In our experiments, both CT and the CTB subunit induced the expression of TGF-β in dermal skin cells and had a similar adjuvant effect in CD4+ T-cell priming. We also obtained similar results in naïve C57BL/6 mice using CTB as both an antigen and an adjuvant. Interestingly, we evaluated whether the response that was elicited by

immunization with HEL and either CT or CTB translated into a DTH response and found ear thickening after an HEL challenge Histone Methyltransferase inhibitor in mice that were previously immunized with HEL in combination with both CT and with CTB. Although CT and CTB induced similar initial primings of CD4+ T cells, CT induced a more vigorous DTH response than CTB 7 days after immunization; this finding could be explained by the lack of inflammation induced by CTB. Surprisingly, we found no differences in the inflammatory cytokines that were expressed in the skin cells following the local administration of CT or CTB (Supporting Information Fig. 5). However, the presence of Vβ8.2+ cells in the ears of the

mice was higher in mice with a DTH response following HEL immunization with CT than with CTB. The DTH response was BMN-673 visible after an HEL challenge given 21 days after immunization, indicating a long-lasting cellular immunity that was induced by immunization with both CT and the CTB. Similar to the contact hypersensitivity response, in which both IFN-γ and IL-17 seem to play a key role 31, the DTH response that was induced by immunization with HEL and CT was dependent on IL-17 and partially dependent on IFN-γ activity. Unlike other reports that showed efficient T-cell proliferation only in the presence

Protein kinase N1 of resident and migrating DCs 22, 23, our results showed efficient T-cell proliferation in mice that were immunized with 0.3 μg HEL and either CT or CTB, even after the ear was removed. Strikingly, after immunization in the ear using a high antigen dose, cytokine expression was only observed in dCLNs, even in the presence of robust proliferation in distal LNs (Supporting Information Fig. 6). Therefore, it was important to determine whether the IFN-γ and IL-17 CD4+ T-cell differentiation that was induced by CT and CTB immunization was dependent on the presence of migrating skin cells. Despite robust T-cell proliferation, only minimal IL-2 expression and no production of IFN-γ and IL-17 in HEL–re-stimulated CD4+ T cells was observed in mice in which the immunization site was removed 90 min after immunization with HEL and either CT or CTB. Consistent with previous reports 32, this result suggests that in our model, sustained antigen presentation (in this case, mediated by DCs that migrate from the ear and arrive at dCLNs) is crucial for inducing CD4+ T cells to differentiate into cytokine-producing cells, even in the presence of strong adjuvants such as CT. Our experiments indicate that migrating cells that arrive after 90 min but within the first 24 h of immunization are important for T-cell differentiation.

Microsurgery 30:397–400, 2010. “
“Autologous breast reconstruction is safe in advanced age, yet no study has examined its effects on the aging abdomen. We, therefore, studied 145 women who participated in a prospective study of abdominal strength following abdominal free flap breast reconstruction, comparing preoperative and late follow-up scores www.selleckchem.com/products/BI-2536.html in patients ≥60 years old (11 unilateral, 13 bilateral) compared with patients <60 (58 unilateral, 63 bilateral). Simple in-office tests were utilized to test abdominal strength. No differences were noted in unilateral absolute scores at either time point, however, a decrease in upper abdominal strength was noted in the younger cohort over time (P = 0.01). Bilateral

analyses revealed absolute score decreases

in upper abdominal strength for both cohorts but no major differences between the two. We conclude that autologous breast reconstruction with abdominal tissue in older patients result in little to no difference in abdominal function as compared with younger patients. © 2012 Wiley Periodicals, Inc. Microsurgery, C646 2013. “
“Background: Large or extensive gouty tophi on the feet can cause functional impairment, drainage sinus, and infected necrosis, finally resulting in complex soft-tissue defects with tendon, joint, bone, nerve, and vessel exposure. Reconstruction of complex soft-tissue defects of the foot is still challenging. The purpose of this report was to review the outcomes of free-flap reconstructive surgery for treating the metatarsal joint defects of the feet caused by chronic tophaceous gout. Methods: Ten patients who had large tophus masses (>5 cm) and ulceration on the feet were admitted to our hospital between September 2006 and September 2010. Six patients underwent free-flap reconstruction after debridement to resurface the circumferential wound, protect the underlying structures, and provide a gliding surface for exposed tendons. The patients’ age, sex, comorbidities, location and size of the defects, reconstructive procedures,

