MD, MPH, Epidemiology Unit, Office of Medical Services, Peace Corps, Washington, DC; Dr Martin Tepper, Raf inhibitor drugs MD, CDCP, D FHP, Canadian Forces Health Services Group Headquarters, DND. The authors state that they have no conflicts of interest to declare. Data sources used provided only de-identified, aggregate information. This study was not undertaken on the behalf of the Department of the Army or the Department of Defense. The opinions or assertions contained herein are the private views of the authors and are not to be construed as official, or as reflecting the views of the Department of the Army or the Department of Defense. “
“1st Ed , (xiv) + 485 pp , hardcover, USD 167.00 , ISBN 978-1-405-18441-0 Enzalutamide . Wiley-Blackwell, Chichester, UK : Eli Schwartz , 2009 . With a record number of international tourist arrivals expected in 20101 and with a myriad of health and safety risks confronting travelers today, those health professionals in the frontline of travel medicine need access to a definitive reference textbook of tropical diseases.

The first edition of Tropical Diseases in Travelers is well positioned to respond to this challenge to inform both the pre-travel and post-travel health consultation.

The first edition of Tropical Diseases in Travelers has a dedication, a table of contents, a list of contributors, Gemcitabine a foreword by Alan Magill (ISTM President 2009–2011), acknowledgments, 43 chapters organized into three main parts, two appendices, and a comprehensive index. There are numerous tables and figures, including a dedicated section with 55 color plates (following p. 274). Major sections include “Part I: Tropical Diseases in Travelers—General Aspects” (six chapters), “Part II: Specific Infections” (29 chapters), and “Part III: Syndromic Approach” (eight chapters). There are two appendices, including “Appendix A: Drugs for Parasitic Infections” and “Section B: Laboratory Tests for Tropical Diseases.” Chapters are consistently presented and have references. Part I of Tropical Diseases in Travelers discusses general aspects of tropical diseases in travelers, which is basically the approach to the post-travel consultation in relation to infectious diseases. There are a number of highlights in part I, including the historical account of travel medicine a century ago, where an address on the “Diagnosis of Fever in Patients from the Tropics” by Sir Patrick Manson is reproduced in full. There are a number of authoritative chapters on important areas of travel medicine, such as “Travelers as Sentinels for Disease Occurrence in Destination Countries” (chapter 4) and “VFR Travelers” (chapter 5).

Skin samples of the injected areas were biopsied under local anes

Skin samples of the injected areas were biopsied under local anesthesia

12 and 24 h after injection. All of the animal experiments were approved by the animal research committee at Tokyo University of Agriculture and Technology. Formalin-fixed, paraffin-embedded skin samples were subjected to histopathological analysis. Frozen skin samples were subjected to immunofluorescence analysis for Dsg1 and Dsg3 using a human pemphigus foliaceus serum containing anti-Dsg1 IgG (Amagai et al., 1994, 1999; Ishii et al., 1997) and an AK15 mouse monoclonal antibody against Dsg3 (Tsunoda et al., 2003) (kind gifts from Dr Masayuki Amagai, Keio University School of Medicine, Tokyo, Japan), Ulixertinib respectively. The anti-Dsg1 IgG serum and the AK15 monoclonal antibody were detected with fluorescein isothiocyanate-conjugated goat anti-human IgG (MP Biomedicals, Solon, OH) and Alexa Fluor 546 goat anti-mouse IgG (Invitrogen Corp., Carlsbad, CA), respectively. Secreted forms of the recombinant proteins representing the entire extracellular domain of canine Dsg1 (cDsg1) and Dsg3 (cDsg3), fused with the hinge region of human IgG1, an E tag and a His tag at their carboxyl termini, were produced using the baculovirus-expression

system as described previously (Nishifuji et al., 2003a, b). Five insect cell DAPT nmr supernatants containing recombinant cDsg1 or cDsg3 were mixed with 10 μg of purified new ORF protein or PBS alone, and incubated at 37 °C for 12 h. Immunoblotting Ribonuclease T1 with rabbit anti-E-tag polyclonal antibody (Bethyl Laboratories, Montgomery, TX) was performed to detect intact and/or degraded cDsg proteins. PCR was performed with the primers 5′-gcggcatgcctaaaacatatgatgaagccgaa-3′ (forward primer) and 5′-tctctatttacattcagagag-3′ or 5′-tctggatccatcttctgattcagctctttttttcaaa-3′ (reverse primers) to amplify two partial regions of the orf gene. The PCR products were resolved by electrophoresis through a 1.2% (w/v) agarose gel,

