Changes from before to after azelnidipine treatment were analyzed using a paired t-test. Values were expressed as means ± standard deviations (SDs). Figure 1 shows the patient classification system using ME average and ME difference as measures. The cut-off values of ME average and ME difference were 135 mmHg and 15 mmHg, respectively. Evaluation was carried out in the following four

groups: those with normal BP PLX3397 in vivo (ME average of <135 mmHg and ME difference of <15 mmHg); those with normal BP with a morning BP surge pattern (ME average of <135 mmHg and ME difference of ≥15 mmHg); those with morning-predominant hypertension (ME average of ≥135 mmHg and ME difference of ≥15 mmHg); and those with sustained hypertension (ME average of ≥135 mmHg and ME difference of <15 mmHg). Changes in the patient distribution based on ME average and ME difference from before to after azelnidipine treatment were evaluated using PD0325901 clinical trial the McNemar test. All tests were two-sided, with the significance level being set at p = 0.05. Adverse events and adverse drug reactions were coded using the Medical Dictionary for Regulatory Activities (MedDRA)/J version 11.0 and classified according to their Preferred

Terms. 3 Results 3.1 Patient Disposition Figure 2 shows the patient disposition. After exclusion of patients with no evening home BP measurement within 28 days prior to the baseline date, 2,590 and 2,546 patients were included in the safety and efficacy analysis populations, respectively. Fig. 2 Patient disposition in the current study. BP blood pressure 3.2 Patient Characteristics Table 1 shows the patient characteristics at baseline. The mean age was 65.1 ± 11.7 years, and 53.6 % of patients were female. The mean baseline home systolic BP (SBP)/diastolic BP (DBP) values were 156.9 ± 16.1/89.7 ± 11.7 mmHg in the morning and 150.2 ± 17.6/85.6 ± 12.2 mmHg in the evening. The mean pulse rates were 72.1 ± 10.2 beats/min in the morning

and 72.5 ± 9.6 beats/min in the evening. During the observation period, morning home BP was usually measured before breakfast and before dosing in a large proportion (86.8 %) of cases. Table 1 Patient characteristics at baseline (n = 2,546) Characteristics Value Gender (n [%])  Male 1,181 [46.4]  Female 1,365 [53.6] Age (years ± SD) Olopatadine 65.1 ± 11.7  15 to <65 years (n [%]) 1,168 [45.9]  65 to <75 years (n [%]) 806 [31.7]  ≥75 years (n [%]) 571 [22.4]  Not specified (n [%]) 1 [0.0] BMI (kg/m2 ± SD) 24.3 ± 3.6  <18.5 kg/m2 (n [%]) 69 [2.7]  18.5 to <25 kg/m2 (n [%]) 1,109 [43.6]  ≥25 kg/m2 (n [%]) 727 [28.6]  Not calculable (n [%]) 641 [25.2] BP and pulse rates  Morning home SBP (mmHg ± SD) 156.9 ± 16.1  Morning home DBP (mmHg ± SD) 89.7 ± 11.7  Morning home pulse rate (beats/min ± SD) 72.1 ± 10.2  Evening home SBP (mmHg ± SD) 150.2 ± 17.6  Evening home DBP (mmHg ± SD) 85.6 ± 12.2  Evening home pulse rate (beats/min ± SD) 72.5 ± 9.6 Patient classification (n [%])  Normal BP 150 [5.

