29 Interestingly, attenuated CD138+ plasma cell generation and Blimp-1 protein expression were discovered in Cox-2-deficient mouse B cells. This provides further evidence

that B-cell terminal differentiation is Cox-2-dependent. Although both Blimp-1 selleck screening library and CD138 expression are attenuated in mouse B-cell cultures, this does not demonstrate that Blimp-1 is directly responsible for the decrease in the frequency of CD138+ cells. However, in the human B-cell cultures, Blimp-1 decreases early after Cox-2 inhibition and precedes CD38+ plasma cell precursor formation, suggesting that reduced Blimp-1 levels are responsible for decreased generation of human plasma cells. Blimp-1 is considered a master regulator of the plasma cell phenotype. Mice deficient in either Blimp-1 or Xbp-1 fail to generate significant numbers of plasma cells and produce relatively little serum antibody.3,26,30 We previously demonstrated that Cox-2-deficient mice immunized with HPV-16 virus-like particles displayed reduced neutralizing antibody titres and B-cell memory responses.15 Lupu et al.16 Y-27632 order provide evidence that Cox-2 selective inhibitors impaired IgG production against T-dependent antigens, namely tetanus and diphtheria toxins. Autoimmune antibody production was also attenuated following treatment with Cox-2 selective inhibitors.31 These observations and our new in vitro results suggest that

impaired in vivo antibody production is a result of decreased B-cell differentiation to antibody-secreting plasma cells. Likewise, our results show reduced human Blimp-1 and Xbp-1 expression in the

presence of Cox-2 inhibitors, which is important in the decreased generation of plasma cell precursors (CD38+ antibody-secreting cells) and overall reduced antibody levels. Our results reveal that Cox-2 is essential for the differentiation B cells to antibody-secreting cells, providing a mechanism Inositol monophosphatase 1 for the involvement of Cox-2 in attenuated antibody production. Use of Cox-2 inhibitors during vaccination or infection could, therefore, impair the generation of plasma cells, which are important regulators of immunity. Without effective generation of plasma cells, patients may be more vulnerable to infections that rely on antibody-mediated immune responses, particularly elderly patients, who often take Cox-2 selective inhibitors and NSAIDs. Ultimately, our findings indicate that taking Cox-2 selective inhibitors or other NSAIDs that inhibit Cox-2 may reduce the efficacy of vaccines, as well as blunt immune responses to invading pathogens. The authors would like to thank Dr Ignacio Sanz and Tam Quach for providing T-cell-depleted human tonsil cells. This work was funded by the National Institutes of Health Grants DE011390, AI071064, ES01247 and the Training Program in Oral Sciences T32-DE007202. The authors have no conflict of interest. “
“Citation Romero R, Kadar N, Vaisbuch E, Hassan SS.

Similarly, pyrosequencing analysis of microbes resident in diabetic Ferroptosis inhibitor foot ulcers identified 38 distinct genera and again yielded a subset of sequences unmatched to any recognized microbial sequences (Dowd et al., 2008b). The microbiome of the healthy oral cavity when examined by cloning and sequencing comprises more than 1000 distinct taxa with over half of them yet to be cultured (Dewhirst et al., 2010). This heretofore unappreciated microbial diversity raises significant questions about the relative importance of the component

organisms, individually and in communities, to health and disease. Much progress has also been made in the examination of bacterial gene expression patterns associated with biofilm formation, including whole transcriptomic studies on multiple microbial species. The vast majority of these studies have been on in vitro biofilms and employ a range of technologies. DNA microarray analysis of microbial transcriptomes has now been accomplished for a variety of organisms associated with human disease, including PLX-4720 ic50 Escherichia coli (Reshamwala & Noronha, 2011), Streptococcus mutans (Shemesh et al., 2010), Streptococcus pyogenes (Kreth et al., 2011), and

