TREM-1 engagement also triggers enhanced production Selleck Ipatasertib of TNF-α, IL-1β, CXCL8, and OPN, suggesting that TREM-1+ H-iDCs infiltrating pathologic tissues are endowed with increased ability to induce angiogenesis and inflammation compared with

TREM-1− iDCs present in normoxic tissues [40, 47-51]. These results are in agreement with previous data supporting a role for TREM-1 as an amplifier of inflammation and in the pathogenesis of many infectious and noninfectious inflammatory disorders [23, 29, 30, 37, 44, 52]. Increased OPN secretion is compatible with a Th1 shift of H-iDC responses [47, 48]. The demonstration that TREM-1 engagement triggers production of IL-12, CCL5, and CCL17, which are implicated in the activation of Th1/Th17-polarized immune responses by recruiting inflammatory T cells and restraining expansion of Treg cells [12, 13, 49, 51, 53-57], provides additional evidence that iDCs generated under chronic hypoxia are polarized toward a Th1/Th17 proinflammatory direction. Indeed, we demonstrate that H-iDCs exhibited increased ability to stimulate EGFR inhibitor allogenic T-cell proliferation and Th1/Th17 cell priming upon

cross-linking with anti-TREM-1 Ab. These findings highlight TREM-1 potential to contribute to the functional reprogramming of iDCs generated at hypoxic sites toward a more mature, Th1/Th17-polarized inflammatory stage. Given the previously reported evidence that TREM-1 engagement also stimulates the Th1/Th17-polarizing activity of H-mDCs and that both TREM-1+ iDC and mDC subsets are enriched in the inflamed juvenile idiopathic arthritis hypoxic joints [23], it is reasonably to suggest that sustained expression of this molecule in DCs may be of pathologic

relevance, representing a potential mechanism of amplification of the local inflammatory process and contributing to chronic inflammation [28, 30, 37]. Although the natural TREM-1 PIK3C2G ligand(s) have not been identified, recent studies have suggested a role for this receptor in the recognition of soluble factors released by necrotic cells as a result of inflammation and/or tissue damage, such as the DAMP molecules high-mobility group box 1 and HSP70 [58, 59]. These proteins are present in inflammatory lesions [60] where they can interact with TREM-1 on myeloid cells amplifying inflammatory responses [58, 61], and the challenge of future studies will be to clarify the effective role played in vivo by TREM-1 putative ligand(s) in triggering H-iDC maturation, proinflammatory cytokine/chemokine production, and Th1/Th17-cell polarization via TREM-1 engagement. In conclusion, our results provide novel mechanistic clues on the contribution of reduced O2 availability to the regulation of immune and inflammatory responses, unraveling the critical role of hypoxia in functionally reprogramming iDCs toward a more mature, Th1/Th17-polarized inflammatory stage.

Another option is to engineer DC genetically to either constitutively express immunosuppressive [e.g. IL-4, IL-10, cytotoxic T lymphocyte antigen (CTLA)-4; [56-60]] or apoptosis-inducing [e.g. Fas, tumour necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL); [61-63]] molecules or, conversely, to inhibit expression of immunostimulatory molecules (e.g. CD80/CD86, IL-12; [64-66]). Other methods of tolDC generation include treatment of DC with immunosuppressive cytokines IL-10/TGF-β [67-69] or rapamycin [70], short-term

stimulation with LPS [71], induction of microRNA-23b expression [72] or increasing Wnt signalling by treatment with Wnt-5a [73]. Many of these ex-vivo-generated tolDC are capable of inhibiting pathogenic autoreactive T cell responses check details in vivo [50]. A variety of tolDC have been tested in animal models of RA. Importantly, a number of tolDC have been shown to have immunotherapeutic potential, i.e. can suppress established arthritis [50, 74]). Not surprisingly, the in-vivo mechanism of action by which these tolDC exert their beneficial effects depends on the type of tolDC administered (reviewed in [74]). For instance, FasL-transduced DC act by

depletion of autoreactive T cells [62], IDO- or CTLA 4 immunoglobulin (Ig)-transduced DC induce FoxP3+ Tregs [75], and dexamethasone/vitamin D3-modulated DC inhibit Th17 cells and enhance IL-10-producing T cells [74]. The positive results from preclinical animal selleck inhibitor models have provided strong support for the concept that tolDC can be applied as an immunotherapeutic agent for the treatment of autoimmune diseases. However, animal models of autoimmune disease do not reflect human disease completely and ultimately the safety, feasibility and effectiveness of tolDC therapy can be tested only through clinical trials. Two tolDC trials (in type I diabetes and RA) have been conducted recently [76, 77], and our tolDC trial in RA has also started recently – see section below for more detail. A tolDC trial in MS has not yet been reported, but a recent study by the Martinez-Caceres/Borras group [78]

