The CS54 island is a 25 kb region found between xseA and yfgJ at centisome 54 in S. Typhimurium (Kingsley et al., 2003) and S. Typhi (Fig. S1r). Five genes are found within this island, which are shdA, ratB, ratA, sinI and sinH (sivH). In S. Typhimurium, ShdA was shown to be an outer membrane protein of the autotransporter family that binds fibronectin, RatB is a predicted secreted protein of

unknown function and SinH is a putative outer membrane protein (Kingsley & Bäumler, 2002; Kingsley et al., 2003; Abd El Ghany et al., 2007). shdA, ratB and sinH (sivH) are all implicated in intestinal colonization of BALB/c mice by S. Typhimurium, but are all pseudogenes in S. Typhi (Kingsley et al., 2003). Fimbriae or pili are proteinous structures Selleckchem HSP inhibitor found on bacteria that can mediate interaction with cells. Fimbriae are normally specific to a receptor and can

be used at different critical times during the infection. Each serovar harbours a unique combination of fimbrial operons (Fig. 2). Whole-genome sequence analysis revealed eight putative fimbrial operons shared by both S. Typhimurium and S. Typhi [bcf, csg (agf), fim, saf, stb, stc, std, sth] (McClelland et al., 2001; Parkhill et al., 2001). Salmonella enterica serovar Typhimurium possesses five unique fimbrial sequences selleck chemicals llc known as lpf, stf, pef, sti and stj (McClelland et al., 2001). These unique fimbriae were not involved in systemic colonization of the spleen, and Lpf was shown to be involved in intestinal colonization of mice (Weening et al., 2005). A type IVB pilus located on SPI-7 is only found within the S. Typhi genome, along with five other unique fimbrial operons (sef, sta, ste, stg and tcf) (Parkhill et al., 2001). For the majority of these fimbriae, little is known about their true function, expression Farnesyltransferase conditions or their importance for virulence during infection. Type IV pili are used by Typhi for adhesion to human monocytes and epithelial cells by interaction with the cystic fibrosis transmembrane conductance regulator receptor (Pier et

al., 1998; Zhang et al., 2000; Tsui et al., 2003; Pan et al., 2005). Tcf was recognized by human sera from patients with typhoid (Harris et al., 2006) and Stg mediates adherence to epithelial cells and reduces phagocytosis (Forest et al., 2007). All fimbrial operons are intact in S. Typhimurium strain LT2, although pseudogenes are found within six fimbrial operons of S. Typhi strain CT18 (fimI, safE, sefA, sefD, bcfC, steA, stgC, sthC, sthE) (Townsend et al., 2001) (http://www.pseudogene.org/cgi-bin/db-gen.cgi?type=Prokaryote). The unique repertoire of fimbrial adhesin systems may explain in part some differences observed between the host tropism colonization niches of these two serovars. In Salmonella, the major subunit of flagella is usually encoded by fliC or fljB, which correspond to the H1 and H2 variants of the H antigen, respectively (Silverman & Simon, 1980).

6b). Intriguingly, protected bands included the SMAG repeat labeled as c in Fig. 6b. The same result was obtained in RNA extension experiments, in which bands of elongation extended over SMAG repeat c only (Fig. 6c). We hypothesize that repeats a and

b fold into one large secondary structure, which is cleaved, and this promotes rapid 3′–5′ degradation of upstream 4478 transcripts. The number of predicted SLSs is significantly higher in prokaryotic genomes existing in nature than in random sequences of comparable GC content (Petrillo et al., 2006). This implies that the ability of a variety of sequences to fold into secondary structures is positively selected in prokaryotic genomes and may have functional significance. A fraction of SLSs is represented by REPs, BGB324 cost sequences shown or hypothesized BMN 673 ic50 to serve different functions. REPs are binding sites for the integration host factor, a protein required for site-specific recombination and DNA replication