Both studies concluded that there is no convincing evidence that mechanical bowel preparation is associated with reduced rates of anastomotic leakage after elective colorectal surgery. Finally in 2009 Kam et al published a systematic review on ICI vs. MD in left-sided colorectal emergencies: they included 1

RCT, 1 prospective comparative trial and 5 prospective descriptive case series and concluded that, although the power of studies is poor and large-scale prospective randomized trial is desirable, no statistical significance could be shown between the two procedures [34]. Recommendation:during segmental resection and primary anastomosis for OLCC (without cecal perforation or evidence of synchronous right colonic cancers), either MD or ICI can be performed as the two techniques selleck screening library are associated with same mortality/morbidity rate. The only significant difference is that MD is a shorter and simpler procedure. Either procedure could be performed, depending of the experience/preference of the surgeon (Grade of recommendation 1A). Endoscopic Colonic Stents (SEMS) Colonic stents were introduced in the 1990 s and have been used for palliation or as a bridge to surgery:

following release of the obstruction with an endoscopic stent the patient is properly staged and offered multidisciplinary treatment and eventually elective or semi-elective surgery [35]. A) Palliation: endoscopic colonic stents (SEMS) vs. colostomy (C) There are three RCTs comparing colostomy vs. SEMS for palliation of malignant selleck compound colonic obstruction [36–38]. Xinopulos et al in 2004 randomized 30 patients. In the SEMS group placement of the stent was achieved in 93.3% (14/15 pt); there was no mortality. In 57% (8/14) of patients in which the stent was successfully placed, colonic obstruction was permanently released (i.e. until death). Mean survival was 21,4 month in SEMS group and 20,9 months in C group. Mean hospital stay was quite high in both groups and significantly higher in group C: 28 days vs. 60 days. This study presented several limitations, and the small sample size might have limited the

ability to discern differences between groups [36] Fiori et al in 2004 randomized 22 patients to either C or SEMS: mortality was 0% in both groups, morbidity was similar. SEMS group had Bacterial neuraminidase shorter time to oral intake, restoration of bowel function, and hospital stay. This study was also limited by the small simple size and by the lack of follow up [37] The Dutch Stent-in I multicenter RCT was planned to randomized patients with incurable colorectal cancer to SEMS or surgery: the study was terminated prematurely after enrolling 21 patients because four stent-related delayed perforations resulting in three deaths among 10 patients in the SEMS group. There are no clear explanation for such a high perforation rate; the authors pointed out that limited safety data existed fort he stent used in their study (WallFlex, Boston Scientific Natick, MA) [38].

Figure 4 displays the results, from which it is obvious that the background in the component R image was lower than that in the RGB image. Hence, the mentioned contrast enhancement algorithm would be acted on the component R of test strip images. The procedure of the proposed algorithm is listed below. Figure SCH 900776 research buy 4 Comparison between RGB and component R. (a) Curve graph in RGB. (b) Curve graph in component R. Consider an image with N pixels and a gray level range of [0, K − 1]. 1. Calculate the average gray value of all pixels named

T. Then, scan all the pixels. These pixels’ value smaller than T will decrease a constant C.   2. Calculate the probability density function (PDF) P(k). P(k) = n k /N, k = 0,1…, K − 1, where n k is the number of pixels with gray level k.   3. Compute an upper limit P u and a lower limit P l with great importance. P u = v · P max, where P max is the highest probability value and v represents the upper threshold normalized to P max (v belongs between 0 and 1). P l is a fixed value, which filters some very low probability values. Herein, P l was set as 0.1%.   4. Define the new PDF. . This step will remove very low probability pixels and limit very GSK126 high probability

pixels (background pixels).   5. Calculate the cumulative distribution function C n(k). .   6. Obtain the output image. O(N) = n · W out · C n(k), where W out is equal to the biggest value subtracting the smallest

