23 per 100,000 population during 2010 7 Meningococcal pneumonia i

23 per 100,000 population during 2010.7 Meningococcal pneumonia is infrequent, is estimated to occur in <5%–15% of patients with invasive meningococcal disease, although the precise incidence is difficult to establish because of uncertainty in establishing the cause of pneumonia.2 and 3 Serogroup Y is more likely than other serogroups to be associated with pneumonia.3 Blood or pleural cultures that yield N. meningitidis establish the diagnosis with certainty. Meningococcal colonization of the nasopharyngeal mucosae is a critical initial step in

the pathogenesis of systemic MAPK Inhibitor Library infection. Several cell surface structures have been identified that function as adhesins in attachment of meningococci to respiratory epithelial cells. After nasopharyngeal colonization, microaspiration of upper respiratory tract secretions containing N. meningitidis probably occurs, with the subsequent

development of pneumonia. Which virulence factors are operative in the production of lung infection and whether they are unique to serogroup Y meningococci are unknown. In addition, the conditions accounting for the increase in serogroup Y infections remain undefined. 2 Other authors have described a predilection of serogroup Y meningococcus for causing respiratory illness, including a large outbreak of predominantly respiratory. Smilack et al. reported a military outbreak that included 12 cases of serogroup Y meningococcal disease (SYMD) among members of an C59 wnt molecular weight army combat training unit. In this series, 5 patients had meningococcemia, 5 had meningitis, and 2 presented with primary meningococcal pneumonia.4 Subsequently, a case series of SYMD was reported in a group of US Air Force recruits in 1971–1974.6 In that series, the predominant manifestation of serogroup Y disease was respiratory; 68 (77%) of 88 patients had meningococcal pneumonia, documented by transtracheal Edoxaban aspirates in 94% of the cases. Only 4 (6%) of the 68 patients with pneumonia had positive blood cultures.5

Among the patients with pneumonia, the response to antibiotic therapy was prompt; 93% of the patients were afebrile within 3 days of antibiotic therapy.2 The outcome of meningococcal pneumonia when treated is generally favorable, but the diagnosis requires a high index of suspicion, testing of respiratory samples, and blood cultures. In conclusion, we report a case of bacteraemic pneumonia caused by N. meningitidis serogroup Y with reduced susceptibility to penicillin in an adult patient. All authors report no conflicts of interest relevant to this study. “
“The recent report on “Red Ginseng and H5N1 influenza infection” in this journal is very interesting [1]. Park et al [1] noted that “the diet with the immune-enhancing Red Ginseng could help humans to overcome the infections by HP H5N1 influenza virus.

Depending on the environment, the metal release from stainless st

Depending on the environment, the metal release from stainless steel is also influenced by other processes including active corrosion and protonation [4], [11] and [14]. The dynamic exchange of proteins between the surface and the solution is important for the metal release process, and depends on various factors including protein concentration and agitation [16]. Surface adsorption

is influenced by the surface charge of stainless steel and of adsorbed species [17], which results in electrostatic (EL) forces (repelling or attractive) [18]. Non-polar (electrodynamic, or Lifshitz-van der Waals – LW), and polar (electron–donor, electron–acceptor, or Lewis acid–base – AB) interactions are both important for any surface adsorption [17], [18] and [19]. These properties can be determined via contact angle measurements using liquids of different and known

GSK 3 inhibitor surface energy components [18]. Dehydration of water at the surface and changes in protein conformation where the driving force is a net gain in entropy, are important in the case of BSA adsorption. This process takes place even if the polarity is the same as the stainless steel surface [20] and [21]. The surface charge is important for the adsorption of proteins (especially for small, hard proteins), since one of the driving forces for protein adsorption on stainless steel is electrostatic [17], [20] and [21]. The zeta potential of massive stainless steel is commonly reported as negative at neutral pH and

the isoelectric point (IEP) was identified between pH 3 and 5 [4], [21], [22], [23] and [24]. Even significantly higher IEPs, between 6 and 8.5, have MK-2206 cost see more been reported for stainless steel particles [25] and [26] and massive sheet of stainless steel (predicted data) [27] and [28]. More positive IEPs of nano- and micron-sized stainless steel particles compared with massive sheet may be explained by differences in surface oxide speciation (such as composition, thickness, crystallinity, phase distribution, and catalytic properties) [29], [30] and [31]. No significant differences in IEP have been reported in the literature [32] for different pure metal particles and their corresponding bulk oxides. However, since all of these particles were treated in NaOH and HNO3 prior to the measurements, this might have influenced the results. Reported IEPs of bulk oxides and hydroxides of iron and chromium vary between 4.5 and 8.5 [33] and [34]. This is higher compared with measurements for massive stainless steel surface oxides made of similar constituents. Somewhat lower IEPs have been reported for several metals and alloys (e.g. stainless steel) [23] and [35] with thin surface oxides (as compared with bulk oxides). The lower IEPs of metals could possibly be explained by a mirror effect of electrons at the metallic interface adjacent to the thin surface oxide [36] and [37].

