Competing neighboring roots can deplete soil nutrient resources and thus inhibit root growth. With other things being equal, plants

grow roots preferentially in areas free of other roots [11]. Plant roots do not interact solely through the depletion of soil resources but may also interact, causing profound consequences for plant growth and competition [12]. Schenk provided an excellent summary of direct interactions between roots, and distinguished between two classes of click here interaction [13]. First, roots may exude toxic substances that cause non-specific inhibitory effects on root development of neighboring plants. Second, genetically identical plants may use non-toxic chemical signals that specifically

affect the roots of neighbors. Increasing numbers of studies have shown that plants produce more root mass when sharing rooting space with a genetically similar neighbor compared with plants growing alone [11] and [14]. This phenomenon has been described as a “tragedy of commons” [15]. However, Hess and Kroon hypothesized that root overproduction in the presence of other plants is consistent with the effects of available larger soil volumes on plants with competition than on those growing alone Lumacaftor in vitro [12]. Earlier, McConnaughay and Loh showed that root mass is a function of the available rooting volume, independent of the available nutrients [16] and [17]. Furthermore, Clomifene some of the observed root overproduction could not be immediately explained solely based on soil volume and nutrient availability [12]. The results observed with competing plants may be an overall effect of the existence of interplant root interactions within a larger

space. Therefore, a thorough understanding of the effects of overlapping roots on maize root growth and nitrogen absorption and utilization will help to explore the effects of plant spacing on maize yields. In recent years, it was proposed that increasing plant populations is a key factor for improvement of maize yields in China [7] and [18], but few reports are available on competition between above-ground and below-ground factors while increasing plant populations. In this study, the differences between root distribution, nutrient absorption and nitrogen utilization under different conditions of plant spacing and nitrogen availability were investigated to provide guidelines for optimizing plant densities in high yield maize production. The field experiment was carried out at the Experimental Farm of Shandong Agricultural University, Tai’an, China (36°18′ N, 117°13′ E) in 2007 and 2008. Only one maize hybrid, Denghai 661, was used because previous experiments confirmed increased grain yield of this cultivar at high plant densities [18]. A box-type soil column cultivation method was adopted.

Lawrence County, NY has documented distinct changes in pH, buffering capacity, elemental concentrations and TSA HDAC manufacturer ratios, and total dissolved solids along their length during long-term average summer discharge volumes (Chiarenzelli et al., 2012). Water from each of the four major rivers (from west to east – Oswegatchie, Grasse, Raquette, and St. Regis) was sampled at points within the three geologic terranes (from south to north – Adirondack Highlands, Adirondack Lowlands, and St. Lawrence River Valley) during typical (non-event) summer flow conditions. During these sampling events distinct changes in water chemistry were noted

from south to north (i.e. downriver) including an increase in pH (e.g. from 4.67 to 7.49 in the Oswegatchie River watershed), decrease in Al (e.g. 373–25 ppb in the Raquette River watershed),

and increase in Ca (e.g. from 4.6 to 47.6 ppm in the Grasse River watershed). The study concluded that the downriver variation in water ICG-001 order chemistry was related to acidification of the headwaters of these rivers, which are underlain by crystalline rocks with limited buffering capacity (Colquhoun et al., 1981), and subsequent buffering by carbonate lithologies downriver in the Adirondack Lowlands (marble and calc-silicate gneisses) and St. Lawrence River Valley (limestone and dolostone). In this follow up study, the control(s) on water chemistry along the length of the Raquette River was investigated during high and low flow events. Compared to previous work, downriver chemical changes were muted during both stormflow and baseflow conditions (Fig. 5); however, these differences provide additional insight into controls on the hydrogeochemistry of the Raquette River drainage basin. The average specific conductance (Table 2; Fig. 4) was greater during baseflow (41.66 μS cm−1) than stormflow (29.50).

