3A). Five chemokines, CCL2, CCL7, CCL8, CXCL9 and CXCL10, were present at high levels in the supernatants of co-culture spheroids, but almost absent or significantly lower in the supernatants of both tumour spheroids and monocyte cultures, buy BAY 57-1293 indicating that co-culturing with tumour cells stimulated the production of these chemokines by the TAMs. When the supernatants of co-culture spheroids of other cancers (prostate, ovarian and breast) were assessed, CCL2, CCL7, CXCL9 and CXCL10 were present at significantly lower levels compared with that of colorectal

cancer (Supporting Information Fig. 5). This implies that TAMs in colorectal cancers secrete more chemokines to attract T cells than TAMs in other cancers Selleck BMS-777607 in which TAMs promote tumour growth. To ascertain that the chemokines present in the supernatants of the colorectal tumour

model were functionally capable of attracting T cells, we performed Transwell assays using two supernatants: supernatants from co-culture spheroids to mimic microenvironment of a tumour with macrophage infiltration, and supernatants from tumour spheroids to mimic microenvironment of a tumour without macrophage infiltration. Indeed, the supernatants of co-culture spheroids attracted significantly more of both CD4+ and CD8+ T cells than the supernatants of tumour spheroids (Fig. 3C), showing that the chemokines in the supernatants of co-culture spheroids were functionally able to attract T cells. As the TAM genes indicated that the

TAMs were involved in antigen presentation (Fig. 3A), and chemokines that attract T cells were present in the co-culture supernatants, we assessed colorectal TAMs for the expression of cell surface molecules involved in interaction with T cells. The TAMs expressed molecules for antigen presentation (HLA-DR, CD74), T-cell co-stimulation (CD40, CD80, CD86) and CD54 (or ICAM-1), an adhesion molecule that stabilises cell contact during T-cell co-stimulation (Fig. 4A, top panel) 15. To obtain an idea of the level of expression of these molecules on colorectal TAMs, we compared them with in vitro differentiated macrophages and freshly isolated monocytes. The median fluorescence intensity (MFI) of the expression of the molecules (Fig. 4A, middle panel) as well as the percentage selleck chemicals llc of cells that expressed the molecules (Fig. 4A, bottom panel) were studied. Colorectal TAMs exhibited higher expression of all the molecules compared with in vitro MCSF-differentiated macrophages, and up-regulated the expression of all molecules except CD74 compared with freshly isolated monocytes. In addition, a significantly larger percentage of TAMs (than macrophages or monocytes) expressed CD74, CD40, CD80 and CD86. This observation indicated that co-culturing with colorectal tumour cells promoted the differentiation of monocytes to TAMs with enhanced expression of antigen presentation and T-cell co-stimulation molecules.

, 2010). They also reported that combination of bacteriophage and ciprofloxacin efficiently kills K. pneumonia biofilm cells and restricts the formation of resistant variants when compared

with individual treatments (Verma et al., 2009). It is well known that environmental cues such as oxygen and carbon substrate concentration can trigger biofilm dispersion (Applegate & Bryers, 1991; Thormann et al., 2005; Gjermansen et al., 2010; Newell et al., 2011). Biofilm dispersion often coincides find more with alteration of the biofilm EPS components. Understanding the modulation of biofilm EPS components and transduction of the dispersion signals would greatly facilitate the development of dispersion-based strategies to control biofilm formation. In recent years, genetic regulators and

signal transduction pathways for biofilm dispersion have been identified from a number of microorganisms. Gjermansen et al. (2010) LY294002 in vitro reported that overexpression of a plasmid-born EAL domain protein reduces intracellular c-di-GMP level and activates the LapG cysteine proteinase in biofilms formed by Pseudomonas putida (Gjermansen et al., 2010). The activated LapG proteinase can digest the LapA protein, which functions both as a surface adhesin and as a biofilm matrix component, and cause dispersion of P. putida biofilms (Gjermansen et al., 2010). Three two-component systems, BfiSR, BfmSR and MifSR, are reported to be essential for regulating P. aeruginosa biofilm development (Petrova & Sauer, 2009). Inhibiting the expression of bfiS, bfmR and mifR genes in mature biofilms leads to biofilm architectural collapse and biomass loss (Petrova & Sauer, 2009). Boles & Horswill (2008) reported that activation of the agr quorum-sensing system of S. aureus by autoinducing peptide addition or glucose depletion can trigger biofilm dispersion via a protease-mediated mechanism (Boles & Horswill, 2008). Genetically engineered regulators are used to DNA ligase manipulate biofilm formation and dispersion. Uppuluri et al. (2010) demonstrated that modulation of NRG1 gene expression