In addition, Korean red ginseng improves arterial stiffness in hy

In addition, Korean red ginseng improves arterial stiffness in hypertension [50]. Overall, these results show the improvement in vasomotor function by ginseng. It has initially been thought that ginseng may increase blood pressure to harmful levels. However, previous studies have shown that ginseng

cures patients with low blood pressure, restoring it to normal levels. In addition, ginseng also reduces blood pressure in patients with high blood pressure [51]. The blood pressure lowering activity of Korean ginseng is attributed to the production of vascular endothelial cell-derived NO [52]. Recent studies have shown that ginseng INCB024360 molecular weight has biochemical and pharmacological activities beneficial for blood pressure control, where lower doses have greater antihypertensive effects than higher doses [53], and improve blood circulation through vasodilation [52]. The antihypertensive effect of ginseng is mediated by the inhibition of myogenic responses on the blood vessels [54]. In addition, ginseng protects against tissue damage and is also a novel therapy Selleckchem Tyrosine Kinase Inhibitor Library for heart failure [55]. Saponins from P. notoginseng protected the heart against doxorubicin-induced cardiotoxicity [56] and blocked the cardiac hypertrophy induced by monocrotaline in rats [57]. Left ventricular hypertrophy produced by aortic coarctation was protected by ginsenoside Rg1 through NO

functions [58]. Electromechanical alternans was suppressed by ginsenoside Re in cardiomyocytes [59], and myocardial infarction after ischemia and reperfusion was preconditionally protected by ginsenoside Rb1 [60]. Another study showed that ginsenoside Rg1 inhibits left ventricular hypertrophy [61]. P. ginseng also suppresses apoptosis in neonatal cardiocytes by modulating Adenosine Bcl-2 and caspase-3 activities during hypoxia and reperfusion [62]. Furthermore, cardiomyocytes have been protected by ginsenoside Rg1 from oxidative injury through antioxidation

and intracellular calcium modulation [63]. Total saponin, panaxadiol, and panaxatriol from ginseng have been able to protect cardiomyocytes from ischemia and reperfusion injuries [64]. Cardiac injury in diabetes induced by streptozotocin has been prevented by ginsenoside Rb1 [65] and unfavorable postmyocardial remodeling was reduced by ginseng [66]. Some studies suggest that cardiac hypertrophy and heart failure are prevented by ginseng through Nhe-1 modulation and reduction of calcineurin activation [67]. Recent studies also show that cardiac protection by NO was facilitated by compound K through the Akt/PI3K pathway [68]. Acute cardiac injury from ischemia and reperfusion has been protected through the GR and estrogen receptor-activated risk pathway by the eNOS-dependent mechanism in rats [69]. Thus, these studies suggest that ginseng preserves heart function after myocardial tissue deterioration.

4) The sub-regional chronologies highlight the strong fidelity b

4). The sub-regional chronologies highlight the strong fidelity between chronologies within group (i.e., BEC unit) and the synchronous WSB outbreak events across the study area, while also emphasizing the unique

outbreak history at smaller spatial scales (Fig. 4 and Fig. 5). For example, chronologies in the very dry-mild BEC unit (FC and FR) are located on south facing slopes of the Fraser or Chilcotin Rivers and were characterized by a pronounced high amplitude signal when compared to the other sub-regional chronologies (Fig. 4). Chronologies from the dry-cool Fraser BEC unit (S1–S2, S5–S6) (Fig. 4), which is characterized by wetter and cooler conditions, have a notable quiescent phase from the early-1700s to early-1800s (Fig. 4 and Fig. 5) that also corresponds to decreased power in the wavelet spectrum (Fig. 6). This suggests that site and/or stand conditions play an important Src inhibitor role in mediating tree response PD-0332991 solubility dmso to WSB outbreaks. For the very dry-mild sites conditions such as steep slopes, thin soils, and availability of