Several elements, on the average, are more concentrated in Raquette River water during stormflow conditions (Table 2; Fig. 3) including Al (3.31x), Ce (4.85x), Fe (2.79x), La (4.44x), Mn (3.70), Nd (3.31x), and Y (3.08). In contrast Ca, K, Mg, Na, Rb, and Sr were slightly more enriched (1.14-1.50x) during baseflow conditions. Terminal deoxynucleotidyl transferase The downriver concentration trends of elements and anions can be visually estimated from Fig. 3 and Fig. 4, and were quantitatively evaluated by determining the correlation coefficients (r2) between water concentration and the distance of sampling sites downriver ( Table 2). During stormflow Ba (0.22), Ca (0.70), Fe (0.84), K (0.23), Mg (0.80), Mn (0.80), Rb (0.05), and Sr (0.34) have positive r2 values indicating a general, but variable, trends of increasing concentrations downriver. In contrast Al, Ce, La, Na, Nd, Y, and Zn have negative correlation coefficients ranging between −0.22 to −0.39, indicating a slight decrease in concentration downriver. Similar trends are shown during baseflow with the exception that Fe (−0.10) and Mn (−0.25) show slight decreases in concentration downriver rather than steep increases.

Following treatments for 24 h, the T cells were removed by centrifugation and the supernatants collected and kept frozen until used. The secreted IL-2 and IFN- in the supernatants were detected using the DuoSet ELISA kits from

R & D System (UK) according to the manufacturer’s instruction. Following treatments, PBMCs (5 × 105 cells) were centrifuged down and the supernatants discarded. The cell pellets were re-suspended in 50 μl staining buffer (2% BSA in PBS). FITC-conjugated anti-CD25 (10 μl), RPE-conjugated anti-CD69 (10 μl) or the appropriate fluorochrome-conjugated mouse IgG (isotype control) were added to the cells and incubated on ice for 30 min in the dark. The cells were then washed twice in staining buffer before analyzed immediately by flow cytometry. This is essentially as described previously (Su et al., 2005). Purified Epacadostat supplier T cells (3 × 106 cells) were co-stimulated see more with anti-CD3 and anti-CD28 for 2 h, washed with cold PBS and fixed with 1 ml paraformaldehyde (4%) for 20 min at room temperature. The cells were permeabilised with PBS containing 3% BSA and 0.2% triton X-100 for 2 min in room temperature. The permeabilised cells were washed twice and resuspended in 100 μl of PBS with 3% BSA and

rabbit anti-p65 antibody (1:50 dilution) for 45 min at room temperature. The cells were then washed and incubated with anti-rabbit antibody conjugated with alexa fluor (1:2000 dilutions) and Hoechst 33348 in a final volume of 200 μl for 30 min in the dark. Following this the cells were washed twice and resuspended in 10 μl PBS: glycerol (50/50, vol/vol). The cells were mounted onto slides and viewed using confocal microscopy. Images were randomly acquired from each sample and cells with NF-κB p65 nuclear localization were counted. A minimum of 500 cells was analyzed for each sample. Following treatments, 2 × 106 cells were washed in PBS and resuspended in 30 μl lysis buffer (0.1 M NaCl, 1 mM Tris HCl at pH7.6, 1 mM EDTA,

1% Triton-X, 1 mM PMSF). The cells in lysis buffer were taken through 3x freeze/thaw cycles Gemcitabine cell line on dry ice. Protein concentration was measured using the Bradford assay (Biorad, Germany). Protein (30 μg) from whole-cell lysates was diluted in loading buffer (2% SDS, 10% Glycerol, 50 mM Tris–HCl pH 6.8, 0.2% Bromophenol Blue and 100 mM DTT) and resolved using SDS-polyacrylamide gel electrophoresis. The polyacrylamide gels used were 7% for PARP and 13% for caspases. The separated proteins were transfer onto Hybond C membrane (Amersham, UK) and probed with antibodies to caspase-8, caspase-3 and PARP. Detection was carried out using chemiluminescence (Amersham). The experimental data were analysed using Student’s t test or One-way analysis of variance followed by Dunnet’s test. In order to determine the immunosuppressive effects of peptidyl-FMK caspase inhibitors on T cell activation, the effects of z-VAD-FMK and z-IETD-FMK on mitogen-induced T cell proliferation were examined.