and visualized by the application of the SYBR safe DNA gel stain (Invitrogen Corp.). Nucleotide sequence data obtained in this study are available in the DDBJ, EMBL and GenBank nucleotide sequence databases under accession number AB569087. During genome sequencing analysis of S. pseudintermedius strain MS5134, an orf with significant homology to a previously reported ET gene was identified. This orf consisted of 843 bp and was predicted to encode a protein of 279 amino acid residues, including a putative signal peptide in the first 32 amino acids (Fig. 1). The mature protein derived from an orf consisting of 247 amino acid residues with an N-terminal sequence beginning with KTYDEAEIIKK, and a predicted molecular weight and pI of 26.9 kDa and 5.86, respectively. The deduced amino acid sequence of the orf was compared with previously isolated ETs including S. aureus ETs (ETA, ETB and ETD), S.

8% and 587 ± 49% of ExPEC strain PCN033 were killed with hyperi

8% and 58.7 ± 4.9% of ExPEC strain PCN033 were killed with hyperimmune mouse sera against OmpC and OmpF, respectively. The results indicated that sera from both OmpC- and OmpF-immunized mice could mediate a significantly higher level of opsonophagocytic killing of ExPEC than sera from mice that received adjuvant

alone. The evidence for recombination signals was found in the E. coli ompC alignment by two programs, SBP and GARD, used for testing recombination. LY2157299 nmr Three potential recombination breakpoints with significant phylogenetic incongruence were identified at the nucleotide positions 492, 744 and 981 in the alignment of ompC. Four non-recombinant alignments together with the relevant trees of topological congruity were generated for the subsequent selection analysis. Based on the FEL inference, the selection profile of the ompC coding region is illustrated in Fig. 5a. The porin showed significant evidence for positive selection, with seven codon sites (47, 189, 223, 237, 322, 324 and 325) under positively selected force. Structural mapping of these sites is shown in Fig. 5b. According to the predicted topology of OmpC by pred-tmbb, all positively selected sites were located in the extracellular space and outer membrane surface. In addition, 48 negatively selected sites were detected at the 0.1 significance level. For ompF, two recombination

breakpoints were identified at the nucleotide positions 234 and 809 in the gene alignment. Notably, none of the positively selected sites was detected in the ompF gene through FEL inference. The E. coli genes ompC and ompF each encode an outer Romidepsin nmr membrane protein. OmpC has a narrower pore and is preferentially expressed under higher osmolar pressure compared with OmpF (Nikaido, 2003). OmpC and OmpF have both been functionally confirmed to be beta barrel porins (Basle et al., 2006), which are important Nabilone for

dynamic interactions with the host immune system (Massari et al., 2003). Additionally, OmpC and OmpF are involved in antibiotic resistance and bacterial virulence (Negm & Pistole, 1999; De et al., 2001; Kumar et al., 2010). In this study, the immunogenic properties of porcine ExPEC OmpC and OmpF were investigated using a mouse model. Both porins OmpC and OmpF of ExPEC can provide high protection against lethal infection with the highly virulent strain PCN033. In addition, OmpC and OmpF both could induce high titers of IgG antibodies, indicating that these two proteins have good immunogenic properties. The type of immune responses was reflected by the two IgG subclasses produced through immunization, IgG1 and IgG2a. In mice, serum IgG1 is associated with a Th2-type response, whereas serum IgG2a is associated with a Th1-type response, which is particularly effective at mediating bacterial opsonophagocytosis (Unkeless et al., 1988). Our study showed that OmpC and OmpF elicited high titers of IgG2a, although less than IgG1, which indicated that OmpC and OmpF could induce significant Th1/Th2 immune responses.