has shown that myelin peptide-pulsed tolDC can induce anergy in myelin-specific T cells from relapsing–remitting MS patients. 4-Aminobutyrate aminotransferase The group are currently preparing for a tolDC trial in MS in the near future (Eva Martinez-Caceres, personal communication). The first clinical trial with tolDC was carried out by the Giannoukakis/Trucco team at the University of Pittsburgh School of Medicine, and the results were published in 2011 [76]. They conducted a randomized, double-blind, Phase I study with tolDC in patients who had insulin-requiring type I diabetes for at least 5 years. Patients were injected with autologous, monocyte-derived DC that were either unmanipulated (control DC; three patients treated) or were treated ex vivo with anti-sense oligonucleotides targeting the CD40, CD80 and CD86 co-stimulatory molecules (tolDC; seven patients treated).

,1 Takumi Yamamoto M.D.,1 Mitsunaga Narushima M.D.,1 Shinya Hayami M.D.,1 Naoya Sawamoto M.D.,1 Munekazu Naito M.D.,2 Isao Koshima M.D.1 In the article entitled “Autologous Groin Lymph Node Transfer for ‘‘Sentinel Lymph Network” Reconstruction after Head-and-Neck Cancer Resection and Neck Lymph Node Dissection: MAPK Inhibitor Library purchase A Case Report,” Microsurgery 2012;32(2):153–7, an inaccurate statement was printed about ethical approval. The corresponding author of this article has notified us that the last sentence in the third paragraph on page 1 of the article inaccurately read: All aspects of this surgery were approved by our institutional review board and informed consent was obtained from the

patient. The sentence Everolimus mouse should have read as follows: Intraoperative ICG lymphography and skin tissue analysis were approved by our institutional review board and informed consent was obtained from the patient. “
“Background: The previously described “perfusion zones” of the abdominal wall vasculature are based

on filling of the deep inferior epigastric artery (DIEA) and all its branches simultaneously. With the advent of the DIEA perforator flap, only a single or several perforators are included in supply to the flap. As such, a new model for abdominal wall perfusion has become necessary. The concept of a “perforator angiosome” is thus explored. Methods: A clinical and cadaveric study of 155 abdominal walls was undertaken. This comprised the use of 10 whole, unembalmed cadaveric abdominal walls for angiographic studies, and 145 abdominal wall Carnitine dehydrogenase computed tomographic angiograms (CTAs) in patients undergoing preoperative imaging of the abdominal wall vasculature. The evaluation of the subcutaneous branching pattern and zone of perfusion of individual DIEA perforators was explored, particularly exploring differences between medial and lateral row perforators. Results: Fundamental differences exist between medial row and lateral row perforators, with medial row perforators larger (1.3 mm vs. 1 mm) and more likely to ramify in the subcutaneous fat toward the contralateral hemiabdomen (98% of

cases vs. 2% of cases). A model for the perfusion of the abdominal wall based on a single perforator is presented. Conclusion: The “perforator angiosome” is dependent on perforator location, and can mapped individually with the use of preoperative imaging. © 2009 Wiley-Liss, Inc. Microsurgery, 2010. “
“Free fibular bone grafting is an effective treatment for early osteonecrosis of the femoral head in young patients. However, recipient vessels are often small rendering microvascular anastomosis difficult. We have developed a novel technique using retrograde flow through the branches of the lateral circumflex femoral artery to use the proximal end of the artery as the recipient vessel. A vessel diameter of up to 5 mm is obtained providing a good match with the peroneal vessels.