value and n represents the number of superposition.   Discussion Characterization of CdSe QDs All the CdSe QDs were prepared by our group’s member [7, 18, 26–29]. The absorption and emission spectrogram is displayed in Figure 5a. The emission wavelength was approximately 625 nm. The HR-TEM pictures (Figure 5b) show that the water-soluble CdSe QDs have a diameter of 5.4 nm. The digital photos of the QD-labeled anti-CagA antibody before and after UV condition are shown in Figure 5c. Figure 5 Characterization of CdSe QDs. (a) Absorption Dimethyl sulfoxide and emission spectrogram. (b) TEM picture of synthesized CdSe QDs. (c) Digital photos of the QD-labeled anti-CagA antibody before and after UV condition. Hardware units Figure 6 shows each component of the device. Figure 6a shows the CCD image sensor with a volume of 29 × 29 × 29 m3. Figure 6c,d represents the excitation light source and the integrated instrument, respectively. Compared with the use of the card acquisition card, that of the CCD image sensor with a USB is more convenient and has less cost. The UV filter is displayed in Figure 6b and could be connected with the CCD image sensor, playing an important role in eliminating interference of the light source. In addition, employing a lithium battery made the device viable without power supply for more than 6 h. Figure 6 Hardware units of the device. (a) CCD image sensor. (b) UV filter. (c) Excitation light source. (d) Integrated instrument.

3 pmV-1 for LiNbO3[26]. The LiNbO3-PDMS-based composite nanogenerator for the e 33 geometry generates stable power even for excessive strain. In Figure  5a, we show the push-pull cycling number dependence of the open-circuit voltage and closed-circuit current. Over a period of 22 h, we continuously applied a compressive strain of up to 105 cycles. Within ±1%, the open-circuit voltage and closed-circuit current were quite stable. The stability of the dielectric constant and electric loss are shown in Figure  5b,c, respectively. The dielectric constant and current–voltage (I-V)

characteristics were similar before and after the application of excessive strain (approximately GSK126 105 cycles). Figure 5 Stability of the LiNbO 3 -PDMS composite nanogenerator. (a) Cycling number-dependent open-circuit voltage and closed-circuit current of the LiNbO3-PDMS composite nanogenerator.

(b) Dielectric constant and (c) current–voltage (I-V) characteristics before and after 105 cycles of excessive strain. In the LiNbO3-PDMS composite nanogenerator, stable power generation depended on the mixing ratio. LiNbO3 has high piezoelectricity, but is fragile and lossy. In contrast, PDMS has flexibility and a low dielectric constant, but no piezoelectricity. buy BGJ398 Nearly the same power generation, dielectric constant, and loss after excessive strain suggest that our LiNbO3-PDMS composite nanogenerator was quite stable; this was attributed to the low volume ratio of LiNbO3 inside the PDMS (approximately 1%). If the volume ratio of LiNbO3 were to increase, then the power generation would increase as well at the expense of a larger dielectric constant; however, the composite devices may become fragile and lossy. Therefore, we suggest that optimization of the mixing ratio is crucial for the application of a lead-free piezoelectric composite nanogenerator. Conclusions We report a lead-free LiNbO3 nanowire-based nanocomposite for piezoelectric power Adenosine generation. Through the ion exchange of Na2Nb2O6-H2O, we synthesized long

(approximately 50 μm) single-crystalline LiNbO3 nanowires having a high piezoelectric coefficient (approximately 25 pmV-1). By blending LiNbO3 and PDMS polymer at a volume ratio of 1:100, we fabricated a flexible nanocomposite nanogenerator. For a similar strain, the piezoelectric power generation for the e 33 geometry was significantly larger than that for the e 31 geometry due to the difference in the d 33 and d 31 piezoelectric coefficients of LiNbO3. For up to 105 cycles of excessive strain, we observed that the output power, dielectric constant, and loss were quite stable. Optimization of the mixing ratio between lead-free piezoelectric materials and flexible polymers is an important factor to consider in the application of an energy-harvesting nanogenerator.