The other possibility is that the BsuM enzyme remained in the cyt

The other possibility is that the BsuM enzyme remained in the cytoplasmic portion of the donor R+ M+ cell in the fusant and that, upon division of the fusants, various quantities of the enzyme were distributed LY2835219 nmr to the progeny cells depending on where the cell division took place. It has been demonstrated that L-form colonies of B. subtilis arise among those of the bacillary form

after PEG-induced cell fusion (Hauser & Karamata, 1992), which indicates that cell division can occur while the fusant is still without the cell wall. As the L-form B. subtilis cell divides by an extrusion–resolution mechanism that is independent of FtsZ (Leaver et al., 2009), it is possible that a similar mechanism was involved in the division of the fused cells that were produced by random collision between the donor and the recipient protoplasts. This may result in incorporation of various parts and quantities of the cytoplasm of the R+ M+ cell into that of the

R− M− protoplast. Thus, upon cell fusion and subsequent cell division, different proportions of the donor and the recipient cell cytoplasms will constitute progeny cells. Cell death by restriction of the recipient chromosome will occur if a higher proportion of the cytoplasm from the R+ M+ donor cell occupies the progeny cell after division. There must be a critical level of the BsuM restriction enzyme under which the recipient DNA is saved from the restriction attack, and this may account for the reduced but significant efficiency of plasmid transfer from the R+ M+ donor to the R− M− recipient cell. We note in this check details respect that the cotransfer efficiencies of pLS32neo and pHV33 from the R+ M+ to R− M− cells were 1/9 to 1/7 of the levels observed for the

fusion between the homologous pairs (see ‘Results’). As the chromosomal DNA in this fraction of the fused cells escaped the restriction attack, it is tempting Glutathione peroxidase to speculate that the cytoplasmic space in the donor R+ M+ cell containing both plasmids but not enough quantities of the BsuM restriction enzyme to destroy the recipient chromosomal DNA corresponds to 1/9 to 1/7 of the space that brings about transfer of both plasmids in the case of homologous pairs. The heterospecific cell fusion between B. subtilis RM125 and either B. stearothermophilus or B. circulans was successful but the efficiencies were relatively low (see ‘Results’). The restriction system(s) in B. stearothermophilus CU21 or B. circulans BM used here has not been studied yet, but it is known that by a rough estimate, most bacteria carry one or more restriction systems (Wilson & Murray, 1991), which may have affected the fusion efficiency in this study. Another possible reason for the low efficiency is that the compositions of the membrane constituents in those bacteria are different from that of B. subtilis RM125, causing inefficient membrane fusion between the heterospecific bacteria.

This is the period over which drug coverage is assessed, and time

This is the period over which drug coverage is assessed, and time-zero represents the point from which prediction of the subsequent outcome VL is made. One rationale for including only patients who had continuous records of prescription and undetectable

VLs was that there was evidence that such patients were actually picking up their prescribed drugs. Patients experiencing at least one DCVL episode were included in the analysis, with one or multiple DCVL episodes contributed by each patient. A DCVL episode was excluded from analyses if the drug coverage period met any of the following exclusion criteria: (i) there was a gap after the end of a prescription to the next prescription or to time-zero longer than 3 months (to exclude the possibility of missing data selleckchem or receipt of antiretroviral drugs from other sources), (ii) the duration of the prescription (i.e. amount of drug) was missing, unless this did not result in any gap in drug coverage, and (iii) time-zero was more than 2 weeks after the end of the last ever (at the time of the analysis) recorded prescription. Furthermore, only episodes with outcome VL up to 30 April 2008 and time-zero

between 1 January 2000 and 1 October 2007 were included. The analysis considered drug coverage measured in two different ways: as a continuous variable (per 10% increase) and categorized as ≤60, 60.1–80, 80.1–95, 95.1–99.9 and 100% Trametinib nmr coverage. The endpoint in this analysis was viral rebound, defined by whether the outcome VL was >200 copies/mL or not. We chose a VL value of 200 copies/mL, because we were interested in predicting even relatively small rises in VL. A modified Poisson regression model, with robust error variances [43], was used to model the association between drug coverage