surgical outcomes, complications, Suplatast tosilate follow-ups, and recurrence of tophaceous gout were reviewed and recorded. Results: The mean patient age was 49.8 years (range, 36–72 years). The average skin defect size was 92.2 cm2. Five patients were treated using free anterolateral thigh flaps, and 1, using a free medial sural flap. These free flaps were safely raised and showed excellent functional and cosmetic results, with a mean follow-up of 31.7 months (range, 7–50 months). Conclusion: Chronic tophaceous gout can cause severe skin infection and necrosis, even resulting in deformity or sepsis if left untreated. Surgical debridement is inevitable in patients with extensive wounds. We reconstructed the large, ulcerative skin and soft-tissue defects on the dorsum of the foot by performing free-flap reconstruction after adequate debridement and achieved good functional and cosmetic results. © C 2011 Wiley Periodicals, Inc. Microsurgery, 2011.

baumannii expression properties that augment the organism’s ability to transition from exponential to stationary phase, as opposed to strain-dependent characteristics. Moreover, characterizing conserved biological processes may, in turn, provide rationale for developing strategies Selleck PLX3397 for the therapeutic intervention of A. baumannii infections. Accordingly, each strain was cultured in LB medium, aliquots were removed during each growth phase, and RNA

was isolated and subjected to microarray analysis. The results presented here are refined to only those changes in gene expression that are conserved across both strains; individual strain expression properties are provided in Supporting Information, Table S1. Results revealed that the gene expression profiles of exponential- and stationary-phase A. baumannii differ dramatically and these differences are relatively well conserved

across the two strains studied. A total of 502 ORFs were determined to exhibit at least a twofold increase (t-test; P ≤ 0.05) in expression during exponential as opposed to stationary phase of growth regardless of the strain studied. Most of these genes belonged to distinct clusters of orthologous functional groups that are related to aspects of cell growth (Fig. 1). For instance, genes associated with amino acid metabolism (n = 43), translation (n = 93), cell wall/envelope PD0325901 in vivo biogenesis (n = 43), nucleotide transport (n = 28), transcription (n = 22), and replication (n = 21) were upregulated during exponential as opposed to stationary phase growth. Conversely, the mRNA levels of 175 genes were upregulated during stationary as opposed to exponential phase

in both strains. Of these, the majority were associated with energy production and conversion (n = 23), lipid transport Olopatadine and metabolism (n = 15), and post-translational modification (n = 11). As described below, a more elaborate analysis of the data indicated that several genes that are likely to contribute to the organism’s ability to cause disease were found to be differentially expressed in a growth phase-dependent manner. Acinetobacter baumannii possesses the ability to survive on common hospital surfaces for weeks at a time, due in part to its ability to tolerate desiccation and form biofilms, subsequently providing a means for the organism to persist in the environment and act as a source for bacterial transmission to susceptible patients (Wendt et al., 1997; Jawad et al., 1998; Espinal et al., 2012). Our microarray data provided potential insight with regard to the biological systems that may contribute to the organism’s ability to form biofilms. More specifically, two members of the trehalose metabolic pathway, trehalose-6-phosphate synthase (A1S_0803), and trehalose-6-phosphate phosphatase (A1S_0804) were among the most highly upregulated stationary phase genes.

9% for Group A, 34.1 ± 4.2% for Group B, and 51.3 ± 3.3% for Group C at 12 weeks. There was no statistical difference between Groups A and C, but Group A was statistically greater when compared to B, and when Group C was Temozolomide in vivo compared to B. In conclusion, acellular nerve allograft demonstrated equal functional recovery when compared to reversed autograft (control), and superior recovery compared to the cabled nerve autograft. © 2013 Wiley Periodicals, Inc. Microsurgery 33:460–467, 2013. “
“From