soil moisture all likely contribute to increasing the sensitivity of these chronologies to negative (e.g., WSB defoliation) and positive (e.g., growing season moisture) stimulus. Conversely, the dry-cool Fraser sites, which were sampled at higher elevation (Table 1) and not from steep slopes, have a dampened sensitivity to environmental factors (Fig. 4). Site factors in combination with cooler and wetter climatic conditions (Table 2) are likely resulting in a more average growth response over time where tree grow is less responsive to events like budworm feeding (Fig. 4). The stand level to

sub-regional scale WSB outbreak dynamics across the study area highlight the complex interactions between: site characteristics, canopy structure and composition, host plant quality, bud phenology, growth Cyclic nucleotide phosphodiesterase rates, tree resistance and climate, which to some extent all play a role in determining the intensity of individual outbreaks and tree growth responses across an area (Kozlowski, 1969, Clancy, 1992, Swetnam and Lynch, 1993, Chen et al., 2001, Maclauchlan and Brooks, 2009 and Nealis, 2012). Synchronous outbreak periods in the Cariboo Forest Region in the 1720s, late-1700s, 1870s and 1930s (Fig. 5) were also present in the reconstructions from locations south of our study area (Campbell et al., 2005, Campbell et al., 2006, Alfaro et al., 2008, Alfaro et al., 2014 and Flower et al., 2014). Notably, the outbreak from 1898 to 1909 was a widespread event that appears in reconstructions in the area directly south of the Cariboo Forest Region (Campbell et al., 2006 and Alfaro et al., 2014), the southern Okanagan (Alfaro et al., 2008 and Alfaro et al., 2014), southern Vancouver Island (Harris et al., 1985), as well as in northeastern Oregon (Swetnam et al., 1995) and in stands found from central Oregon to western Montana (Flower et al., 2014).

Each component was rated on a scale from 1 to 5 Items were score

Each component was rated on a scale from 1 to 5. Items were scored as a 1 if the component never occurred in that session, as a 2 if the component occurred at least once but not in an in-depth manner, as a 3 if it occurred several

times during the session and was covered at least once in a moderately in-depth manner, as a 4 if it occurred frequently and was covered in-depth, and as a 5 if it occurred with high frequency and was covered in considerable depth. The therapist was also rated with regard to overall adherence this website to ACT principles as well as the overall competence of the therapist. Sessions 3 and 10 were rated for Participant 1, and Sessions 4 and 7 were rated for Participant 2. At least one of the rated ACT components was covered frequently in a very in-depth manner (i.e., received a rating of “5”) in each of the rated sessions. The means for each component over the rated sessions were as follows: creative hopelessness/workability = 4.00 Cilengitide datasheet (SD = .82), willingness/acceptance = 4.25 (SD = .96), defusion = 3.5 (SD = 1.29), values/goals = 2.25 (SD = .50),

committed action = 2.25 (SD = .50), and present-moment focus = 4.25 (SD = .50). Therapist overall adherence to the manual was also rated highly (M = 4.75; SD = .50) as well as therapist overall competence (M = 4.25; SD = .50). The therapist was also rated on use of techniques antithetical to an ACT intervention, including challenging cognitions, experiential avoidant change strategies, using a cognitive therapy rationale, and encouraging the idea that thoughts and feelings cause actions. Each

of these items was rated as a 1 across participants, indicating that none of these interventions were observed in any rated sessions. The primary dependent variable was participants’ daily self-monitored binge eating. The baseline phase, treatment phase, and follow-up phases of treatment are presented in Figure 1. Additionally, problematic eating and related outcome variables at pretreatment, Baf-A1 order midpoint, posttreatment, and 3-month follow-up are presented in Table 2 and Table 3. The average number of self-reported binge eating for Participant 1 was 3.0 times per week during the pretreatment period (see Table 2), which is consistent with the criteria for BED. Within the first 2 weeks of the intervention, the average number of binge eating decreased to approximately 1.5 times per week. Throughout the course of the 10-week ACT intervention, Participant 1 engaged in a total of only 5 episodes of binge eating. Her average number of binge eating episodes during the ACT intervention was .5 per week. Participant 1 did not report any episodes of binge eating at 3-month follow-up. The reduction in binge eating paralleled improvement in body image flexibility. Participant 1’s pretreatment level of body image flexibility (BI-AAQ) was 41.