Amoxicillin and risk of viral rebound, after adjusting for other potential confounding variables. Adjustment was made for the following potential confounders: age (per 10-year increase), sex, ethnicity (white, black African and other), risk group (homo/bisexual, heterosexual and other), calendar year of start of HAART, continuous time with undetectable (i.e. ≤50 copies/mL) VL (per 1-year increase), previous virological failures (defined as VL >500 copies/mL while on HAART, classified as 0, 1 and 2 or more), current ART regimen [regimens containing nucleoside reverse transcriptase inhibitors (NRTIs) only, unboosted PIs, ritonavir-boosted PIs, NNRTIs and other], number of previous treatment interruptions (defined as discontinuation of all therapy for at least 2 weeks after having started ART while VL value >500 copies/mL and classified as 0, 1, 2, 3 or more), CD4 cell count at time-zero (<200, 200–350 and >350 cells/μL, and missing) and calendar year of time-zero.

WHO now recommends the use of postpartum antiretroviral therapy,

WHO now recommends the use of postpartum antiretroviral therapy, either maternal HAART or infant nevirapine treatment, to reduce the risk of HIV transmission during the period of breast feeding. As the WHO guidelines are not generally applicable to the UK setting, BHIVA/CHIVA have reviewed the data with a view to providing guidance both to people living with HIV and to healthcare providers with regard to the safety of different feeding practices and the related safeguarding Crizotinib issues. The summary guidance presented below takes into account the substantial number of responses to a public consultation on an earlier draft of this advice, incorporating diverse and often

conflicting views and data interpretations. The Writing Group reconvened Akt inhibitor to address these issues, particularly the concerns expressed by many that any new recommendations should not undermine the extensive and highly successful work to reduce mother-to-child transmission of HIV by complete avoidance of breast feeding. With current interventions, mother-to-child HIV transmission in the UK is now very low, being ∼1% for all

women diagnosed prior to delivery, and 0.1% for women on HAART with a viral load <50 HIV-1 RNA copies/ml plasma [2] at delivery. Current BHIVA/CHIVA pregnancy management guidelines include HAART, the option of managed vaginal delivery for women with an undetectable HIV viral load on HAART at term, pre-labour pre-rupture of membranes caesarean section for women with a detectable viral load, and exclusive feeding with infant formula milk from birth [3]. Mother-to-child HIV transmission can occur through breast feeding, with an ongoing infection risk throughout the breast-feeding period; by contrast, there is no risk of postnatal HIV transmission if the infant is not breastfed [4–6]. The long-term effects of exposing infants to HAART through breast milk are unknown. 1 For these reasons, BHIVA/CHIVA continue

to recommend that, in the UK, mothers known to be HIV-infected, click here regardless of maternal viral load and antiretroviral therapy, refrain from breast feeding from birth. While all other interventions to prevent mother-to-child HIV transmission are provided through HIV commissioned services, it is recognized that infant formula milk is not universally provided and that this lack of provision can be a barrier to the successful implementation of this recommendation. BHIVA/CHIVA therefore recommend that: 2 All HIV-positive mothers in the UK should be supported to formula-feed their infants. This means that: (i) A starter pack (infant formula milk and appropriate equipment) should be freely available as part of the package of care to prevent mother-to-child transmission. 1 Women who are on low incomes and eligible for Healthy Start should be informed about how to purchase infant formula milk with their vouchers (see Appendix 1, which discusses financial support).

, 2003; Grüner et al, 2004; Cowman & Crabb, 2006; Iyer et al, 2

, 2003; Grüner et al., 2004; Cowman & Crabb, 2006; Iyer et al., 2007a, b). Little is known about how the large RH transmembrane proteins mediate their function during erythrocyte invasion, but a crucial step appears to be the proteolytic cleavage during the invasion process (Ogun & Holder, 1994; Triglia et al., 2009). Members of RH have been identified in all Plasmodium species analyzed so far, indicating the conserved function and importance of this protein family to the

malaria parasite (Iyer et al., 2007a; Rodriguez et al., 2008). In the rodent malaria parasite Plasmodium yoelii, selleck kinase inhibitor which has been widely used as a model to study host–parasite interactions (Landau & Gautret, 1998), the RH protein, termed Py235 (235 kDa in mass), has been shown to be a potential virulence factor that allows the parasite to invade a wider range of host erythrocytes (Freeman et al., 1980; Holder & Freeman, 1981). Py235 is also involved in the clonal phenotypic variation of merozoites (Preiser et al., 1999), enabling the parasite to evade immune responses and adapt to changes in PD-0332991 mouse the host environment during the invasion step (Snounou et al., 2000). Previously, a 94 kDa domain of Py235 of P. yoelii, which is highly conserved among the RBLs, has been found to selectively bind ATP and ADP, and is termed the nucleotide-binding domain (NBD94, Ramalingam et al., 2008). The amino acid sequence