(Engelhorn et al., 1995). REPs are targets for the DNA gyrase (Espéli & Boccard, 1997), and repeats located between convergent genes may be a privileged target for the enzyme, in order to counteract the excess of positive supercoiling induced in the chromosome by DNA transcription (Moulin et al., 2005). As RNA elements, REPs may enhance the stability of 5′ proximal mRNA segments (Khemici & Carpousis, 2004). Finally, REPs induce innate immune system stimulation via TLR9, and could play a key role in the pathogenesis of Gram-negative septic shock (Magnusson et al., 2007). Tobes & Ramos (2005) established that, for a palindromic sequence to be considered as REP, the following criteria should be met: (a) be extragenic, (b) range in size from 21 to 65 bp and (c) constitute >0.5% of the total intergenic space. SMAGs meet all these criteria, and constitute the largest set of REPs described so far. SMAGs correspond to the repeats identified by Nunvar et

al. (2010). SMAGs can be sorted into five distinct subfamilies, Ibrutinib chemical structure and come in different genomic formats. Single units make up only 1/5 of the SMAG family. The remaining elements are organized as dimers or are grouped in tandem arrays of variable lengths. Altogether, SMAGs and intermingled DNA occupy 13% of the overall intergenic space, and make up 1.4% of the total chromosome. SMAG families residing in the environmental R551-3 and SKA14 S. maltophilia strains are comparable in size to the repeat family found in K279a. Yet, the sizes of some subfamilies vary, and K279a is enriched in SMAG-3. Most SMAG-3 are organized as HH dimers that feature conserved spacers, and may thus represent a relatively young sequence family variant. Changes in the abundance and chromosomal distribution may make SMAG-3 sequences suitable for use in accurate genotyping and epidemiological studies. Also, the ∼500 REPs identified in the E. coli MG1655 strain have been sorted into subfamilies.

Alkaline extraction of NADH was carried out using the protocol of Caruso et al. (2004), with some modifications. Briefly, a 20-mL aliquot from Xcg cultures grown in LB or RSB for 18 h was centrifuged at 12 500 g for 10 min at 4 °C. The cell pellet was EX-527 washed once with 20 mL phosphate-buffered saline (PBS; 10 mM, pH 7.5) and suspended in 2 mL of chilled KOH (0.5 M). Two volumes of cold milliQ water was added to this alkaline suspension, which was then vortexed for 2 min. The mixture was centrifuged at 12 500 g for 40 min at 4 °C. The supernatant was collected and neutralized by adding 10% volume of KH2PO4 (1 M, pH 6.5). The sample was filtered through a 0.22-μm

filter (Millipore, Bedford, MA) and analyzed using HPLC (Waters, Milford, MA). The C18 column (dimension: 150 × 4 mm) was used for analysis. The sample was loaded into a vial of the autosampler. The mobile phase consisted of buffers A and B [A: 0.1 M KH2PO4, pH 6.0; and B: 0.1 M KH2PO4 (pH 6.0) having 10% (v/v) methanol)]. Buffers were filtered through a 0.22-μm filter

(Millipore) and degassed. Before beginning the analysis of samples, the HPLC system was equilibrated with 50% buffer A/50% buffer B for 30 min. The flow rate was adjusted to 1 mL min−1. The samples were analyzed using the binary gradient (Caruso et al., 2004): 100% buffer A for 2 min, followed by sample injection, 100% buffer A for 5 min, 0–25% buffer B for 6 min, 25–60% buffer B for 2.5 min, 60–100% buffer B for 5 min, 100% buffer B for 7.5 min, and, lastly, 100% see more buffer A for 2 min to

equilibrate the system for the next analysis. The detection of NADH was carried out by measuring the absorbance at 254 nm (Waters 996 Photodiode array detector). Acid extraction of ATP and ADP was carried out based on the method of Giannattasio et al. (2003). Briefly, a 20-mL aliquot from Xcg cultures grown in LB or RSB for 18 h was centrifuged at 12 500 g for 10 min at 4 °C. The cells were washed once with 20 mL PBS (10 mM, pH 7.5) and the pellet was suspended in 4 mL of chilled perchloric acid (0.5 M). The cell suspension was sonicated for 3 min and incubated for a further 45 min with vigorous shaking at 10-min intervals. The acid extract was neutralized with 0.8 × 0.5 M KOH and 0.2 × 1 M KH2PO4 (pH 7.5) and kept Acetophenone on ice for 15 min. The potassium perchlorate precipitate was finally removed by centrifugation (12 500 g for 30 min at 4 °C). The supernatant was filtered through a 0.22-μm filter (Millipore) and subjected to HPLC analysis (Waters) using the C18 column (dimension: 150 × 4 mm). Samples were loaded into a vial of the autosampler. The mobile phase consisted of buffers A [0.1 M KH2PO4, pH 6.0; and 8 mM tetrabutylammonium hydrogen sulfate (TBA)] and B [0.1 M KH2PO4, pH 6.0; 8 mM TBA, and 30% (v/v) acetonitrile].