) and the calcarine fissure (f.c.). The cross-section of the white matter is identical to section 4, only that it

is possible to identify the medial forceps layer (2.), the stratum sagittale internum (5.), and externum (6.) along the entire cross-section of the medial aspect of the occipital horn and between the horn and the calvar avis. These can all be seen with the naked eye. The cross-section of the occipital horn is squared with the dorsal surface being formed by the dorsal forceps, the medial surface by the calcarine fissure, and the inferior surface by the collateral sulcus. The dorsal forceps (1) is rather prominent, the ventral forceps rather weak (4), whilst the medial forceps layer (2) is relatively strong and equally thick as the lateral layer (3). The majority of fibres of the Olaparib manufacturer stratum sagittale

internum (5.) are collected lateral to the ventricle, whilst the fibres of the externum are collected ventral to it (6.). Selleckchem Lumacaftor However, fibres of the latter are still to be found in the lingual gyrus and to a smaller degree in the stem of the cuneus. It is possible to trace a veil from both layers across the medial surface of the occipital horn with the naked eye. 8. This photography shows a coronal section through the temporal lobe of a brain that suffered a stroke. As a consequence of the stroke the occipital cortex and a part of the temporal cortex, especially the first temporal Thalidomide gyrus, ipsilateral to the lesion are damaged. The level of this section is comparable to section 5. The brain stem was removed prior to hardening this specimen. A ramification of the removal is that the temporal lobe anatomy was altered and the cortex shifted more medial. The area of the cut showing the corona radiata of the temporal lobe is bend medially and almost reaches the hippocampus, which caused the unusual form of the lateral horn. The convexity of this section

shows the Sylvian fissure laterally and the sulcus hippocampi (h.) medially. Within the section the following structures are evident: the parallel sulcus (e.), the second and third temporal sulci (s.t. II. and III.), and the collateral sulcus (coll.), which indents the lateral horn from the inside towards the eminentia collateralis Meckelii. The majority of the first temporal gyrus and some of the second temporal gyrus are affected by the stroke. From the second temporal gyrus a bright layer of degenerated fibres runs towards the white mater ditch. From the occipital horn a small remnant of the tapetum is present (1.) lateral to it lies the well-maintained corona radiata of the temporal lobe (2.) whose propagation into the elongation stratum sagittale internum is cut off. The very prominent dark transvers cut through the stratum sagittale externum, as we know it from the healthy brain, is absent.

The eastward currents at 200–450 m EPZ015666 cost depths and 3–5° from the equator are the northern and southern Tsuchiya jets (TJs; Tsuchiya, 1972, Tsuchiya, 1975, Tsuchiya, 1981, McCreary et al., 2002, Furue et al., 2007 and Furue et al., 2009). The structures

of the model TJs agree fairly well with observations, except that the model has westward currents on the equatorward sides of the TJs. The observed field shows another eastward current just south of the primary one, often termed the secondary Tsuchiya Jet, which is much weaker in the model. Note also that the model has other, vertically-coherent, narrow zonal flows at depths farther from the equator. Eddy-resolving models usually have similar, but stronger, flows, sometimes called “striations” or “zonal jets” (Maximenko et al., 2008),

which are thought to be at least partly driven by eddies (e.g., Nakano and Hasumi, 2005 and Richards et al., 2006). These flows are much weaker in our model than in typical eddy-resolving models, likely because our mesoscale eddies are much weaker. There are large-scale bands of high sea-surface salinity between selleck chemicals llc 20 °S°S and 10 °S°S and between 20 °N°N and 30 °N°N (not shown). Waters subducted in these regions flow equatorward in the main pycnocline, forming the tongues of high salinity visible in Fig. 2. Much of this water flows eastward in the EUC, upwells into the mixed layer in the eastern equatorial Pacific, and returns to subtropics near the surface, thereby forming the Pacific’s shallow overturning circulation cells, the Subtropical Cells (STCs; McCreary and Lu, 1994). The tongue from the southern hemisphere is more pronounced partly because surface salinity is higher in the southern hemisphere and partly because the subducted water reaches the equator by a more direct path than

in the northern hemisphere (Lu and McCreary, 1995). As a result, there is a sharp front of salinity in the pycnocline across the equator. The vertical structure of salinity is complicated near the equator because of this feature especially on the northern side. Overall, the model salinity field agrees well with the Argo climatology. The most conspicuous difference is that maximum values Methane monooxygenase of salinity are considerably higher than their observed counterparts both in the northern and southern hemispheres. Indeed, the surface salinity is much higher in our model than in the Argo climatology (not shown), and it is the subduction of this water that leads to the model’s larger subsurface salinities. All solutions follow similar adjustment processes. They include a very fast, initial response due to interactions of gravity and barotropic waves with eddies (Section 3.2.1), a more gradual diffusive, local response (Section 3.2.2), and slower remote adjustments due to wave propagation and advection (Section 3.2.3). Fig. 3 shows δTSEδTSE at z=150z=150 m and t=300t=300 days as an example.