Candida (Sellam et al., 2009). Direct RNA sequencing (RNA Seq) has also been undertaken to distinguish biofilm-specific patterns of gene expression. Dotsch et al. used RNA Seq to compare planktonic cultures of P. aeruginosa with stationary phase cultures and bacteria grown as a biofilm. They found that although there was substantial similarity in the gene expression profiles of stationary phase and biofilm cells, there were also significant differences, indicating that the physiology of biofilm bacteria was not simply surface-attached stationary phase cells. Some studies have begun to examine the transcriptomes of bacteria in vivo. Bielecki et al. (2011) Oxaprozin investigated the expression profiles of three distinct clonal isolates of P. aeruginosa from burn wounds in five different conditions: directly from a burn wound sample, in a plant infection, in a murine tumor infection, and as planktonic and biofilm cultures. They found distinct patterns of

gene expression in each condition, indicating distinct adaptive responses of P. aeruginosa to different environments. Immunohistochemical or immunofluorescent techniques represent another targeted approach to identifying pathogens in host tissue. Polyclonal or monoclonal sera specific to pathogens are routinely used to detect encapsulated pathogens in fluids such as S. pneumoniae, Neisseria meningiditis, and Haemophilus influenzae. These antibodies have not been consistently applied for the detection of bacteria in biofilms often because it is thought the matrix may bind antibodies nonspecifically. However, antibodies can be used by performing parallel controls and careful testing of sera, as well as using blocking steps to reduce nonspecific interactions (Fig. 2) (Hall-Stoodley et al., 2006).

2A. However, the expanded Th17 clones did not exhibit significant alterations of FOXP3 expression and IFN-γ production when the expansion system only included PBMCs but not OKT3. We extended these experiments to the other human Th17 clones and obtained similar results (data not shown). These results indicate a critical role for TCR engagement in IFN-γ-production and FOXP3 expression,

but not IL-17 reduction, in expanded Th17 cells. To further confirm the contribution of TCR stimulation to an unstable lineage phenotype and differentiation plasticity of Th17 cells, E1-Th17 cells were directly stimulated with or without plate-bound OKT3 in the presence or absence of cytokines (IL-1β, IL-6 and IL-23) critical for human Th17 cell development and function, for 7 days, followed INCB024360 by repeated stimulation for another 7 days. We subsequently determined the proportion of IL-17 and IFN-γ-producing cell populations and FOXP3 expression in different cultures of these E1-Th17 cells following two rounds of stimulation. As shown in Fig. 4B and Supporting Information Fig. 3, the percentages of IL-17-producing cell populations decreased dramatically in E1-Th17 cells after in vitro culture with different stimulations, but there was no difference of percentages between the groups stimulated click here with or without OKT3. The addition of cytokines IL-1β, IL-6 and IL-23 to cultures could not

maintain the stability of Th17 cells and did not prevent the reduction of IL-17-producing cells in vitro. We also observed significantly decreased numbers of IL-17-producing cell populations in Th17 clones when cultured with medium only (low IL-2). The combined addition of cytokines did not alter percentages of IFN-γ-producing cells

during the first 7 days of culture, whereas these were increased in the day 14 cultures. However, the addition of these cytokines did not promote FOXP3 expression in Th17 cells in either day 7 or day 14 cultures. When E1-Th17 cells were stimulated with plate-bound OKT3, the percentages of IFN-γ-producing cell populations were not significantly induced during the first 7-day culture but were dramatically increased in day 14 cultures following the eltoprazine second round of stimulation. Furthermore, the percentages of FOXP3+ cell populations in E1-Th17 cells stimulated with plate-bound OKT3 were significantly induced in both 7-day (first stimulation) and 14-day (second stimulation) cultures (Fig. 4B and Supporting Information Fig. 3). However, further combination of the cytokines with OKT3 did not significantly alter IFN-γ-producing cell populations and FOXP3 expression in either day 7 or day 14 cultures, compared with cultures stimulated with OKT3 alone. Interestingly, the combination of these cytokines with OKT3 promoted a reduction in the proportion of IL-17-producing cell populations in Th17 clones compared with those in Th17 cell cultures stimulated with OKT3 only (Fig. 4B and Supporting Information Fig. 3).

A sample of the supernatant was added to SYTOX green nucleic acid stain (1 µM) in a black 96-well plate to quantify NET-DNA fragments by fluorometry BMS-777607 (Twinkle LB970, Berthold Technologies,