During recent years, the awareness of a relationship between long haul travel (LHT) and increased risk of venous thromboembolism (VTE) has risen enormously although this association has been known for decades since the first descriptions by Louvel and Homans in 1951 and 1954, respectively.1,2 Moreover, among travelers and physicians hysteria detectable and was exacerbated by a media hype.3,4 This has been enforced by inconsistent or even controversial recommendations about the necessity of prophylaxis for travelers’ thrombosis (TT). SCH772984 research buy Recently, however, more reliable scientific data about

the pathogenesis of TT and the involved risks have become available. One major step forward to clarify whether LHT could be regarded as an independent important risk factor for thrombosis was the initiation of the WHO Research Into Global Hazards of Travel (WRIGHT)

program by the WHO in 2003. Although phase one of the WRIGHT program focused on the epidemiology and pathophysiology of TT, the efficiency of prophylactic measures was the aim of CX-5461 solubility dmso the second phase of this program resulting in the final goal to develop appropriate preventive recommendations for all travelers. In 2007, the WHO published the final report of the first phase.5 Overall, current data support a weak association between LHT of more than 4 hours and VTE with an approximately twofold increased risk.5–8 However, this risk seems to be significantly higher

for travelers with an increased thrombotic risk.9–15 Compared to other modes of travel, the risk of TT seems to be slightly increased for air travel although published data is somehow conflicting.5,6,9,16,17 The absolute risk of VTE, however, is low and reported with 1 event in 4,656 flights or 215 events per 1 million travelers.10 For air travel of at least 16 hours, the risk increases to 1 event in 1,264 very flights or 798 events per 1 million travelers. Such an association with the duration of the flight or travel in general had also been described by other groups.6,18–20 Against this background, physicians all around the world are faced with the question what kind of thrombosis prophylaxis (TP) would be appropriate for an individual traveler planning a particular journey. As no evidence-based recommendations for prophylactic measures are yet available, this is not an easy task. This is emphasized by the results of a recently published study asking physicians and experts in hemostasis what kind of prophylaxis measures they performed to prevent TT during a long haul flight to Australia.21 Besides age and the perceived individual thrombosis risk (TR), nationality and profession were independent variables for performing a prophylactic measure! Moreover, there is still an ongoing discussion among top experts in the field whether any prophylactic measure to prevent TT are really necessary.

The Gly115Arg mutation present in strains of D was not predicted to result in enzyme inactivation based on sequence analysis alone, making it unclear whether AaxB sequence variations seen in other Chlamydia alter AaxB activity. To further our understanding of this enzyme and determine whether the inactivation Ku-0059436 cost of AaxB is restricted to the human-specific C. trachomatis serovars, we completed an activity panel using variant Chlamydia AaxB proteins in a surrogate E. coli acid shock assay. A pan-chlamydial

anti-AaxB antibody was used to detect enzyme production and processing during the developmental cycle using a cell culture infection model. Collectively, our data indicate that non-C. trachomatis species (and a single C. trachomatis serovar: E) produce active AaxB. Chlamydia strains used in this study include Chlamydia muridarum strain Nigg, C. trachomatis serovar D strain UW-3/CX, Chlamydia psittaci HIF-1 activation strain 6BC, Chlamydia caviae strain SP6 (Binet et al., 2010), and C. trachomatis serovar E strain UW-5/CX. Chlamydia pecorum strain E58 DNA was provided by Patrik

Bavoil (University of Maryland). The previously unreported aaxB sequences for C. caviae SP6 and C. trachomatis E strain UW-5/CX were deposited in GenBank under accession numbers JX287368 and JX287367, respectively. Escherichia coli strain MG1655 was used for the acid resistance complementation assays, while E. coli Rosetta-gami2 (DE3; Novagen) was used for AaxB expression and purification. A pBAD/HisA vector (modified during cloning to remove the histidine tag coding region; Invitrogen) carrying aaxB from C. pneumoniae strain Kajaani 6 or adiA from E. coli strain MG1655 was provided by David Graham (Oak Ridge National Laboratory). Primers used to

amplify the different aaxB variants are listed in Supporting information, Table S1. PCR-amplified products were digested and ligated into the NcoI and HindIII sites on the pBAD/HisA vector (without the histidine tag). Constructs were then electroporated into ΔadiA E. coli strain MG1655. The aaxB gene from C. caviae also was PCR-amplified (primers listed in Table S1) for cloning GNA12 into a pET-19b expression vector (Invitrogen). PCR-amplified products were digested and ligated into the NdeI and BamHI sites on pET-19b and then electroporated into E. coli strain Rosetta-gami2 (DE3). All constructs were sequence verified at the Biomedical Instrumentation Center at the Uniformed Services University. The adiA gene was deleted from E. coli strain MG1655 using the lambda red method of linear recombination with the primers listed in Table S1 (Datsenko & Wanner, 2000). After PCR verification of the constructed ΔadiA::kan mutation, the allele was moved into a clean E. coli MG1655 background via P1L4 transduction (Miller, 1972).