Hand hygiene with the use of an alcohol-based hand rub has become

Hand hygiene with the use of an alcohol-based hand rub has become a key infection click here control measure. We have further promoted hand hygiene by introducing a concept of directly-observed hand hygiene and electronic monitoring of compliance (Cheng et al., 2011a and Cheng et al., 2007b), resulting

in better control of endemic and sporadic pathogens in the hospital (Cheng et al., 2010a and Cheng et al., 2009c). The concept of extensive contact tracing during the SARS outbreak has been harnessed for the control of multiple drug-resistant organisms which are not yet endemic in our healthcare setting (Cheng et al., 2009b and Cheng et al., 2012a). Ten years after the SARS outbreak, our healthcare system is better prepared for the new challenges posed by known and unknown emerging pathogens. “
“Some signs and symptoms in human subjects that may be tentatively associated with neurological involvement or that are clearly associated with West Nile neurological disease (WNND) can also be observed in mice or hamsters (Table 1), the two rodent species AT13387 suitable for WNV investigations. These rodent models have been valuable for understanding the mechanisms of neurological signs and symptoms in human subjects and how they might be managed or treated. Most human WNV cases are subclinical,

or develop a short-term febrile illness, which is referred to as WN fever (Bode et al., 2006, Hayes et al., 2005 and Sejvar, 2007). Fever is often recognized to occur during viremia, but fever is also associated with generalized inflammation of the meninges. Interestingly, WNV-infected hamsters monitored continuously with radiotelemetry do not have a fever during

the Loperamide viremic phase, but can have a temperature spike at days 5–6 when viral induced meningitis is observed (Siddharthan et al., 2009 and Wang et al., 2013a) (Table 1). These data suggest that WN fever in some cases might reflect neurological involvement, and not just the viremic phase. Having an animal model for WNV fever might provide an opportunity to investigate the cause of WNV-induced fever and the neurological implications in human subjects. A small subset of WNV patients develops more serious neurologic deficits (Table 1). Patients can present with meningitis symptoms, which include neck stiffness and light sensitivity (Bouffard et al., 2004, Omalu et al., 2003, Sampson et al., 2000, Sejvar et al., 2003a, Steele et al., 2000 and Weiss et al., 2001). Inflammation of the meninges can be observed in the rodent models (Ben-Nathan et al., 1995, Camenga et al., 1974 and Hunsperger and Roehrig, 2006), which suggests that they also get disease signs of meningitis, but efforts to observe these signs have not been undertaken, except for perhaps the detection of fever associated with CNS infection as described above (Wang et al., 2013a). Encephalitis as an infection of the brain is a more serious development of WNND (Table 1).

However, it also suggested that linking crop insurance to conserv

However, it also suggested that linking crop insurance to conservation compliance and

strengthening and expanding conservation Everolimus nmr compliance provisions could reduce nutrient loads. Daloğlu (2013) and Daloğlu et al. (in press) demonstrated, for example, that DRP load decreased by 6% with conservation compliance that included structural BMPs, as compared to an increase of 8% without compliance. The relatively small percent changes, however, reinforce the recommendation of Bosch et al. (2013) that significantly more BMP implementation is needed. Experiences in other large regions with nutrient problems (e.g., Chesapeake Bay, Gulf of Mexico/Mississippi River) have shown that significantly reducing non-point source loads is difficult. Not only are the sources spatially distributed, but the methods used are primarily voluntary and incentive based and thus difficult to target and track. Reducing non-point inputs of sediments and

nutrients is also difficult because the response time between action and result can be many years or longer, and the results can only be measured cumulatively in space and selleck screening library through time. For these reasons, we recommend the use of an adaptive management approach that sets “directionally correct” interim targets, evaluating the results both in loads and lake response on appropriate time-scales (e.g., www.selleck.co.jp/products/Fludarabine(Fludara).html 5-year running averages), and then adjusting management actions or loading targets, if necessary. Lake Erie is a good candidate for such an approach because its short water residence time (2.6 years) reduces one common time-lag in system response. Such an approach would also allow for more effective testing and post-audits of the ability of models to project the ecosystem’s response and thus improve subsequent assessments

and projections. We see this iteration of research and analysis, management-focused model development and application, management action, and monitoring of results as a particularly effective way to manage large, spatially complex ecosystems. If the monitored results are not as anticipated, returning to research and model refinement establishes a learning cycle that can lead to better informed decisions and improved outcomes. This is publication 13-005 of the NOAA Center for Coastal Sponsored Research EcoFore Lake Erie project, publication # 1681 from NOAA’s Great Lakes Environmental Research Laboratory, and publication 1830 of the U.S. Geological Survey Great Lakes Science Center. Support for portions of the work reported in this manuscript was provided by the NOAA Center for Sponsored Coastal Ocean Research under awards NA07OAR4320006, NA10NOS4780218, and NA09NOS4780234; by NSF grants 0644648, 1313897, 1039043 and 0927643; and the U.S.