Harpenden, UK; excitation 485 nm, emission 525 nm) and recorded as arbitrary fluorescent units (AFU). Neutrophils (1 × 105) suspended in 500 µl RPMI-1640 were seeded into BSA-coated 24-well plates and allowed to settle for 30 min at 37°C, prior to stimulation for 3 h at 37°C [2] and staining of NET-DNA using 1 µM SYTOX green. NETs and cells were observed at room temperature under a fluorescence microscope (Nikon Eclipse TE300, Kingston upon Thames, UK) using a × 20 objective and images captured by digital camera (Nikon CoolPix 450, Kingston upon Thames, UK). The InnoZyme myeloperoxidase activity kit was www.selleckchem.com/products/Everolimus(RAD001).html used according to the manufacturers’ instructions to examine the effect of 3-AT (1 mM) on the activity of purified human MPO (100 ng/ml). ROS generation was quantified

by enhanced chemiluminescence assay [19]. Neutrophils (1 × 105) suspended in PBS supplemented with glucose (10 mM), MgCl2 (1·5 mM) and CaCl2 (1·35 mM) were seeded into a BSA-coated 96-well plate with luminol (450 µM) to detect total ROS, isoluminol (900 µM) plus horseradish peroxidase (7.5 units/ml) to detect extracellular ROS or lucigenin (50 µg/ml) to detect superoxide. Cells were allowed to settle for 30 min at 37°C prior to stimulation. ROS generation was recorded as the peak relative light units (RLU) per second recorded by microplate luminometer (Berthold LB96v) over Reverse transcriptase the 2·5-h incubation period, as reported

previously [19]. Sodium hypochlorite was diluted and the concentration of hypochlorite ions (OCl–) estimated by optical density at 292 nm of pH 12·0 solutions using an extinction coefficient of 350 M/cm [23]. The final pH when used in experiments was approximately the same as the pKa for HOCl (7·5), thus it was assumed that 50% existed as HOCl and 50% existed as OCl–. S. aureus (NCTC 6571) was grown aerobically at 37°C on tryptone soya agar and inoculated into tryptone soya broth. Bacteria were isolated from broth culture by centrifugation, washed three times in sterile PBS and heat-treated at 100°C for 10 min. Opsonization was performed as described previously [24] and stored as a 1·2 × 109 cells/ml suspension at −80°C. Data were analysed using Excel 2007 (Microsoft). Each in vitro experiment was performed at least four times using independent neutrophil donors, and each experiment was performed in quadruplicate. Comparison between groups was made using two-tailed paired t-test where P-values of less than 0·05 were considered significant. It has been reported previously that NADPH oxidase-dependent generation of ROS, and specifically H2O2, is required for NET release [3].

Hence, SD-4 gene deficiency appears to have little to no impact on leucocyte development. Moreover, up to 1 year of age, we observed no morphological nor developmental abnormality. Using functional blockade of SD-4 by antibody or Fc-fusion proteins, we showed previously that SD-4 is the ligand through which DC-HIL mediates its inhibitory function.[7] To study the influence of SD-4 expression on

the regulation of T-cell function, we first examined the capacity of T cells from SD-4 KO mice to mediate the inhibitory function of DC-HIL (Fig. 2). Specificity of the gene deficiency was confirmed by the inability of T cells to express SD-4 after activation (high expression by WT-T cells, see Supplementary selleck screening library material, Fig. S1), even as they were capable of expressing another inhibitory

molecule, PD-1 (Fig. 2a). We then examined the binding of activated T cells to DC-HIL (Fig. 2b), and found that those from WT mice bound strongly to soluble DC-HIL receptor (DC-HIL-Fc), whereas those from KO mice did not. Thereafter, we examined the ability of immobilized DC-HIL-Fc to inhibit T-cell activation triggered by anti-CD3 antibody. CD4+ T cells from WT or KO mice were cultured with immobilized anti-CD3 antibody (increasing doses) and DC-HIL-Fc (constant dose), and their activation was measured as proliferation. AZD0530 DC-HIL-Fc strongly inhibited proliferation of SD-4+/+ CD4+ T cells activated by anti-CD3 antibody at doses < 0·3 μg/ml, although doses > 1 μg/ml rescued the inhibition (Fig. 2c), consistent with our previous results using T cells from BALB/c mice.[6, 7] By contrast, the presence or absence of DC-HIL-Fc had no effect on the proliferation of similarly activated SD-4−/− CD4+ T cells. Loss of responsiveness to DC-HIL was also true for SD-4-deficient CD8+ T cells (Fig. 2d). We also probed the effect of SD-4 deficiency on cytokine expression by anti-CD3 antibody-activated