Chronic cough and expectoration (47%) and breathlessness during exercise (33.9%) were commonly reported. Airflow limitation (AL) was present in 17.2%, low pulmonary diffusing

capacity in 52.2% and emphysema in 10.5−37.7% of patients, depending on the method used for quantification. Most of these abnormalities had not been diagnosed or treated previously. Smoking exposure and previous tuberculosis were the main risk factors for AL, whereas smoking exposure and several variables related to HIV infection appeared to contribute to the risk of emphysema and low diffusing capacity. Despite HAART, pulmonary structural and functional abnormalities are frequent in HIV-positive patients. They are probably attributable to both environmental (smoking and tuberculosis) and HIV-related factors. Most of these abnormalities remain unnoticed and untreated. Given the relatively young age www.selleckchem.com/products/ABT-737.html of these patients, these results anticipate a significant health problem in the next few years as, thanks to the efficacy of HAART, patients survive longer and experience the effects of aging. “
“Whether treatment-experienced HIV-1-infected patients with an acquired K103N mutation after failing nonnucleoside reverse transcriptase inhibitor (NNRTI) regimens can

be treated with rilpivirine is unknown. The aim of this pilot study was to evaluate the efficacy of rilpivirine/tenofovir/emtricitabine SGI-1776 in HIV-1-infected patients with an isolated K103N mutation. A prospective study was carried out in HIV-1-infected adults who acquired the K103N mutation on failing NNRTI regimens. No other mutations in reverse transcriptase were allowed. Patients had to be on second-line regimens with HIV-1 RNA < 200 copies/mL for ≥ 6 months. Exclusion criteria were: use of acid-reducing agents, insufficient caloric intake and impaired renal function. Of primary

interest was virological success Clomifene (HIV-1 RNA < 200 copies/mL) at weeks 6, 12, 24 and 48. Of 1550 HIV-1-infected patients at the Erasmus Medical Center Rotterdam, we identified 10 HIV-1-infected patients with an isolated K103N mutation acquired after NNRTI failure. Five patients were not eligible for inclusion in the study, and two patients refused participation. Three African women (23–35 years of age) were included and were switched from boosted protease inhibitor-based second-line therapies to rilpvirine/tenofovir/emtricitabine. HIV-1 RNA was < 200 copies/mL at weeks 6, 12, 24 and 48 for all patients. No adverse events were observed. All patients had HIV-1 RNA < 200 copies/mL for 6−50 months prior to the switch. This pilot study demonstrates the successful switch of HIV-1-infected patients who acquired an isolated K103N mutation during previous NNRTI therapy to rilpivirine/tenofovir/emtricitabine.

0001). Table 2a summarizes the RR for a detectable VL in

the whole population after fitting a multivariable Olaparib solubility dmso model. In the subset of patients previously on ART for ≥6 months (Table 2b), the proportion of poor prognosis decreased from 45% in 1998 to 12% in 2008. The factors associated with a lower risk of a VL >50 copies/mL were more recent calendar year (with a RR significantly smaller than that estimated in the analysis with the full set of patients), older age, infection via homo/bisexual vs. heterosexual contact, and more recent enrolment year. In contrast, factors associated with a higher risk of VL >50 copies/mL were non-Italian European/North American nationality, living in the

north of Italy compared with the centre, and a higher number of drug switches. Testing for interactions between mode of HIV transmission and calendar year did not yield any improvement Selleckchem BAY 80-6946 in the log-likelihood (P=0.56). Similar risks were also found in the analysis on the subset of patients followed up for at least 1 year, and in those who had their last visit less than 2 years before the date of analysis (data not shown). From 1998 to 2008 there was a decrease in the proportion of patients in the Icona study with an adverse viro-immunological prognosis. The proportion of patients with VL >50 copies/mL decreased from 66% in 1998 to 40% in 2008, and from Chlormezanone 45 to 12% among