According to Marfo GSK1120212 mw et al., 35% of the patients on the waiting list are sensitized with PRA levels > 0%, and 15% are highly sensitized with PRA levels > 80% [1]. In some regions of the United States, the waiting time on the transplant list can exceed five years and due to organ shortage, this scenario is not changing in the near future. It has been thoroughly described that highly sensitized patients have longer waiting times and some may never receive a transplant [1]. In Mexico, roughly 75% of renal transplants are from living donors and approximately 2300 kidney transplants per year have been performed during the last 3 years [8]. Although

there has been a decrease in the mortality rate of patients on dialysis, approximately 15 to 20% still die each year, which emphasizes the importance of early transplantation [4] and [9]. There is an evident financial cost and emotional burden secondary to maintaining

a highly sensitized patient on dialysis in comparison to early transplantation. The impact of kidney MS-275 transplantation on morbidity, mortality, quality of life and medical expenses is undeniable. The main objective of this study was to determine the probability of patients in the deceased donor (DD) waiting list at the National Institute of Medical Sciences and Nutrition (INCMNSZ) in Mexico City to receive a kidney transplant (KT), based on the degree of sensitization determined by % PRA. Acute rejection rate, graft function, patient and graft survival, and causes for patient death/graft loss were also analyzed. This protocol was approved by the Institutional Committee of Medical Ethics and performed in accordance with the revised Declaration of Helsinki content and Good Clinical Practice Guidelines. The renal transplant DD waiting list database was reviewed from January 2005 to August 2012 at the Histocompatibility Laboratory

at INCMNSZ. For each DD event, we documented the donor’s demographic characteristics (age and gender), donor’s blood group (ABO group), the number and ABO group of all the potential recipients considered, the results of the lymphocyte cross-match test [CxM (AHG-CDC)] for each potential recipient considered, Megestrol Acetate the % PRA of each potential recipient (highest % PRA documented in the last three determinations) and which patients consequentially received a DD kidney transplant. Anti-HLA antibodies were tested by the Luminex technique using test kits purchased from One Lambda, Inc., Canoga Park, CA. In the patients on the waiting list, a LabScreen Mixed Classes I & II and a LabScreen PRA Classes I & II were simultaneously performed. Only those with positive results in either test received a Labscreen Single Antigen test. When available, the result of pre-transplant DSA assessment using the LABScreen Single Antigen Classes I & II was gathered for the analysis.

Orcokinin family Talazoparib in vivo peptides have been characterized in many crustacean species. Of the many characterized,

full-length orcokinins [7], glycine, not alanine, is found exclusively at the 11th position in the sequence. Although genomic data for crustaceans is sparse, the available information documents no genes encoding full-length orcokinins with Ala11; furthermore, no genes have been found for any truncated orcokinin variants. This sequence analysis, coupled with our demonstration that isobaric Orc[1-11]-OMe is an extraction artifact, has led us to question the identity of previously published truncated orcokinin family peptides with an alanine, not glycine, at the 11th position. This concern has been supported by our analysis of H. americanus tissues using approaches that either exclude methanol or permit differentiation of Orc[1-11]-OMe/Orc[Ala11], where

we failed to find any evidence of putative Orc[Ala11]. The truncated orcokinin, Orc[Ala11], was first reported by Huybrechts et al. as a novel peptide de novo sequenced from the Jonah crab, C. borealis [21]. For that study, brain and thoracic ganglion selleck chemical tissues from 50 animals were extracted in methanol:water:acetic acid (90:9:1) and peptides were sequenced using ESI-Q-TOF MS/MS. As was the case for H. americanus, this peptide sequence, with an alanine appearing as the 11th residue, is at odds with the sequences of full-length C. borealis orcokinin peptides, which have been established by many MS studies [21] and [32]. We suggest that the peptide reported by Huybrechts et al. is, in fact, Orc[1-11]-OMe; this assertion is supported by work carried out in our laboratory, where we have evidence for the detection of Orc[1-11]-OMe in C. borealis brain tissue extracts