In malaria endemic settings, adults develop Sotrastaurin datasheet protective immunity after repeated exposures (2), but women are more

susceptible to malarial infection when they become pregnant (1). Severe clinical manifestations associated with this infection include premature delivery and intrauterine growth restriction, contributing to low birth weight (LBW), stillbirth, abortion and maternal mortality (3–5). Increased synthesis of inflammatory cytokines like tumour necrosis factor (TNF), interleukin (IL)-2 and interferon (IFN)-γ (6–8) has been shown in malaria during pregnancy, and levels of TNF in particular have been associated with maternal anaemia and LBW (6,9). Interestingly, such pathogenic immune responses to malaria appear to be influenced by host genetic factors. For example, infants homozygous for TNF2, a polymorphism in the TNF promoter region that is associated with increased TNF production (10), are at increased risk of preterm birth and mortality, suggesting that poor birth outcomes in malaria endemic areas are precipitated by a genetically determined maternal tendency to produce high levels of this inflammatory cytokine (11). In mice, the immune response to malaria is complex and varies as a function

of mouse genetic background (12) and anatomical sites analysed. Moreover, it is dependent on parasite species and strain as well as on route of infection. In B6 mice, early production of TNF, IFN-γ, IL-12 (13) and granulocyte–macrophage colony-stimulating factor (14) is required for resistance to Fluorometholone Acetate blood-stage Cell Cycle inhibitor P. chabaudi AS infection. In contrast, susceptible A/J mice mount early, predominantly Th2-biased cytokine responses (15) and succumb to infection (16). Treatment of these mice with recombinant IL-12 early in infection results in increased production of IFN-γ and TNF and facilitates elimination of parasites and survival (17). Interestingly, A/J mice overcome their Th2-cytokine bias later in infection, exhibiting increased TNF expression in the liver and high serum TNF levels coincident with the time that they begin to succumb to infection (18). Recently, we initiated studies of malaria

during pregnancy using P. chabaudi AS infection in B6 mice as a model platform (19–21). This model recapitulates the severe pregnancy outcomes, namely foetal loss, seen in low endemic areas and in some heavily exposed primigravidae (1). Importantly, similar to human malaria during pregnancy (6,9), TNF plays a critical role in embryo loss in this model; antibody-mediated neutralization of this cytokine rescues mid-gestational pregnancy (21). Because TNF is well known to have a negative impact on pregnancy outcomes even in the absence of infection (22,23), the tendency to produce this factor in response to malarial infection may represent a common pathogenic factor that relative to other host elements is central to disease pathogenesis.

05), but not in the ACE/ARB group (P > 0.05). Conclusion:  The findings suggest AZD5363 cell line that ACE/AII inhibitors appeared to have a slower rate of decline in ultrafiltration and RRF, effectively protect against

peritoneal fibrosis in long-term peritoneal dialysis. Long-term follow up seems to be required to draw more conclusions. “
“Diabetic nephropathy (DN) is the most common cause of chronic kidney failure and end-stage renal disease in the Western world. Studies from diabetic animal models and clinical trials have shown that inhibition of the renin-angiotensin system delays the progression of advanced DN. However, a recent large-scale clinical trial has revealed that inhibition of renin-angiotensin system in early phases of DN does not slow the decline of renal function or the development of morphological lesions, suggesting that different mechanism(s) may be involved in the different stages of DN. The role of epithelial-mesenchymal transition in renal fibrosis has been intensively investigated. Recently, endothelial-mesenchymal transition, or endothelial-myofibroblast transition (EndoMT) has emerged as another mechanism involved in both developmental and pathological Talazoparib cost processes. The essential role of EndoMT in cardiac development has been thoroughly studied. EndoMT also exists and contributes to the development and progression of cardiac fibrosis, lung fibrosis, liver fibrosis and corneal fibrosis.

EndoMT

is a specific form of epithelial-mesenchymal transition. During EndoMT, endothelial cells lose endothelial markers and obtain mesenchymal markers. Recent evidence from our laboratory and others suggests that EndoMT plays an important role in the development of renal fibrosis in several pathological settings, including experimental DN. This review considers the evidence supporting the occurrence of EndoMT in normal development and in pathology, as well as the latest findings suggesting EndoMT contributes to fibrosis in DN. Whether experimental findings of EndoMT will be reproduced in human studies remains to be determined. Glomerular and interstitial fibrosis are the key morphological features of diabetic Sitaxentan nephropathy (DN), and both correlate well with the development and progression of renal disease.1 While mesangial cells and podocytes are thought to be major mediators of DN, increasing evidence suggests that renal tubulointerstitial fibrosis also plays a key role in the progression to end-stage renal disease,2 making this an important therapeutic target. Myofibroblasts play a major role in the synthesis and secretion of extracellular matrix in the development and progression of renal fibrosis. In DN, cells expressing α-smooth muscle actin (α-SMA), the putative marker of myofibroblasts, are located primarily in the renal interstitium and to a lesser extent in glomeruli in association with mesangial cell proliferation.