those treated for ≥6 months, which was paralleled by similar decreases in the proportion of patients with a CD4 count ≤200 cells/μL (from 14 to 6% overall and from 14 to 5% in those treated for ≥6 months). Our analysis confirms the results obtained in a previous study conducted in the UK and extends them to a setting with a different distribution of transmission groups, to more recent years, during which new drug classes were available, and to a group of patients who may have had differential access to care and adherence to treatment [17]. Similar improvements in viro-immunological outcomes over time were also observed in patients enrolled in a Swiss cohort although, again, estimates stopped at the year 2005 [18]. There are several possible explanations for our findings. The decrease in the prevalence of patients with an adverse prognosis, for example, may reflect the availability of more effective and tolerable treatments as well as, perhaps, the improved skills of treating physicians in recent years. A change in patients’ attitudes towards therapy and adherence is another factor that is likely to have contributed to the observed improvement in the success rate of ART over time. Overall, the prevalence of patients with immunosuppression or a detectable VL was highest in IDUs.

1). Descriptive baseline characteristics by presence or absence of anal condylomata are shown

in Table 1. The most relevant differences between patients were that a higher percentage of patients with condylomata click here had a history of STIs (46%) and were MSM (84%) compared with patients without condylomata (27% had a history of STIs and 71% were MSM). Accordingly, the percentage of patients practising RAI was also higher in patients with anal condylomata than in those without them (76% vs. 58%, respectively). The overall prevalence of anal condylomata in HIV-infected men was 25% (157 of 640; 95% CI 21–28%). According to sexual behaviour, the prevalence was 28% (132 of 473) in MSM and 15% (25 of 167) in heterosexual HIV-infected men (OR 2.2; 95% CI 1.4–3.5). Condylomatous anal lesions were located in the internal region in 111 of 157 patients (71%), in the perianal area in 13 of 157 patients (8%) Selleckchem Navitoclax and in both locations in 33 of 157 patients (21%) (Fig. 1). The overall prevalence of anal canal HPV infection was 73% (469 of 640; 95% CI 70–77%). The prevalence in patients with anal condylomata was 92% (145 of 157; 95% CI 86–96%) [95.5% (126 of 132) for MSM and 76% (19 of 25) for heterosexuals; χ2 = 11.3; P = 0.001] and that in patients without anal condylomata was 67% (324

of 483; 95% CI 63–71%) [80% (273 of 341) for MSM and 36% (51 of 142) for heterosexuals; χ2 = 88.5; P < 0.001] (with/without anal condylomata, P < 0.001). Moreover,

the prevalence of LR HPV genotypes (63% vs. 19%, respectively; P < 0.001) and that of HR HPV genotypes (83% vs. 62%, respectively; P < 0.001) were considerably higher in the anal canals of HIV-infected men with condylomatous lesions than in those without (Table 2). A higher prevalence of presenting any HPV genotype in the anal canal was associated with having anal condylomata (adjusted OR 8.5; 95% CI 3.2–22). The overall prevalence of single HPV genotype infection was 23% (146 of 640; 95% Paclitaxel CI 20–26%). Similar prevalences of single HPV genotype infection were observed in patients with and without condylomata [18% vs. 24%, respectively; unadjusted OR 0.7; 95% CI 0.4–1.1: in those with condylomata, 14% (19 of 132) for MSM and 36% (nine of 25) for heterosexuals (χ2 = 6.69; P = 0.008); in those without condylomata, 26% (88 of 341) for MSM and 21% (30 of 142) for heterosexuals (χ2 = 1.19; P = 0.275)]. By contrast, the prevalence of HPV infection involving at least two genotypes differed by condylomata status, and this difference was statistically significant: 75% (117 of 157; 95% CI 70–81%) for patients with condylomata [81% (107 of 132) for MSM and 40% (10 of 25) for heterosexuals; χ2 = 18.6; P < 0.001] and 43% (206 of 483; 95% CI 38–47%) for those without condylomata [54% (185 of 341) for MSM and 15% (21 of 142) for heterosexuals; χ2 = 63.8; P < 0.001] (with/without condylomata, adjusted OR 4.0; 95% CI 2.2–7.1).