affects biofilm formation and dispersion by Candida albicans (Uppuluri et al., 2010). Hong et al. (2010a) used random mutagenesis to obtain variants of the global transcriptional regulator Hha, which controls biofilm formation of E. coli probably by activation of proteases (Hong et al., 2010a). One of the obtained Hha variants, Hha13D6 (D22V, L40R, V42I and D48A), causes nearly complete biofilm dispersion by increasing apoptosis (Hong et al., 2010a). The same authors also engineered another global regulator H-NS of E. coli to control its biofilm formation (Hong et al., 2010a b). Analysis of signal transduction molecules involved in biofilm dispersion has led to identification of a series of biofilm dispersion-inducing agents.

Epithelial

cells influence adaptive immunity by affecting the function of antigen presenting cells (APCs). Before the adaptive immune system can respond to inhaled allergens, the allergens have to be presented to them by professional find more APCs such as macrophages, B cells, dendritic cells (DCs) or even by less professional APCs such as basophils and eosinophils [32, 33]. We have recently created TCR transgenic mice reactive to an immunogenic peptide of Der p 1, one of the major allergens of the HDM Dermatophagoides pteronyssinus, to address which APCs present inhaled allergens to naive CD4+ T cells in the draining mediastinal LNs of the lung [34]. Using this novel tool, only mucosal lining DCs were able to present HDM-derived antigens to T cells in the mediastinal nodes, whereas B cells or macrophages were unable to do so. These results are consistent with other reports demonstrating that only DCs, but not basophils, are able to induce Th2 immunity to HDM upon adoptive transfer

to naive mice, and that CD11chi cells (depleted via the CD11cDTR system) are necessary for the development of Th2 immunity to HDM allergens [8]. It is well established that DCs play a role both in the initiation and maintenance of allergic airway inflammation and asthma, and control many aspects of the disease, including BHR and GCM. DCs do so by controlling the recruitment and activation of Th2 cells, Roxadustat manufacturer by producing chemokines that attract eosinophils and Th2 cells, and by expressing co-stimulatory molecules for terminal Teff-cell generation (reviewed in [35]). The exact subtype of DCs exerting all these functions is a matter of intense study [36, 37]. In our hands, Th2 priming

was mainly performed by CD11b+ conventional (c)DCs, and not by CD103+ check details cDCs [34]. The restimulation of Th2 effector cells and recruitment of inflammatory cells was the function of CD11b+CD64+ FceRI+ monocyte-derived DCs [34]. In our previous work, we have found that plasmacytoid DCs induced anti-inflammatory effects and prevented asthma development, possibly by activating Treg cells [38, 39]. As epithelial cells represent the first line of defense to inhaled allergens and also express TLRs, they have the ability to sense the same stimuli as innate immune cells. Triggering of these epithelial cell pattern recognition receptors (PRRs) by PAMPs initiates NF-κB activation and leads to the release of pro-Th2 cytokines such as TSLP, granulocyte-macrophage colony stimulating factor (GM-CSF), IL-1α, IL-25, and IL-33 in mice [40-42]. These cytokines all share the capacity to activate DCs, which then coordinate the subsequent Th2-type immune response. DCs can, however, also be directly activated by stimulation of their PRRs. Additionally, PRR-dependent epithelial cell activation also results in the production of endogenous danger signals such as uric acid, adenosine triphosphate, and lysophosphatidic acid [43].

It is clearly involved in a number of anti-microbial processes but, as discussed in recent reviews, it is also a potentially very harmful inflammatory element [1–3]. There is thus a need for sensitive and robust assays enabling the determination of the concentrations of factors of the complement system in various body

fluids. Initiation of complement activation happens via three different pathways, i.e. the alternative, classical and lectin pathways. The composition of Staurosporine in vivo the two first pathways have long been established, whereas for the lectin pathway new members have been added during recent years [4,10]. In the present report we extend our previous studies of the lectin pathway of the complement system and provide serum concentrations for the last of the known lectin pathway components, namely that of MASP-1. A rat anti-human MASP-1 antibody was obtained after immunization with a peptide corresponding to the C-terminal part of MASP-1. The MASP-1 assay described in this report exploits the binding of this antibody to microtitre wells coated with recombinant protein representing

the last three C-terminal domains of MASP-1. MASP-1 in samples competes with this interaction and the level of inhibition seen is thus a measure of the MASP-1 content of the sample. In principle, such an inhibition assay is dependent only on the number of exposed epitopes and is not influenced by oligomerization of the antigen or whether the antigen is in complex with other proteins. After examining Roxadustat order several buffer compositions, we arrived at one with high salt concentration and calcium. The specificity of the assay was corroborated experimentally (see below). We found a median of 11 µg MASP-1/ml serum in the cohort of 105 Caucasian adult blood donors.