Twenty-four-month-old infants were familiarized with either novel objects or novel names prior to the

referent selection portion of a fast-mapping task. When familiarized with the novel objects, infants retained the novel mapping after a delay, but not when familiarized with the novel words. This suggests familiarity with the object versus the word form leads to differential encoding of the name–object link. We discuss the implications of this finding for subsequent slow mapping. “
“Morgante et al. (in press) find inconsistencies in the time reporting of a Tobii T60XL eye tracker. Their study raises important questions about CYC202 solubility dmso the use of the Tobii T-series in particular, and various software and hardware in general, in different infant eye tracking paradigms. It leaves open the question of the source of the inconsistencies. Here, observations from a Tobii eye Dorsomorphin tracker are presented to elucidate possible sources of timing inconsistencies, including those found by Morgante et al. The ramifications of the reported timing inconsistencies

are related to various infant paradigms. The focus is on the level of concern a researcher should have if any eye tracker displays these timing characteristics, and what corrective measures may be taken. While posing no problems for some paradigms, timing inconsistencies are potentially problematic (but correctable) when assessing event-related looking behavior. Observed timing contraindicates use in fast gaze-contingent displays (<100 ms). General suggestions are made

regarding timing in eye-tracked data collection. “
“This study examined the effects G protein-coupled receptor kinase of program pacing, defined as the rate of scene and character change per minute, on infants’ visual attention to video presentations. Seventy-two infants (twenty-four 6-month-olds, twenty-four 9-month-olds, twenty-four 12-month-olds) were exposed to one of two sets of high- and low-paced commercial infant DVDs. Each DVD was approximately 5-min long, and the order the DVDs were viewed was counterbalanced for pace. Attention was higher during rapidly than slowly paced DVDs, particularly for the 6- and 9-month-old infants. These results support previous research documenting that attention is initially controlled by exogenous qualities (e.g., rapid pace), but with development and experience becomes more influenced by endogenous factors. “
“In the present study, we examined if young infants can extract information regarding the directionality of biological motion. We report that 6-month-old infants can differentiate leftward and rightward motions from a movie depicting the sagittal view of an upright human point-light walker, walking as if on a treadmill. Inversion of the stimuli resulted in no detection of directionality. These findings suggest that biological motion displays convey information for young infants beyond that which distinguishes them from nonbiological motion; aspects of the action itself are also detected.

1). A landmark study of 32 065 haemodialysis patients, mean follow-up of 2.2 years, reported that deaths from cardiac arrests were most common after the long 2

day inter-dialytic break (after long inter-dialytic break, 1.3 vs 1.0 deaths per 100 person-years on other days, P = 0.004).[42] The DOPPS investigators reported similar findings in haemodialysis patients from the United States, Europe and Japan.[43] Possible explanations are manifold, including hypervolaemia, circulatory collapse, or electrolyte and metabolite build-up between dialysis sessions. Potassium is important for regulation of trans-membrane potential of cardiac myocytes, and there is evidence to support the hypothesis that potassium shifts, relative hypokalaemia post-dialysis[44] and pre-dialytic PF-02341066 research buy hypokalaemia predispose to arrhythmia. In one multivariate

Cox regression analysis of the risk factors for SCD in 476 chronic haemodialysis patients, RO4929097 pre-dialytic hyperkalaemia conferred 2.7-fold increase (95% CI = 1.3–5.9).[45] In an observational study of 81 013 haemodialysis patients, the optimum pre-dialysis serum potassium in respect of long-term survival was between 4.6 and 5.3 mmol/L.[46] In a review of 400 dialysis unit cardiac arrests, patients who were dialysed against a low potassium dialysate (0 or 1.0 mmol/L) were twice as likely to have had a cardiac arrest.[47] It has also been reported that a dialysate potassium of <2 mmol/L (or <3 mmol/L, if pre-dialysis potassium is <5 mmol/L) confers increased risk of SCD.[3, 6] Electrical conduction is also dependent on intra-cardiac calcium handling; a low calcium dialysate (1.25 mmol/L) is associated ZD1839 nmr with aberrations in cardiac conduction