9%– using the CG formula) was close to that reported in the EuroSIDA Cohort [3.5% using CG and 4.7% using Modification of Diet in Renal Disease (MDRD) formula] [9], 5.9% in the MACS Cohort [16] and 5.7% in the King’s College Hospital Cohort [17]. This figure

was slightly higher in the Washington University HIV outpatient clinic (7.3%) [18], in the Johns Hopkins HIV Cohort (7%) [19] and in a cross-sectional survey in Barcelona (7.6%) [20]. The epidemiological differences between the studied populations can explain some of the differences between these results; indeed the traditional risk factors of renal insufficiency (high blood pressure, diabetes, dyslipidemia, age and ethnicity) and those specific to HIV disease are differentially distributed in the various studies. The different definitions of RI used in the studies (i.e. acute vs. chronic RI where confirmed value is required, additional see more adjustment of formulae for body surface area) could also contribute to the differences noticed between the studies. Conversely to the overall prevalence of RI, the prevalence of advanced RI is close to what has been reported in the general population: 4.7% in the US population [15], Veliparib supplier 5.7% in a Galician population whose average age was 49.5 years [21] and 5.6% in the control group of a study conducted in Catalonia [20].

In our study, patients with RI were more likely to be female, older, to have

a low BMI, high blood pressure or an exposure to tenofovir or IDV >1 year. Gender, age and BMI reflect the physiological changes nearly of the glomerular filtration rate which are taken into account in the CG formula. These factors are thus logically identified in our study as in most of the available literature [9,10,14,18,19,22]. In one report [20], the presence of lipoatrophy was also independently associated with advanced RI; we did not study this but this finding is compatible with the association of a low BMI with RI. High blood pressure, which is a well-known risk factor for renal function impairment in the general population, was associated with advanced RI within our HIV-infected population, as in previous but not all reports [9,14,18]. The increased risk observed among patients with high blood pressure justifies sensitizing physicians to the screening and treatment of hypertension to reduce the likelihood of developing RI. In contrast to some previous studies [9,14,17,22], we did not identify any association between advanced HIV infection (AIDS stage and low CD4 cell count) and RI. This does not exclude the hypothesis that advanced HIV disease could be associated (through HIVAN) with severe (CC<30 mL/min) and/or end-stage (CC<15 mL/min) renal insufficiency but this has not been tested as too few patients were diagnosed at these RF stages (n=13).

0 (Table 1). The four strains had a wider range of viable temperature and pH conditions than L. plantarum chikuso-1, which can grow at 15–45 °C and at pH 3.5–6.0 (Cai et al., 2003), or L. plantarum NGRI0320, which

can grow at 15 °C but not 45 °C (Tanaka et al., 2000). Therefore, these four strains may be useful for developing an advanced L. plantarum subsp. plantarum-containing inoculant. In rice grains, glucose, maltose, maltotriose, sucrose, raffinose, stachyose, fructose, xylose, raffinose, and arabinose are detectable (Murata et al., 1966; Singh & Juliano, 1977). In hydrolysates of rice straw, glucose, xylose, fructose, and arabinose are major monosaccharides, Selleck GSK1120212 whereas small amounts of fucose, mannose, galactose, and rhamnose also are present (Sugahara et al., 1992; Sulbaran-de-Ferrer et al., 2003). In the analysis of their carbohydrate utilization, the tested strains had unique fermentation patterns compared with the type strains of the L. plantarum group (Table 2). In addition, differences in carbohydrate fermentation patterns were found among the L. plantarum subsp. plantarum strains this website in spite of the high similarity of their genetic backgrounds. For example, strains TO1000 and

TO1001 showed positive reactions for utilization of l-arabinose, whereas TO 1002 and TO 1003 were negative. TO1001 had no ability to use l-rhamnose. Only TO1000 was able to assimilate starch, which is a major constituent of rice grains (Baun et al., 1970;

Perdon et al., 1975; Perez et al., 1975). The potential to utilize carbohydrates might be an important factor in effectiveness of LAB inoculants on silage fermentation quality. Next, Carnitine palmitoyltransferase II we evaluated the four strains as additives for whole crop paddy rice silage. The DM of paddy rice materials used was 43.0%. The pH value of homogenates of the materials was 6.24. Organic acids such as lactic acid, propionic acid, and n-butyric acid were not present at detectable levels. The VBN content was 0.02 g kg−1 FM. Before ensiling, the microbiological composition was LAB (6.66 log CFU g−1 FM), coliform bacteria (6.62), yeasts (8.26), aerobic bacteria (8.28), clostridia (3.00), bacilli (3.18), and molds (4.70). As shown in Table 3, all strains increased fermentation rates in whole crop paddy rice silage, resulting in a significant pH decrease after 30 days of storage. Even within the same subspecies, a significant difference in pH after fermentation was observed between TO1000 and TO1002. Likewise, differences in the content of organic acids and VBN were also found among the treatments (Table 3). For example, the lactic acid content in LAB-treated samples was significantly higher than in the untreated samples, and strain TO1000 had the highest concentration.