January 2000 to May 2008, 50 patients with facial contour deformities underwent soft tissue augmentation with 51 anterolateral thigh (ALT) adipofascial flaps. Fifty flaps survived with no complications; partial fat necrosis occurred in one flap. Mean follow-up was 16 months. Flaps ranged from 10 × 6 cm to 20 × 12 cm. Perforators were found in 50 flaps, 43 musculocutaneous perforators (84.3%) and 7 septocutaneous perforators (13.7%), with a mean of 2.5 perforators per flap. In one flap (2.0%), no perforator was found. In this case, we used an anteromedial thigh adipofascial flap using the medial

branch of the descending branch of lateral circumflex femoral artery as the vascular pedicle. Relatively symmetric facial contour was achieved in 20 cases. In 30 cases, adjunctive procedures including flap debulking, fat injection, and resuspension were necessary, and 23 patients achieved satisfactory outcomes. We conclude that the ALT adipofascial flap can be successfully elevated and transplanted for the correction of soft tissue facial defects. This flap can provide tissue to mafosfamide fill large defects, and posses INCB018424 the qualities of pliability, an excellent blood supply, ease of suspension and fixation, and minimal morbidity at the donor site. © 2010 Wiley-Liss, Inc. Microsurgery 30:368–375, 2010.

“
“The purpose of this study was to examine the current role of the iliac crest osteocutaneous flap in mandibular reconstruction, with a focus on the reliability of its skin island. We reviewed outcomes in 18 cases of immediate mandibular reconstruction with the iliac crest flap. Intraoral mucosal defects were closed with the skin island of the iliac crest flap in 13 patients (iliac crest flap group) and were closed with another free flap, because of poor circulation of the iliac crest skin island, in five patients (double-flap group). Postoperative results were poor in the iliac crest flap group. The rate of partial or total loss of the skin island was 46.2% in the iliac crest flap group and 20.0% in the double-flap group. The presence of a dominant perforator did not reduce the overall rate of recipient-site complications or reoperation. Combined use of another skin flap for intraoral lining provided better results. These results suggest that the skin island of the iliac crest flap should not be used for intraoral lining, unless adequate circulation of the skin island can be confirmed.

The definition of early sexual debut varied across studies and is displayed

for each study in Table 1. Studies that explored the impact of early age at first sexual debut on only high-risk behaviours, perceived risks or determinants of HIV/AIDS risk, such as condom use, multiple partners, other STIs or circumcision, were excluded. The abstracts of all 1572 relevant studies were screened by a single reviewer (NK) after 100% agreement was reached on applying the inclusion criteria to a sample of 250 abstracts between the two reviewers (NK and HS). Following this, the full texts of all studies PI3K Inhibitor Library nmr that could potentially be included in the review were obtained. After removing 13 duplicates, 128 full texts were retrieved and double-screened independently by two reviewers (NK and HS). Any differences in decisions were resolved through discussions. It had been decided that a third reviewer (CW) would be approached if there were differences in decision that could not be resolved; however,

this was not necessary as an agreement was reached on all studies. A total of 26 articles met the inclusion criteria and were included in the review. Two articles Hydroxychloroquine order reported on the same data, and their information was therefore combined in the analysis, and they were treated RG7420 purchase as one study.[12, 13] Information about sample characteristics, setting,

study design, variables adjusted for and statistical results were extracted from the study by one reviewer (NK), and a confirmatory data extraction and quality appraisal were carried out by a second reviewer (HS). The quality appraisal was conducted using seven appraisal questions adapted from the graphical appraisal tool for epidemiological studies (GATE).[30] Each study could obtain a maximum score of 14, indicating the highest level of evidence. For each of the following components, a maximum score of two was given per study: focus of the study, generalisability of the findings, study design, use of adequate control variables, reliable and sensible outcome measures, sensitive reporting of biases and outcomes and ethics. It was agreed that a total score of 0–4 would imply very low quality, 5–8 low quality, 9–11 medium and 12–14 high. Any differences in scoring were resolved through discussions between the two reviewers. The findings of the systematic search first report the unadjusted bivariate associations that emerged in this review. Due to their equivocal outcomes, the multivariate findings of the review were summarised according to the conceptual framework (Fig. 2). Only studies that found a significant association in the unadjusted analysis are examined in the multivariate analysis.