second T cells in the presence or absence of DC-HIL-Fc (Fig. 2e). Interleukin-2 and tumour necrosis factor-α (for CD4+ T cells), and IL-2 and interferon-γ (for CD8+ T cells) were assayed from supernatants of T cells stimulated with anti-CD3 antibody (0·3 μg/ml) plus DC-HIL-Fc or control immunoglobulin. In the absence of DC-HIL (anti-CD3 and control immunoglobulin), there was no significant difference in cytokine production by WT versus KO T cells (CD4+ or CD8+). Consistent with our previous data,[7] co-treatment with DC-HIL markedly inhibited the production of cytokines by SD-4+/+ T cells, whereas it failed to do so for SD-4−/− T cells. Rather, it caused some up-regulation compared with anti-CD3 alone. These results indicate that SD-4 is exclusively responsible for mediating the T-cell-inhibitory function of DC-HIL. SD-4−/− T cells showed similarly strong responsiveness to anti-CD3 antibody stimulation, compared with SD-4+/+ control cells (Fig. 2c,d).

The differentiation of the adipocyte and insulin sensitivity itself is affected by a caspase-1-dependent IL-1β-mediated mechanism. Mice fed a high

fat diet have increased caspase-1 and elevated levels of IL-1β. In contrast, caspase-1-deficient mice have decreased body fat and improved insulin sensitivity 86. In vivo, treatment of obese mice with a caspase-1 inhibitor significantly increases their insulin sensitivity 86. Calorimetry analysis revealed higher fat oxidation rates in caspase-1-deficient animals, and adipocytes from caspase-1-deficient mice or mice deficient in NLRP3 are more metabolically active ex vivo with higher insulin sensitivity and increased production of adiponectin this website as compared with adipocytes from wild-type mice. Gene expression for PPARγ and GLUT4 was also increased in fat from caspase-1- or NLRP3-deficient mice. In the ob/ob obese mouse, fat tissue reveals higher caspase-1 activity with elevated production of active IL-1β. Thus, in addition to blocking IL-1β in type 2 diabetes, targeting IL-1β in pre-diabetic persons with metabolic syndrome should correct some of the abnormalities. These studies are consistent with those reported Selleckchem CH5424802 by Vandanmagsar et al. 89. In those studies, a reduction in adipose tissue expression of NLRP3 was observed

in obese persons WT 2 diabetes following calorie restriction and exercise-mediated weight loss. Not unexpectedly, there was improved insulin sensitivity. Similar to the studies by Stienstra et al. 86, NLRP3-deficient mice did not show obesity-induced inflammasome activation PtdIns(3,4)P2 in fat depots 89. Collectively, both studies 86, 89 establish that caspase-1-dependent cytokines

play an important and possibly causative role in obesity-induced inflammation and insulin resistance. The first clinical proof of a role for IL-1 in the pathogenesis of type 2 diabetes was a randomized, placebo-controlled study of anakinra for 13 wk. In that study, improved insulin production and glycemic control was observed in anakinra-treated patients 90. The fall in glycated hemoglobin was nearly 0.5% lower than that in placebo-treated patients. In addition to improved glycemic control, C-peptide levels increased and the ratio of proinsulin to insulin decreased, both indicators of improved β-cell function. Not unexpectedly, serum IL-6 and CRP levels decreased significantly. In the 39 wk following the 13- wk course of anakinra, patients who responded to anakinra used 66% less insulin to obtain the same glycemic control as compared with baseline requirements 91. The proinsulin to insulin ratio also improved.

This study was supported by Alzheimers Research UK and Alzheimer’s Society through their funding of the Manchester Brain Bank under the Brains for Dementia Research (BDR) initiative. Nancy Allen did immunohistochemistry, all microscopical assessments and data analysis, and helped with paper writing.

Andrew Robinson prepared sections for staining and immunohistochemistry. Julie Snowden helped with statistical advice and clinical data. Yvonne Davidson provided technical support and training. David Mann provided study design, supervision and wrote the paper. “
“Primitive polar spongioblastoma selleck products was first described by Russell and Cairns in 1947. However, the polar spongioblastoma pattern is often seen in many neuroepithelial tumors, and this category was deleted in the previous World Health Organization (WHO) classification. In 2010, Nagaishi et al. reported on a case involving a neuroepithelial

tumor with the typical histological pattern of polar spongioblastoma and suggested that this tumor might click here not be suited to any of the neuroepithelial tumors in the current WHO classification. We report on an autopsy case involving an unclassified high-grade glioma with polar spongioblastoma pattern that was very similar to the case described by Nagaishi et al. A 44-year-old man who presented with a headache exhibited a tumor of the right frontal lobe on MRI. Histological diagnosis of the tumor obtained by gross total resection was high-grade glioma, which was composed of the parallel palisading of spindle tumor cells expressing