Work 17:39–48 Central Statistical Office of the Netherlands (2009) National statistics on sick leave, frequency, period of absence. Heerlen/Voorburg, The Netherlands. Available via: http://​statline.​cbs.​nl. Accessed 6 January 2009 Crown WH, Finkelstein S, Berndt ER, Ling D, Poret AW, Rush AJ, Russell JM (2002) The impact of treatment-resistant depression on health care utilization and costs. J Clin Psychiatry 63:963–971 De Waal MWM, Arnold IA, Eekhof JAH, Van Hemert AM (2004) check details Somatoform disorders in general practice: prevalence, functional impairment and comorbidity with anxiety and depressive disorders. Br J Psychiatry 184:470–476CrossRef Diehl M, Coyle N, Labouvie-Vief G (1996) Age

and sex differences in strategies of coping and defense across the life span. Psychol Aging 11:127–139CrossRef Duijts SFA, Kant IJ, Ribociclib nmr Swaen GMH, van den Brandt PA, Zeegers MPA (2007) A meta-analysis of observational

studies identifies predictors of sickness absence. J Clin Epidemiol 60:1105–1115CrossRef Eaton WW, Martins SS, Nestadt G, Bienvenu OJ, Clarke D, Alexandre P (2008) The burden of mental disorders. Epidemiol Rev 30:1–14CrossRef Escobar JI, Burnam MA, Karno M, Forsythe A, Golding JM (1987) Somatization in the community. Arch Gen Psychiatry 44:713–718 Godin I, Kornitzer M, Clumeck N, Linkowski P, Valente F, Kittel F (2009) Gender specificity in the prediction of clinically diagnosed depression: results of a large cohort of Belgian workers. Soc Psychiatry Psychiatr Epidemiol 44:592–600CrossRef Griffin JM, Fuhrer R, Stansfeld SA, Marmot M (2002) The importance of low control at work and home on depression and anxiety: do these effects vary by gender and social class? Soc Sci Med 54:783–798CrossRef Hardeveld F, Spijker J, De Graaf R, Nolen WA, Beekman AT (2010) Prevalence and predictors of recurrence of major depressive disorder in the adult population. Acta Psychiatr Scand. doi:10.​1111/​j.​1600-0447.​2009.​01519.​x Hensing G, Wahlstrom R (2004) Chapter 7. Sickness absence and psychiatric

disorders. Scand J Public Health 32:152–180CrossRef Montelukast Sodium Hensing G, Brage S, Nygård JF, Sandanger I, Tellnes G (2000) Sickness absence with psychiatric disorders—an increased risk for marginalisation among men? Soc Psychiatry Psychiatr Epidemiol 35:335–340CrossRef Keller MB (2002) The long-term clinical course of generalized anxiety disorder. J Clin Psychiatry 63:11–16 Koopmans PC, Roelen CA, Groothoff JW (2008a) Sickness absence due to depressive symptoms. Int Arch Occup Environ Health 81:711–719CrossRef Koopmans PC, Roelen CA, Groothoff JW (2008b) Frequent and long-term absence as a risk factor for work disability and job termination among employees in the private sector. Occup Environ Med 65:494–499CrossRef Laitinen-Krispijn S, Bijl RV (2000) Mental disorders and employee sickness absence: the NEMESIS study.

When it comes to bile tolerance, Bsh is probably what first comes to mind, since it involves the direct hydrolysis of bile salts. Although the ecological significance of microbial Bsh activity is not yet fully understood, the suggestion was made that it may play a major detoxification role [27]. L. plantarum strains carry four bsh genes (bsh1 to bsh4). Bsh2, bsh3 and bsh4 are highly conserved among L. plantarum species, while bsh1 is not and seems to be the major determinant of the global Bsh activity of L. plantarum strains. Besides, a bsh1-mutant of L. plantarum WCFS1 displayed a decreased tolerance to glycine-conjugated bile salts [49]. In our study, a Bsh1 homologue could only be found

in the most resistant strain in standard PLX3397 molecular weight conditions, PD0325901 but its amount decreased following the strain’s exposure to bile. This result contrasts with the bsh1 gene up-regulation in L. plantarum WCFS1 following bile challenge [45]. Strains from L. acidophilus and L. salivarius on the other hand did not seem to up-regulate their Bsh1 production following bile exposure