Terai et al. [30] reported the results obtained with an assay Sclareol using a biotinylated anti-A-chain antibody (mab 1E2) for development in an assay where the capture antibody was another anti-A chain antibody (mab 2B11). As MASP-1, MASP-3 and MAp44 share the sequence detected by both these antibodies this assay should, in principle, detect all three proteins of these (the latter two had not been discovered at the time when that report was published) with equal sensitivity. Examining 1063 normal sera from Japanese donors, they reported a mean concentration (of MASP-1 + MASP-3 + MAp44) of 6·27 µg/ml serum [30]. We have recently measured the concentrations of MASP-3 and MAp44, which are listed in Table 1. Disregarding possible ethnic differences, the discrepancy is likely to be due to the calibration of the assays against different materials. We found that all the MASP-1 is found in large complexes at sizes indicating an association with MBL and ficolins, suggesting that most MASP-1 is associated with these recognition molecules, and possibly also other proteins.

In addition, SE induces ectopic migration of granule cells into the hilar/CA3 border where they seem to form recurrent excitatory circuitries [72]. Even though it was hypothesized for a long time that aberrant neurogenesis after SE may disturb functional connectivity of the hippocampus, clear evidence that this is indeed the case was missing [76,77]. However, recently it was shown that selective genetic deletion of phosphatase and tensin homologue (PTEN) in NSPCs leads to aberrant migration and maturation of newborn granule cells, which is sufficient to induce epileptic activity. These results support the hypothesis that aberrant seizure-induced neurogenesis contributes

to the epileptic disease process

MI-503 supplier [78]. Thus, current strategies aiming to reduce or normalize seizure-induced neurogenesis are being developed to ameliorate disease symptoms in rodent models of TLE. Regenerative medicine aims at harnessing the potential of pluripotent and somatic stem cells, through the transplantation or activation of resident stem cells in diseased tissues. In the PF-01367338 clinical trial last decade, great advancements have been made in the treatment of blood disorders such as thalassaemia and leukaemia, through the successful development of haematopoietic stem cell therapies. For the treatment of central nervous system (CNS) disorders, neural stem cell therapies have been developed in animal models and are beginning to find their way into human patient clinical trials. To be able to repair a damaged brain, a reliable source of neurones and glia is required. These neural cells can be derived from ES or induced pluripotent stem cell (iPSC) lines and transplanted into brain tissue. Alternatively,

endogenous NSPCs that reside in the human brain also offer a promising source of neurones and glia that are suitable for repair (Figure 3). In animal models of stroke, it has been shown that endogenous SVZ NSPCs are able to migrate to a lesion site in the striatum and differentiate into neurones [79]. This finding suggests that adult NSPCs can contribute to brain repair in response to damage, even outside the neurogenic niche, through increased proliferation and neuronal replacement. In addition, several NSPC transplantation studies in mice have shown promising results, Tacrolimus (FK506) with NSPCs differentiating into functional neurones within lesion sites as well as promoting neuroprotection of surviving neurones through the release of trophic factors and induction of angiogenesis (reviewed by Lindvall and Kokaia [80]). Adult NSPCs have been the focus of many studies for the treatment of diseases affecting neurones. However, it is important to note that NSPC fate is not restricted to the neuronal lineage and that NSPCs can give rise to oligodendrocytes in both neurogenic niches, offering a source of cells for the treatment of demyelinating diseases.