483FNEIKEKLKHYNFDDFVKEE502 in NBD94 has been identified as a nucleotide-binding region as shown by photoaffinity labeling of the nucleotide analogue 8-N3-3′-biotinyl-ATP (Ramalingam

et al., 2008). The preference of MgATP over MgADP recognition is associated with specific structural alterations in the C-terminal domain of NBD94 as depicted by spectroscopic comparison of NBD94 and its C-terminal truncated form, NBD941–550, in which no nucleotide-dependent alteration could be observed (Ramalingam et al., 2008). This nucleotide effect in the recombinant protein is potentially significant, as demonstrated by a strong binding of Py235 to RBCs in the presence of MgATP, which becomes considerably reduced either in the presence of MgADP or in the absence of nucleotides oxyclozanide (Ramalingam et al., 2008). Based on these traits and the absence of significant ATPase activity of NBD94, this domain was suggested to serve as an ATP/ADP sensor during the invasion process (Ramalingam et al., 2008). More recently, the low-resolution solution and crystallographic structure of the smallest structural unit, able to bind nucleotides, and its coupling module, the hinge region, have been determined, respectively (Grüber et al., 2010). The crystal structure of the hinge region, including residues 566–663, called NBD94566–663, consists of two helices 97.8 and 48.6 Å in length, linked by a loop. The region NBD94444–547 (residues 444–547 of NBD94) has been identified to form the nucleotide-binding segment, specific for ATP and ADP.

1a) As expected, the higher the similarity, the higher the signa

1a). As expected, the higher the similarity, the higher the signal intensity, which was consistent at every temperature. Signal intensity decreased with increasing hybridization temperature, with a 10-fold decrease in signal intensity observed from 55 to 75 °C for the perfect match group. The different responses to hybridization temperature are highlighted in Fig. 1b. The signal intensity from mismatches was considerably lower than that of perfect matches, and intensity relative to SAHA HDAC research buy the perfect match decreased with the increase in hybridization temperature. For example, the group with 85–90% similarity had 12%, 5%,

and 1% relative signal intensity compared with the perfect match at 65, 70, and 75 °C, respectively. Previously, long oligonucleotide probes (50–70mer) selleck screening library with around 85–90% of sequence similarity to targets were shown to have 10% relative signal intensity to perfect matches (He et al., 2005). Thus, the specificity of random genomic fragment probes is comparable to

long oligonucleotide probes. In addition, based on the data reported by Goris et al. (2007), most genomic fragment sequences between different species seem to share similarity lower than 90%, a finding consistent with this study. Therefore, our results indicate that the specificity of genomic fragment probes is potentially at species level. In this study, long DNA fragments (around 2000 bp) were selected

as probes because of their high sensitivity (Letowski et al., 2004). Long probes also contain more Demeclocycline sequence information, which makes them advantageous for analysis of microorganisms, many of which are unknown, in the environment (Yokoi et al., 2007; Tobino et al., 2011). Because random 2000-bp fragments may cover two adjacent genes partially, they may however hybridize with target DNA containing one of these genes, which will result in nonspecific signal. Here, target DNA was fragmented to 400 bp to, at least in part, address this concern. When using fragmented DNA, regions flanking the sequence that binds to the probe remain in solution and hence do not contribute to the signal. This situation is similar to what has been observed for whole genome probes, which can provide strain-level specificity even though a given probe (that is, genome) contains genes that are conserved among strains (Wu et al., 2004). However, fragmentation cannot prevent the hybridization of multiple fragments from different strains to the same probe, and hybridization signals obtained with DNA from diverse microbial communities should be interpreted with caution. In conclusion, our results show that the degree of specificity achievable by randomly generated genomic fragment probes on DNA arrays legitimizes their use for microbial diagnostics.