as assessed by electrocardiography, such as increased QTc dispersion or prolonged QT interval.[48] In view of these findings, there is a need for future studies to concentrate on the composition of dialysate in the hope of reducing arrhythmia burden. High rates of fluid removal may result in intra-dialytic hypotension, myocardial stunning and injury. In turn, this may predispose to arrhythmia or circulatory collapse. In DOPPS, a large ultrafiltration volume (>5.7% of post-dialysis weight) conferred an HR of 1.15 for sudden death (defined as deaths due to arrhythmia, cardiac arrest and/or hyperkalaemia).[6] Similarly, in a case-control study of 502 haemodialysis patients who had a sudden cardiac arrest with 1632 age- and dialysis-vintage-matched controls who did not, increased ultrafiltration volumes conferred an adjusted OR of 1.11 (95% CI = 1.02–1.033, P = 0.02). A recent observational study reported that depressed heart rate variability is associated with fluid overload in chronic haemodialysis patients.[49] This may be one of the pathophysiological mechanisms by which fluid overload predisposes to arrhythmias.

The results also showed that the expression level of TIPE2 mRNA in the children with asthma was significantly lower than that in healthy subjects (P = 0.0323) (Fig. 1B). Next, the expression levels of TIPE2 protein were analysed in PBMC from 42 patients with asthma and 39 healthy controls by Western blot as described previously. Consistent with the changes of TIPE2 mRNA levels, the results of Western blot also revealed Selleck XL184 that the expression of TIPE2 protein was lower in patients with asthma

compared with normal controls (Fig. 2), which suggests the downregulation of TIPE2 expression in childhood asthma. As Th1/Th2 imbalance plays an important role in the pathogenesis of asthma, we investigated the levels of Th2-type cytokine IL-4 and Th1-type cytokine IFN-γ in the serum obtained from children with asthma and healthy subjects using ELISA. It was found that serum IL-4 level in the children with asthma was obviously higher than that in healthy subjects (P < 0.001) (Fig. 3A), while serum IFN-γ level was significantly lower in patients with asthma than that in normal controls (P < 0.001) (Fig. 3B).

The results suggest Th2 response is dominated and leads to the development of asthma. It is known that the increase in Th2-type cytokines promotes the production of IgE and terminal differentiation Buparlisib of eosinophils. We next detected serum total IgE and eosinophils in the children with asthma and healthy controls. The results showed the levels of serum total IgE and eosinophil count were significantly increased in children with asthma compared with healthy controls (P < 0.001) (Table 1, Fig. 4A,B), which indicates the important roles of IgE and eosinophil in childhood asthma. To further determine the clinical significance of TIPE2 in childhood asthma, we accordingly analysed the correlations of TIPE2 mRNA expression with IL-4, IFN-γ, IgE and eosinophil. As shown in Fig. 5A–D, the expression level of TIPE2 mRNA was negatively correlated with the serum levels of IL-4 (r = −0.3693,

P = 0.0344). Furthermore, we observed that the expression of TIPE2 mRNA was also inversely related to serum total IgE level (r = −0.5173, P = 0.001) and eosinophil count Branched chain aminotransferase (r = −0.3503, P = 0.0362). However, there was no statistically significant correlation between TIPE2 mRNA expression and serum IFN-γ level (r = 0.1504, P = 0.3959). TIPE2 is a novel negative regulator of innate and adaptive immunity, which is required for maintaining immune homeostasis and preventing deleterious inflammatory responses [19]. TIPE2-deficient mice are easily to develop multiorgan inflammation including lung. Sun et al. [6] reported that both CD4+ and CD8+ T cell- mediated immune responses were significantly augmented in TIPE2−/− mice as compared to their controls, suggesting the regulatory effect of TIPE2 in T cell-mediated immunity. Asthma is one of the most common chronic inflammatory diseases of the airways in childhood [20].

This study showed that caregiver protective behavior, which functions to prevent a child from interacting with a novel stimulus, is an important mechanism to consider when understanding toddler stress responses during novel contexts. “
“Memory based on a one-time experience is an important element of its definition as “episodic.” Infants’

memories for one-time experiences over long delays are largely unexplored. Using elicited imitation, we tested 20- and 16-month-olds’ (Experiment 1) and 13-month-olds’ (Experiment 2) memories as a function of number of experiences and delay. Over 1 month, 20- and 16-month-olds remembered individual actions of one-time events; 20-month-olds also remembered temporal order; with verbal reminders, 16-month-olds did as well. Over AZD2014 chemical structure 3 months, recall depended on multiple experiences. Thirteen-month-olds’ required multiple experiences,