[38, 50]. Such discrepancy in regulation trends of bsh genes suggests that, depending on the considered strains and species, Bsh activity may or may not be a major determinant of bile resistance. Finally, it appeared that the six bile tolerance factors described above may contribute in various ways to the bile tolerance of L. plantarum strains. In particular, strains appeared to regulate key Olopatadine proteins differently following exposure to bile, which suggests that several strategies coexist in the bile adaptation process of L. plantarum species, some strains favoring certain specific pathways, while others downplaying them. Conclusions This work used comparative and functional proteomics to analyze cell-free protein extracts from three L. plantarum strains with different bile resistance properties. This approach showed that the natural protein diversity among L. plantarum strains cultured in standard conditions can reflect their ability to tolerate bile. The results provided an overview of proteomic patterns related to

bile tolerance, and showed a clear effect of bile salts on the level of expression of certain proteins within these patterns. Particularly, 13 out of the 15 proteins of interest were shown to be directly involved in the bile tolerance of L. plantarum, six of which could be part of specific bile adaptation pathways, including protection against oxidative stress (GshR1 and GshR4), maintenance of cell envelope integrity (Cfa2), and active removal of bile-related stress factors (Bsh1, OpuA, and AtpH). Also, analysis of changes in protein expression gave insight into the way the different strains use these pathways for their survival, suggesting complex, strain-specific and probably conflicting molecular mechanisms in the cell’s adaptation strategy to bile.

Proc Natl Acad Sci USA 1972,69(8):2110–2114.CrossRefPubMed 40. Miller VL, Mekalanos JJ: A novel suicide vector and its use in construction of insertion mutations: osmoregulation of outer membrane proteins and virulence determinants in Vibrio cholerae requires toxR. J Bacteriol 1988,170(6):2575–2583.PubMed 41. Craig FF, Coote JG, Parton R, Freer JH, Gilmour NJ: A plasmid which can be transferred between Escherichia coli and Pasteurella haemolytica by electroporation and conjugation.

J Gen Microbiol 1989,135(11):2885–2890.PubMed 42. Figurski DH, Helinski DR: Replication of an origin-containing derivative of plasmid RK2 dependent on a plasmid Mitomycin C datasheet function provided in trans. Proc Natl Acad Sci USA 1979,76(4):1648–1652.CrossRefPubMed

43. Mahenthiralingam E, Coenye T, Chung JW, Speert DP, Govan JR, Taylor P, Vandamme P: Diagnostically and experimentally useful buy MG-132 panel of strains from the Burkholderia cepacia complex. J Clin Microbiol 2000,38(2):910–913.PubMed Authors’ contributions JNRH participated in the design of the study, carried out the majority of experiments and wrote the manuscript. RAMB was involved in plasmid construction, carried out some reporter analysis and critically read the manuscript. STC participated in the design and coordination of the study and final edition of the manuscript. All authors read and approved the final manuscript.”
“Background It is well established that the microbiota of the dental plaque are the primary etiologic agents of periodontal disease in humans [1]. The complex consortium of bacteria in the subgingival plaque biofilm [2] is in a state of dynamic equilibrium with the inflammatory response mounted in the adjacent gingival tissues, resulting in interdependent shifts in the composition of both the bacterial community and the ensuing inflammatory infiltrate. Indeed, it is known

that microbial profiles of plaques harvested from healthy gingival Nintedanib (BIBF 1120) sulci differ from those stemming from gingivitis or periodontitis lesions [3, 4]. Similarly, the cellular and molecular fabric of healthy gingival tissues differs from that of an incipient, early or established periodontitis lesion [5, 6]. A relatively new genomic tool that facilitates the study of the biology of cells, tissues or diseases is gene expression profiling, i.e., the systematic cataloging of messenger RNA sequences, and has provided enormous insights in the pathobiology of complex diseases, particularly in cancer research [7, 8]. Our group was the first to describe gingival tissue transcriptomes in chronic and aggressive periodontitis [9] and recently provided a comprehensive description of differential gene expression signatures in clinically healthy and diseased gingival units in periodontitis patients [10]. To date, a limited amount of data are available characterizing oral tissue transcriptomes in response to bacterial stimuli.