After induction of chronic colitis the colons of both Bim–/–and wild-type mice appeared with an opaque, thickened, more granular mucosa and an altered vascular pattern. Bim–/– animals exhibited significantly higher MEICS score compared to wild-type mice (5·1 ± 1·7, BMS-777607 nmr n = 7 versus 2·7 ± 1·8, n = 5 respectively; Fig. 2b). Spleens of healthy wild-type mice were significantly smaller than those of Bim–/– animals. Upon DSS, the spleen weight increased

significantly in wild-type animals (P < 0·05) and highly significantly in Bim–/– animals (P < 0·01, Fig. 3a). Induction of chronic colitis was followed by a typical reduction of colon length. Shortening of the colon was significant in DSS-receiving Bim–/– animals compared to the respective controls (8·1 ± 0·5 cm upon water, n = 5, versus 7·0 ± 0·8 cm upon DSS, n = 5 for wild-type animals. 8·8 ± 0·4 cm upon water, n = 7, versus 7·8 ± 0·5 cm upon DSS, n = 7, P < 0·05 for Bim–/– mice; Fig. 3b). Increase of spleen weight upon chronic DSS-induced colitis correlated with a decrease in colon length for both wild-type controls and Bim–/– mice Paclitaxel price (P < 0·05). Combining data from wild-type controls and Bim–/– mice upon both water and DSS, no significant relationship between spleen

weight and colon length could be determined because of the significant difference in the spleen weight between wild-type and Bim–/– in mice without inflammation. Also on a microscopic level, more severe these colitis was found for Bim–/– mice compared to wild-type mice. In female animals without chronic DSS-induced colitis, the Bim knock-out did not alter the total histological score compared to the wild-type (1·2 ± 0·6 versus 1·3 ± 0·6, respectively; Fig. 3c). The total histological score for Bim–/– mice with induced chronic colitis was increased significantly compared to the water-treated

mice. The score for epithelial damage considering crypt morphology and loss of goblet cells remained unchanged when comparing DSS-receiving Bim–/– and wild-type mice (Fig. 3c, white bars). In contrast, Bim–/– animals with chronic colitis exhibited a significantly increased inflammatory infiltrate of lymphocytes into the mucosa and submucosa compared to wild-type mice (4·4 ± 0·8 versus 3·1 ± 1·0, respectively; P < 0·05; Fig. 3c, light grey bars). This also led to a significantly higher total histological score for Bim–/– mice with chronic colitis compared to wild-type mice (6·7 ± 1·4 versus 4·9 ± 0·4 respectively; P < 0·05; Fig. 3c, dark grey bars). The results were confirmed in a second experiment of chronic DSS-induced colitis in female mice (n = 5 each group, not shown). In a third experiment in male Bim–/– mice, similar data were obtained (n = 5 each group, not shown). In these animals, more severe inflammation for Bim–/– animals compared to wild-type mice was determined upon chronic DSS-induced colitis.

HIV-1 infection induces a strong and chronic Bortezomib purchase over-activation of the CD8 T cell compartment, measured by the expression of CD38, a glycoprotein present on immature T and B lymphocytes, lost on mature cells and re-expressed during cell activation and acute viral infection [1, 2]. Highly active antiretroviral therapy (HAART), the standard care in paediatric and adult HIV-infected population, leads to virus suppression associated with decreased CD38 expression, increased CD4 T cell counts, recovery of immune function against opportunistic infections and

a good clinical outcome in the majority of patients [3–6]. Undetectable viral load can be achieved in all patients, but this aim is more difficult in children probably due to the characteristic of their immature immune system, poor adherence and availability of new antiretrovirals [4–7]. Moreover, some patients may show incomplete suppression (>50 HIV RNA copies/ml) with a restored CD4 T cell population (>25% of total lymphocytes) (virological discordant response) or undetectable BMS-354825 manufacturer viral load (<50 copies/ml) with scanty CD4 recovery (immunological discordant response). In these patients, CD38 expression on CD8 T cells may provide information

about residual immune activation, while in vitro lymphocyte proliferation, one of the oldest and most widely applied methods for detecting impaired T cell function [8], may describe functional immuno-competence of the restored CD4 population identifying subjects at risk for opportunistic infections [9–14]. Although CD4 percentage and count is a validated surrogate marker of immune competence, the functional evaluation of the CD4 memory T cell proliferation to opportunistic pathogens Rebamipide is reckoned more specific for diagnosing infection susceptibility as compared to response to mitogens, potent stimulators of T cells activation and proliferation regardless of their

antigen specificity. There is evidence that CD38 expression negatively correlates with CD4 cell counts [15, 16] and with CD4 central memory reconstitution in virally suppressed HIV-1-infected adults [17], suggesting that CD38 activation may augment our ability to determine whether therapy has an impact on CD4 recovery. We were interested to study whether the combination of traditional assays (viral load and CD4 T cell immunophenotyping) with the measure of CD38 activation and CD4 T cell function could classify children with a discordant immuno-virological response to HAART more accurately. We performed a retrospective study to establish the diagnostic utility of CD38 expression on CD8 T lymphocytes, for discriminating responders versus non-responders defined on the basis of traditional viral load and CD4 T cell count criteria.