(data not shown), but not for any directly analyzed C. borealis tissues (CoG, SG, PO, brain) (data not shown). Because alanine (A) is isobaric with methylation Oxymatrine at a C-terminal glycine residue (G-OMe), this distinction would not have been revealed from mass measurements. Furthermore, the MS/MS technique used for de novo peptide sequencing in the Huybrechts et al. study would not have provided any obvious flags to distinguish the C-terminal alanine from G-OMe. The orcokinins NFDEIDRSGFA, SSEDMDRLGFA, and NFDEIDRSSFA, all with an alanine as the 11th residue and all detected in tissues that had been analyzed following extraction with acidified methanol, have been reported in other publications [15], [16], [21], [30], [31] and [32]. In summary, our work calls into question the identification of these truncated peptides, which may have Gly-OMe, not Ala, at the C-terminus. A unique issue for the in vitro modification detected in this study is the localized methylation at the C-terminus. Because the Gly-OMe modification is isobaric with Ala-OH, this structural change is not detectable via mass measurements.

If not recognized and treated adequately in time (i.e., strict blood pressure control), hemorrhagic stroke may occur, which subsequently leads to death in up to 40% of patients [2]. The generally accepted definition of post-operative cerebral hyperperfusion

in the context of CEA is defined as an increase in cerebral blood flow (CBF) of >100% over baseline [3]. This occurs in approximately 10% of CEA patients [4] and has been associated with a tenfold higher risk for post-operative intra-cerebral hemorrhage in patients operated under general anesthesia [3] and [5]. Quizartinib Changes in CBF are correlated with changes in the mean blood velocity (Vmean) in the ipsilateral middle cerebral artery (MCA) as measured with TCD [6] and [7]. Currently, during CEA under general anesthesia, an increase in Vmean of >100% three minutes after declamping the ICA, compared to

the pre-clamping Vmean is the most commonly used predictor of CHS [2], [8], [9] and [10]. However, intra-operative TCD monitoring is associated with both false negative and false positive results [2] and [11]. Therefore, a more precise method is needed to predict which patients are at risk for CHS [12]. This study aimed to assess the predictive values of TCD monitoring regarding the development of CHS, by introducing an additional TCD measurement in the first two post-operative hours. Patients who underwent CEA between January 2004 and C59 wnt mouse Sitaxentan August 2010 in the St. Antonius Hospital, Nieuwegein, The Netherlands, were retrospectively included. All patients who underwent CEA for a high degree ICA stenosis and in whom both intra- and post-operative TCD monitoring were performed were included. Surgery was performed under general anesthesia and all patients received the same anesthetic regimen. An intra-luminal shunt was used selectively in case of EEG asymmetry or a decrease of >60% of Vmean measured by TCD [13]. For the TCD registration, a pulsed Doppler transducer (Pioneer TC4040, EME, Überlingen, Germany), gated at a focal

depth of 45–60 mm, was placed over the temporal bone to insonate the main stem of the MCA ipsilateral to the treated carotid artery. The TCD transducer was fixed with a head frame and Vmean was recorded continuously. Vmean values at the following time points were used for further analysis. For the pre-operative Vmean (V1), a TCD measurement was performed 1–3 days prior to operation. During operation, the pre-clamping Vmean (V2) was registered 30 s prior to carotid cross-clamping. The post-declamping Vmean (V3) was determined three minutes after declamping. An additional post-operative Vmean (V4) was measured within the first 2 h after surgery on the recovery ward. The intra-operative increase of Vmean was defined and calculated as (V3 − V2)/V2 × 100%. For calculating the post-operative increase of Vmean the following formula was used (V4 − V1)/V1 × 100%.

Scenario (c), by contrast, is predicted by the P600-as-P3 perspective, while models this website assigning the P600 a specific role in structural/combinatorial processing might require post hoc amendments to explain this scenario. The present study aimed to test these hypotheses. Please note that, in line with recent

calls for dissociating exploratory from confirmatory research (Wagenmakers, Wetzels, Borsboom, van der Maas, & Kievit, 2012), we pre-registered the experiment (German Clinical Trial Registry, ID: DRKS00004596), making our predictions and methods publicly available before data collection was initiated. Twenty monolingually raised native speakers of German (three men; mean age 24.75, range 21–42) participated in the experiment after giving written informed consent. Participants were right-handed, had good auditory acuity and normal or corrected-to-normal vision. All were students of the University of Mainz, receiving course credit for their participation. Experimental stimuli were constructed by a strict scheme, resulting in sentences of the structure shown in example (1). Each sentence consisted of a hyperonym and two potential hyponyms, always presented in that order. Only Ibrutinib these three nouns and their determiners