, 2001), complementing existing freshwater invertebrate surveys o

, 2001), complementing existing freshwater invertebrate surveys of lakes on Macquarie Island (Dartnell et al., 2005). Surveys of stream invertebrates in AD 1992, 2008 and 2010 have already reported large compositional changes at sites exposed to grazing by rabbits (Marchant et al., 2011). In a wider context, the eradication of invasive species is increasingly becoming the goal of conservation management on other sub-Antarctic and oceanic islands around

the world (DOC, 2013, SGSSI, 2013 and SANAP, 2013). www.selleckchem.com/products/BMS-754807.html In all these cases a palaeoecological approach can provide an invaluable long-term perspective for quantifying ecosystem response and recovery after the eradication of the invasive species (Burney and Burney, 2007 and Connor et al., 2012). This study has demonstrated

that the introduction of rabbits on Macquarie Island led to unprecedented and statistically significant changes in Emerald Lake and its catchment from around the late AD 1800s. The scale and magnitude of these changes is unprecedented in at least the last ca. 7200 years. Sediment accumulation rates increased by >100 times due to increases in catchment erosion and within-lake production, and were accompanied by a fourfold increase in the total carbon and total nitrogen content of the sediments. A diverse diatom community was replaced by just two previously rare diatom species Fragilaria capucina and Psammothidium abundans; pioneer colonisers tuclazepam characteristic of rapidly changing environments. This study provides information on the scale of the impact together with one baseline against which the effectiveness of the remedial management, including PLX3397 clinical trial the very successful invasive species eradication programme, can be assessed. As similar eradication programmes are becoming increasingly common on sub-Antarctic islands, and islands elsewhere, this study demonstrates how palaeoecological methods may be used to provide a long-term perspective on both

natural and Anthropogenic forcing of ecosystems, the impact of invasive species and the effectiveness of management programmes aimed at restoring natural biodiversity. This study was funded by an Australian Antarctic Science grant (AAS 2663). Krystyna M. Saunders was funded by an Australian Postgraduate Award and an Australian Institute of Nuclear Science and Engineering Postgraduate Award. Access to Macquarie Island was granted by the Resource Management and Conservation Division, Department of Primary Industry, Parks, Water and the Environment. We would like to thank Donna Roberts for initially establishing the project, Bart Van de Vijver for taxonomic assistance, Keith Springer for background knowledge, technical and logistical support, John Gibson for discussions and contributing to 14C dating, and Sam Hagnauer for laboratory assistance. Comments by two anonymous reviewers helped to improve the manuscript.

To overcome the technical difficulties inherent to cell-based neu

To overcome the technical difficulties inherent to cell-based neutralization assays, we utilized

an electrochemiluminescence detection method, using the MesoScale Discovery (MSD) platform, to develop non-cell-based assays to assess the presence and nature of anti-IFN-β antibodies. In addition to a screening assay for binding Abs, we developed and characterized a non-cell-based assay, based www.selleckchem.com/products/Adriamycin.html on the binding of IFN-β to its receptor, to detect and quantify IFN-β NAbs. We present here the first report of the use of a non-cell-based assay for the assessment of NAbs in clinical samples from IFN-β treated patients. Comparative data from this assay and existing cell-based neutralization assays are also shown. Patients sera have been grouped into 3 distinct cohorts (none overlapping), depending on the available

serum samples and the bioassay previously used. Cohort A (n = 46) includes post-treatment only samples, tested in the MxA protein assay. Cohort B (n = 10) includes post-treatment only samples, tested in the antiviral assay. Cohort C (n = 31) includes sequential samples (baseline and subsequent time-points), tested in antiviral and reporter gene assays. Pooled or individual sera from normal healthy Selleck GW572016 donors were also included in the study (n = 27). Ethical approval and informed consent from patients and donors were obtained in accordance with the guidelines in the Helsinki Declaration for all sera tested. Therapeutic grade IFN-β-1a preparations were supplied to NIBSC directly by the manufacturer and routine supply chains. The recombinant human IFN-α/β R2/Fc chimera was obtained Baf-A1 price from R&D Systems (4015-AB) and the recombinant vaccinia virus-encoded neutralizing type I interferon receptor B18R, was obtained from eBioscience (14-8185). A lyophilized pooled human serum sample from IFN-β treated patients (coded 99/606, available from NIBSC) and a hyperimmune sheep polyclonal anti-IFN-β serum generated at NIBSC served as positive controls. IFN-β-1a was biotinylated with EZ-link