CNVs are frequent in higher eukaryotes and associated with a substantial portion of inherited and acquired risk for various human diseases. CNVs are distributed widely in the genomes of apparently healthy individuals and thus constitute significant amounts of population-based genomic variation. Human CNV loci are check details enriched for immune genes and one of the most striking examples of CNV in humans involves a genomic region containing the chemokine genes CCL3L and CCL4L. The CCL3L–CCL4L copy number

variable region (CNVR) shows extensive architectural complexity, with smaller CNVs within the larger ones and with interindividual variation in breakpoints. Furthermore, the individual genes embedded in this CNVR account for an additional level of genetic and mRNA complexity: CCL4L1 and selleck chemicals llc CCL4L2 have identical exonic sequences but produce a different pattern of mRNAs. CCL3L2 was considered previously as a CCL3L1 pseudogene, but is actually transcribed. Since 2005, CCL3L-CCL4L CNV has been associated extensively with various human immunodeficiency virus-related outcomes, but some recent studies called these associations into question. This controversy may be due

in part to the differences in alternative methods for quantifying gene copy number and differentiating the individual genes. This review summarizes and discusses the current knowledge about CCL3L–CCL4L CNV and points out that elucidating their complete phenotypic impact requires dissecting TCL the combinatorial genomic complexity posed by various proportions of distinct CCL3L and CCL4L genes among individuals. In the last decade, many studies showed

that a major component of the differences between individuals is variation in the copy number of segments of the genome [copy number variation (CNV) or copy number polymorphism (CNP)]. CNVs are distributed widely in the genomes of healthy individuals and thus constitute significant amounts of population-based genomic variation [1–7]. CNV seems to be at least as important as single nucleotide polymorphisms (SNPs) in determining the differences between individual humans [8]. CNV also seems to be a major driving force in evolution, especially in the rapid evolution that has occurred, and continues to occur, within the human and great ape lineage. Compared with other mammals, the genomes of humans and other primates show an enrichment of CNVs. Primate lineage-specific gene CNV studies reveal that almost one-third of all human genes exhibit a copy-number change in one or more primate species [9–12]. To date, almost 58 000 human CNVs from approximately 14 500 regions (CNVRs) have been identified (data from Database of Genomic Variants, http://projects.tcag.ca/variation/). These CNVRs may cover 5–15% of the human genome and encompass hundreds of genes [4,13], and their abundance underscores their substantial contribution to genetic variation and genome evolution [14].

However, these techniques remain limited in their ability to analyse

cell motility and interactions (e.g. between NKT cells and DCs) over extended time and distances in intact tissue, Selleckchem BMN 673 and to distinguish between individual cells in a labelled cell aggregate. As stated by Dr Ron Germain, ‘the most significant advance currently undergoing development in intravital imaging of the immune system is the combination of molecular imaging with measurements of the dynamics of single cells’.[54] The long-term goal is to attribute cellular movement and positioning to causal changes in cell signalling and gene expression in vivo. To achieve this goal, improvements in cell imaging are required and may include increases in the number of different colours used, tissue volume examined and number of cells imaged, duration of imaging sessions, and use of subcellular probes.[51, 54] The successful application of these novel technologies will depend largely on the development of new computer algorithms to analyse complex data sets of system biology approaches, including computer simulations.[135, 136] Additional studies may benefit from the imaging of higher quality sample preparations from less well-characterized tissues (e.g. gastrointestinal tract, pancreas, spleen and lung). Most importantly, it is envisaged that better diagnostic

procedures be achieved in the clinic by introducing selleck chemicals miniaturized imaging instruments and light delivery systems in endoscopes or implantable devices.[54] This work was supported by grants from the National Institutes

of Health, USA, R01 CA100660 and R01 AA020864 (VK) and from the Juvenile Diabetes Research Foundation (JDRF) grants 24-2007-388 (TLD) and 24-2007-362 (VK). Additional support was provided by the Canadian Institutes of Health Research grant MOP 64386 (TLD). cAMP The authors declare no conflict of interest. “
“Cephalosporin-resistant Escherichia coli has been increasingly reported worldwide. In this study, 32 cephalosporin resistant E. coli isolates identified from cancer patients in Cairo, Egypt in 2009–2010 were analyzed. Twenty-three were of phylogenetic group D, seven A and one each B1 and B2. By rep-PCR 15 phylogroup D isolates were grouped in four clusters, one with sequence type (ST) 405 and three ST68. Seventeen isolates showed single patterns. blaCTX-M-15 and aac(6′)-Ib-cr were the most common resistance determinants. blaOXA-48 and blaVIM were also detected. Multidrug resistant E. coli seriously affects healthcare, especially in immunocompromised hosts, such as cancer patients. Escherichia coli is a major cause of both community and healthcare-associated infections [1, 2]. Extra-intestinal infections due to E. coli increase morbidity, mortality, and healthcare costs in hospitalized patients [3]. Their impact can be especially severe in immunocompromised patients, such as cancer patients receiving chemotherapy [4]. Extended spectrum β-lactamases, AmpC and carbapenemase-producing E.