Indeed, in mouse models of rheumatoid arthritis 19 and colitis 25, the lack of a functional immunoproteasome subunit

protected mice from autoimmune diseases. Therefore, the data provided in this manuscript support the conception of the immunoproteasome as a potential new AZD1208 cell line target for the suppression of undesired proinflammatory T-cell responses. C57BL/6 mice (H-2b) mice as well as B6.SJL-PtprcaPep3b/BoyJ (also referred to as “CD45.1-” or “Ly5.1 congenic mice”) were originally obtained from Charles River, Germany. B6.PL (Thy1.1) mice were obtained from The Jackson Laboratory (Bar Harbor, ME, USA). MECL-1 9, LMP2 12 and LMP7 11 gene-targeted mice were kindly provided by Dr. John J. Monaco (Department of Molecular Genetics, Cincinnati Medical Center, Cincinnati, OH, USA); these mice have been bred onto the C57BL/6 background for at least ten generations. TCRtg P14 mice (tg line 318) 26, specific for aa 33–41 (=gp33 epitope, presented on MHC I) of the LCMV glycoprotein were obtained from Dr.

Oliver Planz, Tübingen University. RAG-2-deficient mice bred onto C57BL/6 background were originally obtained from The Jackson Laboratory and bred in individually ventilated cages. Mice were kept in a specific pathogen-free facility and used at 6–12 wk of age. Experimental groups were age and sex matched and the review Ipatasertib cost board of Regierungspräsidium Freiburg has approved experiments. LCMV-WE was originally obtained from F. Lehmann-Grube Phosphoglycerate kinase (Heinrich Pette Institute, Hamburg, Germany) and propagated on the fibroblast line L929. VV-WR was obtained from Professor Hans Hengartner, University Hospital Zurich, Switzerland. The virus was propagated on BSC 40 cells. Mice were infected with 200 PFU or 2×104 PFU LCMV-WE i.v. or with 2×106 PFU VV-WR i.p. BSC 40 is an African green monkey kidney-derived cell line. All cells were grown in MEM 5% FCS. rLM-OVA was kindly provided by Professor Dirk Busch, Technische Universität München, Munich, Germany. The injection cultures were prepared by

inoculation of 10 mL Brain–Heart Infusion Broth with 100 μL of the frozen (−70°C) stock culture. After growing overnight on a shaker at 37°C, the Listeria titer in the culture was estimated by spectrophotometry: 1 OD600 nm unit=109 cfu/mL. The mice were immunised with 2×104 CFU rLM-OVA in 200 μL PBS i.v. To quantify the injection dose, estimated by spectrophotometry, 100 μL of tenfold dilutions of the injection culture were plated on agar plates made of Brain–Heart Agar. Briefly, 24 h after incubation at 37°C, the injection dose was determined by counting the colonies that were growing. All media were purchased from Invitrogen-Life Technologies; Karlsruhe, Germany, supplemented with GlutaMAX, 5 or 10% FCS and 100 U/mL penicillin/streptomycin. T cells from splenocytes of naïve Thy1.

In the thymus, CCRL1 is abundant in cTECs but not mTECs or thymocytes [20]. In fetal mice, CCRL1 regulates the migration of thymocyte precursors before vascularization [19]. It has been reported that CCRL1 deficiency results in thymus enlargement in adult mice, in association with altered thymocyte development and autoimmunity [21]. Thus, CCRL1 is important for optimal thymus homeostasis and normal thymocyte development. To analyze the expression of CCRL1 in TECs during embryogenesis,