Sulfo-NHS-LC-Biotin (Thermo Scientific, 21335). The biotin, resuspended in water, was mixed with IFN-β to give a molecular challenge ratio of label/protein of 2 and the mixture left at room temperature for 1 h to enable the labeling reaction to reach completion. The labeled IFN-β was isolated using a PD-10 desalting column (GE Healthcare, 52-1308-00 AP), recovered in PBS and stored at 4 °C. The labeling of IFN-β-1a with ruthenium-NHS-ester was performed as per manufacturer’s instructions. Briefly, the ruthenium-NHS-ester (labeled Sulfo-Tag, MSD, R91AN-1) was resuspended in cold distilled water and mixed with IFN-β to give a molecular challenge ratio of label/protein of 2. The reaction mixture was incubated for 2 h at room temperature and the conjugated IFN-β isolated by centrifugation using Amicon Ultra 3K centrifugal filters (Millipore, UFC800324), recovered in PBS and stored at 4 °C.

At the same time, residual colonic innate immunity cells, such as

At the same time, residual colonic innate immunity cells, such as neutrophils and macrophages, of WT + DSS mice regressed to WT control baseline levels ( Figure 2B). The adaptive immunity colonic mucosa cells, including Treg, however, did not fully regress (WT vs WT + DSS, P = .048; Figure 2B). This result,

which is in line with gross pathology observation of MLN enlargement at 7 months after DSS treatments, suggests that subtle alterations in local gut adaptive immunity networks may persist for a particularly Caspase phosphorylation long period after the restoration of colonic mucosa architecture and the regression of colitis. In an effort to explain why uPA−/− + DSS mice develop colonic polypoid adenomas in the long term, while WT + DSS ones do not, we next examined the colon of mice at the early time point of 1 week after DSS treatment. We found that WT and uPA−/−controls showed normal colon histology, whereas their DSS-treated counterparts had the typical DSS-associated ulcerative colitis. At this early time point, DSS-treated mice had numerous foci of epithelial dysplasia, characterized by the same histopathologic and immunohistochemical features as those described in polyps (Figure 3A). Colonic

dysplastic foci of uPA−/− + DSS mice, however, were in a more advanced stage of the dysplasia/preneoplasia sequence than those of WT + DSS mice (P = .0001; Figure 3, A and B). A total of 2-minute polyps were found in 2 uPA−/− + DSS mice (2 of 24) and 1-minute polyp was found in the WT + DSS mice (1 of 23). DSS-induced ulcerative lesions, located mostly at the last part of the descending colon and the rectum, consistently presented a larger surface epithelium deficit in the uPA−/− + Y27632 Parvulin DSS mice compared to the same lesions

of the WT + DSS mice (P < .0001; Figure 3C). In the non-ulcerative parts of the gut mucosa, however, colitis in both groups of DSS-treated mice was characterized by comparable levels of inflammatory cell infiltration (P = .1098; Figure 3D). To examine whether the tumor-promoting uPA deficiency is associated with a different inflammatory cell composition of DSS colitis, we labeled in situ and then quantified selected critical inflammatory cell types in the colonic mucosa. We found that the numbers of MPO + neutrophils were significantly higher in both the ulcerative lesions (P = .0052; Figure 4A) and the remaining colonic mucosa (P = .0079; Figure W4A) of uPA−/− + DSS mice compared to topographically matching areas of WT + DSS mice. The presence of neutrophils was unremarkable in both uPA−/− and WT untreated controls ( Figure W4A). Likewise, F4/80 + macrophages were significantly more in the non-ulcerated colonic mucosa of the uPA−/− + DSS compared to the WT + DSS mice (P = .0011; Figure 4B). CD3 + lymphocytes, however, were less in the ulcerative lesions (P = .0039; Figure 4C) and in the colonic lamina propria (P = .0282; Figure W4B) of uPA−/− + DSS mice than those counted in the corresponding areas of WT + DSS mice.