The scanning probe unit scanned the entire tumors www.selleckchem.com/products/PLX-4032.html in several scanning paths with a vertical interval of 0.1 mm. Thus, a magnetic image for the tumor could be constructed, as shown in Figure  2a. SPIONPs under AC field excitation generally expressed the characteristics of AC susceptibility. Therefore, the SSB signal from the in-phase component of the AC susceptibility of SPIONPs was in proportion to the SPIONP concentration [16]. The

3-T MRI (Bruker Biospec System, Karlsruhe, Germany) and a volume coil were used for T2-weighted images. In parallel with the arrangement of the anesthetized mouse, a long tube filled with deionized (DI) water was inserted as the intensity reference to dismiss the instrument drift at various times. Torin 1 nmr Producing the coronal images of each entire mice body at 2-mm intervals required nearly 2 h. In general, the uniformity of the static field and gradient field is distorted by SPIONPs, resulting in the dephasing of the proton nuclear spin and, subsequently, the reduction of nuclear magnetic resonance (NMR) intensity induced by the pulse field of MRI [20]. Hence, the labeled tumor cells using bound SPIONPs expressed a darker image. Therefore, SPIONPs were the contrast agent of the MR images. For ICP examination (EVISA Instruments, PE-SCIEX ELAN 6100 DRC,

High Valued Instrument Center, National Science Council, Kaohsiung, Taiwan), two pieces of tumor tissue from one euthanized mouse were both weighted by a 0.1-g weight

and then dissolved entirely in a HNO3 solution at a concentration of 65%; they were then diluted and examined. To evaluate the incorporation of an anti-CEA SPIONP quantity into the tumor tissue, the difference of Fe concentration between the varied post-injection and pre-injection times at the 0th hour was expressed as ΔC Fe (ppm). The tissue staining was processed (Laboratory Animal Center, National Taiwan University, Taipei, Taiwan), and the × 400 magnification of the optical images was observed using a light microscope. Reverse transcriptase HE staining, PB staining, anti-CEA staining, and CD 31 staining were performed to identify the tumor tissue, Fe element distribution, and anti-CEA SPIONP distribution; and the degree of tumor angiogenesis was related to the transportation of anti-CEA SPIONPs. Results and discussion Figure  1b shows the curve of the magnetism-applied field (M-H) curve of anti-CEA SPIONPs. Based on the ultralow hysteresis in the M-H curve, the anti-CEA SPIONPs expressed superparamagnetic characteristics. Furthermore, the X-ray pattern of the anti-CEA SPIONPs in Figure  1c depicts the crystal structure of anti-CEA SPIONPs obtained by X-ray diffraction. The major peaks correspond with the standard X-ray pattern of Fe3O4 (JCPDS card no. 65–3107), verifying that the magnetic material was Fe3O4, a magnetic iron oxide (IO).

Osteoporos Int. doi:10.​1007/​s00198-009-1052-5 2. Stöckl D, Sluss PM, Thienpont LM (2009) Specifications for trueness and precision of a reference measurement system for serum/plasma 25-hydroxyvitamin D analysis. Clin Chim Acta 408:8–13CrossRefPubMed”
“Introduction

The demonstrated efficacy of a therapy in a randomized clinical trial may not predict its actual effectiveness in clinical practice because of differences in characteristics of patients and level of medical care [1]. As a therapy for osteoporosis, the oral bisphosphonates have been widely utilized in recent years. These bisphosphonates include once-a-week alendronate (marketed in the USA since 2000), once-a-week risedronate (since 2002), and once-a-month ibandronate (since 2005). Since health data on large numbers of bisphosphonate patients BMN673 in clinical practice have now been collected (through administrative billing data, medical records, and registries), many recent observational studies have examined the effectiveness of oral bisphosphonates for reducing clinical fractures. The designs of these observational studies have included comparisons between patient populations with or without a fracture