were varied across sentences. Control sentences (1a), of which subjects heard 150, contained a hyperonym and two hyponyms. Syntactic violation sentences (1b), of which subjects heard 110, consisted of a hyperonym and two of its hyponyms, one of which (balanced across 1st and 2nd positions) was preceded by an article not agreeing in grammatical gender with the hyponym. Agreement violations, including gender mismatches,

have previously been found to elicit P600 effects see more (Hagoort and Brown, 1999 and Molinaro et al., 2011). Semantic violations (1c), of which subjects heard 40, consisted of a hyperonym, one of its hyponyms, and one noun phrase that had been exchanged with a noun phrase from another sentence. Semantic errors of this sort typically induce N400 effects (Kutas & Federmeier, 2011), sometimes followed by an additional P600 (e.g. Roehm et al., 2007 and Sanford et al., 2011). We used a higher number of sentences in the two conditions of primary interest – the control condition and the syntactic violation condition, where we expected to observe a P600 – than in typical studies of sentence processing in order to enable us to conduct single trial analyses. Because we were unable to produce 300 different hyponyms, many hyponyms were shared across sets. However, we ensured that no sentences were repeated verbatim, and neither condition (structural violation, semantic violation or correct) nor violation time point were predictable before the actual violation point/critical point (1st or 2nd hyponym for violation sentences, and 2nd hyponym for control sentences).

T cells from Vav1AA/AA mice also show a proliferative defect when injected into MHC-mismatched recipient animals in a mechanistic GvH mouse model (Fig. 3). The

total number of Vav1AA/AA T cells after 3 days was strongly reduced compared to WT T cells, and 18% of the cells did not divide at all. Interestingly, the majority of Vav1AA/AA T cells reached 6 division cycles, showing that there was no complete block in proliferation. Rather, Vav1AA/AA T cells seemed to have divided more slowly compared to WT T cells, which led to the reduced total numbers of cells. This is in contrast to T cells treated with the strong immunosuppressant CsA, where the majority of T cells did not divide at all. However, in a previous study, T cells from Vav1−/− mice also did not show a complete block in proliferation but a similar delay in proliferation, which was enhanced in T cells from mice deficient in both http://www.selleckchem.com/products/azd9291.html Vav1 and Vav2 [23]. These findings suggest that disruption of Vav1 function only partially affects the TCR-induced proliferative signals which can be overcome by a stronger costimulatory environment in vivo. Vav1 GEF activity seems to be important for the Vav1-mediated proliferative response, as Vav1 GEF inactivation and total Vav1 deficiency have comparable effects. CsA, however, might affect Vav-independent TCR-induced signals Raf targets and also different stimuli

in addition to TCR engagement such as cytokines and costimulatory signals, which also contribute to T cell proliferation [28]. Furthermore, CsA has effects on other cell types and tissues resulting in strong general immunosuppression, which may explain the stronger response compared to Vav1 inactivation. Vav1AA/AA mice show prolonged cardiac allograft survival with a mean survival time of 22 days compared to WT animals which reject the allograft after 7 days (Fig. 4). These findings confirm

the previously observed central role for Vav1 in allograft rejection [23]. Vav1AA/AA as well as Vav1−/− mice have reduced numbers of peripheral T cells due to a defect in thymic development [20], and we cannot exclude a partial effect of this reduction on allograft survival. However, Vav1AA/AA T cells showed a strong defect in allogeneic T cell proliferation and activation in vitro and in vivo when 6-phosphogluconolactonase equal numbers of T cells were used, indicating that the prolonged allograft survival in Vav1AA/AA mice is likely to be caused by defective T cell activation. However, to fully confirm these findings, inducible genetic systems or specific Vav1 inhibitors will be needed. Graft survival in Vav1AA/AA mice is not as pronounced as in Vav1−/− mice which lack the whole Vav1 protein, indicating that the GEF function of Vav1 affects only part of the processes mediating rejection [23]. This could also account for the high variation in allograft survival time observed for the Vav1AA/AA mice.