even over 1 month. The findings speak to the gradual emergence of an important element of episodic memory, namely the ability to preserve memories of one-time experiences Selleck LY2835219 over long periods of time. “
“Toward the end of their first year of life, infants’ overly specified word representations are thought to give way to more abstract ones, which helps them to better cope with variation not relevant to word identity (e.g., voice and affect). This developmental change may help infants process the ambient language more efficiently, thus enabling rapid gains in vocabulary growth. One particular kind of variability that infants must

accommodate is that of dialectal accent, because most children will encounter speakers from different regions and backgrounds. In this study, we explored developmental changes in infants’ ability to recognize words in continuous speech by familiarizing them with words spoken by a speaker of their own region (North Midland-American English) or a different region (Southern Ontario Canadian English), and testing them with passages spoken by a speaker of the opposite dialectal accent. Our results demonstrate that 12- but not 9-month-olds readily recognize words in the face of dialectal variation. Regionally driven dialectal differences produce phonetic variation that straddles the boundary between linguistically relevant and linguistically irrelevant variation. Even for mutually comprehensible very dialectal accents, such as North Midland-American and Southern Ontario Canadian English, phonetic differences affect the realization of contrasts, which may complicate word recognition. As a result of the Canadian shift, both /ae/ and /I/ are lowered and more backed in Southern Ontario Canadian English, compared with North Midland-American English (Labov, Ash, & Boberg, 2006). For example, [ma:p] may be perceived as “map” in this Canadian dialect, but as “mop” in this American dialect. This may fetter perception for American listeners unfamiliar with the variation introduced by this dialect (e.g., Kraljic, Samuel, & Brennan, 2008).

Three in vitro protocols are provided for the analysis of cell migration, one requiring no specialized equipment, one requiring the modified Boyden chamber, and the other employing a flow chamber, which measures cell adhesion, rolling, and migration. Finally, a method is provided for imaging polarized cells by confocal microscopy. Curr. Protoc. Immunol. 88:14.15.1-14.15.14. © 2010 by John Wiley & Sons, Inc. “
“A large acute hemorrhagic conjunctivitis (AHC) outbreak occurred in 2011 in Okinawa Prefecture in Japan. Ten strains of coxsackievirus group A type 24 variant (CA24v) were isolated from patients with AHC and full sequence analysis of the VP3, VP1, 3Cpro and 3Dpol coding

regions performed. To assess time-scale evolution, NVP-AUY922 chemical structure Alpelisib mouse phylogenetic analysis was performed using the Bayesian Markov chain Monte Carlo method. In addition,

similarity plots were constructed and pairwise distance (p-distance) and positive pressure analyses performed. A phylogenetic tree based on the VP1 coding region showed that the present strains belong to genotype 4 (G4). In addition, the present strains could have divided in about 2010 from the same lineages detected in other countries such as China, India and Australia. The mean rates of molecular evolution of four coding regions were estimated at about 6.15 to 7.86 × 10−3 substitutions/site/year. Similarity plot analyses suggested that nucleotide similarities between the present strains and a prototype strain (EH24/70 strain) were 0.77–0.94. Fossariinae The p-distance of the present strains

was relatively short (<0.01). Only one positive selected site (L25H) was identified in the VP1 protein. These findings suggest that the present CA24v strains causing AHC are genetically related to other AHC strains with rapid evolution and emerged in around 2010. "
“Citation Tskitishvili E, Nakamura H, Kinugasa-Taniguchi Y, Kanagawa T, Kimura T, Tomimatsu T, Shimoya K. Temporal and spatial expression of tumor-associated antigen RCAS1 in pregnant mouse uterus. Am J Reprod Immunol 2010; 63: 137–143 Problem  The tumor-associated antigen RCAS1 (receptor-binding cancer antigen expressed on SiSo cells) is considered to play a role in the inhibition of maternal immune response during pregnancy, and participates in the initiation of labor and placental detachment. The aim of our study was to investigate the expression of RCAS1 protein in the uteri of normal pregnant mice. Method of study  Uteri with fetuses were collected from pregnant ICR mice on days 1.5, 3.5, 5.5, 7.5, and 9.5 p.c., and uterine and placental tissues were obtained separately on days 11.5, 13.5, 15.5, and 17.5 p.c. Samples were examined using real-time (RT)-PCR, Western blotting, and immunohistochemical analyses. Results  In normal pregnant mice, RCAS1 protein mRNA was significantly increased on day 7.5 p.c. Antigen localization was detected in the placenta, decidua, and fetus.