GFAP, without microvascular proliferation (MVP) and necrosis. Conventional chemoradiotherapy was performed, but the case was complicated by cerebrospinal fluid (CSF) dissemination that resulted in multiple extraneural metastases through systemic diversionary CSF shunting. Finally, the patient died approximately 13 months after the initial treatment. Both the cerebral and Douglas pouch tumors that were obtained at autopsy were diagnosed as typical glioblastomas, and they were composed of the proliferation of atypical astrocytes with MVP and pseudopalisading necrosis without the formation of rhythmic palisading. Although Afatinib nmr the histological findings were different from that of the first operation, immunohistochemical and genetic profiles demonstrated almost the same results. This tumor was not classified as a typical glioblastoma by the initial findings, but it had the nature of a glioblastoma. These findings suggest that the tumor might be classified as a new subset of glioblastoma called glioblastoma with polar spongioblastoma pattern. “
“The effect of combustion smoke inhalation on the respiratory system is widely reported but its effects on the central nervous system remain unclear. Here, we aimed to determine the effects of smoke inhalation on the cerebellum and hippocampus which are areas vulnerable to hypoxia injury.

[48] This demonstrates that the tolerated, re-transplanted skin graft carried over within it perfectly functional effector T cells, but that FOXP3+ Treg cells were actively blocking their ability to reject and so maintained

the tolerant state within the graft. By studying the changes in gene expression of dendritic cells when they interact with Treg cells,[49, 50] it was found that in addition to the known down-regulation of co-stimulatory ligands and antigen presentation, there was up-regulation of a number of enzymes that either catabolize or use essential amino acids[51] (Fig. 3). In the context of a microenvironment with a restricted availability of nutrients, the local depletion of essential amino acids by these enzymes would Seliciclib mouse be an effective mechanism to control the immune response via the mTOR nutrient sensing pathway. It has also been shown that the intracellular availability of leucine and consequently mTOR activation is controlled by T-cell-receptor-induced expression of the neutral amino acid transporter slc7a5 in Th1 and Th2 cells, where it is essential for their activation LBH589 molecular weight and differentiation, while Treg cells seem not to require this particular transporter.[52] The first example of such amino acid catabolism being able to

control the immune response was the expression of indoleamine 2,3 dioxygenase (IDO) in the placenta during pregnancy, which acts locally to deplete the essential amino acid tryptophan in order to block the maternal immune response to paternal

alloantigens.[53] This tryptophan-depleted microenvironment is sensed by general control non-repressed 2 (GCN2), Mephenoxalone which is one of the initiators of the integrated stress response, and leads to a block in the proliferation of CD8 effector T cells,[54] and is required for the survival of T cells, including CD4+ Treg cells, during periods of amino acid starvation.[51] GCN2, however, was not essential for T cells to sense the absence of essential amino acids in vitro,[51] neither is it required for the induction of tolerance to skin grafts in mice by co-receptor blockade (S. Cobbold, E. Adams and H. Waldmann, unpublished results). The induction of FOXP3 by stimulating naive CD4+ T cells in the presence of low doses of TGF-β in vitro was also unaffected by stimulating the GCN2 pathway with histidinol; whereas, inhibition of the mTOR pathway gave a synergistic increase in FOXP3 induction.[51] It has also now been shown that 1-methyltryptophan mediated blocking of IDO and tryptophan sensing can act via mTOR and PKCθ signalling.[55] Indoleamine 2,3 dioxygenase may have been recognized as the first example of immune regulation due to amino acid catabolism because, of all the essential amino acids, tryptophan is thought to be present at the lowest concentration.

[16, 17, 25] Clearly new therapeutic strategies are required for this deadly disease. Such potential novel therapies can be better designed with comprehensive understanding of the mechanism of infection and its related host defence. Iron uptake from the host by

microorganisms is essential for the establishment and progression of infection since this element is required for the survival of living cells.[26] In a normal host, free iron is restricted by highly efficient iron sequesters such as transferrin, ferritin and lactoferrin.[26] Pathogens either devise strategies to obtain iron from the host by stripping iron from these sequesters (e.g. by siderophore production), or the tightly controlled free iron becomes more available in certain medical conditions. The unique susceptibility of certain patient populations to mucormycosis, but not to other pathogenic check details fungi, point to the importance of iron uptake in the pathogenesis of mucormycosis.[3, 23] These include, hyperglycaemic, DKA and other forms of KPT-330 cost acidosis patients as well as deferoxamine-treated patients. All these patient categories suffer from elevated available serum iron. For example, the excessive glycosylation of proteins such as transferrin and ferritin, due to constant hyperglycaemia result in decreased iron affinity of these sequesters