[2, 3], with or without bisphosphonate use [4, 5], compliant or not compliant with bisphosphonate use [6–19], or between patient populations on different bisphosphonate molecules [20–23]. A key limitation in interpreting any of these comparisons is uncertainty if known or unknown differences in baseline Erismodegib fracture risk between patient populations could account for some or all of the reported results. An approach to directly measure the baseline risk of an outcome within patient populations that has been used in effectiveness studies of other therapies may be applicable to the study of bisphosphonates. In a comparison of patients receiving a bare or drug-eluting stent,

the mortality 2 days after procedure was Monoiodotyrosine used to assess risk of the mortality outcome independent of possible drug effect [24]. In a comparison of patients receiving influenza vaccine or not, the mortality after vaccination but before flu season was used to assess risk of mortality outcome independent of possible vaccination effect [25]. Likewise, following initiation of bisphosphonate therapy, the realization of fracture reduction is likely not immediate. Bone mineral density, a surrogate marker of therapeutic effect, begins to change after start of therapy though does not reach its maximum level of change until at least 1 year on therapy [26]. As changes in bone density and quality take time, correspondingly, fracture reductions have not been noted earlier than 6 months after start of therapy within post hoc, pooled analysis of clinical trials [27, 28].

A total of approximately 30000 transposon mutants were screened and 14 phage resistant mutants were isolated and analyzed. Since two mutants, TM20 and TM22 are defect in the same gene, rmlB, a total of 13 genes was identified, which are essential for phage infection. The transposon VX-809 cell line screen revealed genes important for LPS biosynthesis (see Table 4 for details) like the gene algC which is needed for a complete LPS core in P. aeruginosa [16]. It also revealed the genes rmlA and rmlB, which are involved in the biosynthesis of the LPS core sugars [39, 40]. These findings confirm that the phage JG004 uses LPS as receptor.

Other identified genes involved in LPS biosynthesis are wzz2, selleck inhibitor waaL, migA, PA5000 and PA5001 (Table 4) [40]. Since nine out of 13 identified genes encoded proteins involved in LPS biosynthesis, we additionally isolated LPS from all mutant strains and analyzed it by electrophoresis (see Materials and Methods). Figure 4 shows the LPS profiles of the transposon mutants. The lipid A, which migrates furthest due to its size, is seen as a dark grey spot at the end of the gel. The migration depends on changes in the LPS composition, mostly in the core polysaccharide which

is adjacent to the lipid A [41]. Not all LPS biosynthesis genes cause changes in the LPS which are visible by electrophorsis e.g. migA [42], which appears as wild type LPS. The black line in Figure 4 indicates the migration level of the wild type lipid A. Dramatic changes in the LPS profile which differs clearly from the P. aeruginosa wild type LPS can be seen for the algC, the wzz2 and the PA5001 mutant. Further analysis of the LPS for example Western blot analysis with antibodies specific to the different components of the LPS could provide a better understanding

of the mutants, Olopatadine but was not involved in this phage characterization study. Figure 4 LPS profile of transposon mutants. Silver stained SDS-PAGE illustrating the isolated LPS of the wild type PAO1 and the transposon mutants. Only the gene, interrupted by the transposon of the respective mutant is indicated on top of the lanes, PAO1 is the P. aeruginosa wild type. The arrow points to the black line in the lower part of the gel. This line indicates the migration of wild type lipid A and core sugars of the LPS [42]. As indicated, the LPS of the speD, PA0534, PA0421, PA2555 and migA mutant strains appears similar to wild type LPS. The LPS profile of the remaining mutant strains is different and indicates an altered LPS structure. Interestingly, the biochemical analysis of LPS indicates that gene PA2200 might be involved in biosynthesis or modification of P. aeruginosa LPS due to altered migration. We also identified genes essential for phage infection, which encode proteins of unknown function.