Ribeiro et al. [18] use CCRL1-EGFP-knockin mice, in which EGFP is expressed under the control of CCRL1 gene expression [20]. By crossing CCRL1-EGFP-knockin mice with IL-7-YFP-transgenic Selleckchem Ku 0059436 mice, and by flow cytometry analysis of embryonic TECs, the authors show that CCRL1 expression progressively increases during fetal cTEC development. The emergence of CCRL1-EGFPhigh cells, which are class II MHChigh CD40high cTECs, is diminished in RAG2/IL2Rγ double-deficient mice, in which thymocyte development is arrested at an early stage. From these results, the authors conclude that CCRL1high cTECs represent late-appearing mature cTECs, and that the development of those mature cTECs is regulated by

the signals provided by developing Luminespib manufacturer thymocytes. These results agree with previous reports showing that thymocyte-derived signals are necessary for the late maturation of cTECs [4-6]. Ribeiro et al. [18] also show that CCRL1+UEA1–CD80– cTECs isolated from E15.5 fetal thymus give rise to UEA1+CD80+ mTECs, when cultured in the presence of RANK and CD40 stimulation in RTOCs, suggesting that CCRL1+ fetal cTECs contain mTEC progenitor activity. These results agree with the recent reports discussed above showing that pTECs progress through a stage in which they express cTEC-associated molecules before diversifying into mTECs [11, 14-16] (Fig. 1). Perhaps Isotretinoin more interestingly, Ribeiro et al. [18] go beyond the confirmation of other studies to report that CCRL1-EGFPlow cells in the thymus are not restricted to CD205+ Ly51+ cTECs but also contain UEA1+ mTECs, despite the fact that CCRL1-EGFPhigh cells are

limited to cTECs but not mTECs. The CCRL1-EGFPlow CD80+ UEA1+ mTECs were detectable only after birth. Gene expression analysis showed that this late-appearing subpopulation of mTECs, which was identified by the CCRL1-EGFPlow CD80+ phenotype, contained large amounts of Aire and RANK mRNAs but a nondetectable amount of CCL21 mRNA. Ribeiro et al. [18] further demonstrate that the combination of RANK and CD40 signals, the ligands of which are produced by positively selected thymocytes [8, 10], is important for the development of CCRL1-EGFPlow mTECs. Thus, the analysis of CCRL1-EGFP reporter mice suggests a novel heterogeneity in postnatal mTECs. It has been shown that mTECs are heterogeneous in terms of the expression of various molecules, including class II MHC, CD80, Aire, and CCL21 [22-26]. White et al.

Other authors have reported similar results.[8] The

reconstructed mandible in this case functions well, like other authors have reported in these complex reconstructions in children.[4, 5, 7, 8] As observed in other pathologies, like facial palsy, for example, children tend to have a higher ability to adapt and have better functional outcomes than adults. Once facial growth is complete, additional surgery may be necessary to improve the final aesthetic result and to allow the use of osteointegrated implants, the benefits and risks of which will have to be discussed with the patient and her parents. In summary, this case of mandibular selleck inhibitor reconstruction with fibular osteocutaneous free flap in an 8-month-old girl with a 12-year follow-up is, to our knowledge, the longest reported in such a young patient. “
“Background: An important element in Nivolumab concentration achieving high success rates with free flap surgery has been the use of different techniques for monitoring flaps postoperatively as a means to detecting vascular compromise. Successful monitoring of the vascular pedicle to a flap can potentiate rapid return to theater in the setting of compromise, with the potential to salvage the flap. There is little evidence that any technique

offers any advantage over clinical monitoring alone. Methods: A consecutive series of 547 patients from a single plastic surgical unit who underwent a fasciocutaneous free flap operation for breast reconstruction [deep inferior epigastric artery perforator (DIEP) flap, superficial inferior epigastric artery (SIEA) flap, or superior gluteal artery perforator (SGAP) flap] were included. A comparison was made between the first 426 consecutive patients in whom flap monitoring was performed using clinical monitoring alone and the subsequent 121 patients in whom monitoring was achieved with the Cook-Swartz implantable Doppler probe. Outcome measures

included flap salvage rate and false-positive rate. Results: There was a strong trend toward improved salvage rates with the implantable Doppler probe compared with clinical monitoring (80% vs. 66%, P = 0.48). When combined with the literature (meta-analysis), the data prove statistically significant (P < 0.01). There was no statistical BCKDHB difference between the groups for false-positive rates. Conclusion: Flap monitoring with the implantable Doppler probe can improve flap salvage rates without increasing the rate of false-positive takebacks. © 2009 Wiley-Liss, Inc. Microsurgery, 2010. “
“Supermicrosurgical lymphaticovenular anastomosis (LVA) has become a useful option for the treatment of compression-refractory lymphedema with its effectiveness and less invasiveness. It is important to make as many bypasses as possible for better treatment results of LVA operation. We report a secondary lymphedema case successfully treated using a modified lambda-shaped LVA.