Tetracycline-mediated inhibition of de novo bacterial protein synthesis promotes the loss of ubiquitinated proteins from the AVM. This effect is reversible, as removal of tetracycline restores AVM ubiquitination to pretreatment levels. These results demonstrate a novel mechanism

by which A. phagocytophilum remodels the composition of its host cell-derived vacuolar membrane and present the first example of a Rickettsiales pathogen co-opting ubiquitin during intracellular residence. Anaplasma JNK inhibitor concentration phagocytophilum is a tick-transmitted obligate intracellular bacterium that infects neutrophils to cause the emerging and acute febrile infection, human granulocytic anaplasmosis (HGA) (Chen et al., 1994; Rikihisa, 2011). In nature, A. phagocytophilum is maintained in an enzootic cycle between its tick vector and mammalian hosts. Humans are accidental hosts. HGA clinical manifestations range in severity from asymptomatic to severe disease and death. Although often self-limiting, severe complications such as prolonged fever, shock, leucopenia, thrombocytopenia, high levels of C-reactive protein

and hepatic transaminases, pneumonitis, acute renal failure, and hemorrhages can result. Doxycycline is the drug of choice for treating HGA (Thomas et al., 2009). Following entry, A. phagocytophilum facilitates survival by replicating exclusively within a host cell-derived vacuole that exhibits altered Talazoparib fusogenicity. The A. phagocytophilum-occupied selleck screening library vacuole (ApV) does not mature along the endosomal pathway, does not acidify, avoids lysosomal fusion, and prevents bacterial exposure to reactive oxygen species by avoiding fusion with secretory vesicles and specific granules harboring

NADPH oxidase (Webster et al., 1998; Gokce et al., 1999; Mott et al., 1999; Carlyon et al., 2004; IJdo & Mueller, 2004; Huang et al., 2010a). The ApV is not an inert compartment that is completely sequestered from interfacing with its host cell. Rather, it co-opts membrane traffic, host cell molecules, and cellular processes to camouflage itself and obtain requisite nutrients. For example, the ApV selectively recruits recycling endosome-associated Rab GTPases while excluding Rabs that would otherwise direct A. phagocytophilum to the lysosome (Huang et al., 2010a, b, c). Also, the ApV membrane (AVM) has been shown to accumulate early autophagosomal markers, caveolae markers, and cholesterol, each of which is important for bacterial survival, as well as multiple signaling molecules (Lin & Rikihisa, 2003a, b; Niu et al., 2008). These phenomena serve as harbingers that the A. phagocytophilum likely hijacks additional host cell molecules as part of its intracellular survival strategy. Post-translational modification by ubiquitin is a highly conserved eukaryotic cell-specific process. Ubiquitin is a 76 amino acid protein that is covalently attached to lysine residues of target proteins.

As CD8+ TEM cells persist long-term in the liver (Figure 1), we asked whether these persisting CD8+ TEM cells could also be detected in peripheral blood. CD8+ TEM were found in the blood 8 weeks after challenge and the TCR Vβ profile was the same as that observed 1 week after challenge. Thus, it appears

that once the commitment is made to the expression of a given TCR Vβ repertoire, this expression is maintained long-term. Moreover, the reduced frequency and number of CD8+ TEM observed in the liver 8 weeks after challenge (Table 1) is not because of a selective loss of any TCR Vβ family, but rather a general loss of all CD8+ TEM cells, as would be expected during the contraction phase that occurs after infection. To determine whether any particular www.selleckchem.com/products/MG132.html TCR Vβ is more likely to be expanded in TEM cells, we combined the data from 43 mice (28 analysed in liver, 15 analysed in blood). Results in Figure 7 display the ratio of TCR Vβ expression by CD8+ TEM over CD8+ TN cells, and it represents the expansion or contraction of TEM cells in individual mice. Using an arbitrary cut-off point of p38 MAPK apoptosis 2, the CD8+ TEM cells from at least one mouse analysed had an expansion of a particular TCR Vβ family, except for Vβ3. In addition, some TCR Vβ were more likely to be expanded than others, and common among these were Vβ8.3 (26% of mice), Vβ6 (21%), Vβ7 (16%),