which leads to the release of free ion in the blood stream and in cells.[27] Similarly, DKA and other forms of acidosis cause proton-mediated dissociation of iron from iron-sequestering proteins.[28] The increased levels of available iron enable enhanced growth of Mucorales in serum.[9, 28, 29] It is also known that DKA mice are more susceptible to mucormycosis infection than normal mice and iron chelation therapy using deferiprone or deferasirox protects DKA mice from mucormycosis.[29, 30] Subsequent studies confirmed the efficacy of deferasirox in treating experimental mucormycosis using the Drosophila fly model.[31] Patients with iron overload toxicity were used DNA ligase to be treated with the bacterial iron-siderophore, deferoxamine.

These patients were found to be extremely susceptible to deadly form of mucormycosis.[32-34] Subsequent studies demonstrated that although deferoxamine is an iron chelator from the perspective of the human host, Rhizopus spp. utilise ferrioxamine (the iron-rich form of deferoxamine) as a xeno-siderophore to obtain previously unavailable iron.[35, 36] It was found that ferrioxamine binds to a cell surface receptor on the surface of Rhizopus and through an energy dependent reductive step releases ferrous iron prior to transporting it across the fungal cell membrane without deferoxamine internalisation.[36] Subsequent studies demonstrated that reduction in the high-affinity iron permease FTR1 copies (Mucorales are multinucleated organisms) in R.

The mean diameter of lymphatic vessel used for LVA was 0.240 ± 0.057 mm, and the mean diameter of vein was 0.370 ± 0.146 mm. All lymphatic

vessels were translucent and very thin like human intact lymphatic vessels. In LVA group, intra- and post-operative anastomosis patency rates were 100% (10/10) based on ICG lymphography. In control group, intra- and post-operative patency rates were 0% (0/10). Conclusions: Rat lymphatic vessels are thin, translucent, and fragile similar to intact human lymphatic vessels. The LVA model uses easily accessible lymphatic vessels in the thigh, and is useful for training of supermicrosurgical MLN0128 cost LVA. © 2014 Wiley Periodicals, Inc. Microsurgery, 2014. “
“Peripheral nerve repair requires comprehensive evaluation Selleck IWR 1 of functional outcomes of nerve regeneration; however, autonomic nerve function is seldom evaluated probably due to lack of suitable quantitative methods. This study sought to determine whether autonomic functional recovery could be reflected by cold-induced vasodilation (CIVD) within target skin territory, as monitored by laser Doppler perfusion imaging (LDPI). Rats with sciatic nerve defect injury received autologous nerve grafting, and the plantar surface of the hind feet was subjected to LDPI analysis following nerve repair.

The results indicated that at 3 and 6 months after autologous nerve grafting, the plantar surface of the hind foot exhibited the same level of CIVD as contralateral normal side,

whereas rats in nerve defect group (negative control) showed significantly reduced CIVD. In addition, suitable nerve regeneration and functional recovery were achieved as assessed by pain sensation tests as well as electrophysiological and immunohistological examinations. Based on the potential influence of local autonomic nerve signals on CIVD, it was possible to evaluate functional recovery of autonomic nerves by using LDPI measurements of dermal CIVD. © 2012 Wiley Periodicals, Inc. Microsurgery, 2012. “
“The groin lymph node flap transfer has been used for treatment of extremity lymphedema. The design of this flap is based on the superficial circumflex Vasopressin Receptor iliac artery/vein (SCIA/V), or superficial inferior epigastric artery/vein (SIEA/V). The purpose of this study is to delineate the distribution of lymph nodes in the groin area and their relationship to inguinal vessels by the use of multidirector-row CT angiography (MDCTA). MDCTA was performed in 52 patients who underwent the deep inferior epigastric perforator (DIEP) flap or transverse rectus abdominis musculocutaneous (TRAM) flap for breast reconstruction. The MDCTA data were used to analyze the locations of lymph nodes and their adjacent vascular vessels. The groin region was divided into the superior lateral (I), superior medial (II), inferior lateral (III), and inferior medial (IV) quadrants based on the point where SCIV joined into great saphenous vein.