Vβ9 (16%), Vβ11 (16%) or Vβ4 (14%). In this study, we characterized the TCR Vβ usage by intrahepatic and blood CD8+ T cells during Pbγ-spz immunization

and challenge of C57BL/6 mice. The liver and blood Dichloromethane dehalogenase of unimmunized mice contain very few CD8+ TEM cells but they appear after immunization with γ-spz and increase after challenge with infectious spz. The repertoire CD8+ TN and TCM cells was diverse and it was conserved between individual mice, and did not change with immunization. In contrast, preferential usage of one or more TCR Vβ subset was observed in CD8+ TEM cells after immunization. The particular expanded TCR Vβ varied between individual mice but Vβ4, 6, 7, 8.3, 9 and 11 were the most frequent. In the majority of malaria-related studies, the usage of TCR Vβ chain is usually associated with the pathogenesis of Plasmodia infections. Development of P. berghei cerebral malaria during blood-stage infection is associated with oligoclonal TCR Vβ4, 8.1 and 11 CD8+ T cells in the brains of affected C57BL/6 mice (32,33). In another study, cerebral malaria in B10.D2 mice is associated with an increase in CD8+ peripheral blood lymphocytes (PBLs) expressing Vβ8.1,8.2 (34). In contrast, the Vβ distribution on CD3+ PBLs was not different between patients with malaria (uncomplicated or cerebral malaria) and asymptomatic controls in a cohort of African children (35).

193%) whereas the background staining among TCRβ-positive cells was much lower (0.06%, data not shown).

Last, consistent with iNKT cells being the major PLZF-expressing T-cell population, most PLZF+ αβ T cells expressed NKR-P1A/B at intermediate levels (Fig. 2F). Apart from F344 inbred rats, we also examined the widely used LEW inbred rat strain. The LEW strain is well known for its susceptibility to induced organ-specific autoimmunity, which is not to be found in F344 rats [24-26]. As shown in Figure 2F LEW rats lack the PLZF+ NKR-P1A/B-intermediate T-cell AUY-922 in vitro population found in F344 and show no specific binding of α-GalCer-CD1d dimers (Fig. 2B). Nevertheless, the few cells stained with α-GalCer-CD1d dimers in the liver of LEW rats showed some increase of the DN fraction in comparison with the cells stained with vehicle-CD1d dimers (Fig. 2B). Therefore, it is conceivable that these DN cells are iNKT cells, which may Midostaurin mw be missed due to nonspecific staining of the vehicle control. However, even if it is postulated that all the DN α-GalCer-CD1d-stained cells would be bona fide iNKT cells, their frequency would be a maximum of 0.003% in IHLs (i.e., about 2% of the iNKT cells found in F344 liver). Next, we examined the presence

of iNKT cells in the thymus of both inbred rat strains by flow cytometry and compared it with that of C57BL/6 mice (Fig. 2G). We used both rat and mouse CD1d dimers, but none of them revealed a distinct iNKT-cell population among F344 or LEW thymocytes. In contrast, C57BL/6 thymocytes contained a distinct fraction of α-GalCer-CD1d dimer-stained cells. The analysis of iNKT cells in mouse thymi is commonly carried out after exclusion of HSAhigh (CD24) immature thymocytes. The commercially available anti-rat HSA many mAb does not stain rat thymocytes. Therefore, we analyzed CD8− cells (CD8αβ− in case of rat and CD8αα−/CD8αβ− in case of mouse), stained with anti-TCRβ mAb and CD1d dimers. This approach has been chosen to specifically enrich

the populations among which rat (CD4+, DN, and CD8αα+) or mouse (CD4+, DN) iNKT cells are expected and found to result in an eightfold increase of the relative iNKT-cell frequency among C57BL/6 thymocytes. However, we were still not able to detect a distinct iNKT-cell population among F344 or LEW thymocytes (Fig. 2G). In addition to flow cytometry experiments, we also examined the expression of AV14-containing TCRs by RT-PCR (Supporting Information Fig. 1F). First, we analyzed the expression of TCRα chains comprised by AV14 and AJ18 gene segments. The highest expression levels were found among F344 IHLs, followed by F344 splenocytes, and thymocytes. In contrast, analysis of LEW-derived RNA gave only very weak or no signals. Importantly, the differences between LEW and F344 were already found in thymocytes. AV14-AJ18 rearrangements were also analyzed by sequencing the RT-PCR products.